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Catheter ablation is a procedure that uses radio-frequency energy or other sources to terminate or modify a faulty electrical pathway from sections of the heart of those who are prone to developing cardiac arrhythmias such as atrial fibrillation , atrial flutter and Wolff-Parkinson-White syndrome . If not controlled, such arrhythmias increase the risk of ventricular fibrillation and sudden cardiac arrest . The ablation procedure can be classified by energy source: radiofrequency ablation and cryoablation .
Catheter ablation may be recommended for a recurrent or persistent arrhythmia resulting in symptoms or other dysfunction. Atrial fibrillation frequently results from bursts of tachycardia that originate in muscle bundles extending from the atrium to the pulmonary veins . [ 1 ] Pulmonary vein isolation by transcatheter ablation can restore sinus rhythm . [ 1 ]
Catheter ablation of most arrhythmias has a high success rate. Success rates for Wolff–Parkinson–White syndrome (WPW) have been as high as 95% [ 2 ] For Supraventricular tachycardia (SVT), single procedure success is 91% to 96% (95% Confidence Interval) and multiple procedure success is 92% to 97% (95% Confidence Interval). [ 3 ] For atrial flutter, single procedure success is 88% to 95% (95% Confidence Interval) and multiple procedure success is 95% to 99% (95% Confidence Interval). [ 3 ] For automatic atrial tachycardias, the success rates are 70–90%. [ citation needed ] The potential complications include bleeding, blood clots, pericardial tamponade, and heart block, but these risks are very low, ranging from 2.6 to 3.2%.
For non-paroxysmal atrial fibrillation , a 2016 systematic review compared catheter ablation to heart rhythm drugs. After 12 months, participants receiving catheter ablation were more likely to be free of atrial fibrillation, and less likely to need cardioversion. However, the evidence quality ranged from moderate to very low [ 4 ] A 2006 study, including both paroxysmal and non-paroxysmal atrial fibrillation, found that the success rates are 28% for single procedures. Often, several procedures are needed to raise the success rate to a 70–80% range. [ 5 ] One reason for this may be that once the heart has undergone atrial remodeling as in the case of chronic atrial fibrillation patients, largely 50 and older, it is much more difficult to correct the 'bad' electrical pathways. Young people with AF with paroxysmal, or intermittent, AF therefore have an increased chance of success with an ablation since their heart has not undergone atrial remodeling yet. [ citation needed ] Several experienced teams of electrophysiologists in US heart centers claim they can achieve up to a 75% success rate. [ citation needed ]
Pulmonary vein isolation has been found to be more effective than optimized antiarrhythmic drug therapy for improving quality of life at 12 months after treatment. [ 6 ]
Catheter ablation has been found to improve mental health outcomes in individuals with symptomatic atrial fibrillation. [ 7 ]
A 2018 study showed efficacy of cardiac ablation for treatment of Premature Ventricular Contraction as 94.1%. [ 8 ]
Catheter ablation is usually performed by an electrophysiologist (a specially trained cardiologist ) in a cath lab . [ 9 ]
Catheter ablation procedure involves advancing several flexible catheters into the patient's blood vessels , usually either in the femoral vein , Internal jugular vein , or subclavian vein . The catheters are then advanced towards the heart. The catheters have electrodes at the tips that can measure the electrical signals from the heart. These electrodes create a map of the abnormal pathways causing arrhythmias. Then, the electrophysiologist uses the map to identify areas from which abnormal heart rhythms originate. [ 10 ]
Once the abnormal areas are located, catheters are used to deliver energy via local heating or freezing to ablate (destroy) the abnormal tissue that is causing the arrhythmia. The energy is applied cautiously to avoid damaging healthy heart tissue. [ 10 ] Originally, a DC impulse was used to create lesions in the intra-cardiac conduction system. [ 11 ] However, due to a high incidence of complications, widespread use was never achieved.
In contrast to the thermal methods (extreme heat or cold) electroporation is being used and evaluated as a means of killing very small areas of heart muscle. The cardiac catheter delivers trains of high-voltage ultra-rapid electrical pulses that form irreversible pores in cell membranes, resulting in cell death of cardiac muscle, while not killing adjacent tissues ( esophagus and phrenic nerve ). [ 12 ] It is thought to allow better selectivity than the previous thermal techniques, which used heat or cold to kill larger volumes of muscle. [ 13 ]
One type of catheter ablation is pulmonary vein isolation, where the ablation is done in the left atrium in the area where the 4 pulmonary veins connect. [ 14 ] [ 15 ] Radiofrequency ablation for atrial fibrillation can be unipolar (one electrode) or bipolar (two electrodes). [ 16 ] Although bipolar can be more successful, it is technically more difficult, resulting in unipolar being used more often. [ 16 ] But bipolar is more effective in preventing recurrent atrial arrhythmias. [ 17 ]
During the procedure, the patient's heart rhythm is monitored continuously. The electrophysiologist can observe changes to the patient's cardiac electrical activity to determine the success of the ablation. If the cardiac rhythm shows no abnormal signals or arrhythmias, the catheters are withdrawn from the heart and the incision is closed.
For patients for whom catheter ablations fail, they may then have an epicardial ablation performed. In this type of ablation, instead of a catheter being threaded through a vein in the groin area, the "most direct and safest route to the space outside the heart" is used by going into the subxiphoid region - just under the breastbone at the bottom of the rib cage. [ 18 ]
A needle then enters the pericardial space around the heart, where then a wire is inserted, the needle is removed, and a plastic tube is inserted over the wire. That tube is then where the ablation catheter is threaded to then burn off the offending area of the heart. Following epicardial ablation, often a small plastic tube may be left in place overnight to drain any fluid that may accumulate in the pericardial space. [ 18 ]
At most centers, epicardial ablation is not usually performed, but it is at "selected centers" such as Stanford. [ 18 ]
After catheter ablation the patients are moved to a cardiac recovery unit, intensive care unit, or cardiovascular intensive care unit where they are not allowed to move for 4–6 hours. Minimizing movement helps prevent bleeding from the site of catheter insertion. Some people have to stay overnight for observation, some need to stay much longer and others are able to go home on the same day. This all depends on the problem, the length of the operation and whether or not general anaesthetic was used. [ citation needed ]
Recurrence of atrial fibrillation within three months of an ablation is seen in most patients, but many of those patients become free of atrial fibrillation in the long term. [ 19 ] For this reason the first three months after an ablation are described as the "blanking period," during which no further intervention is to be attempted. [ 19 ] Recurrence during the nine months following the blanking period, occurs in 25% to 40% of patients, the variability greatly affected by obesity and the severity of atrial fibrillation before the ablation. [ 19 ]
Some potential complications associated with the procedure include: [ 20 ]
Patients may also experience a return of the arrhythmia after the procedure, requiring them to undergo further treatment. However, in general this procedure is considered a safe, effective, and minimally invasive method to treat arrhythmias. Studies have shown that the overall complication rate of cardiac ablation procedures is about 6%. [ medical citation needed ]
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A catheterization laboratory , commonly referred to as a cath lab , is an examination room in a hospital or clinic with diagnostic imaging equipment used to visualize the arteries of the heart and the chambers of the heart and treat any stenosis or abnormality found.
Most catheterization laboratories are "single plane" facilities, those that have a single X-ray generator source and an X-ray image intensifier for fluoroscopic imaging. [ 1 ] Older cath labs used cine film to record the information obtained, but since 2000, most new facilities are digital . The latest digital cath labs are biplane (have two X-ray sources) and use flat panel detectors . [ 2 ]
Cardiac catheterization laboratories are usually staffed by a multidisciplinary team. This may include a medical practitioner (normally either a consultant cardiologist or radiologist ), cardiac physiologist , radiographer and nurse . [ 3 ] [ 4 ]
The consultant cardiologist is responsible for gaining arterial access, inserting a sheath into either the radial or femoral artery , passing a wire and catheter into the coronary artery and selectively injecting contrast media into the coronary arteries. They then interpret the images taken to ascertain where the narrowed or blocked artery has the problem. They use a variety of techniques and imaging tools to measure the size of things such as balloons and stents .
Cardiac physiologists usually set up what is known as a transducer to monitor pressure in the arteries. They also have a live view of the patients ECG so they can tell whether or not there is a problem caused by the insertion of the catheter into the heart to the electrical pathways. [ 5 ] [ 6 ] The physiologist will also set up a temporary pacemaker if the procedure is an angioplasty or a percutaneous coronary intervention (PCI). Finally, they also set up defibrillators on to the patient for emergency use if needed. In some locations, some of these responsibilities may be carried out by other personnel, such as trained nurses or technologists. [ 7 ]
Cardiac catheterization is a general term for a group of procedures that are performed in the cath lab, such as coronary angiography . Once a catheter is in place, it can be used to perform a number of procedures including angioplasty , PCI ( percutaneous coronary intervention ) angiography, transcatheter aortic valve replacement , balloon septostomy , and an electrophysiology study or catheter ablation . Devices such as pacemakers may be fitted or rotablation to remove plaque can be performed. [ 8 ] [ 9 ]
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Cathinone ( / ˈ k æ θ ɪ n oʊ n / ; also known as β-ketoamphetamine ) is a monoamine alkaloid found in the shrub Catha edulis (khat) and is chemically similar to ephedrine , cathine , methcathinone and other amphetamines . It is probably the main contributor to the stimulant effect of Catha edulis . Cathinone differs from many other amphetamines in that it has a ketone functional group . Other phenethylamines that share this structure include the stimulants methcathinone , MDPV , mephedrone and the antidepressant bupropion .
Khat has been cultivated in the Horn of Africa and Arabian Peninsula region of the world for thousands of years. It is most commonly chewed for the euphoric effect it produces. The active ingredient was first proposed in 1930, when cathine was identified as a predominant alkaloid in the plant. [ 5 ] Cathine was thought to be the main active ingredient in khat until the 1960s, when it was found that the amount of cathine in the khat leaves is insufficient to produce the effects observed. In 1975, the United Nations Narcotic Laboratory analyzed khat leaves from Yemen , Kenya and Madagascar and found evidence of a different alkaloid, cathinone. [ 5 ] Cathinone is molecularly similar to cathine, but is much more abundant in younger plants. This finding caused scientists to speculate that cathinone was the true active ingredient in khat. [ 5 ]
A study was conducted in 1994 to test the effects of cathinone. Six volunteers who had never chewed khat were given an active khat sample and a cathinone-free placebo sample. [ 6 ] The researchers analyzed the participants' moods, activity levels and blood pressure before and after consuming the khat or placebo. This analysis showed that cathinone produced amphetamine-like effects, leading the researchers to confirm that cathinone, not cathine, is the active ingredient in khat leaves. [ 6 ]
Over 20 million people in the Arabian Peninsula and East Africa chew khat leaves daily. It is an important piece of the culture and economy in this region, especially in Ethiopia (where khat is said to have originated), Kenya, Djibouti , Somalia and Yemen. Men usually chew it during parties or other social gatherings while smoking cigarettes and drinking tea. Farmers and other workers also use khat in the afternoon to reduce fatigue and hunger as the day goes on. It functions like the caffeine in a strong cup of coffee as an anti-fatigue drug. Students and drivers have been known to use it to stay alert for longer periods of time. [ 7 ]
In order to produce its desired effects, khat leaves should be chewed fresh. The fresh leaves have a higher concentration of cathinone. Waiting too long after cultivation to chew the leaf will allow the cathinone to break down into its less potent form, cathine. Because of the need for quick chewing, it is a habit that has historically been prevalent only where the plant grows. However, in the recent years with improvements in road and air transport, khat chewing has spread to all corners of the world.
The cultivation of khat in Yemen is a highly profitable industry for farmers. Khat plants will grow differently depending on the climate they are grown in and each one will produce different amounts of cathinone. [ 8 ] It generally grows best in coastal, hot climates. In Yemen, the khat plant is named after the region in which it is grown. The Nehmi khat plant has the highest known concentration of cathinone, 342.5 mg/100 g. [ 8 ]
Internationally, cathinone is a Schedule I drug under the Convention on Psychotropic Substances . [ 9 ] Circa 1993, the DEA added cathinone to the Controlled Substances Act 's Schedule I.
The sale of khat is legal in some jurisdictions, but illegal in others (see Khat (Regulation) ). Substituted cathinones were also often used as the key ingredient of recreational drug mixes commonly known as " bath salts " in the United States. [ 10 ] [ 11 ] [ 12 ] [ 13 ]
The table below shows the legality of khat and cathinone in various countries:
Cathinone has been found to stimulate the release of dopamine and inhibit the reuptake of epinephrine , norepinephrine and serotonin in the central nervous system (CNS). These neurotransmitters are all considered monoamines and share the general structure of an aromatic ring and an amine group attached by a two-carbon separator. [ 8 ] Because cathinone is a hydrophobic molecule, it can easily cross cell membranes and other barriers, including the blood–brain barrier . [ 33 ] This property allows it to interact with the monoamine transporters in the synaptic cleft between neurons . Cathinone induces the release of dopamine from brain striatal preparations that are prelabelled either with dopamine or its precursors. [ 34 ] It is more specifically a norepinephrine–dopamine releasing agent (NDRA) similarly to amphetamine . [ 31 ] [ 32 ]
The metabolites of cathinone, cathine and norephedrine, also possess CNS stimulation, but create much weaker effects. [ 35 ] The effects of cathinone on the body can be countered by a preceding administration of a dopamine receptor antagonist . [ 35 ] The antagonist prevents synaptic dopamine released by cathinone from exerting its effect by binding to dopamine receptors.
Cathinone can also affect cholinergic concentrations in the gut and airways by blocking prejunctional adrenergic receptors (α 2 adrenergic) and activating 5-HT7 receptors, thereby inhibiting smooth muscle contraction. [ 33 ] It can also induce dry mouth, blurred vision and increased blood pressure and heart rate. [ 8 ]
Cathinone is a weak agonist of the mouse, rat, and human trace amine-associated receptor 1 (TAAR1). [ 36 ] [ 37 ] In contrast to cathinone however, most other cathinones are not human TAAR1 agonists. [ 38 ] [ 37 ] TAAR1 activation may auto-inhibit and constrain the monoaminergic effects of monoamine releasing agents possessing TAAR1 agonism. [ 38 ] [ 39 ]
Khat leaves are removed from the plant stalk and are kept in a ball in the cheek and chewed. Chewing releases juices from the leaves, which include the alkaloid cathinone. The absorption of cathinone has two phases: one in the buccal mucosa and one in the stomach and small intestine . [ 6 ] The stomach and small intestine are very important in the absorption of ingested alkaloids. [ 6 ] At approximately 2.3 hours after chewing khat leaves, the maximum concentration of cathinone in blood plasma is reached. The mean residence time is 5.2 ± 3.4 hours. [ 6 ] The elimination half-life of cathinone is 1.5 ± 0.8 hours. [ 6 ] A two-compartment model for absorption and elimination best describes this data. However, at most, only 7% of the ingested cathinone is recovered in the urine. [ 6 ] This indicates that the cathinone is being broken down in the body. Cathinone has been shown to selectively metabolize into R,S-(-)-norephedrine and cathine. The reduction of the ketone group in cathinone will produce cathine. This reduction is catalyzed by enzymes in the liver. The spontaneous breakdown of cathinone is the reason it must be chewed fresh after cultivation. [ 6 ]
The first documentation of the khat plant being used in medicine was in a book published by an Arabian physician in the 10th century. [ 8 ] It was used as an antidepressant because it led to feelings of happiness and excitement. Chronic khat chewing can also create drug dependence, as shown by animal studies. [ 8 ] In such studies, monkeys were trained to push a lever to receive the drug reward. As the monkeys' dependence increased, they pressed the lever at an increasing frequency. [ 8 ]
Khat chewing and the effects of cathinone on the body differ from person to person, but there is a general pattern of behavior that emerges after ingesting fresh cathinone: [ 8 ]
There are other effects not related to the CNS. The chewer can develop constipation and heartburn after a khat session. Long-term effects of cathinone can include gum disease or oral cancer , cardiovascular disease and depression . [ 8 ] The withdrawal symptoms of cathinone include hot flashes , lethargy and a great urge to use the drug for at least the first two days. [ 8 ]
The synthesis of cathinone in khat begins with L- phenylalanine and the first step is carried out by L-phenylalanine ammonia lyase (PAL), which cleaves off an ammonia group and creates a carbon-carbon double bond, forming cinnamic acid . [ 40 ] After this, the molecule can either go through a beta-oxidative pathway or a non-beta-oxidative pathway. The beta-oxidative pathway produces benzoyl-CoA while the non-beta-oxidative pathway produces benzoic acid . [ 40 ] Both of these molecules can be converted to 1-phenylpropane-1,2-dione by a condensation reaction catalyzed by a ThDP-dependent enzyme (Thiamine diphosphate-dependent enzyme) with pyruvate and producing CO 2 . [ 40 ] 1-phenylpropane-1,2-dione goes through a transaminase reaction to replace a ketone with an ammonia group to form (S)-cathinone. (S)-Cathinone can then undergo a reduction reaction to produce the less potent but structurally similar cathine or norephedrine, which are also found in the plant. [ 40 ]
Aside from the beta- and non-beta-oxidative pathways, the biosynthesis of cathinone can proceed through a CoA-dependent pathway. The CoA-dependent pathway is actually a mix between the two main pathways as it starts like the beta-oxidative pathway and then when it loses CoA, it finishes the synthesis in the non-beta-oxidative pathway. In this pathway, the trans-cinnamic acid produced from L-phenylalanine is ligated to a Coenzyme A (CoA), just like the beginning of the beta-oxidative pathway. [ 40 ] It then undergoes hydration at the double bond. This product then loses the CoA to produce benzaldehyde , an intermediate of the non-beta-oxidative pathway. Benzaldehyde is converted into benzoic acid and proceeds through the rest of the synthesis. [ 40 ]
Cathinone can be synthetically produced from propiophenone through a Friedel-Crafts acylation of propionic acid and benzene. [ 33 ] The resulting propiophenone can be brominated, and the bromine can be substituted with ammonia to produce a racemic mixture of cathinone. A different synthetic strategy must be employed to produce enantiomerically pure (S)-cathinone. This synthetic route starts out with the N-acetylation of the optically active amino acid , S-alanine. [ 33 ] Then, phosphorus pentachloride (PCl 5 ) is used to chlorinate the carboxylic acid forming an acyl chloride. At the same time, a Friedel-Crafts acylation is preformed on benzene with aluminum chloride catalyst. Finally, the acetyl protecting group is removed by heating with hydrochloric acid to form enantiomerically pure S-(-)-cathinone. [ 33 ]
Cathinone can be extracted from Catha edulis (khat), or synthesized from α -bromopropiophenone (which is easily made from propiophenone ). Because cathinone is both a primary amine and a ketone , it is very prone to dimerization , especially as a free base isolated from plant matter. [ 41 ] [ 42 ] These dimers are pharmacologically inactive , and the rapid dimerization reduces active amounts of cathinone in non-fresh khat. [ 41 ] [ 42 ] The rapid formation of dimers also applies to other non- N -substituted cathinones such as methylenedioxycathinone (MDC; normethylone). [ 41 ] [ 42 ]
The structure of cathinone is very similar to that of other molecules. By reducing the ketone, it becomes cathine if it retains its stereochemistry, or norephedrine if its stereochemistry is inverted. Cathine is a less potent version of cathinone and cathinone's spontaneous reduction is the reason that older khat plants are not as stimulating as younger ones. Cathinone and amphetamine are closely related in that amphetamine is only lacking the ketone C=O group. [ 43 ] Cathinone is structurally related to methcathinone , in much the same way as amphetamine is related to methamphetamine . Cathinone differs from amphetamine by possessing a ketone oxygen atom (C=O) on the β (beta) position of the side chain. Advancements in synthesizing cyclic cathinones based on α-tetralone have employed chiral HPLC-CD techniques to determine the absolute configuration of enantiomers, an approach that may contribute to the development of pharmaceutical analogs with antidepressant potential. [ 44 ] The corresponding substance cathine , is a less powerful stimulant. The biophysiological conversion from cathinone to cathine is to blame for the depotentiation of khat leaves over time. Fresh leaves have a greater ratio of cathinone to cathine than dried ones, therefore having more psychoactive effects.
There are many cathinone derivatives that include the addition of an R group to the amino end of the molecule. Some of these derivatives have medical uses as well. Bupropion is one of the most commonly prescribed antidepressants and its structure is Cathinone with a tertiary butyl group attached to the nitrogen and chlorine attached to the benzene ring meta- to the main carbon chain. [ 43 ]
Other cathinone derivatives are strong psychoactive drugs. One such drug is methylone , a drug structurally similar to MDMA .
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The Catholic Church is the largest non-government provider of health care services in the world. [ 1 ] It has around 18,000 clinics, 16,000 homes for the elderly and those with special needs, and 5,500 hospitals, with 65 percent of them located in developing countries. [ 2 ] In 2010, the Church's Pontifical Council for the Pastoral Care of Health Care Workers said that the Church manages 26% of the world's health care facilities. [ 3 ] The Church's involvement in health care has ancient origins.
Jesus Christ , whom the Church holds as its founder, instructed his followers to heal the sick. [ 4 ] The early Christians were noted for tending the sick and infirm, and Christian emphasis on practical charity gave rise to the development of systematic nursing and hospitals. The influential Benedictine rule holds that "the care of the sick is to be placed above and before every other duty, as if indeed Christ were being directly served by waiting on them". During the Middle Ages , monasteries and convents were the key medical centres of Europe and the Church developed an early version of a welfare state. Cathedral schools evolved into a well integrated network of medieval universities and Catholic scientists (many of them clergymen) made a number of important discoveries which aided the development of modern science and medicine .
Albert the Great (1206–1280) was a pioneer of biological field research and is a saint within the Catholic Church; Desiderius Erasmus (1466–1536) helped revive knowledge of ancient Greek medicine , Renaissance popes were often patrons of the study of anatomy, and Catholic artists such as Michelangelo advanced knowledge of the field through sketching cadavers. The Jesuit Athanasius Kircher (1602–1680) first proposed that living beings enter and exist in the blood (a precursor of germ theory). The Augustinian Gregor Mendel (1822–1884) developed theories on genetics for the first time. As Catholicism became a global religion, the Catholic orders and religious and lay people established health care centres around the world. Women's religious institutes such as the Sisters of Charity , Sisters of Mercy and Sisters of St Francis opened and operated some of the first modern general hospitals.
While the prioritization of charity and healing by early Christians created the hospital, their spiritual emphasis tended to imply "the subordination of medicine to religion and doctor to priest". "Physic and faith", wrote historian of medicine Roy Porter "while generally complementary... sometimes tangled in border disputes." Similarly in modern times, the moral stance of the Church against contraception and abortion has been a source of controversy. The Church, while being a major provider of health care to HIV AIDS sufferers, and of orphanages for unwanted children, has been criticised for opposing condom use. Due to Catholics' belief in the sanctity of life from conception, IVF, which leads to the destruction of many embryos, surrogacy, which relies on IVF, and embryonic stem-cell research, which necessitates the destruction of embryos, are among other areas of controversy for the Church in the provision of health care.
Catholic social teaching urges concern for the sick. Jesus Christ , whom the church holds as its founder, placed a particular emphasis on care for the sick and outcast, such as lepers. According to the New Testament , he and his Apostles went about curing the sick and anointing of the sick . [ 5 ] According to the Parable of the Sheep and the Goats , which is found in Matthew 25 , Jesus identified so strongly with the sick and afflicted that he equated serving them with serving him:
For I was hungry and you fed me, thirsty and you gave me drink. I was a stranger and you received me in your homes. Naked and you clothed me. I was sick and you took care of me, in prison and you visited me ... [W]hatever you did for one of these least brothers of mine, you did for me.
In a 2013 presentation to its twenty-seventh international conference in 2013, the President of the Pontifical Council for the Pastoral Care of Health Care Workers , Zygmunt Zimowski , said that "The Church, adhering to the mandate of Jesus, 'Euntes docete et curate infirmos' (Mt 10:6-8, Go, preach and heal the sick), during the course of her history, which by now has lasted two millennia, has always attended to the sick and the suffering."
In orations such as his Sermon on the Mount and stories such as the Parable of the Good Samaritan , Jesus called on followers to worship God (Rpm 12:1-2) through care for our neighbor: the sick, hungry and poor. Such teachings formed the foundation of Catholic Church involvement in hospitals and health care. [ 5 ]
According to James Joseph Walsh , writing in the Catholic Encyclopedia :
Christ Himself gave His followers the example of caring for the sick by the numerous miracles He wrought to heal various forms of disease including the most loathsome, leprosy. He also charged His Apostles in explicit terms to heal the sick (Luke 10:9) and promised to those who should believe in Him that they would have power over disease (Mark 16:18) [...] Like the other works of Christian charity, the care of the sick was from the beginning a sacred duty for each of the faithful, but it devolved in a special way upon the bishops, presbyters, and deacons. The same ministrations that brought relief to the poor naturally included provision for the sick who were visited in their homes. [ 6 ]
The Benedictine rule, which led the profusion of medieval hospitals founded by the Church, requires that "the care of the sick is to be placed above and before every other duty, as if indeed Christ were being directly served by waiting on them". [ 7 ]
Ancient Greek and Roman medicine developed solid foundations over seven centuries, creating, Porter wrote, "the ideal of a union of science, philosophy and practical medicine in the learned physician...". [ 8 ] But Greek and Roman religion did not preach of a duty to tend to the sick. [ 5 ] Christianity emerged into this world as a Jewish sect in the mid-1st century and early Christians from the outset went about tending the sick and infirm. Their priests were often also physicians. [ 5 ] St Luke the Evangelist , credited as one of the authors of The New Testament , was a physician. [ 9 ] Christian emphasis on practical charity was to give rise to the development of systematic nursing and hospitals after the end of the persecution of the early church. [ 6 ]
The early Christian outlook on sickness drew on various traditions, including Eastern asceticism and Jewish healing traditions, while the New Testament wrote of Jesus and his Apostles as healers. [ 10 ] Porter wrote: "While suffering and disease could appear as chastisement of the wicked or a trial of those the Lord loved, the Church also developed a healing mission". [ 11 ] Pagan religions seldom offered help to the sick, but the early Christians were willing to nurse the sick and take food to them. [ 5 ] [ 12 ] Notably during the smallpox epidemic of 165–180 AD and the measles outbreak of around 250 AD, "In nursing the sick and dying, regardless of religion, the Christians won friends and sympathisers", wrote historian Geoffrey Blainey . [ 5 ]
Hospitality was considered an obligation of Christian charity and bishops' houses and the valetudinaria of wealthier Christians were used to tend the sick. [ 6 ] Deacons were assigned the task of distributing alms, and in Rome by 250 AD the Church had developed an extensive charitable outreach, with wealthy converts supporting the poor. [ 11 ] It is believed that the first church hospitals were constructed in the East, and only later in the Latin West. An early hospital may have been built at Constantinople during the age of Constantine by St. Zoticus. St. Basil built a famous hospital at Cæsarea in Cappadocia , later called Basileias , which "had the dimensions of a city". In the West, Saint Fabiola founded a hospital at Rome around 400. [ 6 ] Saint Jerome wrote that Fabiola founded a hospital and "assembled all the sick from the streets and highways" and "personally tended the unhappy and impoverished victims of hunger and disease... washed the pus from sores that others could not even behold" [ 12 ]
Several early Christian healers are honoured as Saints in the Catholic tradition. Cosmas and Damian , brothers from Cilicia in Asia Minor, supplanted the pagan Asclepius as the patron saints of medicine and were celebrated for their healing powers.." [ 13 ] Said to have lived in the late third century AD and to have performed a miraculous first leg transplant on a patient, and later martyred under the Emperor Diocletian , Cosmas and Damian appear in the heraldry of barber-surgeon companies.." [ 13 ] Notable contributors to the medical sciences of those early centuries include Tertullian (born 160 AD), Clement of Alexandria , Lactantius and the learned St. Isidore of Seville (d. 636). St. Benedict of Nursia (480) emphasised medicine as an aid to the provision of hospitality. [ 14 ] The martyr Saint Pantaleon was said to be physician to the Emperor Galerius , who sentenced him to death for his Christianity. Since the Middle Ages, Pantaleon has been considered a patron saint of physicians and midwives. [ 15 ]
The administration of the Eastern and Western Roman Empires split and the demise of the Western Empire by the sixth century was accompanied by a series of violent invasions, and precipitated the collapse of cities and civic institutions of learning, along with their links to the learning of classical Greece and Rome. For the next thousand years, medical knowledge would change very little.." [ 16 ] A scholarly medical tradition maintained itself in the more stable East, but in the West, scholarship virtually disappeared outside of the Church, where monks were aware of a dwindling range of medical texts.." [ 17 ] The legacy of this early period was, in the words of Porter, that "Christianity planted the hospital: the well-endowed establishments of the Levant and the scattered houses of the West shared a common religious ethos of charity.". [ 12 ]
Geoffrey Blainey likened the Catholic Church in its activities during the Middle Ages to an early version of a welfare state: "It conducted hospitals for the old and orphanages for the young; hospices for the sick of all ages; places for the lepers; and hostels or inns where pilgrims could buy a cheap bed and meal". It supplied food to the population during famine and distributed food to the poor. This welfare system the church funded through collecting taxes on a large scale and possessing large farmlands and estates. [ 18 ] It was common for monks and clerics to practice medicine and medical students in northern European universities often took minor Holy orders. Mediaeval hospitals had a strongly Christian ethos and were, in the words of historian of medicine Roy Porter , "religious foundations through and through"; ecclesiastical regulations were passed to govern medicine, partly to prevent clergymen profiting from medicine. [ 19 ]
After a period of decline, the Holy Roman Emperor Charlemagne had decreed that a hospital should be attached to each cathedral and monastery. Following his death, the hospitals again declined, but by the tenth century monasteries were the leading providers of hospital work – among them the Benedictine Abbey of Cluny . [ 6 ] Charlemagne's decree required each monastery and Cathedral chapter to establish a school and in these schools medicine was commonly taught. Gerbert of Aurillac ( c. 946 – 12 May 1003), known to history as Pope Sylvester II , taught medicine at one such school. [ 14 ] Petrus of Spain (1210–1277) was a physician who wrote the popular Treasury of the Poor medical text and became Pope John XXI in 1276. [ 19 ]
Other famous physicians and medical researchers of the Middle Ages include the Abbot of Monte Cassino Bertharius , the Abbot of Reichenau Walafrid Strabo , the Abbess St Hildegard of Bingen and the Bishop of Rennes Marbodus of Angers . [ 5 ] Monasteries of this era were diligent in the study of medicine, and often too were convents. Hildegard of Bingen, a doctor of the church , is among the most distinguished of Medieval Catholic women scientists. Other than theological works, Hildegard also wrote Physica , a text on the natural sciences, as well as Causae et Curae . Hildegard was well known for her healing powers involving practical application of tinctures, herbs, and precious stones. [ 20 ]
In keeping with the Benedictine rule that the care of the sick be placed above all other duties, monasteries were the key medical care providers prior to 1300. Most monasteries offered shelter for pilgrims and an infirmary for sick monks, while separate hospitals were founded for the public. [ 7 ] The Benedictine order was noted for setting up hospitals and infirmaries in their monasteries, growing medical herbs and becoming the chief medical care givers of their districts. [ 5 ] The Capuchin monks sought a revival of the ideals of Francis of Assisi , offering care after plague struck at Camerino in 1523. [ 5 ]
Healing shrines were established and different saints came to be invoked for every body part in the hope of miraculous cures. [ 13 ] Some of the shrines remain to the present day, and were in the Middle Ages great centres for pilgrims, complete with relics and souvenirs. [ 7 ] St Luke or St Michael were invoked for various ailments, and a host of saints for individuals conditions, including St Roch as a protector against plague. [ 13 ] St Roch is venerated as one who provided care to plague suffers, only to fall sick himself and be "healed by an angel". [ 13 ] [ 21 ] Through the devastating Bubonic Plague , the Franciscans were notable for tending the sick. The apparent impotence of medical knowledge against the disease prompted critical examination. Medical scientists came to divide among anti- Galenists , anti-Arabists and positive Hippocratics. [ 14 ]
Crusader orders established several new traditions of Catholic medical care. [ 22 ] The famous Knights Hospitaller arose as a group of individuals associated with an Amalfitan hospital in Jerusalem, which was built to provide care for poor, sick or injured pilgrims to the Holy Land. Following the capture of the city by Crusaders, the order became a military as well as infirmarian order. [ 23 ] The Knights of St John of Jerusalem were later known as the Knights of Malta . The Knights Templar and Teutonic Knights established hospitals around the Mediterranean and through Germanic lands. [ 24 ]
Non-military orders of brothers also took up the service of the infirm. By the 15th century, the brothers of the Order of the Holy Spirit were providing care across Europe, and by the sixteenth century the Spanish-founded Order of St John of God had set up about 200 hospitals in the Americas. [ 24 ] In Catholic Spain amidst the early Reconquista , Archbishop Raimund founded an institution for translations, which employed a number of Jewish translators to communicate the works of Arabian medicine. Influenced by the rediscovery of Aristotelian thought, churchmen like the Dominican Albert Magnus and the Franciscan Roger Bacon made significant advances in the observation of nature.
Small hospitals for pilgrims sprung up in the West during the early Middle Ages, but by the latter part of the period had grown more substantial, with hospitals founded for lepers, pilgrims, the sick, aged and poor. Milan, Siena, Paris and Florence had numerous and large hospitals. "Within hospitals walls", wrote Porter, "the Christian ethos was all pervasive". From just 12 beds in 1288, the Sta Maria Nuova in Florence "gradually expanded by 1500 to a medical staff of ten doctors, a pharmacist, and several assistants, including female surgeons", and was boasted of as the "first hospital among Christians". [ 22 ]
Clergy were active at the School of Salerno , the oldest medical school in Western Europe – among the important churchmen to teach there were Alpuhans , later (1058–1085) Archbishop of Salerno, and the influential Constantine of Carthage , a monk who produced superior translations of Hippocrates and investigated Arab literature. [ 14 ] Cathedral schools began in the Early Middle Ages as centers of advanced education, some of them ultimately evolving into medieval universities . The medieval universities of Western Christendom were well-integrated across all of Western Europe, encouraged freedom of enquiry and produced a great variety of fine scholars and natural philosophers, including Robert Grosseteste of the University of Oxford , an early expositor of a systematic method of scientific experimentation, [ 25 ] and Saint Albert the Great , a pioneer of biological field research. [ 26 ] Porter wrote that, "The great age of hospital building from around 1200 coincided with the flourishing of universities in Italy, Spain, France and England, sustained by the new wealth of the High Middle Ages . ... The Universities extended the work of Salerno in medical education". [ 24 ]
From the 14th century, the European Renaissance saw a revival of interest in Classical learning in Western Europe, coupled with and fuelled by the spread of new inventions like the printing press. The Fall of Constantinople brought refugee scholars from the Greek East to the West. The Catholic scholar Desiderius Erasmus (1466–1536) was interested in medicine and influential in reviving Greek as a language of learning, and the study of the pre-Christian works of Galen . Roy Porter wrote that "after centuries where the Church had taught mankind to renounce worldly goods, for the sake of eternity, Renaissance man showed an insatiable curiosity for the materiality of the here and now...". [ 27 ]
In Renaissance Italy , the Popes were often patrons of the study of anatomy and Catholic artists such as Michelangelo advanced knowledge of the field through such studies as sketching cadavers to improve his portraits of the crucifixion. [ 14 ] It is often wrongly asserted that the papacy banned dissection during the period, though in fact the directive of Pope Sixtus IV of 1482 to the University of Tübingen said that the Church had no objection to anatomy studies, provided the bodies belonged to an executed criminal, and was given a religious burial once examinations were completed. [ 7 ]
In modern times, the Catholic Church is the largest non-government provider of health care in the world. Catholic religious have been responsible for founding and running networks of hospitals across the world where medical research continues to be advanced. [ 28 ] In 2013, Robert Calderisi wrote that the Catholic Church has around 18,000 clinics, 16,000 homes for the elderly and those with special needs, and 5,500 hospitals – with 65 per cent of them located in developing countries. [ 2 ]
Catholic scientists in Europe (many of them clergymen) made a number of important discoveries which aided the development of modern science and medicine. Catholic women were also among the first female professors of medicine, as with Trotula of Salerno the 11th century physician and Dorotea Bucca who held a chair of medicine and philosophy at the University of Bologna . [ 29 ] The Jesuit order, created during the Reformation, contributed a number of distinguished medical scientists. In the field of bacteriology it was the Jesuit Athanasius Kircher (1671) who first proposed that living beings enter and exist in the blood (a precursor of germ theory ). In the development of ophthalmology , Christoph Scheiner made important advances in relation to refraction of light and the retinal image. [ 14 ]
Gregor Mendel , an Austrian scientist and Augustinian friar, began experimenting with peas around 1856. [ 30 ] Mendel had joined the Brno Augustinian Monastery in 1843, but also trained as a scientist at the Olmutz Philosophical Institute and the University of Vienna . The Brno Monastery was a centre of scholarship, with an extensive library and tradition of scientific research. [ 31 ] Observing the processes of pollination at his monastery in modern Czechoslovakia, Mendel studied and developed theories pertaining to the field of science now called genetics . Mendel published his results in 1866 in the Journal of the Brno Natural History Society , and is considered the father of modern genetics. [ 30 ] Where Charles Darwin 's theories suggested a mechanism for improvement of species over generations, Mendel's observations provided explanation for how a new species itself could emerge. Though Darwin and Mendel never collaborated, they were aware of each other's work (Darwin read a paper by Wilhelm Olbers Focke which extensively referenced Mendel). Bill Bryson wrote that "without realizing it, Darwin and Mendel laid the groundwork for all of life sciences in the twentieth century. Darwin saw that all living things are connected, that ultimately they trace their ancestry to a single, common source; Mendel's work provided the mechanism to explain how that could happen". [ 32 ]
Catholic religious institutes, notably those for women, developed many hospitals throughout Europe and its empires. Ancient orders like the Dominicans and Carmelites have long lived in religious communities that work in ministries such as education and care of the sick. [ 33 ] The Portuguese Saint John of God (d. 1550) founded the Brothers Hospitallers of St. John of God to care for the sick and afflicted. The order built hospitals across Europe and its growing empires. In 1898, John was declared patron of the dying and of all hospitals by Pope Leo XIII . [ 34 ] The Italian Saint Camillus de Lellis , considered a patron saint of nurses, was a reformed gambler and soldier who became a nurse and then director of Romes's Hospital of St. James, the hospital for incurables. In 1584 he founded the Camillians to tend to the plague-stricken. [ 35 ] Irishwoman Catherine McAuley founded the Sisters of Mercy in Dublin in 1831. Her congregation went on to found schools and hospitals across the globe. [ 36 ] Saint Jeanne Jugan founded the Little Sisters of the Poor on the Rule of Saint Augustine to assist the impoverished elderly of the streets of France in the mid-nineteenth century. It too spread around the world. [ 37 ]
In 2017, controversy arose when an Associated Press report, which the Vatican criticized, stated that Bambino Gesu (Baby Jesus) Pediatric Hospital, a cornerstone of Italy's health care system and administered by the Holy See, put children at risk between 2008 and 2015 and turned its attention to profit after losing money and expanding services. [ 38 ]
The Spanish and Portuguese Empires were largely responsible for spreading the Catholic faith and its philosophy regarding health care to South and Central America, where the church established substantial hospital networks.
Catholic hospitals were established in the United States in the colonial era. The first was probably Charity Hospital, New Orleans , established around 1727. [ 39 ] American hospitals in the 19th century were largely designed for poor people in the larger cities. There were no paying patients. Very small proprietary hospitals were operated by practicing physicians and surgeons to take care of their own paying patients in better facilities than the charity hospitals offered. By the 1840s, the major religious denominations, especially the Catholics and Methodists, began opening hospitals in major cities. [ 40 ] In the 1840s–1880s era, Catholics in Philadelphia founded two hospitals, for the Irish and German Catholic immigrants. They depended on revenues from the paying sick, and became important health and welfare institutions in the Catholic community. [ 41 ] By 1900 the Catholics had set up hospitals in most major cities. In New York the Dominicans, Franciscans, Sisters of Charity, and other orders set up hospitals to care primarily for their own ethnic group. By the 1920s they were serving everyone in the neighborhood. [ 42 ]
In smaller cities too the Catholics set up hospitals, such as St. Patrick Hospital in Missoula, Montana . The Sisters of Providence opened it in 1873. It was in part funded by the county contract to care for the poor, and also operated a day school and a boarding school. The nuns provided nursing care especially for infectious diseases and traumatic injuries. They also proselytized the patients to attract converts and restore lapsed Catholics back into the Church. They built a larger hospital in 1890. [ 43 ] Catholic hospitals were largely owned and staffed by orders of nuns (who took oaths of poverty), as well as unpaid nursing students. When the population of nuns dropped sharply after the 1960s, the hospitals were sold. The Catholic Hospital Association formed in 1915. [ 44 ] [ 45 ]
The Sisters of Saint Francis of Syracuse, New York, produced Saint Marianne Cope , who opened and operated some of the first general hospitals in the United States, instituting cleanliness standards which influenced the development of America's modern hospital system, and famously taking her nuns to Hawaii to work with Saint Damien of Molokai in the care of lepers. St Damien himself is considered a martyr of charity and model of Catholic humanitarianism for his mission to the lepers of Molokai.
In the 1990s the Catholic Church was still the largest private provider of health care in the United States. [ 46 ] During the 1990s, the church provided about one in six hospital beds in America, at around 566 hospitals, most established by nuns. [ 39 ] The church has carried a disproportionate number of poor and uninsured patients at its facilities and the American bishops first called for universal health care in America in 1919. The church has been an active campaigner in that cause ever since. [ 39 ] In the abortion debate in America, the church has sought to retain the right not to perform abortions in its health care facilities. [ 39 ] In 2012, the church operated 12.6% of hospitals in the US, accounting for 15.6% of all admissions, and around 14.5% of hospital expenses ($98.6 billion dollars). Compared to the public system, the church provided greater financial assistance or free care to poor patients, and was a leading provider of various low-profit health services such as breast cancer screenings, nutrition programs, trauma, and care of the elderly. [ 47 ]
Catholic medical facilities in the United States have refused treatment which runs counter to Papal teachings. Abortions are not allowed. Contraception is a treatment that is not provided, and some Catholic health care providers have refused to treat complications caused by contraceptives. Those seeking treatment within a Catholic facility may be unaware of these restrictions or unaware that their health provider is connected with the Catholic Church until seeking treatment for such an issue. [ 48 ]
During the Middle Ages, Arab medicine was influential on Europe. During Europe's Age of Discovery , Catholic missionaries, notably the Jesuits, introduced the modern sciences to India, China and Japan. Church is a major provider of health care services – especially in Catholic nations like Philippines . [ 49 ]
The famous Mother Teresa of Calcutta established the Missionaries of Charity in the slums of Calcutta in 1948 to work among "the poorest of the poor". Initially founding a school, she then gathered other sisters who "rescued new-born babies abandoned on rubbish heaps; they sought out the sick; they took in lepers, the unemployed, and the mentally ill". Teresa achieved fame in the 1960s and began to establish convents around the world. By the time of her death in 1997, the religious institute she founded had more than 450 centres in over 100 countries. [ 50 ]
French, Portuguese, British and Irish missionaries brought Catholicism to Oceania and built hospitals and care centres across the region. The church remains not only a key provider of health care in predominantly Catholic nations like East Timor but also in predominantly Protestant and secular nations like Australia and New Zealand.
As restrictions were lifted by British authorities on the practice of Catholicism in colonial Australia, Catholic religious institutes founded many of Australia's hospitals. Irish Sisters of Charity arrived in Sydney in 1838 and established St Vincent's Hospital, Sydney , in 1857 as a free hospital for the poor. The Sisters went on to found hospitals, hospices, research institutes and aged care facilities in Victoria, Queensland and Tasmania. [ 51 ] At St Vincent's they trained leading surgeon Victor Chang and opened Australia's first AIDS clinic. [ 52 ] In the 21st century, with more and more lay people involved in management, the sisters began collaborating with Sisters of Mercy Hospitals in Melbourne and Sydney. Jointly the group operates four public hospitals; seven private hospitals and 10 aged care facilities.
The Sisters of Mercy arrived in Auckland in 1850 and were the first order of religious sisters to come to New Zealand; they began work in health care and education. [ 53 ]
The Sisters of St Joseph was founded in Australia by Australia's first Saint, Mary MacKillop , and Fr Julian Tenison Woods in 1867. [ 54 ] [ 55 ] [ 56 ] MacKillop travelled throughout Australasia and established schools, convents and charitable institutions. [ 57 ] The English Sisters of the Little Company of Mary arrived in 1885 and have since established public and private hospitals, retirement living and residential aged care, community care and comprehensive palliative care in New South Wales, the ACT, Victoria, Tasmania, South Australia and the Northern Territory. [ 58 ] The Little Sisters of the Poor , who follow the charism of Saint Jeanne Jugan to "offer hospitality to the needy aged" arrived in Melbourne in 1884 and now operate four aged care homes in Australia. [ 59 ]
Catholic Health Australia is today the largest non-government provider grouping of health, community and aged care services in Australia. These do not operate for profit and range across the full spectrum of health services, representing about 10% of the health sector and employing 35,000 people. [ 60 ] Catholic organisations in New Zealand remain heavily involved in community activities including education, health services, chaplaincy to prisons, rest homes, and hospitals, social justice , and human rights advocacy. [ 61 ] [ 62 ]
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Catholicism has grown rapidly in Africa over the last two centuries. As in all other continents, Catholic missionaries established health care centres across the continent – though limitations on Catholic institutions remain in place for much of Muslim North Africa. Caritas Internationalis is the Church's main international aid and development body and operates in over 200 countries and territories and co-operates closely with the United Nations. [ 63 ]
Pope Paul VI issued the Humanae Vitae Encyclical Letter on the Regulation of Birth in 1968, which outlined opposition to "artificial birth control" on the basis that it would open a "wide and easy road ... towards conjugal infidelity and the general lowering of morality". [ 64 ] In response to the subsequent AIDS epidemic which emerged from the 1980s onward, the United Nations Population Fund (UNFPA) has argued that "comprehensive condom programming is a key institutional priority ... because condoms ... are recognized as the only currently available and effective way to prevent HIV – and other sexually transmitted infections – among sexually active people". [ 65 ] A 2014 report by The U.N. Committee on the Rights of the Child called on the Church to "overcome all the barriers and taboos surrounding adolescent sexuality that hinder their access to sexual and reproductive information, including on family planning and contraceptives". [ 66 ]
In Africa today, the church is heavily engaged in providing care to AIDS sufferers amidst the AIDS epidemic. [ 67 ] [ 68 ] Following the election of Pope Francis in 2013, UNAIDS wrote that the Church "provides support to millions of people living with HIV around the world" and that "Statistics from the Vatican in 2012 indicated that Catholic Church-related organizations provide approximately a quarter of all HIV treatment, care, and support throughout the world and run more than 5,000 hospitals, 18,000 dispensaries and 9,000 orphanages, many involved in AIDS-related activities." UNAIDS co-operates closely with the Church on critical issues such as the elimination of new HIV infections in children and keeping their mothers alive, as well as increasing access to antiretroviral medication. [ 69 ]
In April 2020, the Vatican's Congregation for the Eastern Churches set up a coronavirus fund to address the health crisis of the COVID-19 pandemic. This was a response to Pope Francis' invitation to "not abandon the suffering, especially the poorest, in facing the global crisis caused by the pandemic." [ 70 ]
Catholic Church also supported the government vaccination program by transforming their churches into vaccination sites. Health Secretary Francisco T. Duque affirmed the church's support by saying, ‘we are happy with the CBCP 's offer to have churches as vaccination hubs if needed. Churches really can be alternative sites to areas that lack facility, especially those in hard-to-reach municipalities'. [ 71 ]
In early March 2020, in the United States, Catholic churches practiced avoiding hugs and handshakes as a precautionary measure against spreading the virus. According to Reverend Jeffery Ott of Our Lady of Lourdes in Atlanta, Georgia , the church had to omit the sharing of wine in the chalice during Holy Communion. [ 72 ]
Because the Catholic Church opposes abortion , euthanasia and contraception [ 73 ] and other procedures, Catholic health facilities will not provide most or any such services. [ 74 ] In public debates, particularly among Western nations like the United States, this has raised questions over insurance public/private financial co-operation and government interference and regulation of health facilities. Writing in 2012, the Australian human rights lawyer and Jesuit Frank Brennan , in response to calls for public funding to Catholic hospitals to be contingent on them offering the "full suites of services", said that: [ 75 ]
The nation is the better for policies and funding arrangements that encourage public and private providers of healthcare, including the Churches. The public may need to be patient with Church authorities as they discern appropriate moral responses to new technologies. This is a small price to pay for creative diversity which delivers healthcare of the highest standard with a special character cherished by many citizens, not just Catholics.
The Catholic Church's opposition to abortion has also restricted its hospitals' treatment of miscarriages. [ 76 ] In cases where evacuation of the miscarriage from the uterus is medically indicated, doctors have been prohibited from carrying it out while a fetal heartbeat is still present, "in effect delaying care until fetal heart tones cease, the pregnant woman becomes ill, or the patient is transported to a non–Catholic-owned facility for the procedure." [ 77 ]
A number of controversies have arisen over the application of these treatments in Catholic hospitals, or the lack thereof; [ 76 ] for instance, in the United States, a member of a hospital ethics committee was excommunicated when she approved a therapeutic, direct abortion to save a patient's life, and in Germany a case of two hospitals turning away and refusing to examine or treat a rape victim led to new guidelines from the country's bishops stating that hospitals could provide emergency contraception to victims of rape. [ 78 ]
As regards IVF and surrogacy , the Church's teaching, which states that every human life is sacred from conception until natural death, and that the vulnerable should be protected, therefore finds that this technology, which leads to the death of many embryos for each successful pregnancy, to be an abuse of power at the cost of the weakest. [ 79 ] However, Catholics have been active in developing alternative treatments for infertility and especially addressing its root causes, which, in addition to causing infertility or risk of miscarriage, are likely to have other consequences on health, such as polycystic ovarian syndrome , thyroid conditions and endometriosis . [ 80 ]
In 2016, a woman was refused treatment according to the " Ethical and Religious Directives for Catholic Health Care Services " [ 73 ] for her dislodged IUD , although she was bleeding, cramping and in pain. [ 81 ] [ 82 ] [ 83 ] [ 84 ]
In 2019, a Catholic hospital in Eureka, California , was criticized for not performing a hysterectomy as part of a gender affirming surgery. [ 85 ]
There are a number of patron saints for physicians, the most important of whom are Saint Luke the Evangelist , the physician and disciple of Christ ; Saints Cosmas and Damian , 3rd-century physicians from Syria ; and Saint Pantaleon , a 4th-century physician from Nicomedia . Archangel Raphael is also considered a patron saint of physicians. [ 86 ]
The patron saints for surgeons are Saint Luke the Evangelist , the physician and disciple of Christ , Saints Cosmas and Damian (3rd-century physicians from Syria ), Saint Quentin (3rd-century saint from France), Saint Foillan (7th-century saint from Ireland ), and Saint Roch (14th-century saint from France). [ 87 ]
Various Catholic saints are considered patrons of nursing: Saint Agatha , Saint Alexius , Saint Camillus of Lellis , St Catherine of Alexandria , St Catherine of Siena , St John of God , St Margaret of Antioch , Saint Martín de Porres and Raphael the Archangel . [ 88 ]
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A catlin or catling is a long, double-bladed surgical knife . It was commonly used from the 17th to the mid 19th century, particularly for amputations ; after that its use declined in favor of mechanically driven (and later, electrically driven) oscillating saws.
Surgeon William Clowes wrote about the instrument in a medical treatise written in 1596, that amputation required the use of "a very good catlin, and an incision knife," [ 1 ] Later, surgeon John Woodall referred to a "catlinge" in a work in 1639. By 1693, when British navy surgeon John Moyle described proper amputation techniques, he wrote that "with your Catling, divide the Flesh and Vessels about and between the bones, and with the back of your Catling, remove the Periosteum that it may not hinder the saw, nor cause greater Torment in the Operation,". [ 1 ]
The term was thereafter understood to refer to an interosseous knife. [ 1 ]
This article related to medical equipment is a stub . You can help Wikipedia by expanding it .
This surgery article is a stub . You can help Wikipedia by expanding it .
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Cauda equina syndrome ( CES ) is a condition that occurs when the bundle of nerves below the end of the spinal cord known as the cauda equina is damaged. [ 2 ] Signs and symptoms include low back pain , pain that radiates down the leg , numbness around the anus, and loss of bowel or bladder control. [ 1 ] Onset may be rapid or gradual. [ 1 ]
The cause is usually a disc herniation in the lower region of the back . [ 1 ] Other causes include spinal stenosis , cancer , trauma , epidural abscess , and epidural hematoma . [ 1 ] [ 2 ] The diagnosis is suspected based on symptoms and confirmed by medical imaging such as MRI or CT scan . [ 1 ] [ 3 ]
CES is generally treated surgically via laminectomy . [ 1 ] Sudden onset is regarded as a medical emergency requiring prompt surgical decompression , with delay causing permanent loss of function. [ 4 ] Permanent bladder problems, sexual dysfunction or numbness may occur despite surgery. [ 1 ] [ 3 ] A poor outcome occurs in about 20% of people despite treatment. [ 1 ] About 1 in 70,000 people is affected every year. [ 1 ] It was first described in 1934. [ 5 ]
Signs and symptoms of cauda equina syndrome include:
Severe back pain, saddle anesthesia , urinary or fecal incontinence and sexual dysfunction are considered "red flags", i.e. features which require urgent investigation. [ 8 ]
After the conus medullaris (near lumbar vertebral levels 1 (L1) and 2 (L2), occasionally lower), the spinal canal contains a bundle of nerve fibers (the cauda equina or "horse-tail") that branches off the lower end of the spinal cord and contains the nerve roots from L1–L5 and S1–S5. The nerve roots from L4–S4 join in the sacral plexus which affects the sciatic nerve, which travels caudally (toward the feet). Compression, trauma or other damage to this region of the spinal canal can result in cauda equina syndrome. [ citation needed ]
The symptoms may also appear as a temporary side-effect of a sacral extra-dural injection. [ 9 ]
Direct trauma can also cause cauda equina syndrome. Most common causes include as a complication of lumbar punctures, burst fractures resulting in posterior migration of fragments of the vertebral body, severe disc herniations , spinal anaesthesia involving trauma from catheters and high local anaesthetic concentrations around the cauda equina, penetrating trauma such as knife wounds or ballistic trauma . [ 10 ] Cauda equina syndrome may also be caused by blunt trauma suffered in an event such as a car accident or fall. [ 11 ]
CES can be caused by lumbar spinal stenosis , which is when the diameter of the spinal canal narrows. This could be the result of a degenerative process of the spine (such as osteoarthritis ) or a developmental defect which is present at birth. In the most severe cases of spondylolisthesis cauda equina syndrome can result. [ 10 ]
Chronic spinal inflammatory conditions such as Paget disease , neurosarcoidosis , chronic inflammatory demyelinating polyneuropathy , ankylosing spondylitis , rheumatoid disease of the spine, and chronic tuberculosis can cause it. This is due to the spinal canal narrowing that these kinds of syndromes can produce. [ 10 ]
Individuals most at risk for disc herniation are the most likely to develop CES. Race has little influence with the notable exception that African Americans appear slightly less likely to develop CES than other groups. [ 12 ] [ 13 ] [ 14 ] Middle age also appears to be a notable risk factor, as those populations are more likely to develop a herniated disc; heavy lifting can also be inferred as a risk factor for CES. [ 12 ] [ 14 ]
Other risk factors include obesity and being female. [ 15 ]
Diagnosis is first suspected clinically based on history and physical exam and usually confirmed by an MRI scan or CT scan , depending on availability. [ 4 ] Bladder scanning and loss of catheter sensation can also be used to evaluate bladder dysfunction in suspected cases of cauda equina syndrome and can aid diagnosis before MRI scanning. [ citation needed ] Early surgery in acute onset of severe cases has been reported to be important. [ 4 ]
Early diagnosis of cauda equina syndrome can allow for preventive treatment. Signs that allow early diagnosis include changes in bowel and bladder function and loss of feeling in groin. [ 16 ] Changes in sensation can start as pins and needles leading to numbness. Changes in bladder function may be changes to stream or inability to fully empty the bladder. If a person progresses to full retention intervention is less likely to be successful. [ citation needed ]
The management of true cauda equina syndrome frequently involves surgical decompression. When cauda equina syndrome is caused by a herniated disk early surgical decompression is recommended. [ 17 ]
Sudden onset cauda equina syndrome is regarded as a medical/surgical emergency. [ 4 ] Surgical decompression by means of laminectomy or other approaches may be undertaken within 6, [ 18 ] 24 [ 19 ] or 48 hours of symptoms developing if a compressive lesion (e.g., ruptured disc, epidural abscess, tumor or hematoma) is demonstrated. Early treatment may significantly improve the chance of avoiding long-term neurological damage. [ 17 ] [ 19 ]
Surgery may be required to remove blood, bone fragments, a tumor or tumors, a herniated disc or an abnormal bone growth. If the tumor cannot be removed surgically and is malignant then radiotherapy may be used as an alternative to relieve pressure. Chemotherapy can also be used for spinal neoplasms. If the syndrome is due to an inflammatory condition e.g., ankylosing spondylitis, anti-inflammatory, including steroids can be used as an effective treatment. If a bacterial infection is the cause then an appropriate course of antibiotics can be used to treat it. [ 20 ]
Cauda equina syndrome can occur during pregnancy due to lumbar disc herniation. The risk of cauda equina syndrome during pregnancy increases with age of the mother. Surgery can still be performed and pregnancy does not adversely affect treatment. Treatment for those with cauda equina can and should be carried out at any time during pregnancy. [ 21 ]
Lifestyle issues may need to be addressed post-treatment. Issues could include the person's need for physiotherapy and occupational therapy due to lower limb dysfunction. Obesity might also need to be tackled. [ 20 ]
Rehabilitation of CES depends on the severity of the injury. If permanent damage occurs, then impairment in bladder and bowel control may result. [ 22 ] Once surgery is performed, resting is required until the bladder and bowel dysfunction can be assessed. Urinary catheterization may help with bladder control. Gravity and exercise can help control bowel movement (Hodges, 2004). Pelvic floor exercises assist in controlling bowel movements (Pelvic Floor Exercises, 2010). [ full citation needed ] These exercises can be done standing, lying, or on all fours with the knees slightly separated. Full recovery of bowel and bladder control can take as long as two years. [ citation needed ]
The prognosis for complete recovery is dependent upon many factors. The most important of these is the severity and duration of compression upon the damaged nerve(s). Generally, the longer the time before intervention to remove the compression causing nerve damage, the greater the damage caused to the nerve(s). [ citation needed ]
Damage can be so severe that nerve regrowth is impossible, and the nerve damage will be permanent. In cases where the nerve has been damaged but is still capable of regrowth, recovery time is widely variable. Surgical intervention with decompression of the cauda equina can assist recovery. Delayed or severe nerve damage can mean up to several years' recovery time because nerve growth is exceptionally slow. [ citation needed ]
Review of the literature indicates that around 50–70% of patients have urinary retention (CES-R) on presentation with 30–50% having an incomplete syndrome (CES-I). The latter group, especially if the history is less than a few days, usually requires emergency MRI to confirm the diagnosis followed by prompt decompression. CES-I with its more favourable prognosis may become CES-R at a later stage. [ 23 ]
Various etiologies of CES include fractures , abscesses , hematomas , and any compression of the relevant nerve roots . [ 24 ] Injuries to the thoracolumbar spine will not necessarily result in a clinical diagnosis of CES, but in all such cases it is necessary to consider. Few epidemiological studies of CES have been done in the United States, owing to difficulties such as amassing sufficient cases as well as defining the affected population, therefore this is an area deserving of additional scrutiny. [ 12 ]
Traumatic spinal cord injuries occur in approximately 40 people per million annually in the United States, resulting from traumas due to motor vehicle accidents, sporting injuries, falls, and other factors. [ 13 ] An estimated 10 to 25% of vertebral fractures will result in injury to the spinal cord . [ 13 ] Thorough physical examinations are required, as 5 to 15% of trauma patients have fractures that initially go undiagnosed. [ 25 ]
The most frequent injuries of the thoracolumbar region are to the conus medullaris and the cauda equina , particularly between T12 and L2. [ 13 ] Of these two syndromes, CES is the more common. [ 13 ] CES mainly affects middle-aged individuals, particularly those in their forties and fifties, and presents more often in men. [ 13 ] [ 14 ] [ 26 ] It is not a typical diagnosis, developing in only 4 to 7 out of every 10,000 to 100,000 patients, and is more likely to occur proximally. [ 12 ] [ 13 ] [ 14 ] Disc herniation is reportedly the most common cause of CES, and it is thought that 1 to 2% of all surgical disc herniation cases result in CES. [ 12 ] [ 13 ]
CES is often concurrent with congenital or degenerative diseases and represents a high cost of care to those admitted to the hospital for surgery. [ 13 ] [ 26 ] Hospital stays generally last 4 to 5 days, and cost an average of $100,000 to $150,000. [ 26 ] Delays in care for cauda equina results in the English NHS paying about £23 million a year in compensation. [ 27 ]
Degenerative lumbosacral stenosis (DLSS), also known as cauda equina syndrome, is a pathologic degeneration in the lumbosacral disk in dogs. DLSS affects the articulation, nerve progression, and tissue and joint connections of the disk. [ 28 ] [ 29 ] This degeneration causes compressions in soft tissues and nerve root locations in the caudal area of the medulla , causing neuropathic pain in the lumbar vertebrae . [ 30 ] [ 31 ]
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In law, medicine, and statistics, cause of death is an official determination of the conditions resulting in a human 's death , which may be recorded on a death certificate . A cause of death is determined by a medical examiner . In rare cases, an autopsy needs to be performed by a pathologist. The cause of death is a specific disease or injury , in contrast to the manner of death , which is a small number of categories like "natural", " accident ", " suicide ", and " homicide ", each with different legal implications. [ 1 ]
International Classification of Disease (ICD) codes can be used to record manner and cause of death in a systematic way that makes it easy to compile statistics and more feasible to compare events across jurisdictions. [ 2 ]
A study published in Preventing Chronic Disease found that only one-third of New York City resident physicians reported believing that the present system of documentation was accurate. Half reported the inability to record "what they felt to be the correct cause of death", citing reasons such as technical limitation and instruction to "put something else". Nearly four-fifths reported being unaware that determinations of "probable", "presumed", or "undetermined" could be made, and fewer than three percent reported ever updating a death certificate when conflicting lab results or other new information became available, and cardiovascular disease was indicated as "the most frequent diagnosis inaccurately reported". [ 3 ]
Causes of death are sometimes disputed by relatives or members of the public, particularly when some degree of uncertainty or ambiguity exists in relation to the cause of death. On occasion, such disputes may result from, or sometimes instigate, a conspiracy theory .
Public perception of the relative risk of death by various causes is biased by personal experience and by media coverage. The phrase " hierarchy of death " is sometimes used to describe the factors that cause some deaths to get more attention than others.
Though some opponents of abortion consider it a cause of death, conventionally medical authorities do not confer personhood on fetuses that are not viable outside the womb, and thus abortions are not reported as deaths in these statistics. [ 4 ]
Health departments discourage listing " old age " as the cause of death because doing so does not benefit public health or medical research . [ 5 ] Aging is not a scientifically recognized cause of death; it is currently considered that there is always a more direct cause (although it may be unknown in certain cases and could be one of a number of aging-associated diseases ). As an indirect or non-determinative factor, biological aging is the biggest contributor to deaths worldwide. It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. [ 6 ] In industrialized nations the proportion is much higher, reaching 90%. [ 6 ] In recent years, there have been official claims about a possibility of recognizing aging itself as a disease . [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] If this would be so, the situation would change.
There are also popular notions that someone can be " scared to death" or die of loneliness or heartbreak . Experiencing fear, extreme stress, or both can cause changes in the body that can, in turn, lead to death. For example, it is possible that overstimulation of the vagus nerve —which decreases heart rate in a mechanism related to the behavior of apparent death (also known as "playing dead" and "playing possum")—is the cause of documented cases of psychogenic death . The flight or fight response to fear or stress has the opposite effect, increasing heart rate through stress hormones , and can cause cardiovascular problems (especially in those with pre-existing conditions). This is the proposed mechanism for the observed increase in the death rate due to cardiac arrest after widely experienced acutely stressful events such as terrorism, military attacks, and natural disasters (even among those who are not in the affected area) and for documented deaths in muggings and other frightening events which caused no traumatic physical harm. [ 12 ] [ 13 ] The proximal medical cause of death in these cases is likely to be recorded as cardiac failure or vagal inhibition (which also has other potential causes such as blows to certain parts of the body and nerve injuries). [ 14 ]
One specific condition observed to result from acute stress, takotsubo cardiomyopathy , is nicknamed "broken heart syndrome", but the stress need not be relationship-related and need not be negative. [ 15 ]
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The cause of obsessive–compulsive disorder is understood mainly through identifying biological risk factors that lead to obsessive–compulsive disorder (OCD) symptomology. The leading hypotheses propose the involvement of the orbitofrontal cortex , basal ganglia , and/or the limbic system , with discoveries being made in the fields of neuroanatomy, neurochemistry, neuroimmunology, neurogenetics, and neuroethology.
Many different types of medication can create/induce OCD in patients that have never had symptoms before. A new chapter about OCD in the DSM-5 (2013) now specifically includes drug-induced OCD. [ citation needed ]
Atypical antipsychotics (second generation antipsychotics), such as olanzapine (Zyprexa), have been proven to induce de-novo OCD in patients. [ 1 ] [ 2 ] [ 3 ] [ 4 ]
Although there has been substantial debate regarding the assessment of OCD, current research has gravitated toward structural and functional neuroimaging . These technological innovations have provided a better understanding of the neuroanatomical risk factors of OCD. These studies can be divided into four basic categories: (1) resting studies that compare brain activity at rest in patients with OCD to controls, (2) symptom provocation studies that compare brain activity before and after incitement of symptoms, (3) treatment studies that compare brain activity before and after treatment with pharmacotherapy , and (4) cognitive activation studies that compare brain activity while performing a task in patients with OCD to controls. [ 5 ]
Data obtained from this research suggests that three brain areas are involved with OCD: the orbitofrontal cortex (OFC), the anterior cingulate cortex (ACC), and the head of the caudate nucleus . [ 5 ] Several studies have found that in patients with OCD, these areas: (1) are hyperactive at rest relative to healthy control; (2) become increasingly active with symptom provocation; and (3) no longer exhibit hyperactivity following successful treatment with SRI pharmacotherapy or cognitive-based therapy. [ 6 ] This understanding is frequently cited as evidence that abnormality in these neuroanatomical regions may cause OCD.
The OFC and ACC are intricately connected to the basal ganglia via the Cortico-basal ganglia-thalamo-cortical loop . [ 7 ] Current theories suggest that OCD may be the result of an imbalance between the "direct" and "indirect" pathways through the basal ganglia. The direct pathways are described as running from the cortex to the striatum, then to the globus pallidus internal segment (GPi) and substantia nigra pars reticulate (SNr), then to the thalamus, and finally back to the cortex. The indirect pathways are described as running from the cortex to the striatum, then to the globus pallidus external segment (GPe), the subthalamic nucleus (STN), the GPi and SNr, then thalamus, and finally back to the cortex. [ 8 ] While the net effect of the direct pathway is excitatory, the net effect of the indirect pathway is inhibitory. Thus, it has been hypothesized that excessive relative activity in the direct pathway in OFC/ACC CBGTC loops may result in a positive feedback loop whereby obsessive thoughts are trapped. [ 8 ]
Recent studies suggest that OCD is also associated with reduced functional connectivity between the cerebellum and the cortico-striato-thalamo-cortical (CSTC) circuit, indicating a potential role of cerebellar dysfunction in its pathophysiology. [ 9 ]
Although structural and functional neuroimaging studies have provided a strong basis for this supposition, it is still unclear why patients with OCD develop specific obsessions instead of a generalized obsessive behavior towards everything. While researchers have suggested that a response bias exists toward particular stimuli, such as contamination, the underlying cause is still unclear. [ 10 ]
While there seems to be a ubiquitous understanding that neurochemical functioning is responsible for mediating the symptoms of OCD, recent psychopharmacologic studies have found that the serotonin (5-HT) neurotransmitter system plays a particularly critical role. [ 11 ] In comparison to healthy controls, the long-term administration of selective serotonin reuptake inhibitors (SSRIs) have been found to be more effective than noradrenergic reuptake inhibitors in the treatment of OCD. [ 11 ] For example, Rapoport et al. demonstrated that clomipramine was more effective than desipramine in decreasing several types of repetitive behavior. [ 12 ] Research has also shown that the administration of 5-HT antagonists often exacerbates symptoms of OCD. [ 13 ] If this were to be true, one would expect mirtazapine (which among others is a 5-HT 2A receptor antagonist) and atypical antipsychotics that also have antagonistic effects at this receptor to attenuate the effect of SSRIs. Clinical studies with these drugs, however, have shown the opposite. Mirtazapine , although not effective by itself, has been shown to hasten the effect of paroxetine (Pallanti et al., 2004), and several studies have shown that atypical antipsychotics augment the effects of SSRIs in refractory OCD patients (Bloch et al., 2006). [ 14 ] While these findings do not provide an explicit cause, they do set the stage for the notion that psychiatric conditions can be dissected pharmacologically. Thus, the efficacy in controlling obsessions and compulsions with SSRIs suggests that OCD has an underlying neurochemical etiology.
Dopaminergic systems are implicated in OCD by the efficacy of dopaminergic agents and by various neuroimaging studies. [ 15 ] OCD may be treated with antipsychotic agents, however psychostimulants agents have also shown some promise in alleviating the symptoms of OCD. [ 16 ] Although these need to be reconciled, they both implicate the dopaminergic systems. OCD also has a high comorbidity with ADHD, [ 17 ] which is treated with psychostimulants and may result from increased phasic and decreased tonic signaling of dopaminergic neurons. PANDAS also affects the basal ganglia, where dopamine plays a large role as a neurotransmitter.
The controversial PANDAS hypothesis suggests that neuroimmunological post-streptococcal autoimmunity may be a potential environmental cause of childhood onset OCD. [ 18 ] [ 19 ] [ 20 ] [ 21 ] Following a streptococcal infection, a subgroup of children expressed sudden onset of OCD symptom exacerbations. The primary hypothesis of PANDAS and the broader PANS is that OCD may develop as a consequence of an autoimmune reaction in which antibodies to streptococcal infections attack and damage the basal ganglia. [ 19 ]
Obsessions and compulsions are also very common in several other medical conditions, including: Tourette syndrome , Parkinson disease , epilepsy , schizophrenia , Huntington disease , encephalitis lethargica , Sydenham chorea , and damage to specific brain regions. [ 22 ] Similar to OCD, these disorders also exhibit abnormalities in the basal ganglia. This portion of the brain is responsible for mediating cognition, emotion, and movement. Disruption of the basal ganglia results in a host of symptoms that are characterized by compulsivity (behavioral patterns that are released repeatedly) and impulsivity (behavioral patterns that are released suddenly by various stimuli). [ 5 ] This suggests that in patients with OCD, the disorder may be the result of abnormal functioning of the basal ganglia.
Twin studies [ 23 ] and family association studies have demonstrated that there are definite genetic factors underlying obsessive–compulsive disorder. The majority of family association studies demonstrated that at least some forms of OCD are familial. The rate of OCD among relatives of affected individuals was significantly higher than the estimated population prevalence of OCD and the rate among controls. Relatives of adults with OCD were approximately two times more likely to be affected than the controls, while relatives of children and adolescents with OCD were about ten times more likely to have OCD as well. [ 24 ] However, that familial association could also have been caused by cultural or environmental factors. [ 25 ] Currently, there have been very few studies investigating the environmental factors behind OCD. However, in a retrospective study of environmental risk factors, researchers found that prolonged labor and edema during pregnancy were correlated to OCD, [ 26 ] suggesting that the environment plays some role in determining its manifestation.
As a result, twin studies were performed to show that the symptoms of OCD are heritable and thus genetically related. [ 23 ] Monozygotic, or identical, twins share 100% of their genes, while dizygotic, or fraternal, twins share on average 50% of their genes. The classic twin study compares monozygotic and dizygotic twins. If the monozygotic twins resemble each other much more closely than the dizygotic twins, then it is likely that genetics play a strong role in the development of the trait of interest. These studies showed that the genetic influences on obsessive-compulsive symptoms were 45 to 65% in children. The influence was less in adults, ranging from 27 to 47%. [ 23 ] However, the results of the studies are complicated by the fact that the presence of individuals with OCD in the sample were frequently low. As a result, researchers oftentimes included individuals with obsessive-compulsive symptoms or subclinical OCD. [ 25 ] By doing so, they possibly included subjects with other, related disorders. Early twin studies were replicated later using twins with OCD meeting DSM criteria and ascertainment of probands , but only a few have been performed. [ 23 ]
Early onset OCD, manifesting in childhood or adolescence, is a subtype of OCD etiologically distinct from adult onset OCD. This early onset OCD is reported to be genetically related to tic disorders and Tourette syndrome , as one study has found that patients with early onset OCD have a higher rate of Tourette's and other tic disorders. [ 26 ] Family association studies [ 27 ] have suggested that early onset OCD is correlated to increased familial and possibly genetic risk. The rate of OCD and subclinical OCD among relatives of probands whose OCD manifested in childhood or adolescence was at least twice as high as the rate among relatives of probands whose OCD manifested in adulthood. [ 27 ] Other studies have also indicated that there is an inverse relationship between the age of onset of the proband and the risk of OCD in relatives. [ 28 ] GWAS studies suggest that due to the nature of childhood disorders consisting of multiple small effects originating from multiple genes, OCD is considered a polygenic disorder. [ 29 ] Consequently, it is possible that there are different genetic mechanisms behind the two types of OCD; therefore, it may be necessary to control for age of onset when examining candidate genes.
It is likely that a number of genes are important to the development of OCD. Some of those candidate genes have been identified but none of the candidate gene studies have been consistently replicated except those relating to the glutamate transporter gene, SLC1A1 (solute carrier family 1, member 1), which codes for the glutamate transporter , EAAC1. [ 25 ] It has been suggested that the difficulties in identifying candidate genes may be related to the fact that most gene research has ignored environmental factors.[9] Consequently, it may be necessary to develop models for the interaction between genetic and environmental factors for certain subtypes of OCD to further genetic research. Three genome-wide association studies of OCD have also been completed, which have suggested potential regions of interest, including the region containing SLC1A1, 9p24. [ 25 ] SLC1A1 is expressed in the cortex, striatum, and thalamus (the cortico-striato-thalamocortical circuit) and is related to glutamate neurotransmission. [ 30 ] Neuroimaging, candidate gene, and animal model studies have provided evidence linking SLC1A1 and glutamate signaling to the occurrence of OCD. Neuroimaging studies have found that caudate glutamatergic concentrations are lower in the anterior cingulate and higher in the caudate in early onset OCD patients compared to controls, suggesting that glutamate transport (and in turn, the glutamate transporter gene SLC1A1) is related to the onset of OCD. [ 31 ]
Single nucleotide polymorphisms (SNPs) in the gene SLC1A1 have consistently been found to be related to OCD. In addition to glutamate transport, EAAC1, the transporter coded by SLC1A1, has also been linked to GABA synthesis, which could promote susceptibility to OCD. An initial study demonstrated a significant association between OCD and 3 linked polymorphisms in the SLC1A1 gene. [ 32 ] This result has been replicated in numerous studies. One study tested for four SNPs in the SLC1A1 gene in individuals with early-onset OCD in a Han Chinese population [ 33 ] and found that one SNP, rs10491734, was significantly more frequent in OCD patients than in controls. However, the exact SNPs identified in the different studies vary, though it is possible that this is because the studies were conducted on different ethnic populations. [ 33 ] For example, a family-based association study analyzed the instances of SNPs in and around SLC1A1 in families from throughout the US and found that a different SNP, rs4740788, and a 3-SNP haplotype, rs4740788-rs10491734-rs10491733, were both related to OCD. [ 34 ]
Several mouse models have been developed for the study of obsessive–compulsive disorder. Model organisms are useful for allowing aspects of some psychiatric disorders in one species (in this case, humans) to be explored in other species (in this case, mice). Notably, SLC1A1 null mice demonstrated compulsive behaviors by exhibiting increased aggression and excessive self-grooming resulting in fur loss. However, since these were only two behaviors loosely linked to OCD, this did not provide strong evidence for the relation between the loss of EAAC1 and OCD-like behaviors. Given the strong correlation between the gene SLC1A1 and OCD, this suggests that the lack of EAAC1 only results in OCD-like behaviors when it is combined with other rare mutations in genes related to the CSTC, or cortico-striato-thalamocortical, circuit. [ 35 ]
The vast monolith of psychiatric research has placed an emphasis on proximate mechanisms as the cause for illness. In contrast, evolutionary theory has engendered questions regarding how distal mechanisms may be implicated with pathogenesis. OCD involves several behavioral schemata that may have been preserved over evolutionary history. Numerous species have inherited cognitive patterns that lend to checking for danger, avoiding contamination, and hoarding food. [ 36 ] Theorists have hypothesized that a dysfunction in any of these strategies could lead to the expression of OCD. This conjecture is further supported by evidence that such inherited, species-specific strategies are stored in the basal ganglia. [ 5 ]
When considering the expression of OCD in non-human species, researchers have studied acral lick dermatitis (also known as lick granuloma ) in large canines. This disorder is characterized by excessive licking or scratching that leads to alopecia (hair loss) and subsequent granulomatous lesions (vascular tissue on the surface of a wound). [ 12 ] Rapoport et al. found that this obsessive-compulsive behavior was alleviated in canines after administering clomipramine. [ 12 ] Thus, it is conceivable that evolutionary selected traits could become maladaptive proceeding neurological dysfunction.
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Causes and origins of Tourette syndrome have not been fully elucidated. Tourette syndrome (abbreviated as Tourette's or TS) is an inherited neurodevelopmental disorder that begins in childhood or adolescence, characterized by the presence of multiple motor tics and at least one phonic tic, which characteristically wax and wane. Tourette's syndrome occurs along a spectrum of tic disorders , which includes transient tics and chronic tics. [ 1 ] [ 2 ]
The exact cause of Tourette's is unknown, but it is well established that both genetic and environmental factors are involved. [ 3 ] The overwhelming majority of cases of Tourette's are inherited, although the exact mode of inheritance is not yet known, [ 4 ] and no gene has been identified. [ 5 ] Tics are believed to result from dysfunction in the thalamus , basal ganglia , and frontal cortex of the brain, [ 3 ] involving abnormal activity of the brain chemical, or neurotransmitter , dopamine . In addition to dopamine, multiple neurotransmitters, like serotonin, GABA, glutamate, and histamine (H3-receptor) , are involved. [ 6 ]
Non-genetic factors—while not causing Tourette's—can influence the severity of the disorder. Some forms of Tourette's may be genetically linked to obsessive-compulsive disorder (OCD), while the relationship between Tourette's and attention-deficit hyperactivity disorder (ADHD) is not yet fully understood.
The exact cause of Tourette's is unknown, but it is well established that both genetic and environmental factors are involved. [ 7 ] [ 8 ] [ 9 ] Genetic epidemiology studies have shown that Tourette's is highly heritable, [ 10 ] and 10 to 100 times more likely to be found among close family members than in the general population. [ 11 ] The exact mode of inheritance is not known; no single gene has been identified, and hundreds of genes are likely involved. [ 10 ] [ 11 ] [ 12 ] Genome-wide association studies were published in 2013 [ 13 ] and 2015 [ 8 ] in which no finding reached a threshold for significance. [ 13 ] Twin studies show that 50 to 77% of identical twins share a TS diagnosis, while only 10 to 23% of fraternal twins do. [ 7 ] But not everyone who inherits the genetic vulnerability will show symptoms. [ 14 ] [ 15 ] A few rare highly penetrant genetic mutations have been found that explain only a small number of cases in single families (the SLITRK1 , HDC , and CNTNAP2 genes). [ 16 ]
In some cases, tics may not be inherited; these cases are identified as "sporadic" Tourette syndrome (also known as tourettism ) because a genetic link is missing. [ 17 ]
A person with Tourette syndrome has about a 50% chance of passing the gene(s) to one of their children. Gender appears to have a role in the expression of the genetic vulnerability, with males more likely to express tics than females. [ 5 ] Tourette syndrome is a condition of incomplete penetrance , meaning not everyone who inherits the genetic vulnerability will show symptoms. Tourette's also shows variable expression —even family members with the same genetic makeup may show different levels of symptom severity. The gene(s) may express as Tourette syndrome, as a milder tic disorder (transient or chronic tics), or as obsessive compulsive symptoms with no tics at all. [ 18 ] Only a minority of the children who inherit the gene(s) will have symptoms severe enough to require medical attention. [ 19 ] There is currently no way to predict the symptoms a child may display, even if the gene(s) are inherited.
Recent research suggests that a small number of Tourette syndrome cases may be caused by a defect on chromosome 13 of gene SLITRK1 . Some cases of tourettism (tics due to reasons other than inherited Tourette's syndrome) can be caused by mutation . [ 17 ] The finding of a chromosomal abnormality appears to apply to a very small minority of cases (1–2%).
The exact mechanism affecting the inherited vulnerability has not been established, and the precise cause of Tourette syndrome is not known. Tics are believed to result from dysfunction in the central nervous system , [ 20 ] in the cortical and subcortical regions, the thalamus , basal ganglia , and frontal cortex of the brain. [ 3 ] Neuroanatomic models implicate failures in circuits connecting the brain's cortex and subcortex, [ 5 ] and imaging techniques implicate the basal ganglia and frontal cortex. [ 21 ] [ 22 ] [ 23 ] Research presents considerable evidence that abnormal activity of the brain chemical, or neurotransmitter , dopamine is involved. [ 24 ] Dopamine excess or supersensitivity of the postsynaptic dopamine receptors may be an underlying mechanism of Tourette syndrome. [ 25 ] [ 26 ] [ 27 ] [ 28 ]
Multiple neurotransmitters, like histamine (H3R), dopamine, serotonin, GABA and glutamate are involved in the etiology. [ 6 ] After 2010, the central role of histamine ( H3-receptor in the basal ganglia) came into focus in the pathophysiology of Tourette syndrome. [ 29 ] The striatum is the main input nucleus of the basal ganglia circuit in the disorder, which is linked to the involvement of the histaminergic H3-receptor. [ 30 ]
Psychosocial or other non-genetic factors—while not causing Tourette's—can affect the severity of TS in vulnerable individuals and influence the expression of the inherited genes. [ 31 ] [ 5 ] [ 9 ] [ 11 ] Pre-natal and peri-natal events increase the risk that a tic disorder or comorbid OCD will be expressed in those with the genetic vulnerability. These include paternal age; forceps delivery ; stress or severe nausea during pregnancy; and use of tobacco , caffeine, alcohol , [ 31 ] and cannabis during pregnancy. [ 13 ] Babies who are born premature with low birthweight , or who have low Apgar scores , are also at increased risk; in premature twins, the lower birthweight twin is more likely to develop TS. [ 31 ]
Autoimmune processes may affect the onset of tics or exacerbate them. Both OCD and tic disorders are hypothesized to arise in a subset of children as a result of a post- streptococcal autoimmune process. [ 32 ] Its potential effect is described by the controversial hypothesis called PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), which proposes five criteria for diagnosis in children. [ 33 ] [ 34 ] [ 35 ] PANDAS and the newer PANS (pediatric acute-onset neuropsychiatric syndrome) hypotheses are the focus of clinical and laboratory research, but remain unproven. There is also a broader hypothesis that links immune-system abnormalities and immune dysregulation with TS. [ 8 ] [ 32 ]
Some forms of OCD may be genetically linked to Tourette's, [ 36 ] although the genetic factors in OCD with and without tics may differ. [ 7 ] The genetic relationship of ADHD to Tourette syndrome, however, has not been fully established. [ 37 ] [ 38 ] [ 39 ] A genetic link between autism and Tourette's has not been established as of 2017. [ 40 ]
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Parkinson's disease (PD) is a complicated neurodegenerative disease that progresses over time and is marked by bradykinesia (Slowed movements), tremor (rhythmic shaking), and stiffness. As the condition worsens, some patients may also experience postural instability where one finds it difficult to balance and maintain upright posture. [ 1 ] Parkinson's disease (PD) is primarily caused by the gradual degeneration of dopaminergic neurons (which produces chemical messenger Dopamine in the brain) in the region known as the substantia nigra along with other monoaminergic cell groups throughout the brainstem , [ 2 ] increased activation of microglia , and the build-up of Lewy bodies (clumps of proteins in the brain) and Lewy neurites, which are proteins found in surviving dopaminergic neurons. [ 3 ]
Because the etiology of about 80% of PD cases is unknown, they are classified as idiopathic, whereas the other 20% are thought to be genetic. PD risk is increased by variations in the genetic mix of specific genes. [ 4 ] Research has indicated that the risk of Parkinson's disease (PD) is increased by mutations in the genes encoding leucine-rich repeat kinase 2 ( LRRK2 ), Parkinson's disease-associated deglycase ( PARK7 ), PRKN , PINK1 , or SNCA ( alpha-synuclein ). [ 5 ] [ 6 ]
Exposure to pesticides, metals, solvents , and other toxicants has been studied as a factor in the development of Parkinson's disease. [ 7 ]
Traditionally, Parkinson's disease has been considered a non-genetic disorder. However, around 15% of individuals with PD have a first-degree relative who has the disease. [ 8 ] At least 5–15% of cases are known to occur because of a mutation in one of several specific genes, transmitted in either an autosomal-dominant or autosomal-recessive pattern . [ 9 ]
Mutations in specific genes have been conclusively shown to cause PD. A large number of these genes are linked to translation . [ 10 ] [ 11 ] Genes which have been implicated in autosomal-dominant PD include PARK1 and PARK4, PARK5, PARK8, PARK11 and GIGYF2 and PARK13 which code for alpha-synuclein (SNCA), UCHL1, leucine-rich repeat kinase 2 ( LRRK2 or dardarin) (LRRK2 and Htra2 respectively [ 9 ] [ 12 ] Genes such as PARK2, PARK6, PARK7 and PARK9 which code for parkin (PRKN), PTEN-induced putative kinase 1 ( PINK1 ), DJ-1 and ATP13A2 respectively have been implicated in the development of autosomal-recessive PD [ 9 ] [ 13 ] [ 14 ] Furthermore, mutations in genes including those that code for SNCA, LRRK2 and glucocerebrosidase (GBA) have been found to be risk factors for sporadic PD [ 15 ] In most cases, people with these mutations will develop PD. With the exception of LRRK2, however, they account for only a small minority of cases of PD. [ 16 ] The most extensively studied PD-related genes are SNCA and LRRK2.
At least 11 autosomal dominant and nine autosomal recessive gene mutations have been implicated in the development of PD. The autosomal dominant genes include SNCA , PARK3 , UCHL1 , LRRK2 , GIGYF2 , HTRA2 , EIF4G1 , TMEM230 , CHCHD2 , RIC3 , and VPS35 . Autosomal recessive genes include PRKN , PINK1 , DJ-1 , ATP13A2 , PLA2G6 , FBXO7 , DNAJC6 , SYNJ1 , and VPS13C . Some genes are X-linked or have unknown inheritance pattern; those include USP24 , PARK12 , and PARK16 . A 22q11 deletion is known to be associated with PD. [ 17 ] [ 18 ] An autosomal dominant form has been associated with mutations in the LRP10 gene. [ 19 ] [ 20 ]
The role of the SNCA gene is significant in PD because the alpha-synuclein protein is the main component of Lewy bodies , which appear as a primary biomarker in the disease. [ 9 ] [ 21 ] Missense mutations of the gene (in which a single nucleotide is changed), and duplications and triplications of the locus containing it have been found in different groups with familial PD. [ 9 ] Level of alpha-synuclein expression correlates with disease onset and progression, with SNCA gene triplication advancing earlier and faster than duplication. [ 22 ] Missense mutations in SNCA are rare. [ 9 ] On the other hand, multiplications of the SNCA locus account for around 2% of familial cases. [ 9 ] Multiplications have been found in asymptomatic carriers , which indicate that penetrance is incomplete or age-dependent. [ 9 ]
The LRRK2 gene (PARK8) encodes for a protein called dardarin . The name dardarin was taken from a Basque word for tremor, because this gene was first identified in families from England and the north of Spain. [ 16 ] A significant number of autosomal-dominant Parkinson's disease cases are associated with mutations in the LRRK2 gene [ 23 ] Mutations in LRRK2 are the most common known cause of familial and sporadic PD, accounting for approximately 5% of individuals with a family history of the disease and 3% of sporadic cases. [ 9 ] [ 16 ] There are many different mutations described in LRRK2 , however unequivocal proof of causation only exists for a small number. [ 9 ] Mutations in PINK1 , PRKN , and DJ-1 may cause mitochondrial dysfunction, an element of both idiopathic and genetic PD. [ 22 ] Of related interest are mutations in the progranulin gene that have been found to cause corticobasal degeneration seen in dementia. [ 24 ] This could be relevant in PD cases associated with dementia . [ 24 ]
Mutations in GBA are known to cause Gaucher's disease . [ 9 ] Genome-wide association studies , which search for mutated alleles with low penetrance in sporadic cases, have now yielded many positive results. [ 25 ] Mendelian genetics are not strictly observed in GBA mutations found in inherited parkinsonism. [ 26 ] Incidentally, both gain-of-function and loss-of-function GBA mutations are proposed to contribute to parkinsonism through effects such as increased alpha-synuclein levels. [ 26 ] In patients with Parkinson's disease, the OR for carrying a GBA mutation was 5·43 (95% CI 3·89–7·57), confirming that mutations in this gene are a common risk factor for Parkinson's disease. [ 26 ]
may play a role in maintaining supply of synaptic vesicles in presynaptic terminals;
may regulate release of dopamine [ 30 ]
- Inactivating somatic mutations
- Frequent intragenic deletions
-Mostly point mutations
-Deletions on C-terminus Kinase domain
- Large deletion in L166P
Exposure to pesticides, metals, solvents , and other toxicants has been studied as a factor in the development of Parkinson's disease. [ 7 ] No definitive causal relationship has yet been established. Recent studies also reveal that individuals that sustain mild head injuries (concussions) also have an increased risk of acquiring the disease. [ 42 ] [ 43 ] As discussed below, exercise and caffeine consumption are known to help decrease the risks of acquisition.
Evidence from epidemiological , animal , and in vitro studies suggests that exposure to pesticides increases the risk for Parkinson's disease. [ 7 ] One meta-analysis found a risk ratio of 1.6 for ever being exposed to a pesticide, with herbicides and insecticides showing the most risk. [ 7 ] [ 44 ] Rural living, well-drinking, and farming were also associated with Parkinson's, which may be partly explained by pesticide exposure. [ 44 ] These factors are pertinent to many communities, one of them being South Asian populations. Organochlorine pesticides (which include DDT ) have received the most attention, with several studies reporting that exposure to such pesticides is associated with a doubling of risk for Parkinson's. [ 7 ]
Carbon disulfide is a risk factor, and has been identified in industrial worker case studies and has induced parkinsonism in mice. [ non-primary source needed ] [ 45 ] It is mainly used in the manufacture of viscose rayon, cellophane film, rubber and carbon tetrachloride. [ 46 ]
Lead , which was used in gasoline until 1995 and paint until 1978, is known to damage the nervous system in various ways. [ 7 ] A few studies have found that people with high levels of lead in their body had twice the risk of Parkinson's disease. [ 7 ] Epidemiological studies on lead, however, have found little evidence for a link with Parkinson's. [ 7 ] Iron has been implicated in the etiology of Parkinson's disease, but there is no strong evidence that environmental exposure to it is associated with Parkinson's. [ 7 ]
A 2012 study suggests that players in the National Football League are three times more likely to die from neurodegenerative diseases, including Alzheimer's and Parkinson's diseases, than the general US population. [ 43 ] A 2018 study found 56% increase in risk of Parkinson's disease among US military veterans suffered traumatic brain injury . [ 42 ]
While many environmental factors may exacerbate Parkinson's disease, exercise is considered to be one of the main protective factors for neurodegenerative disorders, including Parkinson's disease. The types of exercise interventions that have been studied can be categorized as either aerobic or goal-based. [ 47 ] Aerobic exercise includes physical activity that increases the heart rate. Aerobic exercise is beneficial to the overall brain through mechanisms that promote neuroplasticity, or the rewiring of the brain circuitry. [ 47 ] Goal-based exercises are often developed with the guidance of a physical therapist to use movement to improve motor task performance and enhance motor learning. [ 47 ] While exercise has consistently been shown to be beneficial, the optimal interventional benefit is still being researched. [ 48 ]
Smokers and nonsmokers with different rates of caffeine consumption were monitored for their susceptibility to PD. The results indicate that higher coffee/caffeine intake is associated with a significantly lower incidence of PD and that this effect appeared to be independent of smoking. [ 49 ]
Emerging research suggests that diet may influence the risk of developing Parkinson's. A 2023 study found that adherence to a Western dietary pattern—characterized by high consumption of red and processed meats, fried foods, high-fat dairy products, and refined grains—is associated with an increased risk of Parkinson's. [ 50 ] Individuals with the highest adherence to this dietary pattern had significantly higher odds—approximately seven times—of developing the disease. Conversely, diets rich in fruits, vegetables, whole grains, and lean proteins have been associated with a reduced risk of Parkinson's, potentially offering protective benefits. Further research is needed to establish causality and better understand the mechanisms underlying these associations.
The CYP2D6 gene is primarily expressed in the liver and is responsible for the enzyme cytochrome P450 2D6. A study showed that those who had a mutation of this gene and were exposed to pesticides were twice as likely to develop Parkinson's Disease; those that had the mutation and were not exposed to pesticides were not found to be at an increased risk of developing PD; the pesticides only had a "modest effect" for those without the mutation of the gene. [ 31 ] [ 51 ]
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Cancer pain can be caused by pressure on, or chemical stimulation of, specialised pain-signalling nerve endings called nociceptors ( nociceptive pain ), or by damage or illness affecting nerve fibers themselves ( neuropathic pain ). [ 1 ]
Infection of a tumor or its surrounding tissue can cause rapidly escalating pain, but is sometimes overlooked as a possible cause. One study [ 2 ] found that infection was the cause of pain in four percent of nearly 300 cancer patients referred for pain relief. Another report [ 3 ] described seven patients, whose previously well-controlled pain escalated significantly over several days. Antibiotic treatment produced pain relief in all patients within three days. [ 4 ]
Tumors can cause pain by crushing or infiltrating tissue, or by releasing chemicals that make nociceptors responsive to stimuli that are normally non-painful ( cf. allodynia ).
Between 40 and 80 percent of patients with cancer pain experience neuropathic pain. [ 1 ]
Brain
Meninges
Spinal cord compression
Nerve infiltration or compression
Dorsal root ganglion inflammation
Brachial plexopathy
Invasion of bone by cancer is the most common source of cancer pain. About 70 percent of breast and prostate cancer patients, and 40 percent of those with lung , kidney and thyroid cancers develop bone metastases . It is commonly felt as tenderness, with constant background pain and instances of spontaneous or movement-related exacerbation, and is frequently described as severe. Tumors in the marrow instigate a vigorous immune response which enhances pain sensitivity, and they release chemicals that stimulate nociceptors. As they grow, tumors compress, consume , infiltrate or cut off blood supply to body tissues, which can cause pain. [ 4 ] [ 8 ]
Fracture
Skull
Pain produced by cancer within the pelvis varies depending on the affected tissue, but it frequently radiates diffusely to the upper thigh, and may refer to the lumbar region. Lumbosacral plexopathy is often caused by recurrence of cancer in the presacral space , and may refer to the external genitalia or perineum . Local recurrence of cancer attached to the side of the pelvic wall may cause pain in one of the iliac fossae . Pain on walking that confines the patient to bed indicates possible cancer adherence to or invasion of the iliacus muscle . Pain in the hypogastrium (between the navel and pubic bone ) is often found in cancers of the uterus and bladder, and sometimes in colorectal cancer especially if infiltrating or attached to either uterus or bladder. [ 4 ]
Visceral pain is diffuse and difficult to locate, and is often referred to more distant, usually superficial, sites. [ 8 ]
Liver
Kidneys and spleen
Abdominal and urogenital hollow organs
Gastrointestinal
Respiratory system
Pancreas
Rectum
Carcinosis of the peritoneum may cause pain through inflammation, disordered visceral motility, or pressure of the metastases on nerves. Once a tumor has penetrated or perforated hollow viscera, acute inflammation of the peritoneum appears, inducing severe abdominal pain. Pleural carcinomatosis is normally painless. [ 10 ]
Invasion of soft tissue by a tumor can cause pain by inflammatory or mechanical stimulation of nociceptors, or destruction of mobile structures such as ligaments, tendons and skeletal muscles. [ 10 ]
Some diagnostic procedures, such as venipuncture , paracentesis , and thoracentesis can be painful. [ 12 ]
Lumbar puncture
Post-dural-puncture headache
Potentially painful cancer treatments include immunotherapy which may produce joint or muscle pain; radiotherapy, which can cause skin reactions, enteritis , fibrosis, myelopathy , bone necrosis , neuropathy or plexopathy ; chemotherapy, often associated with mucositis , joint pain , muscle pain , peripheral neuropathy and abdominal pain due to diarrhea or constipation; hormone therapy, which sometimes causes pain flares; targeted therapies, such as trastuzumab and rituximab , which can cause muscle, joint or chest pain; angiogenesis inhibitors like bevacizumab , known to sometimes cause bone pain; and surgery, which may produce post-operative pain, post-amputation pain or pelvic floor myalgia.
Chemotherapy may cause mucositis, muscle pain, joint pain, abdominal pain caused by diarrhea or constipation, and peripheral neuropathy [ 12 ]
Chemotherapy-induced peripheral neuropathy
Mucositis
Muscle and joint pain
Radiotherapy may affect the connective tissue surrounding nerves, and may damage or kill white or gray matter in the brain or spinal cord.
Fibrosis around the brachial or lumbosacral plexus
Spinal cord damage
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Causes of hearing loss include ageing , genetics , perinatal problems , loud sounds , and diseases . For some kinds of hearing loss the cause may be classified as of unknown cause .
There is a progressive loss of ability to hear high frequencies with ageing known as presbycusis . For men, this can start as early as 25 and for women at 30. Although genetically variable, it is a normal concomitant of ageing and is distinct from hearing loss caused by noise exposure, toxins, or disease agents. [ 1 ] Common conditions that can increase the risk of hearing loss in elderly people are high blood pressure, diabetes, or the use of certain medications harmful to the ear. [ 2 ] [ 3 ] While everyone loses hearing with age, the amount and type of hearing loss is variable. [ 4 ]
Noise exposure is the cause of approximately half of all cases of hearing loss, causing some degree of problems in 5% of the population globally. [ 5 ] The National Institute for Occupational Safety and Health (NIOSH) recognizes that the majority of hearing loss is not due to age, but due to noise exposure. By correcting for age in assessing hearing, one tends to overestimate the hearing loss due to noise for some and underestimate it for others. [ 6 ]
Hearing loss due to noise may be temporary, called a 'temporary threshold shift', a reduced sensitivity to sound over a wide frequency range resulting from exposure to a brief but very loud noise like a gunshot, firecracker, jet engine, jackhammer, etc. or exposure to loud sound over a few hours such as during a pop concert or nightclub session. [ 7 ] Recovery of hearing is usually within 24 hours but may take up to a week. [ 8 ] Both constant exposure to loud sounds (85 dB(A) or above) and one-time exposure to extremely loud sounds (120 dB(A) or above) may cause permanent hearing loss. [ 9 ]
Noise-induced hearing loss (NIHL) typically manifests as elevated hearing thresholds (i.e. less sensitivity or muting) between 3000 and 6000 Hz, centred at 4000 Hz. As noise damage progresses, damage spreads to affect lower and higher frequencies. On an audiogram , the resulting configuration has a distinctive notch, called a 'noise' notch. As ageing and other effects contribute to higher frequency loss (6–8 kHz on an audiogram), this notch may be obscured and entirely disappear.
Various governmental, industry, and standards organizations set noise standards. [ 10 ]
The U.S. Environmental Protection Agency has identified the level of 70 dB(A) (40% louder to twice as loud as normal conversation; typical level of TV, radio, stereo; city street noise) for 24‑hour exposure as the level necessary to protect the public from hearing loss and other disruptive effects from noise, such as sleep disturbance, stress-related problems, learning detriment, etc. [ 11 ] Noise levels are typically in the 65 to 75 dB (A) range for those living near airports or freeways and may result in hearing damage if sufficient time is spent outdoors. [ 12 ]
Louder sounds cause damage in a shorter period of time. Estimation of a "safe" duration of exposure is possible using an exchange rate of 3 dB. As 3 dB represents a doubling of the intensity of sound, the duration of exposure must be cut in half to maintain the same energy dose. For workplace noise regulation, the "safe" daily exposure amount at 85 dB A, known as an exposure action value , is 8 hours, while the "safe" exposure at 91 dB(A) is only 2 hours. [ 13 ] Different standards use exposure action values between 80 dBA and 90 dBA. Note that for some people, sound may be damaging at even lower levels than 85 dB A. Exposures to other ototoxicants (such as pesticides, some medications including chemotherapy agents, solvents, etc.) can lead to greater susceptibility to noise damage, as well as causing its own damage. This is called a synergistic interaction. Since noise damage is cumulative over long periods, persons who are exposed to non-workplace noise, like recreational activities or environmental noise, may have compounding damage from all sources.
Some national and international organizations and agencies use an exchange rate of 4 dB or 5 dB. [ 14 ] While these exchange rates may indicate a wider zone of comfort or safety, they can significantly underestimate the damage caused by loud noise. For example, at 100 dB (nightclub music level), a 3 dB exchange rate would limit exposure to 15 minutes; the 5 dB exchange rate allows an hour.
Many people are unaware of the presence of environmental sound at damaging levels, or of the level at which sound becomes harmful. Common sources of damaging noise levels include car stereos, children's toys, motor vehicles, crowds, lawn and maintenance equipment, power tools, gun use, musical instruments, and even hair dryers. Noise damage is cumulative; all sources of damage must be considered to assess risk. If one is exposed to loud sound (including music) at high levels or for extended durations (85 dB A or greater), then hearing loss will occur. Sound intensity (sound energy or propensity to cause damage to the ears) increases dramatically with proximity according to an inverse square law: halving the distance to the sound quadruples the sound intensity.
In the US, 12.5% of children aged 6–19 years have permanent hearing damage from excessive noise exposure. [ 15 ] The World Health Organization estimates that half of those between 12 and 35 are at risk from using personal audio devices that are too loud. [ 16 ]
Hearing loss due to noise has been described as primarily a condition of modern society. [ 17 ] In preindustrial times, humans had far less exposure to loud sounds. Studies of primitive peoples indicate that much of what has been attributed to age-related hearing loss may be long-term cumulative damage from all sources, especially noise. People living in preindustrial societies have considerably less hearing loss than similar populations living in modern society. Among primitive people who have migrated into modern society, hearing loss is proportional to the number of years spent in modern society. [ 18 ] [ 19 ] [ 20 ] Military service in World War II , the Korean War , and the Vietnam War , has likely also caused hearing loss in large numbers of men from those generations, though proving that hearing loss was a direct result of military service is problematic without entry and exit audiograms. [ 21 ]
Hearing loss in adolescents may be caused by loud noises from toys, music by headphones, and concerts or events. [ 22 ] In 2017, the Centers for Disease Control and Prevention brought their researchers together with experts from the World Health Organization and academia to examine the risk of hearing loss from excessive noise exposure in and outside the workplace in different age groups, as well as actions being taken to reduce the burden of the condition. A summary report was published in 2018. [ 23 ]
In the United States, hearing loss may be more likely among members of the Republican Party due to greater firearm ownership, according to The Washington Post in February 2024. [ 24 ]
Hearing loss can be inherited. Around 75–80% of all these cases are inherited by recessive genes , 20–25% are inherited by dominant genes , 1–2% are inherited by X-linked patterns, and fewer than 1% are inherited by mitochondrial inheritance . [ 25 ]
When looking at the genetics of deafness, there are 2 different forms, syndromic and nonsyndromic . Syndromic deafness occurs when there are other signs or medical problems aside from deafness in an individual. This accounts for around 30% of deaf individuals who are deaf from a genetic standpoint. [ 25 ] Nonsyndromic deafness occurs when there are no other signs or medical problems associated with an individual other than deafness. From a genetic standpoint, this accounts for the other 70% of cases and represents the majority of hereditary hearing loss. [ 25 ] Syndromic cases occur with disorders such as Usher syndrome , Stickler syndrome , Waardenburg syndrome , Chudley-Mccullough syndrome , Alport's syndrome , and neurofibromatosis type 2 . These are diseases that have deafness as one of the symptoms or as a common feature associated with it. Many of the genetic mutations giving rise to syndromic deafness have been identified. In nonsyndromic cases, where deafness is the only finding, it is more difficult to identify the genetic mutation although some have been discovered.
A 2023 systematic review and meta-analysis found that alcohol consumption is associated with an increased risk of hearing loss. [ 35 ]
Some medications may reversibly affect hearing. These medications are considered ototoxic . This includes loop diuretics such as furosemide and bumetanide, non-steroidal anti-inflammatory drugs (NSAIDs) both over-the-counter (aspirin, ibuprofen, naproxen) as well as prescription (celecoxib, diclofenac, etc.), paracetamol, quinine , and macrolide antibiotics . The link between NSAIDs and hearing loss tends to be greater in women, especially those who take ibuprofen six or more times a week. [ 36 ] Others may cause permanent hearing loss. [ 37 ] The most important group is the aminoglycosides (main member gentamicin ) and platinum based chemotherapeutics such as cisplatin and carboplatin . [ 38 ] [ 39 ]
In 2007, the U.S. Food and Drug Administration (FDA) warned about possible sudden hearing loss from PDE5 inhibitors , which are used for erectile dysfunction. [ 40 ]
Audiologic monitoring for ototoxicity allows for the early detection of changes to hearing status presumably attributed to a drug/treatment regime so that changes in the drug regimen may be considered, and audiologic intervention when handicapping hearing impairment has occurred. [ 41 ] Co-administration of anti-oxidants and ototoxic medications may limit the extent of the ototoxic damage. [ 42 ] [ 43 ]
In addition to medications, hearing loss can also result from specific chemicals in the environment: metals, such as lead ; solvents , such as toluene (found in crude oil , gasoline , [ 44 ] and automobile exhaust , [ 44 ] for example); and asphyxiants . [ 45 ] Combined with noise, these ototoxic chemicals have an additive effect on a person's hearing loss. [ 45 ]
Hearing loss due to chemicals starts in the high-frequency range and is irreversible. It damages the cochlea with lesions and degrades central portions of the auditory system . [ 45 ] For some ototoxic chemical exposures, particularly styrene, [ 46 ] the risk of hearing loss can be higher than being exposed to noise alone. The effects are greatest when the combined exposure includes impulse noise . [ 47 ] [ 48 ]
A 2018 informational bulletin by the US Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH) introduces the issue, provides examples of ototoxic chemicals, lists the industries and occupations at risk and provides prevention information. [ 50 ]
Some medications may reversibly affect hearing. These medications are considered ototoxic . This includes loop diuretics such as furosemide and bumetanide, non-steroidal anti-inflammatory drugs (NSAIDs) both over-the-counter (aspirin, ibuprofen, naproxen) as well as prescription (celecoxib, diclofenac, etc.), paracetamol, quinine , and macrolide antibiotics . The link between NSAIDs and hearing loss tends to be greater in women, especially those who take ibuprofen six or more times a week. [ 36 ] Others may cause permanent hearing loss. [ 37 ] The most important group is the aminoglycosides (main member gentamicin ) and platinum based chemotherapeutics such as cisplatin and carboplatin . [ 38 ] [ 39 ]
In 2007, the U.S. Food and Drug Administration (FDA) warned about possible sudden hearing loss from PDE5 inhibitors , which are used for erectile dysfunction. [ 40 ]
Audiologic monitoring for ototoxicity allows for the early detection of changes to hearing status presumably attributed to a drug/treatment regime so that changes in the drug regimen may be considered, and audiologic intervention when handicapping hearing impairment has occurred. [ 41 ]
Co-administration of anti-oxidants and ototoxic medications may limit the extent of the ototoxic damage. [ 42 ] [ 43 ]
There can be damage either to the ear, whether the external or middle ear, to the cochlea, or to the brain centres that process the aural information conveyed by the ears. Damage to the middle ear may include fracture and discontinuity of the ossicular chain. Damage to the inner ear (cochlea) may be caused by temporal bone fracture . People who sustain head injury are especially vulnerable to hearing loss or tinnitus, either temporary or permanent. [ 51 ] [ 52 ]
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A mental disorder is an impairment of the mind disrupting normal thinking, feeling, mood, behavior, or social interactions , and accompanied by significant distress or dysfunction. [ 1 ] [ 2 ] [ 3 ] [ 4 ] The causes of mental disorders are very complex and vary depending on the particular disorder and the individual. Although the causes of most mental disorders are not fully understood, researchers have identified a variety of biological, psychological, and environmental factors that can contribute to the development or progression of mental disorders. [ 5 ] Most mental disorders result in a combination of several different factors rather than just a single factor. [ 6 ]
Risk factors for mental illness include psychological trauma , adverse childhood experiences, genetic predisposition, and personality traits. [ 7 ] [ 8 ] Correlations between mental disorders and substance use are also found to have a two way relationship, in that substance use can lead to the development of mental disorders and having mental disorders can lead to substance use/abuse. This effect is stronger and more reliable in some substance use than others, such as smoking. [ 9 ]
Mental illnesses have risk factors, for instance including unequal parental treatment, adverse life events and drug use in depression , migration and discrimination, childhood trauma, loss or separation in families, and cannabis use in schizophrenia and psychosis , and parenting factors, child abuse, family history (e.g. of anxiety), and temperament and attitudes (e.g. pessimism) in anxiety . Many psychiatric disorders include problems with impulse and other emotional control .
In February 2013, a study [ 10 ] found genetic links between five major psychiatric disorders: autism , ADHD , bipolar disorder , major depressive disorder , and schizophrenia . Abnormal functioning of neurotransmitter systems is also responsible for some mental disorders, including serotonin, norepinephrine, dopamine, and glutamate system's abnormal functioning. Differences have also been found in the size or activity of specific brain regions in some cases. Psychological mechanisms have also been implicated, such as cognitive (e.g. reasoning ) biases, emotional influences, personality dynamics , temperament , and coping style. Studies have indicated [ 11 ] that variation in genes can play an important role in the evolution of mental disorders, although the reliable identification of connections between specific genes and specific disorders has proven more difficult. Environmental events surrounding pregnancy (such as maternal hypertension , [ 12 ] preeclampsia , or infection) and birth have also been implicated. [ 13 ] Traumatic brain injury may increase the risk of developing certain mental disorders. Throughout the years, there have been inconsistent links found to certain viral infections, substance misuse, and general physical health that have been false.
Adverse experiences affect a person's mental health , including abuse , neglect , bullying , social stress , traumatic events , and other overwhelming life experiences. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality , lack of social cohesion, problems linked to migration , and features of particular societies and cultures . The loss of cultural connection can result in cultural bereavement . [ 14 ] Mental stress is a common cause of mental illnesses, so finding a coping solution to cope with mental stress would be beneficial. Many solutions that have helped reduce stress are yoga, exercise, and some medications that may help.
Several theories or models seek to explain the causes ( etiology ) of mental disorders . These theories may differ in regards to how they explain the cause of the disorder, how to treat the disorder, and how they classify mental disorders . Theories also differ about the philosophy of mind they accept; that is, whether the mind and brain are identical or not. [ citation needed ]
During most of the 20th century, mental illness was ascribable to problematic relationships between children and their parents. This view was held well into the late 1990s, in which people still believed this child-parent relationship was a large determinant of severe mental illness, such as depression and schizophrenia. In the 21st century, additional factors have been identified such as genetic contributions, though experience also plays a role. So, the perceived causes of mental illness have changed over time and will most likely continue to alter while more research develops throughout the years.
Outside the West, community approaches remain a focus. [ citation needed ]
A practical mixture of models will explain particular issues and disorders, although there may be difficulty defining boundaries for indistinct psychiatric syndromes .
An overall distinction is also commonly made between a "medical model" (also known as a biomedical or disease model) and a "social model" (also known as an empowerment or recovery model) of mental disorder and disability , with the former focusing on hypothesized disease processes and symptoms, along with latter focusing on hypothesized social constructionism and social contexts.
Biological psychiatry has tended to follow a biomedical model focused on organic or "hardware" pathology of the brain, [ 15 ] where many mental disorders are conceptualized as disorders of brain circuits shaped by a complex interplay of genetics and experience. [ 16 ]
The social and medical models of mental disorders each work to identify and study distinct aspects, solutions, and potential therapies of disorders. The intersection and cross reference between the two models can further be used to develop more holistic models of mental disorders. Many criticisms historically of each model is the exclusivity of the other perspective. Therefore, intersectional research improved the impact and importance of future findings. [ 17 ]
The primary model of contemporary mainstream Western psychiatry is the biopsychosocial model (BPS), which integrates biological, psychological, and social factors. [ 15 ] The Biopsychosocial model was first conceptualised by George Engel in 1977, [ 18 ] suggesting that to understand a person's medical condition it is not simply the biological factors to consider, but also the psychological and social factors . The biopsychosocial approach systematically considers biological, psychological, and social factors and their complex interactions in understanding health, illness, and health care delivery. Biological, psychological, and social factors exist along a continuum of natural systems. The factors within the model contain the following:
This model is commonly used for case conceptualization of psychological disorders as well as chronic pain, [ 19 ] with the view that the pain is a psychophysiological behavior pattern that cannot be categorised into biological, psychological, or social factors alone.
A related view, the diathesis-stress model , posits that mental disorders result from genetic dispositions and environmental stressors, combining to cause patterns of distress or dysfunction. [ 20 ] The model is one way to explain why some individuals are more vulnerable to mental disorders than others. Additionally, it explains why some people may develop a mental disorder after exposure to stressful life events while others do not.
Psychoanalytic theories focus on unresolved internal and relational conflicts. These theories have been predicated as explanations of mental disorders. Many psychoanalytic groups are said to adhere to the biopsychosocial model and to accept an eclectic mix of subtypes of psychoanalysis. Sigmund Freud developed the psychoanalytic theory. This theory focuses on the impact of unconscious forces on human behavior. According to Freud, a personality has three parts: the id , ego , and superego . The id operates under the pleasure principle , the ego operates under the reality principle , and the superego is the "conscience" and incorporates what is and is not socially acceptable into a person's value system. [ 21 ] According to the psychoanalytic theory, there are five stages of psychosexual development that everyone goes through the oral stage , anal stage , phallic stage , latency stage , and genital stage . Mental disorders can be caused by an individual receiving too little or too much gratification in one of the psychosexual developmental stages. When this happens, the individual is said to be in that developmental stage. [ 22 ]
Attachment theory is a kind of evolutionary-psychological approach sometimes applied in the context of mental disorders, which focuses on the role of early caregiver-child relationships, responses to danger, and the search for a satisfying reproductive relationship in adulthood. According to this theory, a child's attachment is to a nurturing adult, the more likely that child will maintain healthy relationships with others in their life. [ 23 ] As found by the Strange Situation experiment run by Mary Ainsworth based on the formulations of John Bowlby , there are four patterns of attachment: secure attachment , avoidant attachment , disorganized attachment , and ambivalent attachment . [ 24 ] Later research found the fourth pattern of attachment is known as disorganized disoriented attachment . [ 25 ] Secure attachments reflect trust in the child-caretaker relationship while insecure attachment reflects mistrust. The security of attachment in a child affects the child's emotional, cognitive, and social competence later in life. [ 24 ]
Evolutionary psychology and evolutionary psychiatry posit that mental disorders involve the dysfunctional operation of mental modules adapted to ancestral physical or social environments but not necessarily to modern ones. Behavioral abnormalities that resemble human mental illness have been found in related species ( great apes ).
Other theories suggest that mental illness could have evolutionary advantages for the species, including enhancing creativity [ 26 ] and stress to enhance survival by activating the flight-or-fight response in anticipation of danger.
Mania and depression could have benefited from seasonal changes by helping to increase energy levels during times of plenty and rejuvenating energy during times of scarcity. In this way, mania was set in motion during the spring and summer to facilitate energy for hunting; depression worked best during the winter, similar to how bears hibernate to recover their energy levels. [ 27 ] This may explain the connection between circadian genes and Bipolar Disorder and explain the relationship between light and seasonal affective disorder .
Biological factors consist of anything physical that can cause adverse effects on a person's mental health. Biological factors include genetics, prenatal damage, infections, exposure to toxins, brain defects or injuries, and substance abuse. Many professionals believe that the cause of mental disorders is the biology of the brain and the nervous system. [ citation needed ]
Mind mentions genetic factors, long-term physical health conditions, and head injuries or epilepsy (affecting behavior and mood) as factors that may trigger an episode of mental illness.
Some rare mental disorders are caused only by genetics such as Huntington's disease .
Family linkage and some twin studies have indicated that genetic factors often play a role in the heritability of mental disorders. The reliable identification of specific genetic variation can cause indication of higher risk to particular disorders, through linkage , Genome Wide Association Scores [ 28 ] or association studies , has proven difficult. This is due to the complexity of interactions between genes, environmental events, and early development or the need for new research strategies. No specific gene results in a complex trait disorder, but specific variations of alleles result in higher risk for a trait. The heritability of behavioral traits associated with a mental disorder may be in permissive than in restrictive environments, and susceptibility genes probably work through both "within-the-skin" (physiological) pathways and "outside-the-skin" (behavioral and social) pathways. Investigations increasingly focus on links between genes and endophenotypes because they are more specific traits. Some include neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive, or neuropsychological, rather than disease categories. Concerning a well-known mental disorder, schizophrenia , it is said with certainty [ by whom? ] that alleles (forms of genes) were responsible for this disorder. Some research has indicated only multiple, rare mutations are thought to alter neurodevelopmental pathways that can ultimately contribute to schizophrenia; virtually every rare structural mutation was different in each individual. [ citation needed ]
Research has shown that many conditions are polygenic meaning there are multiple defective genes rather than only one that is responsible for a disorder, and these genes may also be pleiotropic meaning that they cause multiple disorders, not just one. [ 29 ] Schizophrenia and Alzheimer's are both examples of hereditary mental disorders. [ citation needed ] When exonic genes encode for proteins, these proteins do not just affect one trait. The pathways that contribute to complex traits and phenotypes interact with multiple systems, even though proteins have specific functions. [ 30 ] brain plasticity (neuroplasticity) raises questions of whether some brain differences may be caused by mental illnesses or by pre-existing and then causing them.
Literature reviews published in Biological Psychiatry and in Molecular Psychiatry h ave found the average heritability estimate of ADHD to be from 0.74 to 0.8, based on family , twin studies , and adoption studies . [ 31 ] [ 32 ] Additionally, evolutionary psychiatrist Randolph M. Nesse has argued that the 5:1 male-to-female sex ratio in the epidemiology of ADHD suggests that ADHD may be the end of a continuum where males are overrepresented at the tails , citing clinical psychologist Simon Baron-Cohen 's suggestion for the sex ratio in the epidemiology of autism as an analogue. [ 33 ] [ 34 ] [ 35 ]
Natural selection has been acting against the genetic variants for ADHD over the course of at least 45,000 years, indicating that it was not an adaptive trait in ancient times. [ 36 ] The disorder may remain at a stable rate by the balance of genetic mutations and removal rate (natural selection) across generations; over thousands of years, these genetic variants become more stable, decreasing disorder prevalence. [ 37 ] Throughout human evolution, the executive functions involved in ADHD likely provide the capacity to bind contingencies across time thereby directing behaviour toward future over immediate events so as to maximise future social consequences for humans. [ 38 ]
ADHD has a high heritability of 74%, meaning that 74% of the presence of ADHD in the population is due to genetic factors. There are multiple gene variants which each slightly increase the likelihood of a person having ADHD; it is polygenic and thus arises through the accumulation of many genetic risks each having a very small effect. [ 39 ] [ 32 ] The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder. [ 40 ]
The association of maternal smoking observed in large population studies disappears after adjusting for family history of ADHD, which indicates that the association between maternal smoking during pregnancy and ADHD is due to familial or genetic factors that increase the risk for the confluence of smoking and ADHD. [ 41 ] [ 42 ]
ADHD presents with reduced size, functional connectivity and activation [ 39 ] as well as low noradrenergic and dopaminergic functioning [ 43 ] [ 44 ] in brain regions and networks crucial for executive functioning and self-regulation. [ 39 ] [ 45 ] [ 46 ] Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission. [ 39 ] Those involved with dopamine include DAT , DRD4 , DRD5 , TAAR1 , MAOA , COMT , and DBH. [ 47 ] [ 48 ] [ 49 ] Other genes associated with ADHD include SERT , HTR1B , SNAP25 , GRIN2A , ADRA2A , TPH2 , and BDNF . [ 50 ] A common variant of a gene called latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication. [ 51 ] The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase . The DRD4–7R mutation results in a wide range of behavioural phenotypes , including ADHD symptoms reflecting split attention. [ 52 ] The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with Autism Spectrum Disorder (ASD), schizophrenia , bipolar disorder, and depression make it an interesting candidate causative gene. [ 53 ] Another candidate causative gene that has been identified is ADGRL3 . In zebrafish , knockout of this gene causes a loss of dopaminergic function in the ventral diencephalon and the fish display a hyperactive/impulsive phenotype . [ 53 ]
Behavioral genetic studies have suggested that many chromosomal regions and candidate genes are related to bipolar disorder susceptibility with each gene exerting a mild to moderate effect . [ 55 ] The risk of bipolar disorder is nearly ten-fold higher in first-degree relatives of those with bipolar disorder than in the general population; similarly, the risk of major depressive disorder is three times higher in relatives of those with bipolar disorder than in the general population. [ 56 ]
Although the first genetic linkage finding for mania was in 1969, [ 57 ] linkage studies have been inconsistent. [ 56 ] Findings point strongly to heterogeneity, with different genes implicated in different families. [ 58 ] Robust and replicable genome-wide significant associations showed several common single-nucleotide polymorphisms (SNPs) are associated with bipolar disorder, including variants within the genes CACNA1C , ODZ4 , and NCAN . [ 55 ] [ 59 ] The largest and most recent genome-wide association study failed to find any locus that exerts a large effect, reinforcing the idea that no single gene is responsible for bipolar disorder in most cases. [ 59 ] Polymorphisms in BDNF , DRD4 , DAO , and TPH1 have been frequently associated with bipolar disorder and were initially associated in a meta-analysis , but this association disappeared after correction for multiple testing . [ 60 ] On the other hand, two polymorphisms in TPH2 were identified as being associated with bipolar disorder. [ 61 ]
Due to the inconsistent findings in a genome-wide association study , multiple studies have undertaken the approach of analyzing SNPs in biological pathways. Signaling pathways traditionally associated with bipolar disorder that have been supported by these studies include corticotropin-releasing hormone signaling, cardiac β-adrenergic signaling, phospholipase C signaling, glutamate receptor signaling, [ 62 ] cardiac hypertrophy signaling, Wnt signaling , Notch signaling , [ 63 ] and endothelin 1 signaling. Of the 16 genes identified in these pathways, three were found to be dysregulated in the dorsolateral prefrontal cortex portion of the brain in post-mortem studies: CACNA1C , GNG2 , and ITPR2 . [ 64 ]
Any damage that occurs to a fetus while still in its mother's womb is considered prenatal damage. Mental disorders can develop if the pregnant mother uses drugs or alcohol or is exposed to illnesses or infections during pregnancy. [ citation needed ] Environmental events surrounding pregnancy and birth have increased the development of mental illness in the offspring . Some events may include maternal exposure to stress or trauma , conditions of famine, obstetric birth complications, infections, and gestational exposure to alcohol or cocaine . These factors have been hypothesized to affect areas of neurodevelopment, general development, and restrict neuroplasticity . [ citation needed ]
There have been some findings of links between infection by the parasite Toxoplasma gondii and schizophrenia. [ 67 ]
AIDS has been linked to some mental disorders. Research shows that infections and exposure to toxins such as HIV [ 68 ] and streptococcus cause dementia. [ 69 ] This HIV infection that makes its way to the brain is called encephalopathy which spreads itself through the brain leading to dementia. [ 68 ] The infections or toxins that trigger a change in the brain chemistry can develop into a mental disorder.
Depression and emotional liability may be also be caused by babesiosis .
There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease .
The research on Lyme disease caused by a deer tick and toxins is expanding the link between bacterial infections and mental illness. [ 70 ]
Depression, anxiety, mania, psychosis, vegetative symptoms, cognitive deficit and consciousness impairment may be caused by internal disease as well as endocrine and metabolic disorders, deficiency states and neurologic disorders. [ 71 ]
Any damage to the brain can cause a mental disorder. The brain is the control system for the nervous system and the rest of the body. Without it, the body cannot function properly. [ 72 ]
Increased mood swings, insane behavior, and substance abuse disorders are traumatic brain injury (TBI) examples. Findings on the relationship between TBI severity and prevalence of subsequent psychiatric disorders have been inconsistent, and occurrence relates to prior mental health problems. Direct neurophysiological effects in a complex interaction with personality, attitude, and social influences .
Head trauma classifies as either open or closed head injury. In open head injury , the skull is punctured and the brain tissue is demolished. Closed head injury is more common, the skull is not punctured because there is an impact of the brain against the skull that creates permanent structural damage ( subdural hematoma ). With both types, symptoms may disappear or persist over time. Typically the longer the length of time spent unconscious and the length of post-traumatic amnesia the worse the prognosis for the individual. The cognitive residual symptoms of head trauma are associated with the type of injury (either an open head injury or closed head injury) and the amount of tissue destroyed. Closed injury head trauma symptoms include; Deficits in abstract reasoning ability , judgment, memory, and marked personality changes. Open injury head trauma symptoms tend to be the experience of classic neuropsychological syndromes like aphasia , visual-spatial disorders, and types of memory or perceptual disorders . [ citation needed ]
Brain tumors are classified as either malignant and benign , and as intrinsic (directly infiltrate the parenchyma of the brain) or extrinsic (grows on the external surface of the brain and produces symptoms as a result of pressure on the brain tissue). Progressive cognitive changes associated with brain tumors may include confusion, poor comprehension, and even dementia . Symptoms tend to depend on the location of the tumor in the brain. For example, tumors on the frontal lobe tend to be associated with the sign of impairment of judgment, apathy, and loss of the ability to regulate/modulate behavior. [ 73 ]
Findings have indicated abnormal functioning of brainstem structures in individuals with mental disorders such as schizophrenia , and other disorders that have to do with impairments in maintaining sustained attention. Some abnormalities in the average size or shape of some regions of the brain have been found in some disorders, reflecting genes and experiences. Studies of schizophrenia have tended to find enlarged ventricles and sometimes reduced volume of the cerebrum and hippocampus , while studies of (psychotic) bipolar disorder have sometimes found increased amygdala volume. Findings differ over whether volumetric abnormalities are risk factors or are only found alongside the course of mental health problems, possibly reflecting neurocognitive or emotional stress processes and medication use or substance use. Some studies have also found reduced hippocampal volumes in major depression , possibly worsening with time depression. [ citation needed ]
Abnormal levels of dopamine activity correspond with several disorders (reduced in ADHD and OCD , and increased in schizophrenia). The dysfunction in serotonin and other monoamine neurotransmitters ( norepinephrine and dopamine ) correspond with certain mental disorders and their associated neural networks. Some include major depression , obsessive-compulsive disorder , phobias , post-traumatic stress disorder , and generalized anxiety disorder . Studies of depleted levels of monoamine neurotransmitters show an association with depression and other psychiatric disorders, but "... it should be questioned whether 5-HT [serotonin] represents just one of the final and not the main, factors in the neurological chain of events underlying psychopathological symptoms...."
Simplistic "chemical imbalance" explanations for mental disorders have never received empirical support; and most prominent psychiatrists, neuroscientists, and psychologists have not espoused such ill-defined, facile etiological theories. Instead, neurotransmitter systems have been understood in the context of the diathesis-stress or biopsychosocial models . The following 1967 quote from renowned psychiatric and neuroscience researchers exemplifies this more sophisticated understanding (in contrast to the woolly "chemical imbalance" notion).
Whereas specific genetic factors may be of importance in the etiology of some, and possibly all, depressions, it is equally conceivable that early experiences of the infant or child may cause enduring biochemical changes, that may predispose some individuals to depressions in adulthood. It is not likely that changes in the metabolism of the biogenic amines alone will account for the complex phenomena of normal or pathological affect.
Substance abuse, especially long-term abuse, can cause or exacerbate many mental disorders. Alcoholism is linked to depression while abuse of amphetamines and LSD can leave a person feeling paranoid and anxious .
Correlations of mental disorders with drug use include cannabis , alcohol, and caffeine . At more than 300 mg, caffeine may cause anxiety or worsen anxiety disorders. Illicit drugs can stimulate particular parts of the brain that can affect development in adolescence. Cannabis has also been found to worsen depression and lessen an individual's motivation . Alcohol has the potential to damage " white matter " in the brain that affects thinking and memory . Alcohol is a problem in many countries due to many people participating in excessive drinking or binge drinking .
The term "environment" is very loosely defined in the context of mental illnesses. Unlike biological and psychological causes, environmental causes denote a wide range of stressors that individuals experience in everyday life. They are more psychologically than biologically based. [ 74 ] Events that evoke feelings of loss are the most likely to cause a mental disorder to develop in an individual. [ 14 ]
Environmental factors include but are not limited to dysfunctional home life, poor interpersonal relationships , substance abuse , not meeting social expectations, low self-esteem , and poverty . [ 14 ] The British charity organisation Mind lists childhood abuse , trauma , violence , neglect , social isolation , discrimination , grief , stress, homelessness , social disadvantage, debt, unemployment, caring for a family member or friend, and significant trauma as an adult (such as war , an accident, or being the victim of a violent crime ) as possible triggers of an episode of mental illness. [ 75 ]
Repeating generational patterns, behaviors that are passed down through different familial generations, are also a risk factor for mental illness, especially in children. [ 76 ]
Mistreatment in childhood or adulthood (including sexual -, physical -, and emotional abuse , domestic violence , and bullying ) has been linked to the onset of mental disorders through an interaction of societal, familial, psychological, and biological factors. More generally, negative or stressful life events have been implicated in the development of a range of disorders, including mood and anxiety disorders. [ 77 ] [ 78 ]
The main risks appear to be from the accumulation of such experiences over time, although a single major trauma can sometimes lead to disorders, especially post-traumatic stress disorder . Resilience to such experiences varies; a person may be resistant to some stressors but not to others. The psychological resilience of an individual can be affected by genetics , temperamental characteristics, cognitive flexibility , coping strategies , and previous experiences. [ 79 ] For example, in the case of bipolar disorder , stress is not a specific cause but does place genetically and biologically vulnerable people at risk for more severe forms of the illness. [ 80 ] [ 81 ]
The Adverse Childhood Experiences Study has shown a strong dose–response relationship between adverse childhood experiences or ACEs (such as physical and/or emotional neglect, abuse , poverty, malnutrition , and traumatic experiences) and numerous health, social, and behavioral problems including suicide attempts and the frequency of depressive episodes. [ 82 ] Several such experiences can cause toxic stress . [ 83 ]
ACEs may affect the structural and functional development of the brain and lead to abnormalities, and chronic trauma can disrupt immune responses and cause lasting dysregulated inflammatory response. [ 84 ] A child's neurological development can be disrupted when chronically exposed to stressful events, and his/her cognitive functioning and/or ability to cope with negative emotions can diminish. [ 85 ] Over time, the child may adopt various harmful coping strategies that contribute to later mental and physical problems. [ 86 ] Findings have been mixed, but some studies suggest that cognitive deficit is more related to neglect than other forms of adversity. [ 87 ] [ 88 ]
Poor parenting is a risk factor for depression and anxiety. Separation, grief in families, and other forms childhood trauma are risk factors for schizophrenia . [ 89 ] Children are more susceptible to psychological harm from traumatic events than adults, [ 90 ] but their reaction does vary by individual child, age, the type of event, and the length of exposure.
Neglect is a form of mistreatment in which the responsible caretakers fail to provide the necessary age-appropriate care, supervision, and protection. It is different from abuse in that it is, in this context, not intentional in causing harms. [ 91 ] The long-term effects of neglect can be reduced physical, emotional, and mental health throughout the victim's life. [ 92 ] [ 93 ]
Parental divorce, death, absence, or the lack of stability appears to increase the risk of mental disorders in a child. [ 94 ] Early social privation , and the lack of "ongoing, harmonious, secure, committed" relationships have been implicated in the development of mental illnesses. [ 95 ] Continuous conflict with friends, one's support system, and family can all increase the risk of developing a mental illness or can worsen one's mental health. [ 96 ]
Divorce is a factor that affects adults as well as children. Divorcees may have emotional adjustment problems due to a loss of intimacy and social connections; however, new statistics show that the negative effects of divorce have been overstated. [ 97 ]
Having both too low or too high self-esteem can be detrimental to an individual's mental health. [ 98 ] [ 99 ] Low self-esteem in particular can result in aggression, self-deprecating behavior, anxiety, and other mental disorders. [ 100 ] Being perceived as someone who does not "fit in" can result in bullying and other types of emotional abuse, [ 101 ] [ 102 ] which can lead to the victim experiencing depression, anger, and loneliness. [ 103 ]
Studies show that there is a direct correlation between poverty and mental illness: the lower the socioeconomic status of an individual, the higher the risk of mental illness. Impoverished people in England, defined as those who live in the lowest 20% income bracket, are two to three times more likely to develop mental illness than those of a higher economic class . [ 104 ] This increased risk remains consistent for all poor individuals regardless of any in-group demographic differences, as all disadvantaged families experience economic stressors such as unemployment or lack of housing. A lower or more insecure educational, occupational, economic, or social position is generally linked to more mental disorders. [ 105 ] Children from these backgrounds may have low levels of self-efficiency and self-worth. [ 106 ] Studies have also shown a strong relationship between poverty and substance abuse , another risk factor in the onset of mental disorders. [ 107 ]
Problems in one's community or culture including poverty, unemployment or underemployment , a lack of social cohesion , and migration have been associated with the development of mental disorders. [ 108 ] Personal resources, community factors, and interactions between individual and regional-level income levels have been implicated. [ 109 ] Socioeconomic deprivation in neighborhoods can cause worsen mental health, even after accounting for genetic factors. [ 110 ] According to a 2009 meta-analysis by Paul and Moser, countries with high income inequality and poor unemployment protections have worse mental health outcomes among the unemployed. [ 111 ]
The effects of different socioeconomic factors varies by country. [ 112 ] [ 113 ] Minority ethnic groups, including first or second-generation immigrants , are at a greater risk of developing mental disorders. This has been attributed to the insecurities in their lives and their disadvantages, including racism . [ 114 ] There have been alternate models, such as the drift hypothesis to account for the complex relationship between an individual's social status and mental health. [ 115 ]
Some clinicians believe that psychological characteristics alone determine mental disorders. Others speculate that abnormal behavior can be explained by a mix of social and psychological factors. In many examples, environmental and psychological triggers complement one another resulting in emotional stress, which in turn activates a mental illness. Each person is unique in how they will react to psychological stressors. What may break one person may have little to no effect on another. Psychological stressors, which can trigger mental illness, are as follows: emotional, physical, or sexual abuse, loss of a significant loved one, neglect, and being unable to relate to others. [ 116 ]
The inability to relate to others is also known as emotional detachment . Emotional detachment makes it difficult for an individual to empathize with others or to share their feelings. These individuals tend to stress the importance of their independence and tend to struggle relating to others. An emotionally detached person may try to rationalize or apply logic to a situation to which there is no logical explanation. Often, the inability to relate to others stems from a traumatic event. [ citation needed ]
Mental characteristics of individuals, as assessed by both neurological and psychological studies, have been linked to the development and maintenance of mental disorders. This includes cognitive or neurocognitive factors, such as the way a person perceives, thinks, or feels about certain things; or an individual's overall personality, temperament , or coping style or the extent of protective factors or "positive illusions" such as optimism, personal control and a sense of meaning. [ citation needed ]
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Generally, seizures are observed in patients who do not have epilepsy. [ 1 ] There are many causes of seizures . Organ failure, medication and medication withdrawal, cancer, imbalance of electrolytes, hypertensive encephalopathy , may be some of its potential causes. [ 2 ] The factors that lead to a seizure are often complex and it may not be possible to determine what causes a particular seizure, what causes it to happen at a particular time, or how often seizures occur. [ 3 ]
Malnutrition and overnutrition may increase the risk of seizures. [ 4 ] Examples include the following:
Folic acid in large amounts was considered to potentially counteract the antiseizure effects of antiepileptic drugs and increase the seizure frequency in some children, although that concern is no longer held by epileptologists. [ 13 ]
Those with various medical conditions may experience seizures as one of their symptoms. These include: [ citation needed ]
Other conditions have been associated with lower seizure thresholds and/or increased likelihood of seizure comorbidity (but not necessarily with seizure induction). Examples include depression , psychosis , obsessive-compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), and autism , among many others.
Seizures may occur as an adverse effect of certain drugs. These include: [ medical citation needed ]
Use of certain recreational drugs may lead to seizures in some, especially when used in high doses or for extended periods. These include amphetamines (such as amphetamine , methamphetamine , MDMA ("ecstasy"), and mephedrone ), cocaine , methylphenidate , psilocybin , psilocin , and GHB .
If treated with the wrong kind of antiepileptic drugs (AED), seizures may increase, as most AEDs are developed to treat a particular type of seizure.
Convulsant drugs (the functional opposites of anticonvulsants) will always induce seizures at sufficient doses. Examples of such agents — some of which are used or have been used clinically and others of which are naturally occurring toxins — include strychnine , bemegride , flumazenil , cyclothiazide , flurothyl , pentylenetetrazol , bicuculline , cicutoxin , and picrotoxin .
There are varying opinions on the likelihood of alcoholic beverages triggering a seizure. Consuming alcohol may temporarily reduce the likelihood of a seizure immediately following consumption. But, after the blood alcohol content has dropped, chances may increase. This may occur, even in non-epileptics. [ 15 ]
Heavy drinking in particular has been shown to possibly have some effect on seizures in epileptics. But studies have not found light drinking to increase the likelihood of having a seizure at all. [ citation needed ] EEGs taken of patients immediately following light alcohol consumption have not revealed any increase in seizure activity. [ 16 ]
Consuming alcohol with food is less likely to trigger a seizure than consuming it without. [ 17 ]
Consuming alcohol while using many anticonvulsants may reduce the likelihood of the medication working properly. In some cases, it may trigger a seizure. Depending on the medication, the effects vary. [ 18 ]
Some medicinal and recreational drugs can dose-dependently precipitate seizures in withdrawal, especially when withdrawing from high doses and/or chronic use. Examples include drugs that affect GABAergic and/or glutamatergic systems, such as alcohol (see alcohol withdrawal ), [ 19 ] benzodiazepines , barbiturates , and anesthetics , among others.
Sudden withdrawal from anticonvulsants may lead to seizures. It is for this reason that if a patient's medication is changed, the patient will be weaned from the medication being discontinued following the start of a new medication.
A missed dose or incorrectly timed dose of an anticonvulsant may be responsible for a breakthrough seizure, even if the person often missed doses in the past, and has not had a seizure as a result. [ 20 ] Missed doses are one of the most common reasons for a breakthrough seizure . A single missed dose is capable of triggering a seizure in some patients. [ 21 ]
In children between the ages of 6 months and 5 years, a fever of 38 °C (100.4 °F) or higher may lead to a febrile seizure . [ 25 ] About 2-5% of all children will experience such a seizure during their childhood. [ 26 ] In most cases, a febrile seizure will not indicate epilepsy. [ 26 ] Approximately 40% of children who experience a febrile seizure will have another one. [ 26 ]
In those with epilepsy, fever can trigger a seizure. Additionally, in some, gastroenteritis , which causes vomiting and diarrhea , can lead to diminished absorption of anticonvulsants, thereby reducing protection against seizures. [ 27 ]
In some epileptics, flickering or flashing lights, such as strobe lights , can be responsible for the onset of a tonic clonic , absence , or myoclonic seizure. [ 28 ] This condition is known as photosensitive epilepsy and, in some cases, the seizures can be triggered by activities that are harmless to others, such as watching television or playing video games, or by driving or riding during daylight along a road with spaced trees, thereby simulating the "flashing light" effect. Some people can have a seizure as a result of blinking one's own eyes. [ 29 ] Contrary to popular belief, this form of epilepsy is relatively uncommon, accounting for just 3% of all cases. [ 30 ]
A routine part of the EEG test involves exposing the patient to flickering lights to attempt to induce a seizure, to determine if such lights may be triggering a seizure in the patient, and to be able to read the wavelengths when such a seizure occurs. [ 29 ]
In photosensitive epilepsies, epileptic activity only appears for few seconds after eye-closure. In some non-photosensitive epilepsies, seizures may be triggered by the loss of central vision during eye-closure, in an phenomenon called fixation-off sensitivity (FOS), where the epileptic activity persists for the total duration of eye-closure. Though unrelated phenomena, photosensitive and non-photosensitive epilepsies can occur together in some patients. [ 31 ] [ 32 ] [ 33 ]
A severe head injury , such as one sustained in a motor vehicle accident , fall , assault , or sports injury , can result in one or more seizures that can occur immediately after the fact or up to a significant amount of time later. [ 34 ] This could be hours, days, or even years following the injury.
A brain injury can cause seizure(s) because of the unusual amount of energy that is discharged across of the brain when the injury occurs and thereafter. A disruption of the supply of oxygen may cause damage to the temporal lobe of the brain. [ 35 ]
The risk of seizure(s) from a closed head injury is about 15%. [ 36 ] In some cases, a patient who has had a head injury is given anticonvulsants, even if no seizures have occurred, as a precaution to prevent them in the future. [ 37 ]
Hyperglycemia , or high blood sugar, can increase frequency of seizure. The probable mechanism is that elevated extracellular glucose level increases neuronal excitability. [ 38 ]
Curiously, hypoglycemia , or low blood sugar, can also trigger seizures. [ 39 ] The mechanism is also increased cortical excitability. [ 40 ]
In catamenial epilepsy , seizures become more common during a specific period of the menstrual cycle .
Sleep deprivation is the second most common trigger of seizures. [ 15 ] In some cases, it has been responsible for the only seizure a person ever has. [ 41 ] However, the reason for which sleep deprivation can trigger a seizure is unknown. One possible thought is that the amount of sleep one gets affects the amount of electrical activity in one's brain. [ 42 ]
Patients who are scheduled for an EEG test are asked to deprive themselves of some sleep the night before to be able to determine if sleep deprivation may be responsible for seizures. [ 43 ]
In some cases, patients with epilepsy are advised to sleep 6-7 consecutive hours as opposed to broken-up sleep (e.g., 6 hours at night and a 2-hour nap) and to avoid caffeine and sleeping pills in order to prevent seizures. [ 44 ]
In some cases, certain parasites can cause seizures. The Schistosoma sp. flukes cause Schistosomiasis . Pork tapeworm and beef tapeworm cause seizures when the parasite creates cysts at the brain. Echinococcosis , malaria , toxoplasmosis , African trypanosomiasis , and many other parasitic diseases can cause seizures.
Seizures have been associated with insect stings. Reports suggest that patients stung by red imported fire ants ( Solenopsis invicta ) and Polistes wasps had seizures because of the venom. [ 45 ] [ 46 ]
In endemic areas, neurocysticercosis is the main cause behind focal epilepsy in early adulthood. All growth phases of cysticerci (viable, transitional and calcified) are associated with epileptic seizures. Thus, anti-cysticercus treatment helps by getting rid of it thus lowers the risk of recurrence of seizures in patients with viable cysts. Symptomatic epilepsy can be the first manifestation of neuroschistosomiasis in patients without any systemic symptoms. The pseudotumoral form can trigger seizures secondary to the presence of granulomas and oedemas in the cerebral cortex. [ 47 ]
Stress can induce seizures in people with epilepsy , and is a risk factor for developing epilepsy. Severity, duration, and time at which stress occurs during development all contribute to frequency and susceptibility to developing epilepsy. It is one of the most frequently self-reported triggers in patients with epilepsy. [ 48 ] [ 49 ]
Stress exposure results in hormone release that mediates its effects in the brain. These hormones act on both excitatory and inhibitory neural synapses , resulting in hyper-excitability of neurons in the brain. The hippocampus is known to be a region that is highly sensitive to stress and prone to seizures . This is where mediators of stress interact with their target receptors to produce effects. [ 50 ]
"Epileptic fits" as a result of stress are common in literature and frequently appear in Elizabethan texts, where they are referred to as the "falling sickness". [ 51 ]
A breakthrough seizure is an epileptic seizure that occurs despite the use of anticonvulsants that have otherwise successfully prevented seizures in the patient. [ 52 ] : 456 Breakthrough seizures may be more dangerous than non-breakthrough seizures because they are unexpected by the patient, who may have considered themselves free from seizures and, therefore, not take any precautions. [ 53 ] Breakthrough seizures are more likely with a number of triggers. [ 54 ] : 57 Often when a breakthrough seizure occurs in a person whose seizures have always been well controlled, there is a new underlying cause to the seizure. [ 55 ]
Breakthrough seizures vary. Studies have shown the rates of breakthrough seizures ranging from 11 to 37%. [ 56 ] Treatment involves measuring the level of the anticonvulsant in the patient's system and may include increasing the dosage of the existing medication, adding another medication to the existing one, or altogether switching medications. [ 57 ] A person with a breakthrough seizure may require hospitalization for observation. [ 52 ] : 498
Music (as in musicogenic epilepsy ) [ 59 ] [ 60 ] [ 61 ]
In the case of patients with seizures associated with medical illness, the patients are firstly stabilized. They are attended to their circulation, airway, and breathing. Next vital signs are assessed through a monitor, intravenous access is obtained, and concerning laboratory tests are performed. Phenytoin or fosphenytoin supplemented with benzodiazepines are administered as the first line of therapy if the seizure persists for more than 5 –10 minutes. Through neuroimaging, clinical assessments, and spinal-fluid examination the patients are screened for intrinsic neurological anomalies. The patients are analyzed for non-epileptic seizures . Early electroencephalography is recommended if there is a possibility of non-convulsive or subtle status epilepticus. They are examined for disorders such as sarcoidosis , porphyria , and other unusual systemic disorders. Information is gathered on the drug, medication history, and its withdrawal. For seizures associated with alcohol, intravenous pyridoxine and other specific antidotes are prescribed. The patient is checked for proconvulsant exposure. All underlying potential causes are considered. For instance, in a patient with an end-stage renal disease where there is a probability of hypertensive encephalopathy , blood pressure is analyzed. [ 2 ]
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A caustic pencil (or silver nitrate stick) is a device for applying topical medication containing silver nitrate and potassium nitrate , used to chemically cauterize skin, providing hemostasis or permanently destroying unwanted tissue such as a wart , skin tag , aphthous ulcers , or over-production of granulation tissue . [ 1 ] They are not used as a treatment for minor skin cuts, and are not to be confused with a styptic pencil .
The silver and potassium nitrates in caustic pencils is in a dried, solid form at the tip of a wooden or plastic stick. When the material is applied to a wound or lesion, the tissue moisture or blood dissolves the dried nitrate salts, which then chemically burn the tissue. It requires moisture for activation.
Silver nitrate sticks are often used for minor hemostasis where patients are not under general anesthesia, and where electrocautery would be painful and inconvenient. One common use of silver nitrate sticks is in emergency medicine, to control epistaxis (nosebleed). The stick is rolled on the affected mucous membrane or visible blood vessel in the nares (nostril) where the chemical cauterization stops the minor bleeding.
If the bleeding is too copious, the chemical cautery may not be effective, as the flowing blood can wash away the chemical before it can react with the tissue. It can also be accidentally spread to undesirable locations where it can cause skin staining and tissue burns. This is especially important, as it is often used in the nose where accidental aerosolization can occur, splattering the clinician or other parts of the patient and causing unintentional burns. Accidental application to unintended tissue is treated with copious water irrigation, and saline solution will inactivate the chemical reaction. [ 2 ]
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Cauterization (or cauterisation , or cautery ) is a medical practice or technique of burning a part of a body to remove or close off a part of it. It destroys some tissue in an attempt to mitigate bleeding and damage, remove an undesired growth, or minimize other potential medical harm, such as infections when antibiotics are unavailable. [ 1 ]
The practice was once widespread for treatment of wounds. Its utility before the advent of antibiotics was said to be effective at more than one level:
Cautery was historically believed to prevent infection, but current research shows that cautery actually increases the risk for infection by causing more tissue damage and providing a more hospitable environment for bacterial growth. [ 2 ] Actual cautery refers to the metal device, generally heated to a dull red glow, that a physician applies to produce blisters , to stop bleeding of a blood vessel , and for other similar purposes. [ 3 ]
The main forms of cauterization used today are electrocautery and chemical cautery —both are, for example, prevalent in cosmetic removal of warts and stopping nosebleeds . Cautery can also mean the branding of a human .
Cauterize is a Middle English word borrowed from the Old French cauteriser , from Late Latin cauterizare "to burn or brand with a hot iron", from Ancient Greek καυτηριάζειν ( kauteriazein ), from καυτήρ ( kauter ), "burning or branding iron", and καίειν ( kaiein ) "to burn" (of caustic). [ 4 ]
Cauterization has been used to stop heavy bleeding since antiquity. The process was described in the Edwin Smith Papyrus [ 5 ] and Hippocratic Corpus . [ 6 ] It was primarily used to control hemorrhages, especially those resulting from surgery, in ancient Greece . Archigenes recommended cauterization in the event of hemorrhaging wounds, and Leonides of Alexandria described excising breast tumors and cauterizing the resulting wound in order to control bleeding. [ 7 ] The Chinese Su wen recommends cauterization as a treatment for various ailments, including dog bites. [ 8 ] Indigenous peoples of the Americas , ancient Arabs , and Persians also used the technique. [ 9 ]
Tools used in the ancient cauterization process ranged from heated lances to cauterizing knives. The piece of metal was heated over fire and applied to the wound. [ 10 ]
Cauterization continued to be used as a common treatment in medieval times. The Babylonian Talmud (redacted in 500 AD), alluding to the practice, states: "... and the effect of the hot iron comes and removes the traces of the stroke." [ 11 ] While mainly employed to stop blood loss, it was also used in cases of tooth extraction and as a treatment for mental illness. In the Muslim world , scholars Al-Zahrawi and Avicenna wrote about techniques and instruments used for cauterization. [ 12 ]
As late as the 20th-century, Bedouins of the Negev in Israel had it as their practice to take the root of the shaggy sparrow-wort ( Thymelaea hirsuta ), cut the root into splinters lengthwise, burn the splinter in fire, and then apply the red-hot tip of a splinter to the forehead of a person who was ill with ringworm ( dermatophytosis ). [ 13 ]
The technique of ligature of the arteries as an alternative to cauterization was later improved and used more effectively by Ambroise Paré .
Electrocauterization is the process of destroying tissue (or cutting through soft tissue) using heat conduction from a metal probe heated by electric current. The procedure stops bleeding from small vessels (larger vessels being ligated ). Electrocautery applies high frequency alternating current by a unipolar or bipolar method. It can be a continuous waveform to cut tissue, or intermittent to coagulate tissue.
The electrically produced heat in this process inherently can do numerous things to the tissue, depending on the waveform and power level, including cauterize, coagulate, cut, and dry (desiccate). Thus electrocautery, electrocoagulation, electrodesiccation, and electrocurettage are closely related and can co-occur in the same procedure when desired. Electrodesiccation and curettage is a common procedure.
In unipolar cauterization, the physician contacts the tissue with a single small electrode. The circuit's exit point is a large surface area, such as the buttocks, to prevent electrical burns. The amount of heat generated depends on the size of contact area, power setting or frequency of current, duration of application, and waveform. A constant waveform generates more heat than intermittent. The frequency used in cutting the tissue is higher than in coagulation mode.
Bipolar electrocautery passes the current between two tips of a forceps-like tool. It has the advantage of not disturbing other electrical body rhythms (such as the heart) and also coagulates tissue by pressure. Lateral thermal injury is greater in unipolar than bipolar devices. [ 14 ]
Electrocauterization is preferable to chemical cauterization, because chemicals can leach into neighbouring tissue and cauterize outside of intended boundaries. [ 15 ] Concern has also been raised regarding toxicity of the surgical smoke electrocautery produces. This contains chemicals that, through inhalation, may harm patients or medical staff. [ 16 ]
Ultrasonic coagulation and ablation systems are also available.
Many chemical reactions can destroy tissue, and some are used routinely in medicine, most commonly to remove small skin lesions such as warts or necrotized tissue, or for hemostasis . [ 17 ] Because chemicals can leach into areas not intended for cauterization, laser and electrical methods are preferable where practical. [ 18 ] Some cauterizing agents are:
Frequent nosebleeds are most likely caused by an exposed blood vessel in the nose, usually one in Kiesselbach's plexus .
Even if the nose is not bleeding at the time, a physician may cauterize it to prevent future bleeding. Cauterization methods include burning the affected area with acid, hot metal, or lasers. Such a procedure is naturally quite painful. Sometimes, a physician uses liquid nitrogen as a less painful alternative, though it is less effective. A physician may apply cocaine in the few countries that allow it for medical use. Cocaine is the only local anesthetic that also produces vasoconstriction , [ 23 ] making it ideal for controlling nosebleeds.
More modern treatment applies silver nitrate after a local anesthetic. The procedure is generally painless, but after the anesthetic wears off, there may be pain for several days, and the nose may run for up to a week after this treatment.
Nasal cauterization can cause empty nose syndrome . [ 24 ] [ 25 ] [ 26 ]
Cauterization has been used for the circumcision of infants in the United States and Canada . The College of Physicians and Surgeons of Manitoba advises against its use in neonatal circumcision. [ 27 ] This method of circumcision resulted in several infants having their penises severely burned. [ 28 ] [ 29 ] [ 30 ] [ 31 ] [ 32 ] [ 33 ]
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Cavitations are an area of dead or dying bone . They are caused by infections, physical trauma, or a dearth of blood flow to that part of the bone. [ 1 ]
There is little evidence to support the theory of cavitation in the jawbone, and their diagnosis is highly controversial. [ 2 ] Proponents claim they primarily affect the jawbone, yet that cavitations are able to affect any bone. [ 3 ] Jawbone cavitations, also called neuralgia-inducing cavitational osteonecrosis (NICO) if they are associated with pain, might be extraction sites in the jaw that have not healed. [ 4 ]
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Cecectomy is a surgical procedure in which the cecum is removed partially or totally. [ 1 ] It can be done in cases like carcinoid syndrome , primary or secondary cancer .
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CellNetix Pathology & Laboratories, LLC, headquartered in Tukwila, Washington , is a premier anatomic pathology provider in the Pacific Northwest, with 60 physicians and more than 300 total staff. Services include cytology , histology , fine needle aspiration (FNA) services, flow cytometry , immunohistochemistry , immunofluorescence , UroVysion™, and molecular diagnostics.
CellNetix institutes pollution prevention planning [ 1 ] and receives technical assistance from Washington State Department of Ecology.
CellNetix uses a subspecialized case allocation process [ 2 ] in which specimens arrive in the pathology laboratory and staff allocate them by subspecialty: breast cases to breast pathologists, gastroenterology (GI) cases to GI pathologists, genitourinary cases (GU) cases to GU pathologists, etc. In a typical case allocation process in a non-specialized pathology practice, cases are manually allocated to pathologists based on workload, without regard to the type of case. Tests are interpreted by board-certified pathologists who have experience in breast core biopsies, GI biopsies, Pap tests, and prostate biopsies. [ citation needed ]
CellNetix is expanding the utilization of molecular biology to identify the root cause of abnormalities within the genetic material of the cell itself. The CellNetix molecular pathology department tests for breast, gastric, colon and lung cancers, as well as melanoma. A women's health subspecialty provides high-risk HPV testing, testing for the detection of Neisseria gonorrhoeae (GC) and Chlamydia trachomatis (CT), as well as vaginosis/vaginitis testing. [ 3 ]
CellNetix uses a specimen tracking system in which each specimen is labeled with a bar code and scanned up to 15 times during transit—from pickup at the hospital or clinic, to arrival at the lab, to final report. [ 4 ]
Early in 2012, the company invested in whole-slide imaging which views a live capture of the slide on a microscope . This is done using an ultra-high resolution scanner to image the complete slides and store them digitally. [ 5 ]
CellNetix spent 6 months validating WSI for use in diagnostic processes. It is now in daily use for digital IHC reads by pathologists at remote locations. They are also using WSI for HER2/neu diagnosis after a lengthy validation (comparing diagnosis by glass slide vs. digital image) for many cases by different pathologists. [5]
CellNetix is a physician- and employee-owned partnership formed in 2005 by the merger of three independent pathology groups—Black Hills Pathology (Olympia), Associated Pathology (Everett) and Washington Pathology Consultants (Seattle), with the addition of Northwest Pathology Group in 2008. [ citation needed ]
In 2007, CellNetix opened a 48,000-square-foot pathology and laboratory facility in downtown Seattle, where most of the testing is conducted. CellNetix provides diagnostic services for nine hospitals across western Washington as well as physicians and patients in Washington and Alaska. [ 6 ]
On December 4, 2012, Spokane, Wash.-based PAML (Pathology Associates Medical Laboratories) and CellNetix signed a letter of intent in which PAML agreed to purchase a minority ownership interest in CellNetix, LLC. As part of this partnership, CellNetix and PAML will form a jointly owned molecular pathology esoteric testing division. PAML employs approximately 1,400 staff and is 75% owned by Providence Health & Services and 25% by CHI (Catholic Health Initiative). By agreement, PAML and CellNetix will have a seat on each other's boards. [ citation needed ]
On May 2, 2013, PAML and CellNetix announced that PAML had completed a minority investment in the technical laboratory business division owned by CellNetix. The two companies also stated that they entered into an agreement to work together to form a “jointly owned national Esoteric Anatomic Pathology reference laboratory offering.” [ 7 ]
On February 28, 2017, just a week after Laboratory Corp. of America Holdings announced its plan to buy PAML, CellNetix bought back the 22% minority share from PAML to regain complete ownership. With this transaction, CellNetix Pathology and Laboratories became one of the largest independent, pathologist-owned groups in the country. [ 8 ]
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Cellular Oncology is a bimonthly peer-reviewed medical journal published by Springer Science+Business Media . [ 1 ] The journal was established in 1989 as Analytical Cellular Pathology , obtaining its current name in 2003. [ 2 ] [ 3 ] It is an official publication of the International Society for Cellular Oncology and is published six times a year. The journal covers basic cancer research . [ 1 ]
According to the Journal Citation Reports , the journal has a 2022 impact factor of 6.6. [ 4 ]
This article about an oncology journal is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Cellular_Oncology
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Cellular cardiomyoplasty , or cell-based cardiac repair, is a new potential therapeutic modality in which progenitor cells are used to repair regions of damaged or necrotic myocardium. The ability of transplanted progenitor cells to improve function within the failing heart has been shown in experimental animal models and in some human clinical trials. [ 1 ] In November 2011, a large group of collaborators at Minneapolis Heart Institute Foundation at Abbott Northwestern found no significant difference in left ventricular ejection fraction (LVEF) or other markers, between a group of patients treated with cellular cardiomyoplasty and a group of control patients. [ 2 ] In this study, all patients were post MI, post percutaneous coronary intervention (PCI) and that infusion of progenitor cells occurred 2–3 weeks after intervention. In a study that is currently underway (February 2012), however, more positive results were being reported: In the SCIPIO trial, patients treated with autologous cardiac stem cells post MI have been reported to be showing statistically significant increases in LVEF and reduction in infarct size over the control group at four months after implant. Positive results at the one-year mark are even more pronounced. [ 3 ] Yet the SCIPIO trial "was recently called into question". [ 4 ] [ 5 ] Harvard University is "now investigating the integrity of some of the data". [ 4 ] The Lancet recently published a non-specific ‘Expression of concern’ about the paper. [ 6 ] Subsequently, another preclinical study also raised doubts on the rationale behind using this special kind of cell, [ 7 ] as it was found that the special cells only have a minimal ability in generating new cardiomyocytes. [ 8 ] Some specialists therefore now raise concerns to continue. [ 8 ]
To date, the ideal progenitor cells have not been found or created. With the goal of recreating human tissue, the use of embryonic stem cells (ESC) was the initial logical choice. These pluripotent cells can conceptually give rise to any somatic cell line in the human body and while animal studies have shown restoration of cardiac function, immunologic rejection issues and teratoma formation have rendered ESC's a high risk. [ 9 ] [ 10 ]
Human-induced pluripotent stem cells (iPSCs) are a cell line derived from somatic cells which have been induced through a combination of transcription factors . The iPSC line is very similar or identical to ESCs in many regards and also shows great promise in cardiac potential. [ 11 ] This cell line, however, is also less than ideal in that this cell type has been unable to mature into a homogeneous cell culture, making it immunogenic and teratogenic . [ 12 ] A third cell line that shows great promise and has no known safety concerns is the adult stem cell derived from bone marrow or from cardiac tissue explants. It has been shown in several studies that adult stem cells do have cardiogenic potential. [ 13 ] [ 14 ] [ 15 ]
Presently, the success of adult stem cells in regenerating human myocardium is just a fraction of what it could be. Three major challenges have been observed. Adult stem cells exhibit a minimal [ clarification needed ] commitment to engraft into the damaged myocardium, they have low survival rates and they have limited proliferation. [ 16 ] The positive effects observed in clinical trials today are a result of the work of donated stem cells that persist in the damaged myocardium for just days to weeks after delivery. Clearly, if cell survival is prolonged, these effects could be greatly enhanced. [ citation needed ] This is where a majority of research is being done today and several methodologies hold great promise. [ 17 ] [ 18 ]
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In dental anatomy , the cementoenamel junction ( CEJ) is the location where the enamel , which covers the anatomical crown of a tooth , and the cementum , which covers the anatomical root of a tooth, meet. Informally it is known as the neck of the tooth. [ 1 ] The border created by these two dental tissues has much significance as it is usually the location where the gingiva (gums) attaches to a healthy tooth by fibers called the gingival fibers . [ 2 ]
Active recession of the gingiva reveals the cementoenamel junction in the mouth and is usually a sign of an unhealthy condition. The loss of attachment is considered a more reliable indicator of periodontal disease . The CEJ is the site of major tooth resorption . A significant proportion of tooth loss is caused by tooth resorption, which occurs in 5 to 10 percent of the population. The clinical location of CEJ which is a static landmark, serves as a crucial anatomical site for the measurement of probing pocket depth (PPD) and clinical attachment level (CAL). The CEJ varies between subjects, but also between teeth from the same person. [ 1 ]
There exists a normal variation in the relationship of the cementum and the enamel at the cementoenamel junction. In about 60–65% of teeth, the cementum overlaps the enamel at the CEJ, while in about 30% of teeth, the cementum and enamel abut each other with no overlap. In only 5–10% of teeth, there is a space between the enamel and the cementum at which the underlying dentin is exposed. [ 3 ]
In the tooth bud, regions where enamel formation is completed, the enamel organ gives rise to Hertwig's epithelial root sheath, composed of two epithelial layers derived from the external and internal epithelia. The sheath is irregularly fragmented in time and space as it promotes cementum deposition on the newly formed dentin. After this fragmentation, Hertwig's epithelial root sheath also participates in cementogenesis and formation of the periodontal ligament , giving rise to the epithelial rests of Malassez. This irregular fragmentation of Hertwig's epithelial root sheath yields an equally irregular limit of cervical enamel and an irregular onset of formation and deposition of cementum. Consequently, the relationship between cementum and enamel at the CEJ presents an irregular contour, as observed during scanning electron microscope (SEM) analysis of the primary teeth.
Fragmentation of Hertwig's epithelial root sheath and exposure of dentin covered by a thin layer of intermediate cementum are fundamental for the onset of cementogenesis . If Hertwig's epithelial root sheath is not fragmented, there will be enamel deposition and it will be transformed into reduced epithelium, thus preventing cementum deposition on its surface. [ 4 ]
The shape and location of the cementoenamel junction (CEJ) on each tooth surface should be considered. CEJs differ from tooth to tooth in terms of their anatomy. The curvature of the CEJ is greatest on anterior teeth due to the narrow profile of these teeth. [ 6 ] On the anteriors, the distal aspect's curvature is usually one mm lower than the mesial aspect. Posterior teeth have flatter CEJ curvatures on the inter-proximal surfaces in comparison to the anteriors. [ 7 ]
Root resorption often starts at cementoenamel junction (CEJ) in teeth. Types of tooth resorption include internal resorption and external resorption. [ 8 ]
There are two types of internal resorption - root canal (internal) replacement resorption and internal inflammatory resorption.
External resorption can be classified into four categories by its clinical and histologic manifestations: external surface resorption, external inflammatory root resorption, replacement resorption, and ankylosis . External inflammatory root resorption can be further categorized into cervical resorption with or without a vital pulp (invasive cervical root resorption) and external apical root resorption. [ 8 ]
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Cementum [ 1 ] is a specialized calcified substance covering the root of a tooth . The cementum is the part of the periodontium that attaches the teeth to the alveolar bone by anchoring the periodontal ligament . [ 2 ]
The cells of cementum are the entrapped cementoblasts, the cementocytes. Each cementocyte lies in its lacuna , similar to the pattern noted in bone. These lacunae also have canaliculi or canals. Unlike those in bone, however, these canals in cementum do not contain nerves, nor do they radiate outward. Instead, the canals are oriented toward the periodontal ligament and contain cementocytic processes that exist to diffuse nutrients from the ligament because it is vascularized.
After the apposition of cementum in layers, the cementoblasts that do not become entrapped in cementum line up along the cemental surface along the length of the outer covering of the periodontal ligament. These cementoblasts can form subsequent layers of cementum if the tooth is injured.
Sharpey fibers are part of the principal collagenous fibers of the periodontal ligament embedded in the cementum and alveolar bone to attach the tooth to the alveolus. [ 3 ]
If cementum can be observed on teeth, it can imply that the roots are exposed, showing that the clinical crown (the exposed part of the tooth) is bigger than the anatomical crown (the surface of the tooth covered by enamel). [ 4 ] This is often due to gingival recession and may be an indication of periodontal disease . [ 5 ]
The cementum joins the enamel to form the cementoenamel junction (CEJ), which is referred to as the cervical line .
Three possible types of transitional interfaces may be present at the CEJ. The traditional view was that certain interfaces dominated in certain oral cavities. The CEJ may exhibit all of these interfaces in an individual's oral cavity, and there is even considerable variation when one tooth is traced circumferentially. [ 6 ]
When the cementoid reaches the full thickness needed, the cementoid surrounding the cementocytes becomes mineralized, or matured, and is then considered cementum. The dentinocemental junction (DCJ) is formed because of the apposition of cementum over the dentin. [ 7 ] This interface is not as defined, either clinically or histologically, as that of the dentinoenamel junction (DEJ), given that cementum and dentin are of common embryological background, unlike that of enamel and dentin. [ 8 ]
The dentinocemental junction (DCJ) is a relatively smooth area in the permanent tooth, and attachment of cementum to the dentin is firm but not understood completely. [ 9 ]
The different categories of cementum are based on the presence or absence of cementocytes, as well as whether the collagen fibres are extrinsic or intrinsic . It is thought that fibroblasts , and some cementoblasts , secrete extrinsic fibres, but only cementoblasts secrete intrinsic fibres. [ 10 ] The extrinsic fibres within acellular extrinsic fibre cementum, travel perpendicular to the surface of the root and allow the tooth to attach to the alveolar bone by the periodontal ligament (PDL), continuous with the cementodentinal junction (CDJ). [ 11 ] Acellular cementum only contains extrinsic collagen fibres. Whereas, cellular cementum is quite thick and contains both extrinsic and intrinsic collagen fibres. [ 11 ] The first cementum to be formed during tooth development is acellular extrinsic fibre cementum. [ 12 ] [ 13 ] The acellular layer of cementum is living tissue that does not incorporate cells into its structure and usually predominates on the coronal half of the root; cellular cementum occurs more frequently on the apical half. [ 9 ] In summary, the main types of cementum are as follows: acellular afibrillar cementum (AAC), acellular extrinsic fibres cementum (AEFC), cellular intrinsic fibres cementum (CIFC) and mixed stratified cementum (MSC) which displays both cellular and acellular cementum. [ 11 ] [ 14 ]
Cellular cementum contains cells and is the medium of attachment of collagen fibres to the alveolar bone. It is also responsible for minor repair of any resorption by continued deposition to keep the attachment apparatus intact. [ 15 ] Acellular cementum does not contain cells and has a main purpose of adaptive function. [ 16 ]
Cementum is slightly softer than dentin and consists of about 45% to 50% inorganic material ( hydroxylapatite ) by weight and 50% to 55% organic matter and water by weight. [ 17 ] The organic portion is composed primarily of collagen and proteoglycans . [ 18 ] Cementum is avascular, receiving its nutrition through its own imbedded cells from the surrounding vascular periodontal ligament . [ 19 ]
The cementum is light yellow and slightly lighter in color than dentin . It has the highest fluoride content of all mineralized tissue. Cementum also is permeable to a variety of materials. It is formed continuously throughout life because a new layer of cementum is deposited to keep the attachment intact as the superficial layer of cementum ages. Cementum on the root ends surrounds the apical foramen and may extend slightly onto the inner wall of the pulp canal.
Cementum is secreted by cells called cementoblasts within the root of the tooth and is thickest at the root apex (the end of the root where the nerves and blood vessels enter the tooth). These cementoblasts develop from undifferentiated mesenchymal cells in the connective tissue of the dental follicle or sac. Cementoblasts produces cementum in a rhythmic manner on intervals indicating periods of activity and periods of rest, producing so-called incremental lines of Salter. Incremental lines of Salter are the only incremental lines in the tooth that are hypercalcified, because there is a much smaller organic portion (collagen fibers) than inorganic portion (hydroxyapatite crystals) of cementum, so when the cementoblasts rest they leave a space for the inorganic portion. Conversely, in enamel ameloblasts (incremental lines of Retzius) and dentin odontoblasts (incremental lines of von Ebner), the inorganic portion is much greater than the organic portion, so when ameloblasts and odontoblasts rest, they leave a space for the organic portion and become hypocalcified. [ 9 ]
Unlike ameloblasts and odontoblasts , which leave no cellular bodies in their secreted products, during the later steps within the stage of apposition , many of the cementoblasts become entrapped by the cementum they produce, becoming cementocytes. Thus again, cementum is more similar to alveolar bone, with its osteoblasts becoming entrapped osteocytes . [ 20 ]
Cementum is capable of repairing itself to a limited degree, but cannot regenerate. It is not resorbed under normal conditions. [ 12 ]
A 2010 archeological study has found that cementum has five times the amount of mitochondrial DNA compared to dentin , which is commonly sampled. [ 26 ] Teeth are increasingly utilized as a source of nuclear DNA to aid identification of human remains. DNA extraction and the results of genetic analysis from the tissue are extremely variable and to some extent unpredictable. However, the quantity of DNA available in dentin is affected by age and dental disease, whereas that in cementum is not. [ 27 ]
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Cenderitide (also known as chimeric natriuretic peptide or CD-NP ) is a natriuretic peptide developed by the Mayo Clinic as a potential treatment for heart failure . [ 1 ] [ 2 ] [ 3 ] Cenderitide is created by the fusion of the 15 amino acid C-terminus of the snake venom dendroaspis natriuretic peptide (DNP) with the full C-type natriuretic peptide (CNP) structure. [ 2 ] This peptide chimera is a dual activator of the natriuretic peptide receptors NPR-A and NPR-B and therefore exhibits the natriuretic and diuretic properties of DNP, as well as the antiproliferative and antifibrotic properties of CNP. [ 1 ] [ 3 ]
When faced with pressure overload, the heart attempts to compensate with a number of structural alterations including hypertrophy of cardiomyocytes and increase of extracellular matrix (ECM) proteins. [ 4 ] [ 5 ] Rapid accumulation of ECM proteins causes excessive fibrosis resulting in decreased myocardial compliance and increased myocardial stiffness. [ 5 ] [ 6 ] The exact mechanisms involved in excessive fibrosis are not fully understood but there is evidence that supports involvement from local growth factors FGF-2 , TGF-beta and platelet-derived growth factor. [ 7 ] [ 8 ] [ 9 ] TGF-β1 plays an important role in cardiac remodelling through the stimulation of fibroblast proliferation, ECM deposition and myocyte hypertrophy. [ 10 ] [ 11 ] [ 12 ] The increase in TGF-beta 1 expression in a pressure-overloaded heart correlates with the degree of fibrosis, suggesting TGF-beta 1 involvement in the progression from a compensated hypertrophy to failure. [ 13 ] [ 14 ] Through an autocrine mechanism, TGF-beta 1 acts on fibroblasts by binding TGF-beta 1 receptors 1 and 2. Upon receptor activation, the receptor-associated transcription factor Smad becomes phosphorylated and associates with Co-Smad. [ 15 ] This newly formed Smad-Co-Smad complex enters the nucleus where it acts as a transcription factor modulating gene expression. [ 15 ] Cardiac remodelling of the ECM is also regulated by the CNP/NPR-B pathway as demonstrated by the improved outcomes in transgenic mice with CNP over-expression subjected to myocardial infarction. [ 16 ] [ 17 ] Binding of CNP to NPR-B catalyzes the synthesis of cGMP, which is responsible for mediating the anti-fibrotic effects of CNP. [ 18 ] Fibrotic heart tissue is associated with an increase risk of ventricular dysfunction which can ultimately lead to heart failure . [ 5 ] [ 19 ] Thus, anti-fibrotic strategies are a promising approach in the prevention and treatment of heart failure .
As cenderitide interacts with both NRP-A and NRP-B, this drug has antifibrotic potential. [ 1 ] Binding of cenderitide to NRP-B elicits an antifibrotic response by catalyzing formation of cGMP similar to the response seen with endogenous CNP. Additionally, in vitro study of human fibroblasts demonstrates that cenderitide reduces TGF-beta 1 induced collagen production. [ 1 ] [ 20 ] These two proposed mechanisms illustrate therapeutic potential for the reduction of fibrotic remodelling in the hypertensive heart. Through combined effects of CNP and DNP, cenderitide treatment results in a reduction in stress on the heart (through natriuresis/diuresis) and inhibition of pro-fibrotic, remodeling pathways. [ 1 ]
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Cenesthopathy (from French : cénestopathie , [ 1 ] formed from the Ancient Greek κοινός ( koinós ) "common", αἴσθησῐς ( aísthēsis ) "feeling", "perception" + πᾰ́θος ( páthos ) "feeling, suffering, condition"), also known as coenesthesiopathy , [ 2 ] is a rare psychiatric term used to refer to the feeling of being ill and this feeling is not localized to one region of the body . [ 3 ] Most notably, cenesthopathies are characterized by aberrant and strange bodily sensations (for example, a feeling of wires or coils being present within the oral region ; tightening, burning, pressure, tickling etc. occurring in various parts of the body, and so on). [ 4 ]
The established occurrence of coenesthetic hallucinations in 18% of individuals with a psychiatric diagnosis of schizophrenia has led to the formulation of a separate subgroup of schizophrenia in the ICD-10 , called cenesthopathic schizophrenia . [ 2 ] [ 6 ] Cenesthopathic schizophrenia is included (but not defined) within the category "other schizophrenia" ( F20.8 ) in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems . [ 7 ] [ 8 ]
Cenesthopathy (originally French : cénestopathie ) is a term created in 1907 by the French neuro-psychiatrists Ernest Ferdinand Pierre Louis Dupré and Paul Camus. [ 1 ] [ 9 ] [ 10 ]
This medical symptom article is a stub . You can help Wikipedia by expanding it .
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A center of excellence ( COE or CoE ), also called an excellence center , is a team, a shared facility or an entity that provides leadership , best practices , research , support, or training for a focus area.
Due to its broad usage and vague legal precedent, a "center of excellence", in one context, may have completely different characteristics from another. The focus area might be a technology (such as Java ), a business concept (such as BPM ), a skill (such as negotiation ) or a broad area of study (such as women's health ). A center of excellence may also be formed to revitalize stalled initiatives. [ 1 ] The term may also refer to a network of institutions collaborating with each other to pursue excellence in a particular area. [ 2 ] (e.g. the Rochester Area Colleges Center for Excellence in Math and Science ).
Within an organization, a center of excellence may refer to a group of people, a department or a shared facility. It may also be known as a competency center , or as a capability center , or as an excellence center . Stephen Jenner and Craig Kilford, in Management of Portfolios , mention COE as a coordinating function which ensures that change initiatives are delivered consistently and well, through standard processes and competent staff. [ 3 ] In technology companies, the center of excellence concept is often associated with new software tools, technologies or associated business concepts such as service-oriented architecture or business intelligence . [ 4 ] [ 5 ]
In academic institutions, a center of excellence often refers to a team with a clear focus on a particular area of research; such a center may bring together faculty members from different disciplines and provide shared facilities. [ 6 ]
The governments of Guyana and India jointly formed the Centre for Excellence in Information Technology (CEIT) at the University of Guyana in 2019. [ 7 ]
In Australia, the Australian Research Council (ARC) funds a competitive grant program for centres of excellence which link a number of institutions within the country and internationally in a specific field of research. [ 8 ] New centres are funded every three years and each run for seven years. [ 8 ]
2020-2027:
2017-2024:
2014-2021:
2011-2018
2004/5-2013
In the Philippines , a center of excellence (COE) is a certification given by the Commission on Higher Education to departments within a higher education institution (e.g. a college within a university) which "continuously demonstrates excellent performance in the areas of instruction, research and publication, extension and linkages and institutional qualifications". Candidates for this certification are referred as centers of development (CODs) by the education body. [ 9 ]
In Russia, the Center of Excellence status (in Russian it is used notion Leading scientific school ) is granted by the Council for Grants of the President of the Russian Federation since 1996. [ 10 ] To obtain the COE status, a group of scientists, usually based on a department at a university or a laboratory at an academic institute, and its leader should have a high scientific reputation and should submit an application, which presents a plan of scientific and educational work for the period of two years, to the council. The council issues a special certificate of the COE status to the leader of the group. [ 11 ]
In the United Kingdom, schools and sixth forms specialising in an area of curriculum are known as specialist schools . These schools are recognised as centres of excellence in their specialist subject areas. [ 12 ] [ 13 ] Schools that attained Beacon status were also recognised as centres of excellence, [ 14 ] however this status has been discontinued. [ 15 ]
Walmart is designating certain employee healthcare venues as centers of excellence. In 2013, several regions of the country (Dallas-Fort Worth; Northern Arkansas; Orlando, FL) Walmart is offering employees free treatment when they use the designated CoEs. Treatments are administered to covered employees, who travel to the centers, along with a caregiver, for a course of treatment at the center. Depending on the budgetary outcome, Walmart will be sharing its operational results with other employers, as a method of controlling its healthcare costs. [ 16 ]
Ford Motor Company opened its Ford Ion Park battery center of excellence, meant to centralize a cross-functional team to accelerate the development of battery and battery cell technology. Electrical batteries would then serve as the basis for all-electric vehicles. [ 17 ]
Northrop Grumman has invested in a manned aircraft design center of excellence in Melbourne, Florida . It uses modeling and simulation tools at the center of excellence which predict the performance of its test-bed aircraft, as a method for reducing risk during the process of developing the B-21. [ 18 ] In 2013, it designated five centres for excellence in the U.S. [ 19 ]
Huntington Ingalls Industries is building out an Unmanned Systems center of excellence, which is working on Boeing's project for the Navy's Extra Large Unmanned Undersea Vehicle. [ 20 ]
Asda 's merchandising centre of excellence in Leeds contains "a full-size model store for mocking up different shelf layouts and a state-of-the-art virtual reality lab, where Asda and its suppliers can test store layouts and construction plans". [ 21 ]
Unum opened its IT centre of excellence in Carlow , Ireland in 2008, [ 22 ] expanding it in 2020 [ 23 ] promoting business technology in the U.S. [ 24 ] and abroad [ 25 ] [ 26 ]
IBM Consulting launched its center of excellence for transformative generative AI in 2023. [ 27 ]
Alliant Techsystems , Otis Elevator , Alcoa , Greatbatch , and GE have each used centers of excellence as organizational mechanisms to gain economies of scale , when discovering and sharing efficiencies of operation. [ 28 ]
In the healthcare sector, the term often refers to a center that provides sufficient and easily accessible medical services to patients. [ 29 ]
The National Institutes of Health (NIH) of the United States, in 2023, allocated $24 million to create 10 maternal health research centers of excellence. [ 30 ]
In the British NHS , the term is almost always used sarcastically , following its popularisation by Dr Peter Gooderham on the Doctors.net.uk fora. [ 31 ] It can often be heard being used to describe tertiary centres by staff working in district general hospitals.
In the European defense community, the European Centre of Excellence for Countering Hybrid Threats is a response to hybrid warfare on its periphery; the COE seeks to inform, and also protect its non- NATO components, as well as its non- PESCO members. [ 32 ] The US Department of Defense (DoD) intends to use CoEs that focus on key technologies, such as drones, and commercial satellite imagery. [ 33 ]
The Army maintains numerous Centers of Excellence (CoE) at major universities, [ 34 ] training installations, and other locations:
TRADOC oversees ten of these Centers of Excellence, each focused on a separate area of expertise within the Army. These centers train over 500,000 Soldiers and service members each year. [ 49 ]
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The Central Brain Tumor Registry of the United States (CBTRUS) is the primary national database of malignant and benign tumors of the brain, "other central nervous system (CNS), tumors of the pituitary and pineal glands, olfactory tumors of the nasal cavity, and brain lymphoma and leukemia." [ 1 ] A non-profit , it was established in 1992. [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ]
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Central Regional Dental Testing Service ( CRDTS ) is one of five examination agencies for dentists in the United States . The other examination agencies are, West Regional Examining Board , Northeast Regional Board of Dental Examiners , Southern Regional Testing Agency , and Council of Interstate Testing Agencies . These were organized to standardize clinical exams for licensure.
Member states that help create the exam are: Colorado , Georgia , Hawaii , Illinois , Iowa , Kansas , Minnesota , Missouri , Nebraska , New Mexico , North Dakota , South Carolina , South Dakota , Washington , West Virginia , Wisconsin , and Wyoming .
Other states that accept the exam for licensure: Alabama , Arizona , Arkansas , Colorado Connecticut , Georgia , Idaho , Illinois , Indiana , Iowa , Kansas , Kentucky , Maine , Maryland , Massachusetts , Michigan , Minnesota , Missouri , Montana , Nebraska New Hampshire , New Mexico , North Dakota , Ohio , Oregon , Pennsylvania , Rhode Island , South Carolina , South Dakota , Tennessee , Texas , Utah , Virginia , Washington , West Virginia , Wisconsin , Wyoming , and Vermont .
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The central governor is a proposed process in the brain that regulates exercise in regard to a neurally calculated safe exertion by the body. In particular, physical activity is controlled so that its intensity cannot threaten the body’s homeostasis by causing anoxic damage to the heart muscle . The central governor limits exercise by reducing the neural recruitment of muscle fibers. This reduced recruitment causes the sensation of fatigue . The existence of a central governor was suggested to explain fatigue after prolonged strenuous exercise in long-distance running and other endurance sports, but its ideas could also apply to other causes of exertion-induced fatigue.
The existence of a central governor was proposed by Tim Noakes in 1997, but a similar idea was suggested in 1924 by Archibald Hill . It was first published as a full theory by Tim Noakes, Alan St Clair Gibson and Vicki Lambert in five linked articles in the British Journal of Sports Medicine in 2004-2005 [ 1 ]
In contrast to this idea is the one that fatigue is due to peripheral "limitation" or "catastrophe." In this view, regulation by fatigue occurs as a consequence of a failure of homeostasis directly in muscles.
The 1922 Nobel Prize in Physiology or Medicine winner Archibald Hill proposed in 1924 that the heart was protected from anoxia in strenuous exercise by the existence of a governor.
the heart is able to regulate its output, to some extent, in accordance with the degree of saturation of the arterial blood ... we suggest that, in the body (either in the heart muscle itself or in the nervous system), there is some mechanism which causes a slowing of the circulation as soon as a serious degree of unsaturation occurs, and vice versa . This mechanism would tend, to some degree, to act as a ‘governor’, maintaining a reasonably high degree of saturation of the blood: the breathing of a gas mixture rich in oxygen would produce a greater degree of saturation of the blood and so allow the output to increase until the ‘governor’ stopped it again. We realise the danger of a hypothesis partly suggested by teleological reasoning: in this case, however, we can see no other explanation of our experimental results pp. 163 [ 2 ]
This hypothesis was disregarded and further research upon exercise fatigue was modeled in terms of it being due to a mechanical failure of the exercising muscles ("peripheral muscle fatigue"). This failure was caused either by an inadequate oxygen supply to the exercising muscles, lactic acid buildup, or total energy depletion in the exhausted muscles. [ 3 ]
Tim Noakes , a professor of exercise and sports science at the University of Cape Town , in 1997 [ 4 ] has renewed Hill’s argument on the basis of modern research. Along with collaborators Alan St Clair Gibson and Vicki Lambert, they suggested that the power output by muscles during exercise is continuously adjusted in regard to calculations made by the brain in regard to a safe level of exertion. These neural calculations factor in earlier experience with strenuous exercise, the planning duration of the exercise, and the present metabolic state of the body. These brain models [ 5 ] ensure that body homeostasis is protected, and an emergency reserve margin is maintained. [ 6 ] [ 7 ] [ 8 ] [ 9 ] This neural control adjusts the number of activated skeletal muscle motor units, a control which is subjectively experienced as fatigue . This process, though occurring in the brain, is outside conscious control.
the rising perception of discomfort produced by exhausting exercise progressively reduces the conscious desire to over-ride this control mechanism, which, if it were to be reduced, would lead to the recruitment of more motor units. Thus the presence of conscious over-ride would be undesirable because it would increase or maintain the exercise intensity, thereby threatening homoeostasis ... as exercise performance is centrally regulated by the CNS, then fatigue should no longer be considered a physical event but rather a sensation or emotion, separate from an overt physical manifestation—for example, the reduction in force output by the active muscles. Rather we now suggest that the physical manifestation of any increasing perception of fatigue may simply be an alteration in the subconsciously regulated pace at which the exercise is performed. Hence the novel suggestion is that the conventional understanding of fatigue is flawed because it makes no distinction between the sensation itself and the physical expression of that sensation which, we suggest, is the alteration in the subconsciously regulated pacing strategy consequent on changing motor unit recruitment/derecruitment by the CNS. [ 10 ]
Noakes, St Clair Gibson and Lambert created the idea of the central governor in the context of prolonged endurance exercise. However, they have noted that the central processes involved might also underlie the existence of other kinds of fatigue:
This new interpretation is the first to allow a more reasonable description of a number of phenomena that defy rational explanation according to the traditional ‘‘limitations’’ models of fatigue. These include, among many others, the chronic fatigue syndrome, in which affected individuals experience evident fatigue at rest, and the role of psychological and motivational factors, centrally (brain) acting pharmaceutical agents, hypnosis, shouting or sudden unexpected gunshots, or other forms of distraction including music or premeditated deception on human exercise performance. [ 11 ]
In support of this, placebos (which must be mediated by a central process) have a powerful effect upon not only fatigue in prolonged exercise, [ 12 ] [ 13 ] but also upon short term endurance exercise such as sprint speed, [ 14 ] the maximum weight that could be lifted with leg extension, [ 15 ] and the tolerance of ischemic pain and power when a tourniqueted hand squeezes a spring exerciser 12 times. [ 16 ]
The existence of a central governor over physiology has been questioned since ‘physiological catastrophes’ can and do occur in athletes (important examples in marathons have been Dorando Pietri , Jim Peters and Gabriela Andersen-Schiess ). This suggests that humans can over-ride ‘the central governor’. [ 17 ] Moreover, a variety of peripheral factors in addition to those such as lactic acid build up can impair muscle power and might act to protect against "catastrophe". [ 18 ] Another objection is that models incorporating conscious control also provide an alternative explanation [ 19 ] (see Noakes’ reply). [ 20 ]
Exercise fatigue has also been attributed to the direct effects of exercise upon the brain such as increased cerebral levels of serotonin , reduced level of glutamate secondary to uptake of ammonia in the brain, brain hyperthermia, and glycogen depletion in brain cells. [ 21 ] [ 22 ]
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Central hypoventilation syndrome ( CHS ) is a sleep-related breathing disorder that causes ineffective breathing, apnea , or respiratory arrest during sleep (and during wakefulness in severe cases). CHS can either be congenital (CCHS) or acquired (ACHS) later in life. The condition can be fatal if untreated. CCHS was once known as Ondine's curse.
ACHS can develop as a result of severe injury or trauma to the brain or brainstem . [ 1 ] Congenital cases are very rare and involve a failure of autonomic control of breathing. In 2006, there were only about 200 known cases worldwide. As of 2008, only 1000 total cases were known. [ 2 ] The diagnosis may be delayed because of variations in the severity of the manifestations or lack of awareness in the medical community, particularly in milder cases. [ 3 ] However, as there have been cases where asymptomatic family members also were found to have CCHS, it may be that these figures only reflect those found to require mechanical ventilation. In all cases, episodes of apnea occur in sleep, but in a few patients, at the most severe end of the spectrum, apnea also occurs while awake.
Although rare, cases of long-term untreated CCHS have been reported and are termed late onset CCHS (LO-CCHS). [ 4 ] There have, however, even been cases of LO-CCHS where family members found to have it have been asymptomatic. [ 5 ] Again, lack of awareness in the medical community may cause such a delay. [ 6 ] CCHS susceptibility is not known to be affected by sex or race. [ 3 ]
CHS is associated with respiratory arrests during sleep and, in some cases, to neuroblastoma (tumors of the sympathetic ganglia ), Hirschsprung disease (partial agenesis of the enteric nervous system ), [ 7 ] dysphagia (difficulty swallowing) and anomalies of the pupilla. Other symptoms include darkening of skin color from inadequate amounts of oxygen, drowsiness, fatigue, headaches, and an inability to sleep at night. Patients with CHS also have a sensitivity to sedatives and narcotics, which makes respiration even more difficult. A low concentration of oxygen in the red blood cells also may cause hypoxia-induced pulmonary vasoconstriction and pulmonary hypertension, culminating in cor pulmonale or a failure of the right side of the heart. [ 8 ] Associated complications may also include gastro-esophageal reflux, ophthalmologic issues, seizures, recurrent pneumonia, developmental delays, learning disabilities, episodes of fainting, and temperature disregulation. [ 9 ]
CHS is exhibited typically as a congenital disorder, but in rare circumstances, can also result from severe brain or spinal trauma or injury (such as after an automobile accident , stroke , asphyxiation , brain tumor , encephalitis , poisoning , as a complication of neurosurgery ) or due to particular neurodegenerative conditions such as Parkinson's disease , multiple system atrophy , or multiple sclerosis . Long and Allen (1984) were the first to report the abnormal brainstem auditory evoked responses in an alcoholic woman who recovered from Ondine's curse. These investigators hypothesized that their patient's brainstem was poisoned — not destroyed — by her chronic alcoholism. [ 10 ]
Medical investigation of patients with this syndrome has led to a deeper understanding of how the body and brain regulate breathing on a molecular level. PHOX2B , a transcription factor involved in the development of neurons, [ 11 ] can be associated with this condition. [ 12 ] [ 13 ] [ 14 ] [ 15 ] This homeobox gene is important for the normal development of the autonomic nervous system . [ 16 ]
The disease used to be classified as a " neurocristopathy ", [ 17 ] [ 18 ] or disease of the neural crest because part of the autonomic nervous system (such as sympathetic ganglia) derives from the neural crest. However, this denomination is no longer favored because essential neurons of the autonomic nervous system, including those that underlie the defining symptom of the disease (respiratory arrests), are derived from the neural tube (the medulla ), not from the neural crest, which may be the case in other mixed embryological origins and neurocristopathies. [ 19 ]
Children with CCHS develop life-threatening episodes of apnea with cyanosis , usually in the first months of life. Medical evaluation excludes lesions of the brain, heart, and lungs but demonstrates impaired responses to build-up of carbon dioxide ( hypercapnia ) and decreases of oxygen in the circulation ( hypoxia ), the two strongest stimuli to regulate breathing rate. [ 20 ]
Polysomnography shows that hypoventilation is most marked during slow-wave sleep . Specifically, infants with CCHS usually display lower tidal volumes during sleep, meaning they inhale less air during a normal breath. [ 21 ] In the most severe cases, hypoventilation is present during other nonrapid eye movement sleep stages and even wakefulness. A subset of CCHS patients are at very high risk for developing malignant neural crest-derived tumors , such as neuroblastoma .
Sequencing of the gene PHOX2B revealed mutations in 91% of the cases within a French cohort. [ 7 ]
Physicians unable to recognize the disorder should seek help from a neurologist and a pulmonologist. In some locations, such as France, optimal management of patients, once identified, has been aided by the creation of a national registry and the formation of a network of centers. [ citation needed ]
People generally require tracheostomy and lifetime mechanical ventilation on a ventilator in order to survive. However, it has been shown that biphasic cuirass ventilation can effectively be used without the need for a tracheotomy. Other potential treatments for CCHS include oxygen therapy and medicine for stimulating the respiratory system. Problems may arise with the extended use of ventilators, including fatal infections and pneumonia. [ 22 ]
There are two primary organisations focused on delivering new treatments for CCHS. These are Keep Me Breathing , a UK based research charity which focuses solely on CCHS and The CCHS Network , a US based research charity which focuses the vast majority of its funding on CCHS scientific research.
Most people with CCHS (unless they have the Late Onset form) do not survive infancy, unless they receive ventilatory assistance during sleep. An alternative to a mechanical ventilator is diaphragm pacing . [ 23 ]
CCHS was first described in 1962 by Severinghaus and Mitchell in three patients following surgery to the upper cervical spinal cord and brainstem . [ 24 ]
Its name is a reference to the story of Ondine and Hans, characters in Ondine , a 1938 play by Jean Giraudoux based on traditions tracing back through Undine (a novella of 1811) to earlier European folk tales. The water-spirit Ondine tells her future husband Hans, whom she had just met, that "I shall be the shoes of your feet ... I shall be the breath of your lungs". Ondine reluctantly makes a pact with her uncle the King of the Ondines that if Hans ever deceives her he will die. After their honeymoon, Hans is reunited with his first love Princess Bertha. Ondine leaves Hans in an attempt to protect him, but she is recaptured by a fisherman and Hans is stricken by the King's curse. On meeting Ondine again, Hans tells her that "all the things my body once did by itself, it does now only by special order ... A single moment of inattention and I forget to breathe". Hans and Ondine kiss, after which he dies.
Since being coined in 1962 the name has become controversial in medical literature, as later summaries frequently misunderstood the plot of Ondine and its connection to the diagnosis. Most frequently, Ondine was inaccurately blamed for cursing Hans, but other mistakes sometimes changed the nature of the curse itself. Such errors led to confusion in defining the medical condition. [ 25 ]
In season 7 episode 20 of Chicago Med named End of the Day, Anything Can Happen , a mob boss daughter named Eva Corluka was diagnosed with a mild congenital form of this disease after exome genome testing post-appendectomy.
In the 1987 thriller film Black Widow the villainess uses carefully formulated drugs to induce respiratory failure in her wealthy older male victims, making the cause of their deaths to appear to be due to Ondine’s Curse.
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Central venous pressure ( CVP ) is the blood pressure in the venae cavae , near the right atrium of the heart . CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), [ 1 ] although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure (where central venous pressure increases, but right atrial pressure stays the same; VR = CVP − RAP).
CVP has been, and often still is, used as a surrogate for preload , and changes in CVP in response to infusions of intravenous fluid have been used to predict volume-responsiveness (i.e. whether more fluid will improve cardiac output ). However, there is increasing evidence that CVP, whether as an absolute value or in terms of changes in response to fluid, does not correlate with ventricular volume (i.e. preload ) or volume-responsiveness, and so should not be used to guide intravenous fluid therapy. [ 2 ] [ 3 ] Nevertheless, CVP monitoring is a useful tool to guide hemodynamic therapy .
The cardiopulmonary baroreflex responds to an increase in CVP by decreasing systemic vascular resistance while increasing heart rate and ventricular contractility in dogs. [ 4 ]
Pulmonary capillary wedge pressure
Normal CVP in patients can be measured from two points of reference: [ citation needed ]
CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP. [ citation needed ]
In most intensive care units , facilities are available to measure CVP continuously. [ citation needed ]
Normal values vary between 4 and 12 cm H 2 O.
Factors that increase CVP include: [ citation needed ]
Factors that decrease CVP include:
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In dentistry, centric relation is the mandibular jaw position in which the head of the condyle is situated as far anterior and superior as it possibly can within the mandibular fossa/glenoid fossa .
It is defined as, "The maxillo-mandibular relationship in which the condyles articulate with the thinnest avascular portion of their respective discs with the complex in the anterior-superior position against the slopes of the articular eminences. This position is independent of tooth contact. This position is clinically discernible when the mandible is directed superiorly and anteriorly. It is restricted to a purely rotary movement about the transverse horizontal axis". — GPT.
This position is used when restoring edentulous patients with removable or either implant -supported hybrid or fixed prostheses. Because the dentist wants to be able to reproducibly relate the patient's maxilla and mandible, but the patient does not have teeth with which to establish his or her own vertical dimension of occlusion , another method has been devised to achieve this goal. The condyle can only be in the same place as it was the last time it was positioned by the dentist if it is consistently moved to the most superior and anterior position within the fossa.
It is a physiologic position that is used for reproducibility. The Temporomandibular Joint is not restricted to Centric Relation in function. At the most superior position, the condyle-disc assemblies are braced medially, thus centric relation is also the midmost position. A properly aligned condyle-disc assembly in centric relation can resist maximum loading by the elevator muscles with no sign of discomfort. It also allows for the most repeatable and recordable position, and therefore should be used when designing an appropriate occlusion.
Methods of Recording Centric Relation:
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https://en.wikipedia.org/wiki/Centric_relation
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A cephalotribe was a medical instrument used in obstetrics to crush the skull of stillborn fetuses ( cephalotripsy ). It was used in cases of obstructed labor (dystocia) to aid delivery . [ 1 ] [ 2 ]
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Cerebellar degeneration is a condition in which cerebellar cells, otherwise known as neurons , become damaged and progressively weaken in the cerebellum . [ 1 ] There are two types of cerebellar degeneration; paraneoplastic cerebellar degeneration , and alcoholic or nutritional cerebellar degeneration. [ 2 ] As the cerebellum contributes to the coordination and regulation of motor activities, as well as controlling equilibrium of the human body, any degeneration to this part of the organ can be life-threatening. Cerebellar degeneration can result in disorders in fine movement, posture, and motor learning in humans, due to a disturbance of the vestibular system . This condition may not only cause cerebellar damage on a temporary or permanent basis, but can also affect other tissues of the central nervous system , those including the cerebral cortex , spinal cord and the brainstem (made up of the medulla oblongata , midbrain , and pons ). [ 2 ]
Cerebellar degeneration can be attributed to a plethora of hereditary and non-hereditary conditions. More commonly, cerebellar degeneration can also be classified according to conditions that an individual may acquire during their lifetime, including infectious, metabolic, autoimmune , paraneoplastic , nutritional or toxic triggers. [ 3 ]
Patients with cerebellar degeneration experience a progressive loss of nerve cells ( Purkinje cells ) throughout the cerebellum. As well as this, it is common to incur an elevated blood protein level and a high volume of lymph cells within the cerebrospinal fluid , resulting in swelling and enlargement of the brain. The most characteristic signs and symptoms experienced by patients with cerebellar degeneration include: [ 2 ] [ 4 ]
Scientific studies have revealed that psychiatric symptoms are also common in patients with cerebellar degeneration, [ 5 ] [ 6 ] where dementia is a typical psychiatric disorder resulting from cerebellar damage. Approximately 50% of all patients experience dementia as a result of paraneoplastic cerebellar degeneration. [ 2 ]
The root cause of incurring a cerebellar degenerative condition can be due to a range of different inherited or acquired (non-genetic and non-inherited) conditions, including neurological diseases, paraneoplastic disorders, nutritional deficiency, and chronic heavy alcohol use . [ 7 ]
A neurological disease refers to any ailment of the central nervous system, including abnormalities of the brain, spinal cord and other connecting nerve fibres. [ 8 ] Where millions of people are affected by neurological diseases on a worldwide scale, [ 8 ] it has been identified that the number of different types of neurological diseases exceeds six hundred, [ 9 ] any of which an individual can incur. Some of the most prevalent types include Alzheimer's disease , cerebral palsy , epilepsy , Parkinson's disease and stroke . [ 10 ] More specifically, the neurological diseases that can cause cerebellar degeneration include: [ 11 ]
Paraneoplastic disorders are a combination of non-inherited conditions that are activated by an individual's autoimmune response to a malignant tumour . These disorders prevail when T-cells (also known as white blood cells) begin to harm familiar cells in the central nervous system rather than the cancerous cells, [ 2 ] resulting in degeneration of neurons in the cerebellum. Other signs and symptoms that commonly result from the incursion of a paraneoplastic disorder include an impaired ability to talk, walk, sleep, maintain balance and coordinate muscle activity, as well as experiencing seizures and hallucinations . [ 18 ] Paraneoplastic disorders are prevalent among middle-aged individuals, typically those with lung, lymphatic , ovarian or breast cancer. [ 19 ]
Nutritional deficiency relates to an insufficient amount of macronutrients and micronutrients being provided to the body. Nutrient deficiencies are most prevalent among infants, the elderly, the poverty-stricken, and individuals with eating disorders. [ 20 ] Alcohol use disorder is the diagnosis of which an individual frequently consumes excessive amounts of alcohol, and thus becomes dependent on the intoxicating substance. Studies show that men of every age group consume more alcohol than women, where the prevalence is higher in some regions of the world than others, such as across Western Europe and Australia. [ 21 ] [ 22 ] Nutritional deficiency is a non-inherited condition that lead to impaired absorption or utilisation of the vitamin thiamine (B-1) by the body, thus causing temporary or permanent damage to cerebellar cells. [ 2 ] Alcoholic degeneration of cerebellar cells is the most common trigger of spinocerebellar ataxia. [ 23 ]
To select an appropriate and accurate diagnostic test for cerebellar degeneration, it is crucial that a range of factors specific to each patient are taken into consideration. These include; the patient's age, acuity of their signs and symptoms, associated neurological conditions, and family history of hereditary forms of cerebellar degeneration. [ 3 ] A diagnosis for cerebellar degeneration is regarded after any of the aforementioned signs and symptoms surface. For genetically classified forms of cerebellar degeneration, genetic testing can be carried out in order to confirm or deny the diagnosis, where this form of testing is only possible if the gene responsible for the cause of the condition is recognised. [ 24 ] In saying this, for most conditions the genetic cause of cerebellar degeneration is unidentified, hence these patients cannot proceed with genetic testing. [ 1 ] In cases where cerebellar degeneration is acquired, a diagnosis can be established using imaging methods such as computerised tomography (CT scans) and magnetic resonance imaging (MRI) , necessary to detect brain abnormalities in patients with cerebellar degeneration. [ 25 ]
Like any other disease, treatment for cerebellar degeneration is contingent on the underlying cause, unique to each patient. As of present time, hereditary forms of cerebellar degeneration are incurable, though they can be managed. Management is centred around coping with symptoms and improving a patient's quality of life. In these cases, immediate management of inherited cerebellum damage should involve consultation with a neurologist , followed by specific management approaches based on the signs and symptoms experienced by each unique patient. [ 3 ] These management approaches aim to provide supportive care to the patient, consisting of physical therapy to strengthen muscles, occupational therapy , and speech pathology . Long-term management of inherited cerebellar degeneration involves an ongoing commitment to supportive care therapies, as well as a longitudinal relationship with a neurologist. In some instances adjustments need to be made in the patients home, to improve accessibility and mobility in and around their living environment, to optimise safety. [ 3 ] The cerebellum is highly reactive to transcranial direct current stimulation, a technique which may improve ataxia. [ 26 ]
For non-hereditary types of cerebellar degeneration, some physical and mental indicators can be reversed by treating the fundamental cause. [ 27 ] For instance, the signs and symptoms of paraneoplastic cerebellar degeneration can be managed by initially terminating the underlying cancer with treatments such as surgery, radiation therapy and chemotherapy . In cases of nutritional or alcoholic cerebellar degeneration, symptoms of these conditions can be relieved by initially consuming a balanced diet and discontinuing the consumption of alcohol respectively, followed by dietary supplementation with thiamine. [ 2 ]
The long-term prospect for patients with cerebellar degeneration differs according to the underlying cause of the disease. [ 1 ] Each inherited or acquired disease that results in cerebellar degeneration has its own specific prognosis; however, most are generally poor, progressive and often fatal. [ 3 ]
Cerebellar degeneration continues to carry a considerable burden on the health of the world population, as well as on health agencies and governing bodies across the globe. Cerebellum-related disorders generally transpire in individuals between the ages of 45 and 65 years; however, the age of symptomatic onset differs in accordance with the underlying cause of the degenerative disorder. [ 1 ] For paraneoplastic cerebellar degeneration, the average age of onset is 50 years, generally affecting a greater population of males than females. [ 2 ] Nutritional and alcoholic cerebellar degeneration, being more prevalent than paraneoplastic cerebellar degeneration, affects individuals with a thiamine deficiency and dipsomaniacs , respectively. [ 2 ] Recent epidemiological studies on cerebellar degeneration estimated a global prevalence rate of 26 per 100,000 cases of cerebellar degeneration in children. [ 28 ]
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Cerebellar hypoplasia is a neurological condition in which the cerebellum is smaller than usual or not completely developed. [ 1 ] It has been reported in many animal species. [ 2 ]
The cerebellum is the brain's main control center for planning, adjusting, and executing movements of the body, the limbs and the eyes. It plays a major role in several forms of motor learning, including balance and posture. [ 3 ]
In the past, the evidence for a role for the cerebellum in cognitive functions was rather weak. [ 4 ] However, investigations into the cognitive neuroscience of the cerebellum are rapidly advancing, extending far beyond the traditional view. For humans, current theories support that what the cerebellum does to sensorimotor and vestibular control , it also does to cognition, emotion, and autonomic function . [ 5 ] [ 6 ] How it functions in cognition, emotion, or autonomic function in animals is still largely unknown. In 2012, a study in mice provided direct evidence that subtle disruptions in cerebellar architecture can have pronounced effects on behaviors typically associated with "autistic-like" behavior. [ 7 ]
Development of the cerebellum starts in a fetus in utero and, depending on the species, may continue for some period after birth. Postnatal development periods vary by species including: dogs up to 75 days, cats to 84 days, calves up to six months. [ 8 ]
The severity of the condition is dependent upon the time of infection and the portion of the cerebellum that is affected. The condition is not usually diagnosed by a test, but rather by a conclusion based on the symptoms observed in their behavior. There is no treatment for this because of how it arises, but there is a way for it to be prevented. It is prevented by vaccinating mothers before becoming pregnant. The vaccination is against panleukopenia [ 9 ] (a white blood cell infection).
There are very minor differences to a cat's life with cerebellar hypoplasia. [ 10 ] Usually, they are more prone to falls and being attacked. A simple solution is keeping them indoors. The condition is not infectious in any way. Some accommodations that might be needed are easier access to the litter box or higher food and water bowls.
Symptoms [ 11 ]
A hereditary link to cerebellar hypoplasia has been established in some animals, including certain breeds of cows [ 2 ] and dogs. [ 12 ]
There are numerous other potential causes for cerebellar hypoplasia. It is suspected that the most common cause is animal parvoviruses. [ 13 ]
In dogs, along with parvoviruses, it can be caused by canine herpes virus. The time frame to receive cerebellar hypoplasia is prenatal all the way up to four weeks old. Some non-infectious causes include injuries, heredity, and random events during development. [ 11 ]
In cattle, cerebellar hypoplasia is the most frequent result of bovine virus diarrhea virus. [ 14 ] This happens because the virus destroys brain cells in the immature cattle fetus. Loss of cells specifically in the cerebellum of the cattle fetus results in lesions that reduce the size of the cerebellum and cause cerebellar hypoplasia.
Feline panleukopenia ( a.k.a. feline distemper [ 15 ] or Feline Parvo) virus has long been known to cause cerebellar hypoplasia in neonatal kittens through in utero or perinatal infection. [ 16 ] In utero , the virus can pass from the dam to the developing fetus and may then disrupt the development of its cerebellum by hindering cell division. This can happen when the dam is actively infected with the virus or given a modified-live feline parvovirus vaccine when pregnant. [ 17 ] Kittens are particularly vulnerable to cerebellar hypoplasia, in particular when the protective antibodies present in their mothers' milk are no longer present at four to twelve weeks of age. Unvaccinated adult cats are also prone to developing the condition. [ 18 ]
In most cases, the cause is unknown. However, in dogs and cats, it is thought to be most likely related to in utero viral infections, toxins or genetic disorders. [ 19 ]
Other possible causes, if they occurred during the development period of the cerebellum and inhibit its growth, include: [ 20 ]
The veterinarian performs a physical exam and a neurological assessment to diagnose cerebellar hypoplasia. They will perform the physical exam to rule out other possibilities [ 11 ]
which include:
If needed, an MRI can affirm the presence of the condition, though this is not always necessary due to the usual lack of severity with cerebellar hypoplasia.
In 2004, a study was published that linked ketamine to post-anesthetic cerebellar dysfunction in cats. [ 25 ] Eleven cats that did not have any indication of cerebellar deficits before surgery developed deficits post-surgery. All of these cats were Persian crossbreeds. Ketamine can cause erratic and spastic, jerky movements and muscle tremors and is slow to be metabolized out of the system. [ citation needed ] The 2018 American Association of Feline Practitioner's Feline Anesthesia Guidelines [ 26 ] lists numerous alternatives. Gas anesthesia offers a number of advantages in many circumstances. In cats, the rapid recovery is its primary advantage. [ citation needed ]
Source [ 11 ]
The basis of care of these animals is making it easier and safer for them to move around/live as normally as possible. These are only a couple more common examples, and they are not the rule for caring for them, but the easiest and most effective ways that have been found to make these animals live comfortably.
If the root cause of the cerebellar hypoplasia impacted other parts of the developing brain and/or body, the overall health and life-span may or may not be impacted. For instance, fetuses infected in utero by feline panleukopenia virus that survive, and kittens less than a few weeks of age that become infected with it, can also have retinal dysplasia , and optic neuropathy . [ 27 ]
The level of severity and mode of infection (if any) both play a role in determining the prognosis for animals that have cerebellar hypoplasia. At worst, the animal will not survive ex-utero; at best, the animal will live for the length of time that is considered normal for its species. If the root cause of the cerebellar hypoplasia impacted other parts of the developing brain and/or body, the overall health and life-span may or may not be impacted. For instance, feline fetuses infected in utero by FPLV that survive ex-utero, and kittens less than a few weeks of age that become infected with it, can also have retinal dysplasia , and optic neuropathy .The symptoms of cerebellar hypoplasia can also affect the prognosis of the animal. In severe cases, mobility issues can negatively affect the quality of life outcomes associated with the animal. In most cases, the symptoms of cerebellar hypoplasia can cause the animal to become more vulnerable to injuries or attacks. [ 10 ] Most animals affected by cerebellar hypoplasia adapt to their disability but will need extra support and care to survive.
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A cerebral arteriovenous malformation ( cerebral AVM , CAVM , cAVM , brain AVM , or BAVM ) is an abnormal connection between the arteries and veins in the brain —specifically, an arteriovenous malformation in the cerebrum . [ 1 ]
The most frequently observed problems related to a cerebral arteriovenous malformation (AVM) are headaches and seizures , cranial nerve afflictions including pinched nerve and palsy , [ 2 ] [ 3 ] backaches, neckaches, and nausea from coagulated blood that has made its way down to be dissolved in the cerebrospinal fluid . Perhaps 15% of the population at detection are asymptomatic . [ 3 ] Other common symptoms are a pulsing noise in the head, progressive weakness , numbness and vision changes as well as debilitating, excruciating pain . [ 4 ] [ 5 ]
In serious cases, blood vessels rupture and cause bleeding within the brain ( intracranial hemorrhage ). [ a ] In more than half of patients with AVM, this is the first symptom. [ 7 ] Symptoms due to bleeding include loss of consciousness , sudden and severe headache, nausea, vomiting , incontinence , and blurred vision , amongst others. [ 4 ] Impairments caused by local brain-tissue damage on the bleed site are also possible, including seizure, one-sided weakness ( hemiparesis ), a loss of touch sensation on one side of the body and deficits in language processing ( aphasia ). [ 4 ] Ruptured AVMs are responsible for considerable mortality and morbidity. [ 8 ]
AVMs in certain critical locations may stop the circulation of the cerebrospinal fluid, causing it to accumulate within the skull and giving rise to a clinical condition called hydrocephalus . [ 5 ] A stiff neck can occur as the result of increased pressure within the skull and irritation of the meninges . [ 9 ]
A cerebral AVM is an abnormal anastomosis (connection) between the arteries and veins in the brain due to the lack of a capillary bed , and is most commonly of prenatal origin. [ 10 ] [ 11 ]
In normal cerebral circulation , oxygen-enriched blood from the heart travels in sequence through smaller blood vessels going from arteries, to arterioles and then capillaries . [ 10 ] Oxygen is removed in the capillaries to be used by the brain. [ 10 ] After the oxygen is removed, blood reaches venules and later veins which will take it back to the heart and lungs . [ 10 ] A cerebral AVM causes blood to be shunted directly from arteries to veins because the capillary bed is lacking, causing a disrupted circulation . [ 10 ] [ 11 ]
The overall annual incidence of haemorrhage from a ruptured AVM is 2-4%. Smaller AVMs have a greater propensity for haemorrhaging, whereas larger AVMs tend to more often cause seizures instead. [ 12 ]
A cerebral AVM diagnosis is established by neuroimaging studies after a complete neurological and physical examination. [ 5 ] [ 13 ] Three main techniques are used to visualize the brain and search for an AVM: computed tomography (CT), magnetic resonance imaging (MRI), and cerebral angiography . [ 13 ] A CT scan of the head is usually performed first when the subject is symptomatic. It can suggest the approximate site of the bleed. [ 3 ] MRI is more sensitive than CT in the diagnosis, and provides better information about the exact location of the malformation. [ 13 ] More detailed pictures of the tangle of blood vessels that compose an AVM can be obtained by using radioactive agents injected into the blood stream. If a CT is used in conjunction with an angiogram, this is called a computerized tomography angiogram; while, if MRI is used it is called magnetic resonance angiogram . [ 3 ] [ 13 ] The best images of a cerebral AVM are obtained through cerebral angiography. This procedure involves using a catheter , threaded through an artery up to the head, to deliver a contrast agent into the AVM. As the contrast agent flows through the AVM structure, a sequence of X-ray images are obtained. [ 13 ]
A common method of grading cerebral AVMs is the Spetzler-Martin (SM) grade. [ 14 ] This system was designed to assess the patient's risk of neurological deficit after open surgical resection (surgical morbidity), based on characteristics of the AVM itself. Based on this system, AVMs may be classified as grades 1–5. This system was not intended to characterize risk of hemorrhage. [ 15 ]
" Eloquent " is defined as areas within the brain that, if removed will result in loss of sensory processing or linguistic ability, minor paralysis, or paralysis. These include the basal ganglia, language cortices, sensorimotor regions, and white matter tracts. [ 16 ] Importantly, eloquent areas are often defined differently across studies [ 17 ] where deep cerebellar nuclei, cerebral peduncles, thalamus, hypothalamus, internal capsule, brainstem, and the visual cortex could be included.
The risk of post-surgical neurological deficit (difficulty with language, motor weakness, vision loss) increases with increasing Spetzler-Martin grade. [ 18 ]
A limitation of the Spetzler-Martin Grading system is that it does not include the following factors: Patient age, hemorrhage, diffuseness of nidus, and arterial supply. In 2010 a new supplemented Spetzler-Martin system (SM-supp, Lawton-Young) was devised adding these variables to the SM system. Under this new system AVMs are classified from grades 1–10. It has since been determined to have greater predictive accuracy than SM grades alone. [ 19 ]
Treatment depends on the location and size of the AVM and whether there is bleeding or not. [ 20 ]
The treatment in the case of sudden bleeding is focused on restoration of vital function . [ 21 ]
Anticonvulsant medications such as phenytoin are often used to control seizure; medications or procedures may be employed to relieve intracranial pressure. Eventually, curative treatment may be required to prevent recurrent hemorrhage. However, any type of intervention may also carry a risk of creating a neurological deficit. [ 22 ]
Surgical elimination of the blood vessels involved is the preferred curative treatment for many types of AVM. [ 20 ] Surgery is performed by a neurosurgeon who temporarily removes part of the skull ( craniotomy ), separates the AVM from surrounding brain tissue, and resects the abnormal vessels. [ 20 ] While surgery can result in an immediate, complete removal of the AVM, risks exist depending on the size and the location of the malformation. The AVM must be resected en bloc, for partial resection will likely cause severe hemorrhage. [ 8 ] The preferred treatment of Spetzler-Martin grade 1 and 2 AVMs in young, healthy patients is surgical resection due to the relatively small risk of neurological damage compared to the high lifetime risk of hemorrhage. Grade 3 AVMs may or may not be amenable to surgery. Grade 4 and 5 AVMs are not usually surgically treated. [ 23 ]
Radiosurgery has been widely used on small AVMs with considerable success. The Gamma Knife is an apparatus used to precisely apply a controlled radiation dosage to the volume of the brain occupied by the AVM. While this treatment does not require an incision and craniotomy (with their own inherent risks), three or more years may pass before the complete effects are known, during which time patients are at risk of bleeding. [ 20 ] Complete obliteration of the AVM may or may not occur after several years, and repeat treatment may be needed. Radiosurgery is itself not without risk. In one large study, nine percent of patients had transient neurological symptoms, including headache, after radiosurgery for AVM. However, most symptoms resolved, and the long-term rate of neurological symptoms was 3.8%. [ 24 ]
Embolization is performed by interventional neuroradiologists and the occlusion of blood vessels most commonly is obtained with ethylene vinyl alcohol copolymer ( Onyx ) or n-butyl cyanoacrylate . These substances are introduced by a radiographically guided catheter, and block vessels responsible for blood flow into the AVM. [ 25 ] Embolization is frequently used as an adjunct to either surgery or radiation treatment. [ 20 ] Embolization reduces the size of the AVM and during surgery it reduces the risk of bleeding. [ 20 ] However, embolization alone may completely obliterate some AVMs. In high flow intranidal fistulas balloons can also be used to reduce the flow so that embolization can be done safely. [ 26 ]
A first-of-its-kind controlled clinical trial by the National Institutes of Health and National Institute of Neurological Disorders and Stroke focuses on the risk of stroke or death in patients with an AVM who either did or did not undergo interventional eradication. [ 27 ] Early results suggest that the invasive treatment of unruptured AVMs tends to yield worse results than the therapeutic (medical) management of symptoms. [ 28 ] [ b ] Because of the higher-than-expected experimental event rate (e.g. stroke or death), patient enrollment was halted by May 2013, while the study intended to follow participants (over a planned 5 to 10 years) to determine which approach seems to produce better long-term results. [ 28 ]
The main risk is intracranial hemorrhage. This risk is difficult to quantify since many patients with asymptomatic AVMs will never come to medical attention. Small AVMs tend to bleed more often than do larger ones, the opposite of cerebral aneurysms . [ 29 ] If a rupture or bleeding incident occurs, the blood may penetrate either into the brain tissue ( cerebral hemorrhage ) or into the subarachnoid space , which is located between the sheaths (meninges) surrounding the brain ( subarachnoid hemorrhage ). Bleeding may also extend into the ventricular system ( intraventricular hemorrhage ). Cerebral hemorrhage appears to be most common. [ 3 ] One long-term study (mean follow up greater than 20 years) of over 150 symptomatic AVMs (either presenting with bleeding or seizures) found the risk of cerebral hemorrhage to be approximately 4% per year, slightly higher than the 2–4% seen in other studies. [ 30 ] [ 6 ] The earlier an AVM appears, the more likely it is to cause hemorrhage over one's lifetime; e.g. (assuming a 3% annual risk), an AVM appearing at 25 years of age indicates a 79% lifetime chance of hemorrhage, while one appearing at age 85 indicates only a 17% chance. [ 6 ] Ruptured AVMs are a significant source of morbidity and mortality; following a rupture, as many as 29% of patients will die, with only 55% able to live independently. [ 8 ]
The annual new detection rate incidence of AVMs is approximately 1 per 100,000 a year. The point prevalence in adults is approximately 18 per 100,000. [ 3 ] AVMs are more common in males than females, although in females pregnancy may start or worsen symptoms due to the increase in blood flow and volume it usually brings. [ 31 ] There is a significant preponderance (15–20%) of AVM in patients with hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu syndrome). [ 6 ]
Footnotes
Citations
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https://en.wikipedia.org/wiki/Cerebral_arteriovenous_malformation
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Cerebral circulation is the movement of blood through a network of cerebral arteries and veins supplying the brain . The rate of cerebral blood flow in an adult human is typically 750 milliliters per minute , or about 15% of cardiac output . Arteries deliver oxygenated blood, glucose and other nutrients to the brain. Veins carry "used or spent" blood back to the heart , to remove carbon dioxide , lactic acid , and other metabolic products. The neurovascular unit regulates cerebral blood flow so that activated neurons can be supplied with energy in the right amount and at the right time. [ 1 ] Because the brain would quickly suffer damage from any stoppage in blood supply, the cerebral circulatory system has safeguards including autoregulation of the blood vessels . The failure of these safeguards may result in a stroke . The volume of blood in circulation is called the cerebral blood flow . Sudden intense accelerations change the gravitational forces perceived by bodies and can severely impair cerebral circulation and normal functions to the point of becoming serious life-threatening conditions.
The following description is based on idealized human cerebral circulation. The pattern of circulation and its nomenclature vary between organisms.
Blood supply to the brain is normally divided into anterior and posterior segments, relating to the different arteries that supply the brain. The two main pairs of arteries are the internal carotid arteries (supply the anterior brain) and vertebral arteries (supplying the brainstem and posterior brain). [ 2 ] The anterior and posterior cerebral circulations are interconnected via bilateral posterior communicating arteries . They are part of the circle of Willis , which provides backup circulation to the brain. In case one of the supply arteries is occluded, the circle of Willis provides interconnections between the anterior and the posterior cerebral circulation along the floor of the cerebral vault, providing blood to tissues that would otherwise become ischemic . [ 3 ]
The anterior cerebral circulation is the blood supply to the anterior portion of the brain including eyes . It is supplied by the following arteries:
The posterior cerebral circulation is the blood supply to the posterior portion of the brain, including the occipital lobes , cerebellum and brainstem .
It is supplied by the following arteries:
The venous drainage of the cerebrum can be separated into two subdivisions: superficial and deep.
The superficial system is composed of dural venous sinuses , sinuses (channels) within the dura mater . The dural sinuses are therefore located on the surface of the cerebrum. The most prominent of these sinuses is the superior sagittal sinus which is located in the sagittal plane under the midline of the cerebral vault, posteriorly and inferiorly to the confluence of sinuses , where the superficial drainage joins with the sinus that primarily drains the deep venous system. From here, two transverse sinuses bifurcate and travel laterally and inferiorly in an S-shaped curve that forms the sigmoid sinuses which go on to form the two jugular veins . In the neck, the jugular veins parallel the upward course of the carotid arteries and drain blood into the superior vena cava . The veins puncture the relevant dural sinus, piercing the arachnoid and dura mater as bridging veins that drain their contents into the sinus. [ 5 ]
The deep venous system is primarily composed of traditional veins inside the deep structures of the brain, which join behind the midbrain to form the great cerebral vein (vein of Galen). This vein merges with the inferior sagittal sinus to form the straight sinus which then joins the superficial venous system mentioned above at the confluence of sinuses .
The maturation of blood vessels in the brain is a critical process that occurs postnatally. [ 6 ] It involves the acquisition of key barrier and contractile properties essential for brain function. During the early postnatal phase, endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) undergo significant molecular and functional changes.
Endothelial cells begin to express P-glycoprotein , a crucial efflux transporter that helps protect the brain by expelling harmful substances. [ 7 ] This efflux capacity is progressively acquired and becomes fully functional by the postnatal period. Additionally, VSMCs, which initially populate the arterial network, start to express contractile proteins such as smooth muscle actin (SMA) and myosin-11 , transforming VSMCs into contractile cells capable of regulating blood vessel tone and cerebral blood flow.
The expression of Myh11 in VSMCs acts as a developmental switch, with significant upregulation occurring from birth to the age of 2 to 5 years. [ 6 ] This is a critical period needed for the establishment of vessel contractility and the overall functionality of the cerebral circulation.
Cerebral blood flow (CBF) is the blood supply to the brain in a given period of time. [ 8 ] In an adult, CBF is typically 750 millilitres per minute or 15.8 ± 5.7% of the cardiac output . [ 9 ] This equates to an average perfusion of 50 to 54 millilitres of blood per 100 grams of brain tissue per minute. [ 10 ] [ 11 ] [ 12 ]
The ratio index of cerebral blood flow/cardiac output (CCRI) decreases by 1.3% per decade, even though cardiac output remains unchanged. [ 9 ] Across the adult lifespan, women have a higher CCRI than men. [ 9 ] CBF is inversely associated with body mass index . [ 9 ]
CBF is tightly regulated to meet the brain's metabolic demands. [ 10 ] [ 13 ] Too much blood (a clinical condition of a normal homeostatic response of hyperemia ) [ 1 ] can raise intracranial pressure (ICP), which can compress and damage delicate brain tissue. Too little blood flow ( ischemia ) results if blood flow to the brain is below 18 to 20 ml per 100 g per minute, and tissue death occurs if flow dips below 8 to 10 ml per 100 g per minute. In brain tissue, a biochemical cascade known as the ischemic cascade is triggered when the tissue becomes ischemic, potentially resulting in damage to and the death of brain cells . Medical professionals must take steps to maintain proper CBF in patients who have conditions like shock , stroke , cerebral edema , and traumatic brain injury .
Cerebral blood flow is determined by a number of factors, such as viscosity of blood, how dilated blood vessels are, and the net pressure of the flow of blood into the brain, known as cerebral perfusion pressure , which is determined by the body's blood pressure . Cerebral perfusion pressure (CPP) is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP). In normal individuals, it should be above 50 mm Hg. Intracranial pressure should not be above 15 mm Hg (ICP of 20 mm Hg is considered as intracranial hypertension). [ 14 ] Cerebral blood vessels are able to change the flow of blood through them by altering their diameters in a process called cerebral autoregulation ; they constrict when systemic blood pressure is raised and dilate when it is lowered. [ 15 ] Arterioles also constrict and dilate in response to different chemical concentrations. For example, they dilate in response to higher levels of carbon dioxide in the blood and constrict in response to lower levels of carbon dioxide. [ 15 ]
For example, assuming a person with an arterial partial pressure of carbon dioxide ( PaCO2 ) of 40 mmHg (normal range of 38–42 mmHg) [ 16 ] and a CBF of 50 ml per 100g per min. If the PaCO2 dips to 30 mmHg, this represents a 10 mmHg decrease from the initial value of PaCO2. Consequently, the CBF decreases by 1ml per 100g per min for each 1mmHg decrease in PaCO2, resulting in a new CBF of 40ml per 100g of brain tissue per minute. In fact, for each 1 mmHg increase or decrease in PaCO2, between the range of 20–60 mmHg, there is a corresponding CBF change in the same direction of approximately 1–2 ml/100g/min, or 2–5% of the CBF value. [ 17 ] This is why small alterations in respiration pattern can cause significant changes in global CBF, specially through PaCO2 variations. [ 17 ]
CBF is equal to the cerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR): [ 18 ]
Control of CBF is considered in terms of the factors affecting CPP and the factors affecting CVR. CVR is controlled by four major mechanisms:
Increased intracranial pressure (ICP) causes decreased blood perfusion of brain cells by mainly two mechanisms:
Cerebral perfusion pressure is the net pressure gradient causing cerebral blood flow to the brain (brain perfusion ). It must be maintained within narrow limits; too little pressure could cause brain tissue to become ischemic (having inadequate blood flow), and too much could raise intracranial pressure .
Arterial spin labeling (ASL), phase contrast magnetic resonance imaging (PC-MRI), and positron emission tomography (PET) are neuroimaging techniques that can be used to measure CBF. ASL and PET can also be used to measure regional CBF (rCBF) within a specific brain region.
rCBF at one location can be measured over time by thermal diffusion [ 19 ]
ocular group: central retinal
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https://en.wikipedia.org/wiki/Cerebral_circulation
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Cerebral salt-wasting syndrome ( CSWS ), also written cerebral salt wasting syndrome , is a rare endocrine condition featuring a low blood sodium concentration and dehydration in response to injury (trauma) or the presence of tumors in or surrounding the brain . In this condition, the kidney is functioning normally but excreting excessive sodium. [ 1 ] The condition was initially described in 1950. [ 2 ] Its cause and management remain controversial. [ 3 ] [ 4 ] In the current literature across several fields, including neurology , neurosurgery , nephrology , and critical care medicine , there is controversy over whether CSWS is a distinct condition, or a special form of syndrome of inappropriate antidiuretic hormone secretion (SIADH) . [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ]
Signs and symptoms of CSWS include large amounts of urination (polyuria, defined as over three liters of urine output over 24 hours in an adult), high amounts of sodium in the urine, low blood sodium concentration, [ 1 ] excessive thirst (polydipsia), extreme salt cravings, dysfunction of the autonomic nervous system (dysautonomia), and dehydration . Patients often self-medicate by consuming high amounts of sodium and by dramatically increasing their water intake. Advanced symptoms include muscle cramps , lightheadedness, dizziness or vertigo , feelings of anxiety or panic, increased heart rate or slowed heart rate , low blood pressure and orthostatic hypotension which can result in fainting . [ 12 ] Other symptoms frequently associated with dysautonomia include headaches , pallor , malaise , facial flushing, constipation or diarrhea , nausea , acid reflux , visual disturbances, numbness, nerve pain, trouble breathing , chest pain, loss of consciousness, and seizures . [ 12 ]
Although the pathophysiology of CSWS is not fully understood, it is usually caused by neurological injury, most commonly aneurysmal subarachnoid hemorrhage . [ 5 ] It is also reported after surgery for pituitary tumor, acoustic neuroma, calvarial remodeling, glioma and with infections including tuberculous meningitis , viral meningitis , metastatic carcinoma , and cranial trauma . [ 5 ]
CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. [ 1 ] The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume [ 3 ] whereas SIADH is consistent with a normal or high blood volume (due to water reabsorption via the V2 receptor). [ 1 ] If blood-sodium levels increase when fluids are restricted, SIADH is more likely. [ 13 ] Additionally, urine output is classically low in SIADH and elevated in CSWS. [ 1 ]
While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement. [ 1 ] The mineralocorticoid medication fludrocortisone can also improve the low sodium level. [ 1 ] [ 14 ]
In 1858, Claude Bernard first raised the possibility of a direct relationship between the central nervous system and renal excretion of osmotically active solutes. He found that a unilateral lesion in the reticular substance at the floor of the fourth ventricle produced a diuresis of chloride, but not glucose. Bernard reproduced this syndrome through renal denervation. [ 15 ] Through medullary lesioning in animals, Jungmann and Meyer from Germany induced polyuria and increased urinary salt excretion in 1913. Water intake restriction did not stop the polyuria, and salt continued to be excreted in the urine despite. [ 16 ] In 1936, McCance defined the consequences of salt depletion in normal human. Patients with extra-renal salt losses complicated by hyponatremia were found to be common-place, and consistent with McCance's description, they excreted urine virtually free of sodium. [ 17 ]
Shortly after World War II, the flame photometer was developed. The availability of the flame photometer made clinical determinations of the serum sodium concentration possible. Berry, Barnes and Richardson shared the production of this new device to measure sodium and potassium in solution of biological materials by means of the flame photometer in 1945. [ 18 ] [ 19 ] [ 20 ] Yale was one of the first medical centers to have that new device, the flame photometer, so some of the first published observations about hyponatremia came from Yale. [ 21 ]
Almost a century after the pioneering work of Bernard in animals, Peters et al., in 1950, reported three patients seen at Yale New Haven Hospital with hyponatremia associated with varying cerebral pathologies and severe dehydration. In each patient, urine sodium losses persisted despite hyponatremia and a high-salt diet. All three patients were unable to prevent urinary sodium loss despite low serum sodium levels and no evidence of extrarenal sodium loss. Their hyponatremia responded to salt therapy. They postulated that this provided evidence of an extra-pituitary cerebral structure mediating normal sodium metabolism but were unsure of its location or mechanism of action. A subsequent paper from the group at Yale attributed hyponatremia in neurologic disease to SIADH. [ 22 ]
The normal regulatory mechanism of renal adjustment of salt and water balance was better understood in 1950s. The responsibility for the maintenance of a normal volume and tonicity of the body fluids devolves on the kidneys. This modern concept of renal physiology described the transformation of a large volume of glomerular filtrate to a much smaller volume of bladder urine which has been altered. The proximal portion of renal tubule is largely responsible for the decrease in volume of the filtrate and, to less extent, for alterations in composition. However, it is in the distal tubule that induced fine adjustment of water and sodium balance. [ 23 ] In 1953, Leaf et al., demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intravascular volume. Vasopressin-ADH administration to normal humans was shown to result in water retention and urinary loss of electrolytes (primarily sodium) in other studies at the time. [ 24 ]
The term "cerebral salt wasting" (CSW) was coined by Cort in 1954. The title of a paper by Cort describing a patient with a thalamic glioma resulting in hydrocephalus and raised intracranial pressure (although it is prudent to note that the earlier-described work by Peters, Welt and colleagues in 1950 was presented in a paper entitled "A salt-wasting syndrome associated with cerebral disease"). This patient was hyponatremic and clinically dehydrated with initial salt therapy not reversing this. Salt restriction resulted in ongoing natriuria. Recommencement of salt therapy subsequently increased serum sodium. Treatment with adrenocorticotropic hormone (ACTH) and deoxycortone acetate (having potent mineralocorticoid activity) had no effect. The author postulated an external influence on renal function not adrenal or pituitary in origin. Unfortunately, the patient died three and a half weeks later in "circulatory failure with terminal shock". At autopsy, the pituitary and adrenal glands were normal. Given Bernard's ability to create a chloride diuresis without glycosuria though renal denervation, Cort postulated the existence of a neuronal connection between the hypothalamus and proximal tubule of the kidney influencing electrolyte reabsorption. In all above-described cases, there was evidence of hyponatremia and dehydration. In the ensuing years, however, hyponatremia in cerebral pathology was described without clinical or laboratory evidence of dehydration. Renal and adrenal function appeared intact, but, unlike in the earlier case of "cerebral salt wasting" described by Cort, an increase in renal absorption and plasma concentration of sodium occurred with administration of ACTH and deoxycortone acetate. [ 25 ] [ 26 ] A study on a 5-month-old female infant with diffuse cerebral damage and hyponatremia in 1957 suggested that on normal fluid intakes the child was unable to excrete solute-free water in a normal manner. This may represent the result of damage to the cerebral osmoreceptors as part of generalized brain damage. The data do not support the concept that the hyponatremia resulted from true salt-wasting, either cerebral or renal in mediation. If correction of such a state is desirable, the most useful therapeutic measure would appear to be limitation of the intake of fluid to slightly more than the amount needed to cover water expenditure from insensible losses, obligatory urine volume and growth requirements. [ 27 ]
The term "cerebral hyponatremia" was suggested in the work of Epstein, et al. 1961. Inappropriate release of endogenous vasopressin is probably responsible for hyponatremia in tuberculous meningitis. Inability to excrete water normally is also a feature of the salt wasting of certain hyponatremic patients with pulmonary tuberculosis. Similarly, it has been suggested that inappropriate release of vasopressin is the cause of hyponatremia and renal salt wasting in certain diseases, including bronchogenic carcinoma, cerebral injuries, and malformations. [ 28 ]
In 1981, Nelson et al. studied hyponatremia in neurosurgical patients, primarily subarachnoid hemorrhage, and found that isotopically measured blood volumes were contracted; he attributed this finding to cerebral salt wasting (CSW). Following these publications, the term "CSW" vanished from the literature for over two decades with hyponatremia in patients with cerebral pathology assumed to result from SIADH. Then, in 1981, a study of twelve neurosurgical patients mainly with SAH found ten to have decreased red blood cell mass, plasma volume, and total blood volume despite "fulfilling laboratory criteria" for SIADH. [ 29 ] Other authors associated hyponatremia in subarachnoid hemorrhage with increased levels of natriuretic peptides, negative sodium balance, and low central venous pressure. [ 30 ] [ 31 ] [ 32 ]
A valid diagnosis of "salt wasting" requires evidence of inappropriate urinary salt losses and a reduced "effective arterial blood volume". Unfortunately, there is no gold standard to define inappropriate urinary sodium excretion. "Effective arterial blood volume" is a concept, not a measurable variable; in fact, we often define it clinically by looking at urine sodium excretion. [ 33 ]
William Schwartz (1922–2009) attended Duke University after serving in the US Army in World War II. He observed that sulfanilamide increased excretion of sodium in patients with heart failure. This observation was the basis for the discovery and development of modern diuretic drugs. Frederic Bartter (1914–1983) worked on hormones affecting the kidney that led to the discovery of syndrome of inappropriate antidiuretic hormone (SIADH) in 1957 and Bartter syndrome in 1963. Schwartz-Bartter syndrome is named after these two scientists. The first reports of hyponatremia and renal sodium loss corrected by fluid restriction in patients with bronchogenic carcinoma were published by Bartter. At that time, no direct measurement of vasopressin was done. [ 34 ]
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https://en.wikipedia.org/wiki/Cerebral_salt-wasting_syndrome
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A cerebral shunt is a device permanently implanted inside the head and body to drain excess fluid away from the brain. They are commonly used to treat hydrocephalus , the swelling of the brain due to excess buildup of cerebrospinal fluid (CSF). If left unchecked, the excess CSF can lead to an increase in intracranial pressure (ICP), which can cause intracranial hematoma , cerebral edema , crushed brain tissue or herniation . [ 1 ] The drainage provided by a shunt can alleviate or prevent these problems in patients with hydrocephalus or related diseases.
Shunts come in a variety of forms, but most of them consist of a valve housing connected to a catheter, the lower end of which is usually placed in the peritoneal cavity . The main differences between shunts are usually in the materials used to construct them, the types of valve (if any) used, and whether the valve is programmable or not. [ 2 ]
The location of the shunt is determined by the neurosurgeon based on the type and location of the blockage causing hydrocephalus. All brain ventricles are candidates for shunting. The catheter is most commonly placed in the abdomen but other locations include the heart and lungs. [ 11 ] Shunts can often be named after the route used by the neurosurgeon. The distal end of the catheter can be located in just about any tissue with enough epithelial cells to absorb the incoming CSF. Below are some common routing plans for cerebral shunts.
It is located on the parietal bone, above the lambdoid suture, 3 to 4 cm lateral to the midline and 6 cm above the inion . [ 12 ] It is a common site for ventricular cannulation in the context of inserting a ventriculoperitoneal shunt for the treatment of hydrocephalus. It was first described by C H Frazier in 1928. [ 13 ]
A subgaleal shunt is usually a temporary measure used in infants who are too small or premature to tolerate other shunt types. The surgeon forms a pocket beneath the epicranial aponeurosis (the subgaleal space) and allows CSF to drain from the ventricles, creating a fluid-filled swelling on the baby's scalp. These shunts are normally converted to VP or other shunt types once the infant is big enough. [ 14 ]
Below is a short list of known complications that can lead to hydrocephalus requiring shunting.
There are a number of complications associated with shunt placement. Many of these complications occur during childhood and cease once the patient has reached adulthood. Many of the complications require immediate shunt revision (the replacement or reprogramming of the already existing shunt). The common symptoms often resemble a new onset of hydrocephalus, such as headaches, nausea, vomiting, double vision, and an alteration of consciousness. This can result in damage to an individual's short-term memory. [ 11 ] In the pediatric population, the shunt failure rate two years after implantation has been estimated to be as high as 50%. [ 24 ] Those patients with advanced age, prolonged hospital stay, GCS score of less than 13, extra-ventricular drains in situ, or excision of brain tumors are more likely to have early shunt malfunction. [ 25 ]
Infection is a common complication that normally affects pediatric patients because they have not yet built up immunities to a number of different diseases. Normally, the incidence of infection decreases as the patient grows older and the body gains immunity to various infectious agents. [ 11 ] Shunt infection can occur in up to 27% of patients. Infection can lead to long term cognitive defects, neurological problems, and in some cases death. Common microbial agents for shunt infection include Staphylococcus epidermidis , Staphylococcus aureus , and Candida albicans . Further factors that can lead to shunt infection include shunt insertion at a young age (less than six months old) and the type of hydrocephalus being treated. There is no strong correlation between infection and shunt type. [ 26 ] Though the symptoms of a shunt infection are generally similar to the symptoms seen in hydrocephalus, infection symptoms can also include fever and elevated white blood cell counts. [ 27 ]
Treatment of a CSF shunt infection generally includes removal of the shunt and placement of a temporary ventricular reservoir until the infection is resolved. [ 28 ] [ 29 ] There are four main methods of treating ventriculoperitoneal (VP) shunt infections: (1) antibiotics; (2) removal of infected shunt with immediate replacement; (3) externalization of shunt with eventual replacement; (4) removal of infected shunt with external ventricular drain (EVD) placement and eventual shunt re-insertion. The last method has the highest success rate at over 95%. [ 30 ]
Initial empiric therapy for CSF shunt infection should include broad antibiotic coverage for gram-negative aerobic bacilli including pseudomonas as well as for gram-positive organisms including Staphylococcus aureus and coagulase-negative staphylococcus, such as a combination of ceftazidime and vancomycin. Some clinicians add parenteral or intrathecal aminoglycosides to enhance pseudomonas coverage, although the efficacy of the aminoglycosides is not clear. Meropenem and aztreonam are additional antibiotic options that are effective against gram-negative bacterial infections. [ 31 ]
To evaluate the benefit of surgical shunt removal or externalization followed by removal, Wong et al. compared two groups: one with medical treatment alone, and another with medical and surgical treatment simultaneously. 28 patients with infection after ventriculoperitoneal shunt implantation over an 8-year period in their neurosurgical center were studied. 17 of these patients were treated with shunt removal or externalization followed by removal in addition to IV antibiotics while the other 11 were treated with IV antibiotics only. The group receiving both surgical shunt removal and antibiotics showed lower mortality – 19% versus 42% (p = 0.231). Despite the fact that these results are not statistically significant, Wong et al. suggest managing VP shunt infections via both surgical and medical treatment. [ 32 ]
An analysis of 17 studies published over the past 30 years regarding children with CSF shunt infections revealed that treating with both shunt removal and antibiotics successfully treated 88% of 244 infections, while antibiotic therapy alone successfully treated the CSF shunt infection in only 33% of 230 infections. [ 29 ] [ 33 ]
While typical surgical methods of handling VP shunt infections involve removal and reimplantation of the shunt, different types of operations have used with success in select patients.
Steinbok et al. treated a case of recurrent VP shunt infections in an eczematous patient with a ventriculosubgaleal shunt for two months until the eczema healed completely. This type of shunt allowed them to avoid the area of diseased skin that acted as the source of infection. [ 30 ] Jones et al. have treated 4 patients with non-communicating hydrocephalus who had VP shunt infections with shunt removal and third ventriculostomy. These patients were cured of the infection and have not required shunt re-insertion, thus showing the effectiveness of this procedure in these types of patients. [ 34 ]
Another leading cause of shunt failure is a blockage of the shunt at either the proximal or distal end. At the proximal end, the shunt valve can become blocked due to the buildup of excess protein in the CSF. The extra protein will collect at the point of drainage and slowly clog the valve. The shunt can also become blocked at the distal end if the shunt is pulled out of the abdominal cavity (in the case of VP shunts), or from similar protein buildup. Other causes of blockage are overdrainage and slit ventricle syndrome. [ 11 ]
Over drainage occurs when a shunt has not been adequately designed for the particular person.
First, when the CSF drains too rapidly, extra-axial fluid collection can occur. In this condition the brain collapses on itself resulting in the collection of CSF or blood around the brain. This can cause severe brain damage by compressing the brain, and a subdural hematoma may develop. Extra-axial fluid collection can be treated in three different ways depending on the severity of the condition. Usually the shunt will be replaced or reprogrammed to release less CSF, and the fluid that has collected around the brain will be drained. [ 35 ]
Studies have shown that over drainage of CSF due to shunting can lead to acquired Chiari I malformation . [ 36 ] It was previously thought that Chiari I Malformation was a result of a congenital defect but new studies have shown that overdrainage of Cysto-peritoneal shunts used to treat arachnoid cysts can lead to the development of posterior fossa overcrowding and tonsillar herniation , the latter of which is the classic definition of Chiari Malformation I. Common symptoms include major headaches, hearing loss, fatigue, muscle weakness and loss of cerebellum function. [ 37 ]
Slit ventricle syndrome may occur, when CSF overdrains slowly over several years. [ 35 ] Slit ventricle syndrome is an uncommon problem associated with shunted people, but results in a large number of shunt revisions. It occurs several years after shunt implantation. The most common symptoms are similar to normal shunt malfunction, with several key differences. First, the symptoms are often cyclical and will appear and then subside several times over a lifetime. Second, the symptoms can be alleviated by lying prone. In the case of shunt malfunction neither time nor postural position will affect the symptoms. [ 38 ]
The condition is thought to occur during a period where overdrainage and brain growth occur simultaneously. In this case, the brain fills the intraventricular space, leaving the ventricles collapsed. Furthermore, the compliance of the brain will decrease, which prevents the ventricles from enlarging, thus reducing the chance for curing the syndrome. The collapsed ventricles can also block the shunt valve, leading to obstruction. Since the effects of slit ventricle syndrome are irreversible, constant care in managing the condition is needed. [ 35 ] [ 36 ]
Rarely, overdrainage causes cervical myelopathy from neck vein congestion, which compress the cervical cord or cervical nerve roots, or impact blood circulation it is called Miyazaki syndrome. People do not have signs of overshunting, i.e. intracranial hypotension. [ 39 ]
An intraventricular hemorrhage can occur at any time during or after a shunt insertion or revision. Intraparenchymal hemorrhages that are multi-focal in nature have also been described in the pediatric population following ventriculoperitoneal shunting. [ 40 ] The hemorrhage can cause an impairment in shunt function which can lead to severe neurological deficiencies. [ 36 ] Studies have shown that intraventricular hemorrhage can occur in nearly 31% of shunt revisions. [ 41 ]
Though there have been many cases of patients reaching "shunt independence", there is no general agreement among doctors on how to determine which patients might survive without a shunt. It can be very difficult to discern whether a patient could be shunt independent, except under some very specific circumstances. Overall, the permanent removal of a shunt is a rare but not unheard of procedure. [ 42 ]
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A cerebral vasodilator is a drug which acts as a vasodilator in the brain . [ 1 ] [ 2 ] They are used to improve blood flow in people with cerebrovascular insufficiency and to treat neurological disorders secondary to this condition. [ 2 ] A number of different cerebral vasodilators exist. [ 2 ] [ 1 ] [ 3 ] An example is ifenprodil , which has been marketed for use as a cerebral vasodilator in France , Hong Kong , and Japan . [ 4 ] [ 5 ] [ 6 ] Other examples include buphenine (nylidrin), isoxsuprine , oxyfedrine , suloctidil , and tinofedrine . [ 7 ]
Similar drugs include cerebral activators , or cerebral metabolism activators, like bifemelane , indeloxazine , and teniloxazine , which are also used to treat cerebrovascular disease . [ 8 ] [ 9 ] [ 10 ] [ 11 ]
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Cerebrospinal fluid diversion is a procedure that is used to drain fluid from the brain and spinal cord . A shunt is placed in a ventricle of the brain and threaded under the skin to another part of the body, usually the abdomen . It is used to treat hydrocephalus and idiopathic intracranial hypertension .
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The cerebrospinal venous system (CSVS) consists of the interconnected venous systems of the brain (the cerebral venous system ) and the spine (the vertebral venous system ).
The anatomic connections between the cerebral and vertebral venous systems was accurately depicted in 1819 by Gilbert Breschet , a French physician later to become Professor of Anatomy at Faculté de médecine de Paris. [ 1 ] However, the significance and physiology of this venous complex remained obscure for more than a century, until the seminal work of Oscar Batson. Batson, a Professor of Anatomy at the University of Pennsylvania, in 1940 detailed the anatomy and physiology of the cerebrospinal venous system and its role in the spread of metastases. [ 2 ] Batson’s work remains primarily known for its accurate depiction of the vertebral venous system as the route of metastasis of cancer from the prostate to the spine, and the vertebral venous system is often referred to as Batson venous plexus or Batson’s plexus. It is less commonly recognized that Batson’s detailed experiments also demonstrated the direct anatomic connection between the vertebral and cerebral venous system, an anatomical and physiological fact that was later confirmed by others. [ 3 ] [ 4 ] [ 5 ] [ 6 ] It was later recognized that the cerebrospinal venous system represents a main route for efflux of venous blood from the brain. [ 4 ] [ 5 ] [ 6 ] Modern imaging methodology, including MR scanning , have detailed the anastomoses of the cerebral and spinal venous systems in the suboccipital region. [ 7 ] [ 8 ] Batson, and others had recognized that blood flow in the cerebrospinal venous system was bi-directional, a unique feature that was enabled by a general lack of venous valves in these venous plexuses. [ 9 ] [ 10 ] [ 11 ] This bi-directional flow was thought to have physiologic significance with regard to the maintenance of pressure hemostasis within the cranium with changes in posture. [ 12 ] [ 13 ] The terms “cerebrospinal venous system” and “CSVS” were coined in a 2006 review [ 14 ] that has itself been cited in a number of subsequent articles and reviews. [ 15 ] [ 16 ] [ 17 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ]
Beginning in 1937 Batson began a series of injection experiments investigating the anatomy and physiology of the cerebrospinal venous system. [ 2 ] His carefully documented results demonstrated the continuity of the venous systems of the brain and the spine, as injections of contrast dyes into venous systems feeding into the spinal venous plexus led to the appearance of contrast material in the cerebral veins (Figures 5 and 7, Batson 1940). [ 2 ] [ 9 ] Batson noted "the extensive filling of the vertebral veins, the superior longitudinal sinus, transverse sinus as well as other dural and cerebral veins" following injection of radiopaque material into a superficial venule in the left breast (Batson 1940, Figure 5, page 143). Subsequent studies by multiple independent authors replicated Batson's findings of the continuity of the cerebral and vertebral venous systems, and the important physiological consequences of this continuity. For example, in 1996, Arnautovic et al., summarizing the results of their own work and that of others, stated: "In addition to confirming that the vertebral venous plexus is a direct continuation of the cranial venous sinuses, our study showed that it is also indirectly connected to these sinuses via the suboccipital cavernous sinus . The vertebral venous plexus is involved in regulating intracranial pressure, transmitting the influence of the respiratory and cardiac pressures to the intracranial compartment and equalizing the pressures within the venous system. [ 8 ] ". The continuity of the cerebral and vertebral venous systems was therefore essential to an understanding of both normal physiology, as well as to an understanding of the distribution of tumor metastases, as Batson had so elegantly demonstrated.
It is now recognized that the cerebrospinal venous system represents not only a route for dissemination of metastases, but also a route for dissemination of infection throughout the cerebrospinal axis, in both directions. [ 17 ] [ 22 ] [ 23 ]
In 1957 Batson wrote, ""It seems incredible that a great functional complex of veins would escape recognition as a system until 1940 .... In the first four decades of the last [19th] century, our knowledge of the vertebral veins was developed and then almost forgotten. [ 9 ] ". During the past half century, our appreciation of Batson's findings and concepts has grown, expanding beyond his explanation for previously inexplicable routes of tumor metastasis. In 2011, researchers from the Department of Neurological Surgery at Ohio State Medical Center summarized the significance and current understanding of several aspects of the CSVS in their review article: "Today, the vertebral venous plexus is considered part of the cerebrospinal venous system, which is regarded as a unique, large-capacitance, valveless plexiform venous network in which flow is bidirectional that plays an important role in the regulation of intracranial pressure with changes in posture and in venous outflow from the brain, whereas in disease states, it provides a potential route for the spread of tumor, infection, or emboli.". [ 20 ]
The cerebrospinal venous system may serve as a route for therapeutic delivery of large molecules to the brain [ 24 ] and spinal cord , [ 25 ] as discussed: "... the drug enters the brain through the cerebrospinal venous system..."( Sun Sentinel , December 9, 2012, page 21A). [ 26 ]
Glymphatic system
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Certified Professional Electrologist (CPE) credential signifies that an electrologist 's knowledge has been tested and measured against a national standard of excellence. The credential was developed and is administered through the American Electrology Association 's International Board of Electrologist Certification (IBEC). The CPE must obtain seventy-five hours of continuing education, in a five-year period, to maintain this voluntary credential, or be re-tested.
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The American Society of Anesthesia Technologists & Technicians , or ASATT , based in Oak Creek, Wisconsin , is a nonprofit , educational organization responsible for the standards of technologist/technician competency in all areas of anesthesia .
ASATT's mission is to establish a professional entity for the anesthesia technician that will positively affect health care and standards of quality in patient care by providing a safe anesthetic environment.
ASATT has the only nationally recognized certification for technicians ( Cer.A.T. ) and technologists ( Cer.A.T.T. ). [ 2 ]
Beginning July 25, 2015, ASATT will be phasing out the technician exam (Cer.A.T.) and on-the-job training for the Anesthesia Technology profession. The certification is still valid for those who hold it. [ 3 ]
Technologist (Cer.A.T.T.) exam.
A certified anesthesia technician ( Cer.A.T. ) is person that has met the experience and examination requirements set for this certification established by ASATT. The certification exam is no longer offered. ASATT requires any candidate seeking certification (Cer.A.T.) to meet one of the following requirements: [ 4 ]
A certified anesthesia technologist ( Cer.A.T.T. ) is a person who has met the experience and examination requirements for this certification established by ASATT. Requirements to sit for the certified anesthesia technologist (Cer.A.T.T.) examination are [ citation needed ] the successful completion of a 2- or 4-year CAAHEP accredited / CoA-ATE approved program through ASATT. Current certified anesthesia technicians are re-certified every 2-years after the Cer.A.T.T. designation was granted. 30 hours of continuing education credits are needed every 2 years to recertify.
The Society produces a quarterly publication known as The Sensor , which provide its readers information on anesthesia-related topics, and a forum for learning and discussion. [ 5 ]
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https://en.wikipedia.org/wiki/Certified_anesthesia_technician
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The American Society of Anesthesia Technologists & Technicians , or ASATT , based in Oak Creek, Wisconsin , is a nonprofit , educational organization responsible for the standards of technologist/technician competency in all areas of anesthesia .
ASATT's mission is to establish a professional entity for the anesthesia technician that will positively affect health care and standards of quality in patient care by providing a safe anesthetic environment.
ASATT has the only nationally recognized certification for technicians ( Cer.A.T. ) and technologists ( Cer.A.T.T. ). [ 2 ]
Beginning July 25, 2015, ASATT will be phasing out the technician exam (Cer.A.T.) and on-the-job training for the Anesthesia Technology profession. The certification is still valid for those who hold it. [ 3 ]
Technologist (Cer.A.T.T.) exam.
A certified anesthesia technician ( Cer.A.T. ) is person that has met the experience and examination requirements set for this certification established by ASATT. The certification exam is no longer offered. ASATT requires any candidate seeking certification (Cer.A.T.) to meet one of the following requirements: [ 4 ]
A certified anesthesia technologist ( Cer.A.T.T. ) is a person who has met the experience and examination requirements for this certification established by ASATT. Requirements to sit for the certified anesthesia technologist (Cer.A.T.T.) examination are [ citation needed ] the successful completion of a 2- or 4-year CAAHEP accredited / CoA-ATE approved program through ASATT. Current certified anesthesia technicians are re-certified every 2-years after the Cer.A.T.T. designation was granted. 30 hours of continuing education credits are needed every 2 years to recertify.
The Society produces a quarterly publication known as The Sensor , which provide its readers information on anesthesia-related topics, and a forum for learning and discussion. [ 5 ]
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Certified anesthesiologist assistants (CAAs) are master’s degree level non-physician anesthesia care providers in North America. CAAs are members of the anesthesia care team as described by the American Society of Anesthesiologists (ASA). This designation must be disambiguated from the Certified Clinical Anesthesia Assistant (CCAA) designation conferred by the Canadian Society of Respiratory Therapists . All CAAs possess a baccalaureate degree, and complete an intensive didactic and clinical program at a postgraduate level. CAAs are trained in the delivery and maintenance of most types of anesthesia care as well as advanced patient monitoring techniques. The goal of CAA education is to guide the transformation of student applicants into competent clinicians. [ 1 ]
Prior to acceptance into their respective graduate programs all anesthesiologist assistant students must possess an undergraduate degree. [ 2 ] The anesthesiologist assistant works under the medical direction of a physician anesthesiologist as a part of the anesthesia care team . Anesthesiologist assistants administer all forms of anesthetic medications, IV fluids and blood products. [ 3 ]
Anesthesiologist assistants generally work in the hospital setting but can work at any location (with the presence/direction of a physician anesthesiologist) such as pain clinics, dental offices, and outpatient surgical centers. Anesthesiologist assistants work in most facets of surgical environments such as endoscopy, conscious sedation, abdominal surgery, orthopedic surgery, as well as cardiac surgery , neurosurgery , transplant surgery , and trauma surgery centers. Currently Certified Anesthesiologist Assistants are able to practice in twenty one states, the District of Columbia , and Guam . [ 3 ] In each of these states, the anesthesiologist assistant falls under the regulatory authority and licensing of the State Board of Medicine. [ 3 ]
As of 2017 [update] there are twelve anesthesiologist assistant training programs in the United States [ 4 ] all of which offer degrees at the Master's level. [ 5 ] Approximately 97% of currently working anesthesiologist assistants hold a master's degree (some early anesthesiologist assistant graduates held bachelor's degrees). [ citation needed ] All newly credentialed and future anesthesiologist assistants must complete an accredited Master's program for anesthesiologist assistants. Upon completion of the educational program, graduates must sit for a credentialing exam that is co-validated by the National Board of Medical Examiners and National Commission for Certification of Anesthesiologist Assistants. All anesthesiologist assistant programs are credentialed by the Commission on Accreditation of Allied Health Educational Programs (CAAHEP). [ 6 ]
In the 1960s, three anesthesiologists, Joachim S. Gravenstein, John E. Steinhaus, and Perry P. Volpitto, were concerned with the shortage of anesthesiologists in the country. These academic department chairs analyzed the spectrum of tasks required during anesthesia care. The tasks were individually evaluated based on the level of professional responsibility, required education and necessary technical skill. The result of this anesthesia workforce analysis was to introduce the concept of team care and to define a new type of anesthesia provider called a mid-level anesthesia practitioner linked to a supervising anesthesiologist. This new professional - the Anesthesiologist Assistant or AA - was an answer to help alleviate this shortage [ citation needed ]
The chairmen's vision became reality in 1969 when the first AA training programs began accepting students at Emory University in Atlanta, Georgia, and at Case Western Reserve University in Cleveland, Ohio. [ 7 ] [ 8 ]
A master's level education is required to train anesthesiologist assistants to collect patient data, assist in the evaluation of patients’ physical and mental status, document the surgical procedures planned, and administer the therapeutic plan for patient care that has been formulated by the anesthesiologist. [ 9 ] There are twenty one programs available for the Anesthesiologist Assistant master's degree in the United States. All programs are accredited by the Commission on Accreditation of Allied Health Education (CAAHEP).
To enroll in an AA program, candidates require a bachelor's degree in any field,have to obtain a minimum of eight hours of documented anesthesia exposure by observation in the operating room. [ 9 ] [ 10 ] All programs require an entrance exam (either GRE or MCAT , MCAT preferred). [ 11 ] [ 12 ] [ 13 ]
Program lengths range from 24 to 28 months with didactic and clinical instruction. [ 9 ] [ 10 ] Didactic training includes courses such as physiology , pharmacology , airway management , simulation laboratory, Basic Life Support (BLS) certification, Pediatric Advanced Life Support (PALS) certification, Advanced Cardiac Life Support (ACLS) certification, anatomy, monitoring, and applied principles and practices. In addition to class work, programs include 2000 to 2700 clinical hours per student. [ 14 ] Students gain preoperative, intra-operative and post-operative experience with a variety of patients in a variety of surgical settings. [ 9 ] [ 10 ] [ 11 ] In addition, each program may have additional educational experiences; for example, Nova Southeastern University provides students with courses on scientific research and publishing. [ 11 ] All programs must have at least one board-certified, licensed anesthesiologist serving as a director. Additionally, each AA program must be based at, or in collaboration with, a university that has a medical school. [ 3 ]
Graduates from an accredited educational program are eligible to take the initial certifying examination and can do so up to 6 months before graduating from the program. The certifying examination for anesthesiologist assistants is a written exam administered by the National Board of Medical Examiners (NBME), which is contracted by the National Commission for Certification of Anesthesiologist Assistants (NCCAA). Once successfully completed, the NCCAA will award a time-limited certificate to each candidate. In order to maintain certification, anesthesiologist assistants need to register for 40 hours of Continuing Medical Education (CME) every two years and successfully complete a Continued Demonstration of Qualifications (CDQ) examination every six years. [ 15 ] [ 16 ]
Anesthesiologist assistants are mid-level providers who work under the direction of licensed physician anesthesiologists as integral members of the Anesthesia Care Team (ACT) . [ 17 ] The following list is obtained from the American Academy of Anesthesiologist Assistants (AAAA), which states anesthesiologist assistant responsibilities may include but are not limited to: [ 3 ]
The AA scope of practice may differ slightly in relation to local practice and is always defined by the medically directing anesthesiologist, the hospital's clinical protocol procedures, the state's board of medicine, and state regulations.
The American Medical Association (AMA) states that "AAs are most commonly employed in larger facilities that perform procedures such as cardiac surgery , neurosurgery , transplant surgery , and trauma care ." [ 6 ] Studies by the AMA found entry-level salaries for 2006 Anesthesiologist Assistant graduates to be between $120,000 and $150,000 for the 40-hour work week plus benefits and consideration of on-call activity. They also found the high end of the salary range to be around $190,000 to $220,000 for experienced anesthesiologist assistants. [ 18 ] Salaries vary by region and individual employer.
Anesthesiologist assistants are currently able to work in twenty one states plus the District of Columbia and the territory of Guam either by licensure or through physician delegation. AAs are recognized by the federal government and are authorized to work at all Veteran Affairs hospitals using the TRICARE insurance program. [ 19 ]
Licensure defines the practice of AAs and is achieved through state law or by approval of the individual state board of medicine. Physician delegation is achieved through recognition of AAs by the state board of medicine or through statutes included in the state's medical practice act. The board of medicine affords Anesthesiologist's the right to delegate the responsibilities of their realm of practice to qualified individuals. Delegating authority requires that the physician remain ultimately responsible for the patient. In all states, the practice of anesthesiologist assistants is guided by the board of medicine. Any attempt to employ AAs under delegating authority should be made through the individual state's board of medicine. [ 3 ]
States and territories where AAs practice through license and certification: [ 19 ]
States where AAs practice through physician delegation:
Anesthesiologist Assistants are employed at Veteran Affairs (VA) and Department of Defense facilities under the TRICARE health system since Dec 22, 2006. [ 7 ]
The Veterans Health Administration Handbook 1123 on Anesthesia Service, includes the profession of anesthesiologist assistant as an allied health professional . Information in regards to required qualifications, coverage criteria, billing, and payment for Medicare services under the TRICARE program for anesthesiologist assistants is published by the Department of Health and Human Services . [ 22 ]
AA's are currently classified as GS-0601, General Health Science Series employees, as defined by The Handbook of Occupational Groups and Families from the U.S. Office of Personnel Management . [ 23 ]
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A Certified Registered Nurse Anesthetist ( CRNA ) is a type of advanced practice nurse who administers anesthesia in the United States . CRNAs account for approximately half of the anesthesia providers in the United States and are the main providers (80%) of anesthesia in rural America . [ 1 ] Historically, nurses have been providing anesthesia care to patients for over 160 years, dating back to the American Civil War (1861–1865). The CRNA credential was formally established in 1956. [ 2 ] CRNA schools issue a Doctorate of nursing anesthesia degree to nurses who have completed a program in anesthesia, which is 3 years in length. [ 3 ]
Scope of practice and practitioner oversight requirements vary between healthcare facility and state, with 25 states and Guam granting complete autonomy as of 2024. [ 4 ] In states that have opted out of supervision, the Joint Commission and CMS recognize CRNAs as licensed independent practitioners. [ 5 ] In states requiring supervision, CRNAs have liability separate from supervising practitioners and are able to administer anesthesia independently of physicians, such as Anesthesiologists . [ 6 ] [ 7 ] [ 8 ] [ 9 ]
Among the first American nurses to provide anesthetics was Catherine S. Lawrence during the American Civil War . It was during the Second Battle of Bull Run in 1863 that she administered chloroform to wounded soldiers who needed emergency operations in the battlefield. [ 10 ] Nevertheless, it still took several years for nurses to step forward and formally answer the call to provide anesthesia. Reasons for this delay included lack of training, the non-emergency nature of civilian surgical practice after the war was over, and the paucity of role models and sponsors. However, the wartime concept of nurses providing anesthesia care gradually took root as surgeons trained and encouraged nurses to take on this important role. [ 11 ]
Catholic nuns played an important role in the training of nurses and also in anesthesia. The earliest recorded nurse to specialize in anesthesia was Sister Mary Bernard Sheridan, a Catholic nun who practiced in 1877 at St. Vincent's Hospital in Erie, Pennsylvania . [ 11 ] Her influence spread throughout the Midwest, and many other Catholic nuns who were also nurses began training to administer anesthesia. Nuns of the Third Order of the Hospital Sisters of St Francis from Münster established a community in Springfield, Illinois , and on June 22, 1879, they founded St John's Hospital . [ 12 ] At St John's, the administration of chloroform and ether was taught to the nurses by surgeons, and many of the Franciscan Sisters were assigned as anesthetists throughout the Midwest. Nurse anesthesia became “undoubtedly a prevailing practice in many Catholic hospitals”. [ 13 ] [ 14 ]
In 1883, Minnesota was devastated by a tornado . Mother Alfred Moes and the Sisters of Saint Francis proposed building a hospital to aid the sick and injured in Southern Minnesota. However, they stipulated that William Worrall Mayo (1819-1911) and his sons work at the hospital. The Mayos agreed, and in 1889, St Mary's Hospital opened with 27 beds. [ 15 ] Although Catholic nuns seemed to be the most influential force in teaching nurses to administer anesthesia in the late 1800s, it was William W. Mayo who should be credited for promoting the popularity of nurse anesthesia practice. [ 16 ] Mayo and his sons William J. Mayo and Charles H. Mayo were well known for their surgical skills. Surgeons traveled from across the country to their clinic in Minnesota to observe operations and learn their surgical techniques. However, the visiting surgeons also took note of the nurses administering anesthesia at the head of the operating table. [ 15 ]
One of the most well-known nurse anesthesia pioneers was Alice Magaw , who came to St Mary's Hospital in Rochester, Minnesota, in 1893. She was trained by the Graham sisters, Edith and Dinah, and began working as a nurse anesthetist for Charles H. Mayo, who bestowed on her the title of “Mother of Anesthesia” due to her natural aptitude and mastery of safe administration of open-drop ether . [ 17 ] In addition to being skilled at anesthesia administration, Magaw documented and evaluated all her anesthesia procedures, culminating with a landmark article in nurse-anesthesia history. [ 18 ] An even larger work (A Review of Over Fourteen Thousand Surgical Anesthesias) was published in 1906, reporting huge number of open-drop ether anesthetics, incredibly without a single fatality. [ 19 ] Magaw's work highlighted the benefits of the trained anesthetist, allowing great advances in the practice of medicine. As the reputation and success of the Mayo Clinic spread, so did the renown of the Mayo Clinic nurse anesthetists. [ 20 ]
The sustainability and historical longevity of the practice of nurse anesthesia can be attributed to excellent working relationships between nurse anesthetists and surgeons in these early years of the practice. Impressed by the provision of superior anesthesia by nurses at St Mary's, and following the example of the Mayo Clinic, prominent Cleveland surgeon George Washington Crile recruited Agatha Cobourg Hodgins as his personal anesthetist in 1908. [ 21 ]
Several notable nurse anesthetist from the early 20th century are revered by their modern counterparts. Agnes McGee taught at the Oregon Health Science Center. [ 22 ] Alice Hunt was appointed instructor in anesthesia with university rank at the Yale University School of Medicine beginning in 1922 and continuing for 26 years. [ 23 ] She authored the 1949 book Anesthesia, Principles and Practice, likely the first nurse anesthesia textbook. [ citation needed ]
The first challenge to the nurse's right to administer anesthesia came in 1911 from Francis Hoeffer McMechan, a native Cincinnati physician, who felt that the field of anesthesia should belong solely to physicians. McMechen challenged the practice of nurse anesthesia with the Ohio Medical Board, which along with Ohio State Attorney General ruled in 1916 that only a registered physician could administer anesthesia. [ 24 ] Surgeons at the Lakeside Hospital in Cleveland, such as Crile, initially obeyed the ruling; however, in 1917, Crile and his supporters successfully lobbied the Ohio legislature to create an exemption within the Medical Practice Act for nurses who were educated appropriately to administer anesthesia under the supervision of a physician. [ 25 ]
Perhaps the most noteworthy challenge occurred in 1934, when nurse anesthetist Dagmar Nelson was charged by an anesthesiologist, William VaneChalmer-Francis, with practicing medicine and violating California Medical Practice by administering anesthesia without a license. The case went all the way to the California Supreme court, but Nelson was given a favorable ruling at each level of the case. [ 26 ] The Dagmar Nelson case was won via precedents set by early nurse anesthetists. The California Supreme Court reasoned that Nelson's practice of anesthesia was in “accordance with the uniform practice in operating rooms” not only in Los Angeles but also throughout the country including the Mayo Clinic , where Nelson had trained and “where...one hundred thousand surgical operations had been performed” with anesthetic administered by nurses. [ 27 ]
Despite the rapid growth of the nurse anesthetist profession following the Great War , World War II again precipitated a shortage of anesthetists. A recruitment campaign was begun, but this was quickly followed by concern about the emergence of “ill advised and unjustified schools”. [ 27 ] Helen Lamb in turn stressed the importance of maintaining educational standards even in times of shortages. By the end of WWII, the military had trained more than 2000 nurses to provide anesthesia using a program patterned by the NANA. The quality of nurse anesthesia education was again upgraded following WWII, and although university affiliation was advised, most programs were still hospital based. In 1933, the NANA established an Education Committee to develop educational standards, and by 1952, formal accreditation standards were in place. [ 28 ]
Under US law, Frank v. South , [ 29 ] Chalmers-Francis v. Nelson [ 30 ] and other court decisions established that anesthesia was the practice of nursing as well as medicine. [ 31 ] As such, the practice of anesthesia in the US may be delivered by either a nurse anesthetist or an anesthesiologist. The decisions have not been challenged since the Dagmar Nelson case. [ 32 ] In addition to legal decisions, individual hospital and surgical facility policies also regulate the granting of anesthesia clinical privileges and are often based on contractual agreements with provider groups. [ citation needed ]
The first school of nurse anesthesia was formed in 1909 at St. Vincent Hospital, Portland, Oregon . Established by Agnes McGee, the course was seven months long, and included courses on anatomy and physiology , pharmacology , and administration of the few common anesthetic agents available at the time. [ 22 ] Within the next decade, approximately 19 schools opened. All consisted of post-graduate anesthesia training for nurses and were about six months in length. These included programs at Mayo Clinic , Johns Hopkins Hospital , Barnes Hospital , New York Post-Graduate Hospital, Charity Hospital in New Orleans, Grace Hospital in Detroit, among others. [ 33 ] During those early days of administering anesthetics, knowledge and available anesthetic options were extremely limited and programs provided what little education they could for all levels of health providers. For example, in 1915, chief nurse anesthetist Agatha Hodgins established the Lakeside Hospital School of Anesthesia in Cleveland, Ohio . This program was open to nurses, physicians , and dentists . The training was only six months and the tuition was $50. In its first year, it graduated six physicians, eleven nurses, and two dentists. [ 34 ]
Among the oldest schools in the U.S., Ravenswood Hospital in Chicago, opened in 1925 by Mae Cameron, which in 2001 became the NorthShore University HealthSystem School of Nurse Anesthesia, was the first school to be accredited by the Council on Accreditation of Nurse Anesthesia Educational Programs in 1952. [ 35 ] [ 36 ]
In 1981, the Nursing Council on Accreditation developed guidelines for master's degrees . In 1982, it was the official position of the AANA board of directors that registered nurses applying for a school of anesthesia shall be, at minimum, baccalaureate prepared and then complete a master's level anesthesia program. [ 37 ] As early as 1978, the Kaiser Permanente California State University program had evolved to a master's level program. All programs were required to transition to a master's degree beginning in 1990 and complete the process by 1998. [ 38 ] Currently, the American Association of Colleges of Nursing has endorsed a position statement that will move the current entry level of training and education of nurse anesthetists in the United States to the Doctor of Nursing Practice (DNP) or Doctor of Nurse Anesthesia Practice (DNAP). [ 39 ] This move will affect all advance practice nurses , with a mandatory implementation by the year 2015. [ 40 ] In August 2007, the AANA announced its support of this advanced clinical degree as an entry level for practice of all nurse anesthetists, with a target compliance date of 2025. In accordance with traditional grandfathering rules, all those in current practice would not be affected and neither would the training provided to those now receiving the DNP or DNAP designation. [ 39 ] Currently, more than 50% of the 120 nurse anesthesia programs have already transitioned to the DNP or DNAP entry level format. [ 41 ]
The didactic curricula of nurse-anesthesia programs is governed by the COA standards. Accredited programs provide supervised experiences for students with patients of all ages who require medical, surgical, obstetrical, dental, and pediatric interventions. [ 42 ] Programs require study in methods of scientific inquiry and statistics, as well as active participation in a student-generated and faculty-sponsored research project.
Before becoming a nurse anesthetist, one must complete a few years of a bachelor's-level registered nursing. A minimum of one year of full-time work experience as a registered nurse in a critical care setting is required before applying to CRNA school. The average experience of RNs entering nurse anesthesia educational programs is 2.9 years. [ 43 ] Nurse anesthetists are required to attend accredited educations programs covering all areas of anesthesia. This education provides training about the anesthetics needed for patients in any type of procedure or surgery. [ 44 ] After completing an accredited program, CRNAs must pass a national certification exam to acquire this designation. [ 45 ] It is important to have the best education for this field for the significance of anesthesia. By 2025 the Council on Accreditation, the organization which accredits nurse anesthetist programs, will require all graduating CRNAs to be doctorate prepared. [ 46 ]
Nurse anesthetists serve in the United States armed forces . In some military treatment facilities, nurse anesthetists function as the only licensed independent anesthesia practitioners, including U.S. Navy ships at sea. They also provide anesthesia for the Veterans Administration and Public Health Service medical facilities. [ citation needed ]
During World War I , America's nurse anesthetists cared for troops in France . From 1914 to 1915, three years prior to America entering the war, Dr. George Crile and nurse anesthetists Agatha Hodgins and Mabel Littleton served in the Lakeside Unit at the American Ambulance at Neuilly-sur-Seine in France. [ 47 ] [ 48 ] In addition, they helped train the French and British nurses and physicians in anesthesia care. In 1917, the American participation in the war resulted in the U.S. military training nurse anesthetists for service. The Army and Navy sent nurses anesthesia trainees to various hospitals, including the Mayo Clinic at Rochester and the Lakeside Hospital in Cleveland before overseas service. [ 49 ]
Among notable nurse anesthetists are Sophie Gran Winton. She served with the Red Cross at an army hospital in Château-Thierry , France, and earned the French Croix de Guerre in addition to other service awards. [ 50 ] In addition, Anne Penland was the first nurse anesthetist to serve on the British Front and was decorated by the British government. [ 51 ]
American nurse anesthetists also served in World War II and Korea . [ 25 ] Second Lieutenant Mildred Irene Clark provided anesthesia for casualties from the Japanese attack on Pearl Harbor . [ 52 ] During the Vietnam War , nurse anesthetists served as both CRNAs and flight nurses , and also developed new field equipment. [ 53 ] Nurse anesthetists have been casualties of war. Lieutenants Kenneth R. Shoemaker Jr. and Jerome E. Olmsted, were killed in an air evac mission en route to Qui Nhon, Vietnam. [ 54 ]
At least one nurse anesthetist was a prisoner of war . Army Nurse anesthetist Annie Mealer endured a three-year imprisonment by the Japanese in the Philippines , and was released in 1945. [ 55 ] During the Iraq War , nurse anesthetists provide care at forward positioned medical treatment facilities. [ 56 ] In addition, they play a role in the continuing education and training of Department of Defense nurses and technicians in the care of wartime trauma patients.
Board certification and recertification process is governed by the National Board on Certification and Recertification of Nurse Anesthetists (NBCRNA). The NBCRNA exists as an autonomous not-for-profit incorporated organization. CRNAs also have continuing education requirements and recertification check-ins every two years thereafter, plus any additional requirements of the state in which they practice. The new recertification pathway focuses on: maintenance of certification, lifelong learning, and continued competence. The Continued Professional Certification (CPC) Program consists of 8-year periods, and each period comprises two four-year cycles. [ 57 ]
The degree of independence or supervision by a licensed provider (physician, dentist, or podiatrist) varies with state law. [ 58 ] Some states use the term collaboration to define a relationship where the supervising physician and the CRNA work together to provide the anesthetic. Other states require the consent or order of a physician or other qualified licensed provider to administer the anesthetic. [ 59 ]
The licensed CRNA is legally authorized to deliver care under the particular Nurse Practice Act of each state. Scope of CRNA practice is commonly further defined by the practice location's clinical privilege and credentialing process, anesthesia department policies, or practitioner agreements. Clinical privileges are based on the scope and complexity of the expected clinical practice, CRNA qualifications, and CRNA experience. This allows the CRNA to provide core services and activities under defined conditions with or without supervision. [ 60 ]
In 2001, the Centers for Medicare and Medicaid Services (CMS) published a rule in the Federal Register that allows a state to be exempt from Medicare's physician supervision requirement for nurse anesthetists after appropriate approval by the state. [ 58 ] To date, 22 states and Guam have opted out of the federal requirement, instituting their own individual requirements instead. [ 61 ]
According to the U.S. Bureau of Labor Statistics , a CRNA salary is around $225,555. Salaries within the US vary by state. Connecticut is the highest-paying state for CRNAs at an average salary of $276,540. It is followed by New Jersey ($263,850), Illinois ($250,280), and West Virginia ($247,650). [ 44 ] Overall employment for nurse anesthetists and other medical professions is projected to grow 45 percent from 2020 to 2030. [ 62 ]
CRNAs typically work in healthcare settings such as emergency rooms, intensive care units, and operating rooms. Their environment is with medical and surgical teams with procedures that can occur anytime. Some partnerships they work with are dentists, surgeons, podiatrists and other healthcare providers in serving patients who need of receiving anesthesia. Nurse anesthetists are an essential part of everyday medical facilities. The need of CRNAs is anticipated to grow. [ 44 ]
Nurse anesthetists practice independently (depending on the state law) or they practice in collaboration with anesthesiologists, surgeons, and doctors to supply anesthetics to patients. CRNAs are responsible for communicating with the surgeon or team about the patient's health history and designing a plan for anesthesia. The procedures that nurse anesthetists offer include:
CRNAs have important roles when it comes to patient care. They need to meet all patient standards and help ensure the patient is in good condition before receiving an anesthesia plan. Some of the skills a CRNA requires include:
Subsequent to the COVID-19 pandemic , there has been an increase in the number of individuals who need respiratory assistance. [ 64 ]
The AANA recognizes Certified Registered Nurse Anesthetist , CRNA , nurse anesthetist , and nurse anesthesiologist as equivalent titles. [ 65 ] The use of nurse anesthetist is substantially more common than the use of nurse anesthesiologist; [ 66 ] terms anesthesia nurse and anesthetist nurse are unheard of.
Use of the term nurse anesthesiologist has been criticized by those who argue that the term anesthesiologist should be limited to medical doctors . [ 66 ] For example, groups representing anesthesiologists and other medical doctors, such as the American Medical Association (AMA) and American Society of Anesthesiologists (ASA), oppose the use of this phrase to describe CRNAs and call it misleading. [ 67 ] [ 68 ]
In 2021, after a year-long rebranding effort, the American Association of Nurse Anesthetists changed its name to the American Association of Nurse Anesthesiology. The name change was condemned by physician groups, including the AMA, ASA, American Board of Anesthesiology , American Board of Medical Specialties , and American Osteopathic Association . Physicians' organizations said that the name change was "title misappropriation" that was deceptive, misleading to patients, and cause confusion in care settings. [ 69 ] [ 70 ] [ 71 ]
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The cervical branch of the facial nerve is a nerve in the neck . It is a branch of the facial nerve (VII). It supplies the platysma muscle , among other functions.
The cervical branch of the facial nerve is a branch of the facial nerve (VII). It runs forward beneath the platysma muscle , and forms a series of arches across the side of the neck over the suprahyoid region. One branch descends to join the cervical cutaneous nerve from the cervical plexus .
The lateral part of the cervical branch of the facial nerve supplies the platysma muscle . [ 1 ] [ 2 ]
This article incorporates text in the public domain from page 905 of the 20th edition of Gray's Anatomy (1918)
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Cervical cancer staging is the assessment of cervical cancer to determine the extent of the spread of cancer beyond the cervix. [ 12 ] This is important for determining how serious the cancer is and to create the best treatment plan. [ 13 ]
Cervical cancer is a type of gynecological cancer that begins from cells lining the cervix, the lower part of the uterus. [ 14 ] Cervical cancer begins when the cells that line the cervix become abnormal and grow in a pattern that is atypical for non-cancerous cells. [ 14 ] Cervical cancer is typically first identified with an abnormal pap smear . [ 14 ] The final diagnosis of cervical cancer, including the stage of the cancer, is confirmed with additional testing. [ 12 ]
Cancer staging is determined by where the tumor is located, the size of the tumor, and how much the tumor has spread beyond where it originally began, such as to nearby lymph nodes or different parts of the body. [ 13 ]
Cancer staging is described on a spectrum from stage 0 to stage IV. Stage 0 describes pre-cancerous or non-invasive types of tumors. Stage IV is used to describe cancers that have spread throughout a significant part of the body. In general, the greater the stage of cancer, the more aggressive the disease and the worse the prognosis. [ 13 ]
Cervical cancer staging is described by the International Federation of Gynecology and Obstetrics ( FIGO ). [ 12 ] [ 15 ] In 2018, FIGO released the most recent guidelines for cervical cancer staging. [ 16 ] These guidelines recommend the use of various physical examinations, types of imaging , and biopsies to determine the stage of cervical cancer. [ 16 ]
Cervical cancer is the abnormal growth of the cells that line the cervix, resulting in the cells growing out of control and potentially spreading to areas outside of the cervix. [ 14 ]
The cervix is the lower part of the uterus . It connects the upper part of the uterus with the vagina. The cervix is divided into two parts based on the types of cells. The outer portion of the cervix is called the ectocervix, while the inner portion of the cervix is the endocervix. These two portions of the cervix have different types of cells. The area where the endocervix and ectocervix meet is known as the transformation zone. Most cervical cancers arise from the cells in the transformation zone. [ 14 ]
Cervical cancer screening occurs with pap smears performed by an obstetrician-gynecologist. During a pap smear, doctors collect a sample of the cells from the cervix to look at under a microscope to examine for any abnormalities or signs of pre-cancerous changes. [ 17 ] While many abnormalities on pap smears are not indicative of cervical cancer, [ 14 ] the doctor may recommend additional testing to gain a better understanding of the cervical cells. [ 18 ] Additional testing that may be performed includes an endocervical curettage , colposcopy , or cervical conization . [ 18 ] Each of these procedures allows for the collection of a biopsy of the cells of the cervix. [ 18 ]
Abnormalities of cervical cells, or dysplasia, develop over time and along a continuum. There are several types of abnormalities of cervical cells known as pre-cancerous changes. These pre-cancerous changes are known as cervical intraepithelial neoplasm (CIN) and squamous intraepithelial lesion (SIL), based on whether the results are from a biopsy or a pap smear. CIN and SIL are graded from 1 to 3 based on the degree of change observed. CIN 1, 2, and 3 all represent pre-cancerous findings. [ 14 ]
The main types of cervical cancer include squamous cell carcinomas and adenocarcinomas. Nearly 90% of cervical cancers are squamous cell carcinomas. Cervical cancers may also be a mix between squamous cell carcinomas and adenocarcinomas, known as adenosquamous carcinoma. [ 14 ]
Cervical cancer spreads directly from the cervix into surrounding organs and via the lymphatic system. [ 16 ] When spreading via the lymphatic system, cervical cancer will spread to nearby lymph nodes, including the obturator, external iliac, and internal iliac lymph nodes. [ 16 ] Nearby structures that cervical cancer may spread to directly include the peritoneum, vagina, uterus, bladder, and rectum. [ 16 ] If cervical cancer has spread to distant organs, such as the liver, lungs, or skeleton, this represents a late finding and significant disease. [ 16 ] The degree of spread of cancer to areas beyond the cervix is important in determining the stage of cervical cancer. [ 16 ]
Staging is the process of determining the type of cervical cancer and the extent the cancer has spread beyond the cervix to local or distant parts of the body. [ 12 ] To determine the stage of the cancer, various modalities may be used including physical examination , biopsies , pathological examinations, and imaging , including MRI , ultrasound , CT , and PET scans. [ 16 ] The information gathered from all of these modalities is put together to determine the cancer stage. [ 16 ] FIGO guidelines recommend assigning a lower stage whenever possible. [ 16 ] The cervical cancer stage assigned at initial diagnosis cannot be altered later, regardless of recurrence or later disease spread. [ 19 ]
A biopsy , or sample of the tissue, is the first step in determining the type and extent of cancer. This biopsy may be obtained through a punch biopsy, LEEP (loop electrosurgical excision procedure), or cone biopsy . These procedures allow the doctor to obtain a sample of the cancerous tissue to look at under a microscope. By examining the size of the cancer, the margins of the biopsy sample, and the type of abnormal cells, the type of cancer can be determined. [ 16 ]
Biopsy of nearby lymph nodes may also be necessary to determine if the cervical cancer has spread lymphatically. This may be done via fine-needle aspiration , minimally invasive surgery , or laparotomy (open incision of the abdomen). [ 16 ] Typically, these procedures are not done until after there is confirmation of cervical cancer and after imaging is performed, if possible.
Following the collection of biopsies of the cervical cancer and areas where it may have spread, the cells of the cancer will be looked at under a microscope. This is vital in determining the stage of the cancer. There are several different ways that pathologists may classify the cancer. All cancers of the cervix must be confirmed under a microscope and are determined to be cervical in origin if the primary source of the cancer is the cervix. [ 16 ]
The histopathologic stage describes the type of cells seen under the microscope. There are 10 histopathologic types of cervical cancers: [ 16 ]
The grade of the cancer is another method to describe the appearance of the tumor cells under a microscope. This describes how different the cells look from typical cells of the cervix. [ 20 ] It may also indicate the speed at which the cancer cells grow. [ 20 ] The grades are described below, with grade 3 being the most aggressive. [ 16 ]
Imaging modalities , including ultrasound , MRI , CT , and positron emission tomography (PET), may be beneficial in helping to determine the stage of the disease, where resources permit. These imaging modalities allow for the visualization of the tumor size, degree of spread of the cancer to lymph nodes and surrounding organs, and to evaluate for distant metastasis. [ 16 ]
For primary tumors over 10mm in size, MRI is the best imaging modality to evaluate the primary tumor. PET-CT scans are the imaging modality of choice to evaluate for lymph node metastasis. Ultrasound may also be a beneficial method of evaluating the extent of cancer spread when performed by an experienced sonographer. [ 16 ]
Overall, imaging has the benefit of providing greater information on cancer, including the size of the tumor and its spread beyond the cervix. This information is critical in determining the stage of the cancer and building the best treatment plan. [ 16 ]
If there is evidence that the cervical cancer has spread to local or distant organs, such as the bladder, rectum, or lungs, additional imaging or procedures may be necessary to determine the extent of cancer spread. This may include a chest X-ray to evaluate for lung metastasis, a cystoscopy (camera in the bladder) to look for bladder metastasis, a renal ultrasound to evaluate for the tumor blocking the ureter (tubes connecting the kidney to the bladder), and a sigmoidoscopy (camera in the rectum) to evaluate for cancer that has spread to the colon. The performance of these procedures and imaging modalities is highly individualized based on the symptoms the patient has and the evidence of disease progression. [ 16 ]
Following the collection and interpretation of all imaging and pathology reports, the stage of cervical cancer is determined. [ 16 ] Stages of cervical cancer range from stage I to stage IV, with stage 1 indicating local cancerous cells at the cervix, to stage IV indicating advanced disease and the spread of cancer cells to distant parts of the body. [ 12 ] Stage 0 represents the presence of precancerous cells, but does not represent a cervical cancer diagnosis. [ 13 ] [ 20 ] Controversially, the presence of the spread of cervical cancer to nearby lymph nodes does not change the stage of the diagnosis but is important to note as it may alter the treatment plan. Additionally, the involvement of the body of the uterus does not factor into the stage of cervical cancer. [ 16 ] [ 21 ]
The precancerous cells are confined to the surface layer (cells lining) of the cervix . [ 16 ] This is also known as carcinoma in situ (CIS). [ 20 ]
Cervical cancer is confined only to the cervix. The size of the cancer may include the corpus or fundus (upper portion of the uterus), but there is no cancer growth beyond the cervix or the uterus. Stage I is subdivided based on the depth of the cancer as follows: [ 16 ] [ 19 ] [ 22 ]
Cervical cancer invades beyond the uterus , but does not extend to the pelvic wall or the lower third of the vagina . [ 16 ] [ 19 ] [ 22 ]
Cervical cancer has spread to involve any or all of the following: lower third of the vagina, pelvic wall , pelvic or para-aortic lymph nodes (more distant lymph nodes), is causing hydronephrosis (blockage of the kidney), and/or is causing a non-functioning kidney. [ 16 ] [ 19 ] [ 22 ]
The cancer has spread beyond the true pelvis (the internal reproductive organs , bladder , and colon) or has involved the mucosa of the bladder or rectum . Spread to the bladder or rectum must be biopsy-proven. [ 16 ] [ 19 ] [ 22 ]
The drive to develop a staging for gynecological malignancies, including cancer of the cervix, was the need to have a uniform method to describe the extent of the disease. Comparing outcomes from different treatments could only be possible if the comparison were made for groups of patients with a similar degree of disease burden. [ 23 ]
Source: [ 23 ]
1929 - League of Nations Classification for Cervical Cancer
1937 - First annual report of statistics on radiotherapy outcomes in cervical cancer patients
1938 - Atlas of Cervical Cancer Staging (Heyman and Strandquist)
1950 - The International Classification of the Stages of Carcinoma of the Uterine Cervix
1954 - Founding of FIGO
1958 - FIGO becomes the official publisher of the Annual Report
1973 - Commencement of triennial publication of the Annual Report on the Results of Treatment in Gynecological Cancer
1976 - The American Joint Committee on Cancer accepts the FIGO stage grouping for gynecological cancers
2018 - Latest triennial FIGO Cancer Report [ 22 ]
The most recent updates to cervical cancer staging included in the 2018 edition marked a departure from a system based mainly on clinical evaluation to one that allows imaging and pathological methods to help determine tumor size and extent of disease to assign the stage. A major topic of debate was the impact that newer diagnostic modalities would have on low- and middle-income countries, which bear most of the disease burden . [ 21 ] The final recommendations make findings from imaging and pathology optional for staging rather than a requirement. [ citation needed ]
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Cervical cerclage , also known as a cervical stitch , is a treatment for cervical weakness , when the cervix starts to shorten and open too early during a pregnancy causing either a late miscarriage or preterm birth. In women with a prior spontaneous preterm birth and who are pregnant with one baby, and have shortening of the cervical length less than 25 mm, a cerclage prevents a preterm birth and reduces death and illness in the baby. [ 1 ]
The treatment consists of a strong suture sewn into and around the cervix early in the pregnancy, usually between weeks 12 to 14, and then removed towards the end of the pregnancy when the greatest risk of miscarriage has passed. The procedure is performed under local anaesthesia , usually by way of a spinal block . It is typically performed on an outpatient basis by an obstetrician-gynecologist . Usually the treatment is done in the first or second trimester of pregnancy, for a woman who has had one or more late miscarriages in the past. [ 2 ] The word "cerclage" means encircling, hooping or banding in French. [ 3 ]
The success rate for cervical cerclage is approximately 80–90% for elective cerclages, and 40–60% for emergency cerclages. A cerclage is considered successful if labor and delivery is delayed to at least 37 weeks (full term). After the cerclage has been placed, the patient will be observed for at least several hours (sometimes overnight) to ensure that she does not go into premature labor. The patient will then be allowed to return home, but will be instructed to remain in bed or avoid physical activity (including sexual intercourse) for two to three days, or up to two weeks. Follow-up appointments will usually take place so that her doctor can monitor the cervix and stitch and watch for signs of premature labor. [ citation needed ]
For women who are pregnant with one baby (a singleton pregnancy) and at risk for a preterm birth, when cerclage is compared with no treatment, there is a reduction in preterm birth and there may be a reduction in the number of babies who die ( perinatal mortality ) [ 2 ] There is no evidence that cerclage is effective in a multiple gestation pregnancy for preventing preterm births and reducing perinatal deaths or neonatal morbidity. [ 4 ] Various studies have been undertaken to investigate whether cervical cerclage is more effective when combined with other treatments, such as antibiotics or vaginal pessary, but the evidence remains uncertain. [ 5 ]
There are three types of cerclage: [ 6 ]
While cerclage is generally a safe procedure, there are a number of potential complications that may arise during or after surgery. These include: [ citation needed ]
The Arabin Pessary is a silicone device that has been suggested to prevent spontaneous preterm birth without the need for surgery. [ 11 ] The leading hypotheses for its mechanisms were that it could help keep the cervix closed similarly to the cerclage, as well as change the inclination of the cervical canal so that the pregnancy weight is not directly above the internal os . However, large randomized clinical trials in singleton [ 12 ] and twin pregnancies [ 13 ] found that the cervical pessary did not result in a lower rate of spontaneous early preterm birth. Therefore, the Society for Maternal-Fetal Medicine recommendation is that placement of cervical pessary in pregnancy to decrease preterm birth, should be used only in the context of a clinical trial or research protocol. [ 14 ]
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Cervical conization refers to an excision of a cone-shaped portion of tissue from the mucous membrane of the cervix . Conization is used for diagnostic purposes as part of a biopsy and for therapeutic purposes to remove pre-cancerous cells ( cervical intraepithelial neoplasia ) or early stage cervical cancer . [ 1 ] Ablative treatments are also available to treat abnormal cervical cells. The decision to perform a cervical conization procedure is made with consideration of a patient's pap smear, colposcopy, and HPV test results. ACOG recommends that decisions regarding excision should be based on risk of CIN3+. [ 2 ] A conization can be performed in the office or in the operating room, depending on the type of conization performed. This procedure carries few risks, with the most common one being bleeding after the procedure. [ 1 ] [ 3 ]
Prior to the introduction of the speculum , cervical cancer was only found once it was advanced. With the invention and use of a speculum, changes in the cervix could be appreciated. First, they were evaluated macroscopically and eventually were also assessed using a microscope. In 1927, H. Hinselmann discovered the transformation zone, where metaplastic squamous epithelium is found between the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix. The transformation zone is clinically significant, as it is where almost all cervical cancers and precancerous lesions arise. [ 4 ]
All current cervical conization methods can be traced back to amputation of the ectocervix which was developed by Marion Sims in 1861. Prior to this, any excisions of cervical carcinomas were mainly a palliative care treatment option. A. Sturmdorf was the first to describe an excision of a cone shape from the ectocervix, however he utilized this as a treatment for cervicitis. J. E. Ayre was the first to introduce cold knife conization in 1948 and stressed the importance of evaluating the excised tissue in serial sections to assess the extent of invasion. This method of cold knife conization has been utilized and eventually options for excisions using electrocautery were developed as well. Initially, excised tissue utilizing electrocuatery was not satisfactory for evaluation, but as the loops used have become finer, the quality of the surgical specimens have improved to rival those of cold knife conization. Presently, electrocuatery methods are often preferred to cold knife conization due to greater ease of procedure. [ 4 ]
The cervix connects the uterine cavity to the vagina . The cervix can be viewed by placing a speculum in the vagina. The part of the cervix that can be directly viewed upon placing a speculum in the vagina is the ectocervix. The beginning of the endocervix is called the cervical os. The endocervix leads from the vagina into the uterine cavity. The area where the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix meet is called the transformation zone or the squamocolumnar junction (SCJ). This is the area of the cervix that is most susceptible to human papillomavirus (HPV) infection and is where the vast majority of cervical precancers and cancers arise. This is the tissue that is sampled during a pap smear as a screening test to find abnormal cells or the presence of an HPV infection. [ 1 ]
Types of conization include: [ 5 ] [ 6 ]
Abnormal cervical cells found on pap smear and colposcopy are the basis for the recommendation of a conization procedure. The amount of irregularity will be graded by the pathologist after the colposcopy as CIN1, CIN2, or CIN3. CIN3 represents the most irregular appearing cells of the possible grading options. Conization may be recommended once the risk of CIN3 is greater than 25%. [ 2 ] Conization prior to a radical hysterectomy is associated with better outcomes for early -stage cervical cancers as well, so it may be recommended even when hysterectomy will be the definitive surgical option. [ 7 ] The American Society for Colposcopy and Cervical Pathology has developed a tool to aid in decision -making with abnormal cervical cancer screening and abnormal colposcopy results. [ 8 ]
The vagina is prepped using antimicrobial scrub or iodine. Draping is placed to maintain a sterile surgical field. Some physicians may choose to drain the bladder using a catheter. The speculum will be placed and the cervix visualized. The tissue is then excised from the cervix. The tissue will include the transformation zone and will be shaped like a cone, as the procedure name suggests. The physician will ensure hemostasis has been achieved prior to removing the speculum and ending the procedure. Typically the physician will place a suture at the 12 o'clock region of the excised tissue to serve as a reference point during histological examination. [ 1 ] [ 9 ]
The main difference between cold knife conization and LEEP is the instrument used to excise the tissue. In a LEEP, a thin wire loop electrode is used to remove the cone-shaped surgical specimen. During a cold knife cone, a scalpel is used to excise the tissue. Both LEEP and cold knife cone have shown equal effectiveness, so the decision for which procedure is often based on physician comfort with each procedure or other clinical considerations. Cold knife cone is performed with a scalpel and one advantage to this procedure is that the margins of the excised tissue will be free from thermal damage that would be present in the excised tissue from a LEEP. This can allow for more accurate analysis of the margin of the specimen. [ 1 ] [ 9 ]
Contraindications to completing the procedure are cervicitis , pelvic inflammatory disease , or anticoagulation. Pregnancy is a relative contraindication, meaning that decisions of whether to perform the procedure in pregnant patients would be made on an individual basis. [ 1 ]
After treatment, screenings will continue. HPV screening is recommended 6 months after conization. Regular cervical cancer screening will resume as well, with the schedule of screening being determined by the type of abnormal cells that were present in the cervix. HPV vaccination may also be recommended as a part of treatment plan with the goal of reducing the chances of abnormal cervical cells developing again. [ 3 ]
The most common complication of cervical conization is bleeding during the procedure or within a few weeks after the procedure. Infection after the procedure is possible but very rare. There is the possibility of cervical stenosis or cervical insufficiency . The data regarding risk of preterm birth and low birth weight in future pregnancies is mixed, however it is generally accepted that for patients desiring to carry future pregnancies, limiting the amount of cervical tissue that is excised is the best option to limit this risk. However, taking less tissue does produce increased risk that the margins of the excised specimen will be positive, so the decision on how aggressive of an excision is preformed must be discussed between patient and physician. [ 5 ] [ 6 ] [ 1 ] [ 9 ]
Cervical conization effectively reduces the risk of cancer developing or spreading. The chances of cancer recurrence and premature birth depends on the type of conization. Cold knife conization is associated with 7% chance of the cancer recurring and 16% chance of premature birth, laser conization comes with 6% cancer recurrence and 13% premature birth, and loop excision comes with 10% recurrence and 11% premature birth. [ 5 ] [ 6 ]
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Cervical dislocation is a common method of animal euthanasia . It refers to a technique used in physical euthanasia of small animals by applying pressure to the neck and dislocating the spinal column from the skull or brain . [ 1 ] The aim is to quickly separate the spinal cord from the brain [ 2 ] so as to provide the animal with a fast, painless, and easy death. [ 1 ]
Firm pressure is applied at the base of the skull, along with a sharp pinching and twisting of the thumb and forefinger. At the same time, the tail is pulled backward. [ 3 ] This severs the spinal cord at the base of the brain or within the cervical spine area (the upper third of the neck). [ 2 ] According to the Canadian Council on Animal Care (CCAC), cervical dislocation is normally only conducted on small animals. [ 1 ]
The University of Iowa and some veterinary associations consider the technique to be an ethically acceptable method for killing small rodents such as rats, mice, squirrels, etc. [ 4 ]
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Cervical pessary is a medical device used to treat an incompetent (or insufficient) cervix (cervix starts to shorten and open too early). Early in the pregnancy a round silicone pessary is placed at the opening to the cervix to close it, and then it's removed later in the pregnancy when the risk of a preterm birth has passed.
Pregnant women are at risk of giving birth too early when their cervix begin to efface (shorten) and dilate (open). Different treatments have been tried to prevent a late miscarriage or preterm birth. A common treatment is cervical cerclage or stitch when a suture is stitched around the opening of the cervix around 12–14 weeks into the pregnancy. [ 1 ] A cervical pessary is being studied as an alternative to cervical cerclage since there are fewer potential complications . [ 2 ] More medical studies are needed to decide whether a cervical pessary is equal to or the best treatment. [ 2 ] [ 3 ]
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Cervical Spondylotic Myelopathy (CSM) is a disorder characterised by the age-related deterioration of the cervical spinal cord. [ 1 ] Referred to be a range of different but related terms, a global consensus process selected Degenerative Cervical Myelopathy as the new overarching disease term . [ 2 ] It is a neurological disorder related to the spinal cord and nerve roots . [ 3 ] The severity of CSM is most commonly associated with factors including age, location and extent of spinal cord compression .
Incidence of CSM increases with age, where spinal cord compression is bound to be present people aged 55 or above. [ 4 ]
Pain, numbness, issues with balance and coordination are symptoms widely representative of most common cases of CSM. [ 5 ] It primarily results from spinal cord compression due to the degenerative changes in the cervical region of the spine . [ 6 ] A wide range of tests and medical care are available to help diagnose and treat CSM, respectively, due to the relatively high incidence of CSM.
Numerous CSM symptoms are present which primarily vary according to the relative location and extent of the spinal cord compression. Most common symptoms are: [ 7 ]
Pain in the neck, arms and legs are characterised by the inflammation in the respective regions of nerve root compressions. [ 7 ] It is common for CSM patients to experience a sudden onset of a concentrated, sharp and burning sensation in the affected area. [ 8 ] This pain is accompanied by loss of sensation or a tingling sensation in the limbs; observable characteristics associated with the inability to grasp objects or walk properly. [ 7 ] Damage to the spinal cords and nerve roots typically result in muscle weakness in regions concerning both upper and lower limbs. This results in lack of cohesiveness in movement coordination of the arms and legs. Compression at the superior cervical region can lead to compensatory compression at inferior levels (for example, the lumbar spine ) and affect control over bowel or bladder function. [ 4 ] The severity of such symptoms tend to progress over time and occur more frequently amongst older patients. [ 5 ]
CSM symptoms can be unilateral or bilateral, depending on the lateral regions where compression of the spinal cord and nerve roots occur. [ 9 ] If left untreated, CSM can lead to long-term or permanent damage to the spinal cord and nerve roots. [ 5 ]
The general cause of CSM is the compression of the spinal cord and related nerve roots as a result of the deterioration of the spinal column . The narrowing of the spinal canal due to the inability of the disc to structurally support the vertebrae results in compression. [ 10 ] As the disc continues to lose its elasticity from progressive wear and tear, spinal cord compression increases.
As an age-related disorder, the severity of CSM increases with age. Although, further degeneration can be accelerated via daily practices including poor posture or sedentary behaviours. Prolonged poor posture can misalign the spinal column to apply uneven distribution of weight on the spinal cord and nerve roots. [ 10 ] Absence of physical activity also contributes to exacerbating CSM symptoms, as lack of exercise and muscular strength cannot provide adequate support to the spine.
Spinal arthritis [ 11 ] – most commonly osteoarthritis – is the inflammation of superior and inferior facet joints within the spine . This leads to the formation of Osteophytes [ 11 ] which grow around the joints. This contributes to narrowing the spinal canal and compressing the spinal cord in the corresponding region.
Herniated disk due to tearing of the spinal disk over time, causes the disk to protrude and exert pressure on surrounding spinal nerve tissue. Consequent compression on the spinal cord at the cervical region causes CSM. [ 12 ]
Osteoporosis is the weakening of the bones due to progressive decrease in bone density. [ 13 ] In older patients, the low bone density of the spine is unable to support the weight of the body. This gives rise to CSM via vertebral compression fractures [ 14 ] promoting further compression of the spinal cord and nerve roots.
Spinal tumors can be classified into primary tumours or metastatic tumours which originate from or disseminate to the site of compression, respectively. As the tumours surrounding the spinal column grow in size, the spinal canal is narrowed and therefore results in pressure to be exerted directly on the spinal cord and nerve roots. [ 15 ]
A patient presenting with signs of CSM must see a doctor to perform a wide variety of diagnostic tests. Physical examination is used to determine the severity of the disease by examining the extent of observable CSM symptoms. [ 7 ] [ 16 ] The severity of CSM symptoms indicates of the amount of pressure the cervical spine is under. Physical examination involves flexibility of the neck, strength and reflexes of limb muscles, gait patterns , etc. [ 12 ]
Imaging studies may be used to understand the fundamental cause of the CSM symptoms. This includes: [ 12 ] [ 17 ]
By nature of the CSM as an age-related degenerative condition, there are ways to minimise or delay the onset of CSM, but averting CSM completely can be difficult. [ 19 ] Risks of this condition may be reduced by:
The fundamental principle behind treating CSM lies in decompressing the pressure put on the spinal cord and nerve roots. Although, the treatment options vary depending on the severity and duration of CSM symptoms as determined by a medical professional.
Physical therapy is an appropriate treatment option for mild to moderate stages of CSM to help enhance muscle strength. [ 7 ] Stronger core stability helps correct posture which releases intraspinal pressure exerted on the spinal cord and therefore reduces CSM-related pain.
Upper and lower limb pain caused by inflammation at the corresponding nerve roots can be treated with nonsteroidal anti-inflammatory drugs (NSAIDs) or steroid injections . [ 7 ] CSM medications include: [ 21 ] [ 22 ]
Other medications including acetaminophen , oral corticosteroids, and muscle relaxants are used in conjunction with NSAIDS to address both pain and inflammation. [ 17 ]
A ring-shaped cushion that is secured around the neck with velcro. This is a form of a cast that restricts neck movement and relaxes the neck muscles in daily activities. Usage must be controlled as prolonged usage may permanently weaken the neck muscles. [ 17 ]
Injection of steroids and anaesthetics into the affected area of interest is devised for achieving short-term benefits with treating the disease. [ 12 ]
Surgery is often involved in severe cases of CSM to manually relieve the pressure exerted on the spinal cord and related nerve roots. [ 23 ] Laminectomy is a common surgical procedure for spinal decompression , wherein a part of the vertebrae is excised to alleviate compression on the spinal cord. [ 7 ] [ 24 ]
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The chain of survival refers to a series of actions that, properly executed, reduce the mortality associated with sudden cardiac arrest . Like any chain, the chain of survival is only as strong as its weakest link. [ 1 ] [ 2 ] The six interdependent links in the chain of survival are early recognition of sudden cardiac arrest and access to emergency medical care, [ 3 ] early CPR , early defibrillation, early advanced cardiac life support , and physical and emotional recovery. The first three links in the chain can be performed by lay bystanders, while the second three links are designated to medical professionals. [ 4 ] Currently, between 70 and 90% of cardiac arrest patients die before they reach the hospital. [ 4 ] However, a cardiac arrest does not have to be lethal if bystanders can take the right steps immediately. [ 4 ]
According to the American Heart Association, out-of-hospital cardiac arrest can affect more than 300,000 people in the United States each year. [ 5 ] Three minutes after the onset of cardiac arrest, a lack of blood flow starts to damage the brain, and 10 minutes after, the chances of survival are low. [ 6 ] Therefore, bystanders have only a few minutes to act to optimize a person's chances of survival and recovery. [ citation needed ]
To improve survival outcomes for people who have experienced out-of-hospital cardiac arrest, the American Heart Association–International Liaison Committee on Resuscitation recommended the chain of survival concept in the early 2000s. [ 3 ] Originally, the chain consisted of four steps: early access to emergency medical care was the first link, the second link was early CPR, early defibrillation was the third link, and the final link was early advanced cardiac life support. [ 3 ] Over the years, the American Heart Association has added two new links to the chain: post-resuscitation care in 2010, [ 7 ] [ 3 ] and physical and emotional recovery in 2020. [ 4 ] Also in 2020, the American Heart Association issued a new pediatric chain of survival for infants, children, and adolescents. [ 8 ]
Mary M. Newman, co-founder and president/CEO of the Sudden Cardiac Arrest (SCA) Foundation and previous executive director of the National Center for Early Defibrillation at the University of Pittsburgh, [ 9 ] developed the chain of survival metaphor and first described it [ 6 ] in an article she wrote for the Journal of Emergency Medical Services in 1989, [ 10 ] and further promoted in an editorial she wrote for the first issue of Currents in Emergency Cardiac Care in 1990. [ 11 ] The American Heart Association later adopted the concept and elaborated on it in its 1992 guidelines for cardiopulmonary resuscitation and emergency cardiac care, [ 12 ] [ 13 ] The International Liaison Committee on Resuscitation (ILCOR) echoed the concept in 1997. [ 1 ] The links of the Chain of survival are described below.
Ideally, someone must recognize an impending cardiac arrest or otherwise witness the cardiac arrest and activate the EMS system as early as possible with an immediate call to the emergency services. Unfortunately, many persons experiencing symptoms (for example, angina) that may lead to a cardiac arrest ignore these warning symptoms or, recognizing these warning symptoms correctly, fail to activate the EMS system, preferring to contact relatives instead (e.g., the elderly often contact their adult offspring rather than contact emergency services). [ citation needed ]
To be most effective, bystanders should provide CPR immediately after a patient collapses. In their 2015 guidelines , the American Heart Association re-emphasized the importance of more bystanders performing hands-only CPR until EMS personnel arrive because, at present, fewer than 40% of people who have an out-of-hospital cardiac arrest receive CPR from a bystander. [ 4 ] The guidelines recommend lay rescuers start CPR on a person with presumed cardiac arrest because the overall risk of harm to patients from CPR is low, even if their heart hasn't stopped beating. [ 4 ] Properly performed CPR can keep the heart in a shockable rhythm for 10–12 minutes longer. [ citation needed ]
Most adults who can be saved from cardiac arrest are in ventricular fibrillation or pulseless ventricular tachycardia , which means their heart has fallen out of rhythm. [ 14 ] Early defibrillation is the link in the chain most likely to improve survival since defibrillation can help shock the heart back into a regular beat. [ 15 ] Early, rapid defibrillation is considered the most important link in the chain of survival. [ 15 ] Rapid defibrillation outside of the hospital improves the chances of survival by as much as 30%, and involves using an automated external defibrillator (AED) to shock the patient's heart. [ 16 ]
While CPR keeps blood flowing artificially, [ 17 ] rapid defibrillation is the only way to restart the heart and reset it to a healthy rhythm. [ 18 ] And while only 40% of adults experiencing cardiac arrest receive CPR, fewer than 12% receive shocks from an AED before EMS arrival. [ 8 ] What is more, the chances of the patient's survival decrease by as much as 10% with every minute that they do not receive rapid defibrillation. [ 19 ]
AEDs are becoming more common in businesses, schools, and even the home as the public becomes more aware of the importance of rapid defibrillation. [ 20 ] [ 6 ] AEDs come with pre-recorded instructions and are easy to use. [ 18 ] If an AED is not available, bystanders will need to continue CPR until emergency responders arrive with a defibrillator, which is why it is important to recognize cardiac arrest and call for help quickly. [ 21 ] [ 6 ]
Public access defibrillation may be the key to improving survival rates in out-of-hospital cardiac arrest, [ 1 ] but is of the greatest value when the other links in the chain do not fail.
Early advanced cardiac life support by paramedics is another critical link in the chain of survival. In communities with survival rates > 20%, a minimum of two of the rescuers are trained to the advanced level. [ citation needed ]
Some ACLS ambulance providers will administer medications to manage pain, arrhythmias, shock, and pulmonary congestion; monitor the heart rhythm to identify any potentially lethal cardiac arrhythmias; or initiate transcutaneous pacing. [ 15 ] ACLS ambulance providers use the mnemonic "MONA" (morphine, oxygen, nitroglycerin, and aspirin) to reflect the out-of-hospital therapies they will use for cardiac arrest. [ 15 ]
Often, ACLS ambulance providers will attach an electrocardiogram to the patient and transmit its findings to the receiving hospital or care facility, which leads to earlier diagnosis of a heart attack, and significantly reduces time to treatment at the hospital. [ 15 ] This prearrival ECG and notification has been shown to improve patient outcomes. [ 15 ] In the event of a complication at the scene of the event or on the way to the hospital, ACLS ambulance providers can administer life saving therapies, including CPR, rapid defibrillation, airway management, and intravenous medications. [ 15 ]
In October 2020, the American Heart Association added the recovery phase as the sixth link in the chain of survival. [ 4 ] Recovery consists of cardiac arrest survivors receiving treatment, surveillance, and rehabilitation at a hospital. [ 4 ] It also includes an assessment for anxiety, depression, and post-traumatic stress, which can all lead to future repeated events. Before being discharged from the hospital, the American Heart Association recommends that cardiac arrest survivors receive rehabilitation assessment and treatment for physical, neurologic, cardiopulmonary, and cognitive impairments. [ 4 ] [ 8 ] They also recommend that cardiac arrest survivors and their caregivers receive comprehensive, multidisciplinary discharge planning to include medical and rehabilitative treatment recommendations and return to activity and work expectations. [ 4 ] [ 8 ]
A patient's recovery from cardiac arrest continues long after their initial hospitalization following the event, so the American Heart Association recommended in their 2020 guidelines that patients have formal assessment and support for their physical, cognitive, and psychosocial needs. [ 8 ]
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Chalky teeth is a colloquialism used to describe teeth that are abnormal in some way. The term usually refers to tooth enamel that is visibly different in colour, consistency or shape ( morphology ). Hence, by analogy to blackboard chalk , "chalky enamel" is discoloured, opaque, soft, porous and prone to degradation or staining – unlike normal enamel which is translucent, hard and impermeable. Chalky teeth and derivative terms ("chalky molars", "chalky enamel") have received widespread exposure as a metaphor for malformed teeth with elevated risk of tooth decay . A public "Chalky Teeth Campaign" highlights the major socioeconomic burdens of this medico-dental problem and desirability of research into prevention . [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] The gritty sensation elicited by oxalate -rich foods such as spinach may also be described as "chalky teeth'. [ 6 ]
Since 1920, various derivatives of "chalky teeth" have appeared in the academic literature to describe specific dental anomalies. Most references are to enamel defects that have a chalky appearance (white, cream or brown) and are of developmental origin (i.e. amelogenesis imperfecta , enamel hypomineralisation, dental fluorosis , molar hypomineralisation ). Additionally, researchers have described the earliest stage of tooth decay as "chalky white spots", and an iconic toothpaste advertisement featuring school teacher "Mrs Marsh" used a chalk metaphor in this context. [ 1 ] [ 2 ] [ 7 ]
Developmental types of chalky teeth (i.e. those due to abnormal tooth development inside the jaw) are thought to reflect one or more pathological disturbances, raising the prospect for medical prevention. [ 2 ] [ 3 ] [ 4 ] For example, enamel hypomineralisation is attributed to local trauma or various medical conditions (e.g. fever , respiratory disease , vitamin D deficiency , adverse drug reaction ), and dental fluorosis results from excessive consumption of fluoride during enamel development. Usually only one or several teeth are chalky in these instances where the primary cause isn't genetic – such acquired disorders are often accessible to prevention. Conversely, amelogenesis imperfecta is a relatively rare genetic disorder that distinctively may cause all teeth to be chalky. [ 2 ] [ 3 ] [ 4 ]
Links between chalky teeth and accelerated tooth decay have long been recognised at academic and societal levels but largely overlooked by public health, dentistry, maternal and child health policy makers. Evidence that the commonest type of chalky teeth (termed "chalky molars" or molar hypomineralisation) affects 1-in-5 children worldwide makes this association particularly concerning. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] In 2007, a translational research and education network (The D3 Group for developmental dental defects ) was formed to advocate for and facilitate research into the management and prevention of chalky teeth. The D3 Group recognised that medico-dental research outcomes could lead to substantial reductions in childhood tooth decay and allied socioeconomic burdens. In 2013, they launched a public-awareness initiative (The Chalky Teeth Campaign) and an online education resource, aiming to increase understanding of this issue across society. Educational materials for non-specialist audiences, including a children's storybook about chalky molars, were central to this initiative. Subsequent activities involving public, professional and academic audiences have promoted "the fight against chalky teeth" as an attractive opportunity for jointly improving oral and paediatric health worldwide. "Chalky teeth" is thereby growing from a nebulous colloquialism into a social-good mission and translational nomenclature that is being incorporated into other languages. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 8 ] [ 9 ]
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The Chalmers Medal is the major mid-career award of the Royal Society of Tropical Medicine and Hygiene . [ 1 ] The Chalmers Medal was initially awarded biennially, then annually, "in recognition of research of outstanding merit contributing to our knowledge of tropical medicine or tropical hygiene" [ 2 ] and now "to researchers in tropical medicine or international health who obtained their last relevant qualification between 15 and 20 years ago, allowing for career breaks, who demonstrate evidence of mentoring and professional development of junior investigators, and other forms of capacity-building in line with Dr Chalmers’ own values". [ 3 ] It is named in honour of Albert John Chalmers MD, FRCS, DPH, who was acclaimed for his work on tropical medicine on the Indian sub-continent.
The award was established in 1921 following a donation by Mrs Chalmers, the widow of Dr Chalmers, and consists of a silver gilt medal bearing the image of Dr Chalmers and the society's motto Zonae torridae tutamen (Guardian of the torrid zone) on one side, and a representation of Anopheles gambiae above a spray of the cinchona plant on the other.
Source: RSTMH
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The Chamber of Physicians and Dentists ( Polish : Naczelna Izba Lekarska ) together with the regional chambers of physicians and dentists are the organizational bodies of the professional self-government of physicians and dental practitioners who are associated in the chambers with equal status. Chambers of physicians and dentists deal with all kinds of matters concerning the exercise of medicine and dentistry in Poland .
The organs of The Polish Chamber of Physicians and Dentists are: General Assembly, Supreme Medical Council (implements resolutions of the General Assembly, supervises the correct execution of tasks of the self-government of physicians and dentists, coordinates and supervises activities of regional medical councils), The Supreme Screener for Professional Liability (conducts proceedings in cases involving professional liability of physicians and dentists), The Supreme Medical Court (hears cases involving professional liability of physicians and dentists), The Supreme Audit Committee (controls financial and business activities of the Polish Chamber of Physicians and Dentists).
The regional chamber of physicians and dentists registers as its members those physicians and dentists who hold a right to practice the profession and intend to practice as a physician or dentist within the jurisdiction of the given chamber. [ 1 ]
The Medical Code of Ethics was passed at the 2nd General Medical Assembly in 1991. It was significantly amended at the 3rd General Medical Assembly in 1993 and at the 7th General Medical Assembly in 2003 in order to update the Code according to the current developments, e.g. new provisions on the relations between the physician and the medical industry were introduced.
The Polish Chamber of Physicians and Dentists is active in the works of the following international organizations of doctors and dental practitioners:
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The Chanchlani Global Health Research Award is a Canadian health sciences award that recognizes a world leading scholar in the area of Global Health. Each year a discipline within Global Health (i.e. Determinants of Health, Policy Development, and Innovative Solutions) is chosen by the internal review committee at McMaster University . The review committee then selects the leading researcher based on interview and impact in the field. The award recipient receives a monetary prize of $5,000 and opportunity to present their research findings to researchers and students. [ citation needed ]
The award provides opportunities for informal scientific exchanges between the scientist/scholar and faculty, postdoctoral fellows, graduate and undergraduate medical students. The award was created by the Chanchlani Family through $1 Million endowment along with a $250,000 donation at the McMaster University in 2012. [ 1 ]
Source: McMaster University
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The Charing Cross Trunk Murder took place in a third floor office at 86 Rochester Row in the City of Westminster in London on 4 May 1927. [ 1 ]
On 6 May 1927, [ 2 ] John Robinson, a 35-year-old estate agent, took a cab to Charing Cross railway station , where he deposited a large black trunk in the left-luggage office. [ 1 ] On 10 May after a "dreadful smell" was noted, the police opened the trunk to find the dismembered body of a woman, with each limb separately wrapped in brown paper. [ 1 ]
The shopowner who sold the trunk and the cab driver were traced, and the police that visited the office at No 86 said it was "hastily vacated but scrupulously clean". [ 1 ] Although the identity parade failed to pick out Robinson, a more careful search of the property found a matchstick in the bin with a small spot of blood.
A laundry tag on the dead woman's knickers for "P Holt" was traced to a Mrs Holt in Chelsea, who had employed ten women as servants over the past two years, and all were traced except for a "Mrs Rolls". [ 1 ] [ 3 ] [ 4 ] Holt confirmed that the head of the dead woman was that of Mrs Rolls, who turned out to be Minnie Alice Bonati, who had left her Italian waiter husband to live with a Mr. Rolls, and now used his name. [ 1 ] [ 3 ]
Bonati was working as a domestic servant and supplementing her income with prostitution . She had met Robinson at Victoria station , and they had gone to his office for sex. [ 1 ] [ 3 ] She died after an argument about money, with Robinson claiming that she attacked him, leading him to push her away, causing Bonati to fall, hit her head and die. [ 1 ] [ 3 ] He claimed that he panicked, bought a knife and trunk and disposed of the body, because he thought that no one would believe him. [ 1 ] [ 3 ] Robinson's story was contradicted by forensic pathologist Bernard Spilsbury , who said that Bonati had died of asphyxiation after being knocked unconscious, which could not have been caused by a fall as Robinson claimed. [ 3 ]
During his investigation Detective Inspector Grosse of the Metropolitan Police also pursued enquiries on behalf of a newspaper, an action which some held to be "reckless and unscrupulous" and argued should lead to the withdrawal of his pension. [ 2 ] After being produced as a trial exhibit, the trunk was retained in the collections of its private "Black Museum" (now the Crime Museum ), where it was the subject of Episode 47 of the 1952 radio crime drama The Black Museum , with Orson Welles as both the host and narrator of the show. [ 5 ] [ 6 ] A version of the story (with names and dates changed) was dramatised in Dec 1951 as 'The Founier Case' episode of Whitehall 1212 (radio show) . [ 7 ] A third dramatisation was broadcast as 'The Family Solicitor' in the 1949-51 series The Secrets of Scotland Yard with Clive Brook as the narrator [ 8 ]
The trunk was also loaned from the Crime Museum to the Crime Museum Uncovered exhibition at the Museum of London from October 2015 to April 2016. [ 9 ] [ 10 ]
Robinson was tried at the Old Bailey and convicted by Spilsbury's evidence that Bonati had been deliberately asphyxiated. He was sentenced to death by Mr. Justice Swift and hanged at Pentonville Prison on 12 August 1927. [ citation needed ]
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Charles Augustus Hawley (March 13, 1861 – July 22, 1929) was an American orthodontist who developed the Hawley retainer which is used in the field of orthodontics. He attended Angle School of Orthodontia and graduated in 1905. [ 1 ] [ 2 ]
He was born in Avery, Ohio in 1861. He attended high school in Columbus, Ohio and then attended Ohio State University for his college degree. He then attended University of Michigan School of Dentistry and graduated in 1893. He then became the Professor of Operative Faculty soon after graduation. He was one of the first people to have used nitrous oxide as an anesthetic for the removal of teeth. [ 1 ] He attended Angle School of Orthodontia and graduated in 1905. He moved to Washington, D.C. after and became the first person to specialize in orthodontics in that city. [ 3 ]
He was married to Evelyn Frank Hawley, and had two children. He died on July 22, 1929 at the Garfield Hospital in Washington DC , following complications from an operation. [ 3 ]
In the field of orthodontics, he is best known for his introduction of a refined type of retention plate called the Hawley Bite Plate. Two of Dr. Hawley's papers Determination of the Normal Arch and Its Application to Orthodontia and An Accurate Method in Orthodontia were read before 4th International Dental Congress and New York Institute of Stomatology . [ citation needed ]
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Charles Antzelevitch is an American cardiovascular research scientist in the fields of cardiac electrophysiology and cardiac arrhythmia syndromes. [ 1 ]
Antzelevitch graduated from Queens College, City University of New York with a BA in biology. He earned a PhD in pharmacology from State University of New York Upstate Medical University in 1978. [ 1 ] From 1977 to 1980, he held a postdoctoral fellowship in the department of experimental cardiology at the Masonic Medical Research Laboratory (MMRL) in Utica , New York. [ 2 ]
After his fellowship, he joined the staff of the MMRL as a research scientist. In 1984, he was named executive director and director of research at the MMRL and was appointed the Gordon K. Moe Scholar, an endowed chair in experimental cardiology, in 1987. [ 2 ]
Antzelevitch was a member of the faculty at State University of New York Upstate Medical University in Syracuse , New York , from 1980 until 2015. In 1980, he received an appointment as assistant professor in the department of pharmacology there. In 1983, he was promoted to associate professor and then in 1986, to research professor. He became professor of pharmacology in 1995. [ 2 ] [ 3 ] In 2015, Antzelevitch moved to the Lankenau Institute for Medical Research (LIMR), where he was appointed professor and executive director of cardiovascular research and director of research at the Lankenau Heart Institute. In 2020, he was designated as distinguished professor emeritus at LIMR. [ 4 ] [ 1 ]
Antzelevitch was president of the International Cardiac Electrophysiology Society from 1996 to 1998 [ 5 ] and has served as secretary/treasurer since 1998. [ 6 ] He serves as Associate Editor of Heart Rhythm journal as well as on the editorial board of several other peer-reviewed medical publications, including Journal of Electrocardiology [ 7 ] and Journal of the American College of Cardiology . [ 8 ] He received the Distinguished Scientist Award from the North American Society of Pacing and Electrophysiology (NASPE), currently the Heart Rhythm Society (HRS 2002), [ 9 ] Excellence in Cardiovascular Science Award from the NE Affiliate of the American Heart Association (AHA 2003), [ 10 ] Carl J. Wiggers Award from the American Physiological Society (2007), [ 11 ] [ 12 ] Distinguished Scientist Award from the American College of Cardiology (ACC 2011), [ 9 ] [ 13 ] Distinguished Service Award from the Cardiac Electrophysiology Society (2015), [ 14 ] the Douglas P. Zipes Lecture Award from the Heart Rhythm Society (2016) [ 10 ] and the Lifetime Achievement Award from the American College of Cardiology (ACC 2020). [ 15 ]
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Charles Edward Wallis (26 March 1869 – 4 January 1927), otherwise known as the 'father' of the London School Dental Service, was a physician and dental surgeon in London in the early 20th century. As one of the first assistant medical officers to London County Council , his research led to the establishment of a school dental treatment service and an improvement in child welfare.
He was an active member of the British Dental Association (BDA) and a keen historian of medicine, participating in the activities of the Royal Society of Medicine's (RSM) History of Medicine Section , later renamed society.
Between his medical and dental training, Wallis took up a post as a ship’s surgeon, a position he pursued again later to travel much of the world and learn dental procedures. He was particularly skilled in the bilateral molar extraction before the use of local anaesthetic.
As a King's College Hospital dental surgeon, Wallis also published extensively in the British Dental Journal , ultimately being an important part of its editorial board.
His legacy is honoured through a fund left by his brother to the RSM.
Charles Edward Wallis was born on 26 March 1869 in Lambeth , his mother being called Fanny Margaret and his father, Augustus Wallis, an insurance clerk. His early education was at Bedford Grammar School , following which he gained the conjoint medical diploma from King's College Hospital in 1894. [ 1 ]
Wallis became a ship's surgeon on the Royal Microscopical Society's RMS Garth Castle ( Union-Castle Line ), after fulfilling two house appointments. Later, he would use vacations to travel to Canada, the United States, South Africa and the Antarctic [ 3 ] and learn new dental techniques. Subsequently, he went to study in Paris and then again in London. [ 1 ]
At one time, Wallis was Joseph Lister 's dresser (assistant). [ 4 ]
In 1897, he gained the Licentiate in Dental Surgery of the Royal College of Surgeons of England from the Dental Hospital of London , [ 1 ] later named the Royal Dental Hospital which subsequently merged with Guy's Dental School and became the United Medical and Dental Schools of Guy's and St Thomas' Hospitals . [ 5 ] Wallis then set up practice in Queen Anne Street , London and joined the BDA where he remained an active member for 22 years. He wrote extensively for the British Dental Journal from 1908 to 1919 and became chairman of its editorial board from 1914. In 1899, Wallis was appointed dental assistant at KCH and subsequently took over from Professor Swayne Underwood as dental surgeon in 1911. [ 1 ]
In 1905, Wallis was appointed assistant medical officer to the London County Council. Wallis was mainly responsible for the formation of its school dental service. [ 1 ]
Prior to the advent of local anaesthesia, Wallis would perform the bilateral molar extraction by simultaneously pulling out the two teeth whilst an assistant held the head. This avoided experiencing pain twice. [ 6 ]
In addition to his concern with dental health, as an assistant medical officer to the London County Council , Wallis maintained his overall interest in child welfare. [ 7 ]
Wallis was interested in archaeology and history. Writing extensively on the history of dentistry and sitting next to Lilian Lindsay at meetings, Wallis spent a considerable time with activities related to the history of medicine section at the Royal Society of Medicine in Wimpole Street, London. [ 1 ]
He was considered expert in the histories of Paris and London and published on dentistry in ancient times. [ 1 ]
Wallis died at the age of 59 years in King’s College hospital on Tuesday 4 January 1927 [ 8 ] from bronchopneumonia . He left with his writing an unfinished history of Harley Street. His brother, Ferdinand bestowed a C.E Wallis prize in preventive dentistry for undergraduates at King’s. [ 1 ] Ferdinand Wallis also presented the RSM with £100 to establish a ‘CE Wallis Lecture’ on the history of dentistry in memory of his brother. [ 9 ] This is jointly arranged by the odontology section of the RSM and the history of medicine society and is given every five years. [ 10 ] It was emphasised that the lecturer must be a fluent and interesting speaker and should provide “illustrations such as lantern slides”. [ 11 ] The first person given the honour of presenting the memorial lecture was Lilian Lindsay . She remembered Wallis as a personal friend who sat next to her at meetings of the History of Medicine Section at the RSM. Other notable speakers have included W. Fraser-Moodie in 1971, [ 11 ] J. R. Garrett in 1975, [ 12 ] Frank Colyer , Zachary Cope [ 10 ] and Stanley Gelbier . [ 1 ]
Tributes continued through to 2017 with Malcolm Bishop recalling how Wallis was a model mover and shaker of his time. Previously, John Davy Rolleston had prepared a special reference to Wallis in Philadelphia in 1926, at the 7th International Dental Congress called 'Recollections of Lister'. Following Wallis's death, Dr E Graham Little MP, honoured a lecture on the 'Art of War' which Wallis had centred on the Latin text De Re Militari (Concerning Military Matters). Lilian Lindsay commented how "his retentive memory provided material for his entertainment of children whom he delighted with his stories and recitations". [ 7 ]
He became known as the 'father' of the London School Dental Service . [ 1 ]
Past lectures and speakers include:
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Charles P. Friedman is a medical health informatician and educator, and an academic. He is a professor in the Department of Learning Health Sciences at the University of Michigan Medical School .
Friedman's research focuses on biomedical and health informatics, as well as the processes of education and learning.
Friedman is a distinguished fellow of the American College of Medical Informatics , and a founding fellow of the International Academy of Health Sciences Informatics.
Friedman completed his B.S. in Physics in 1971 from the Massachusetts Institute of Technology (MIT). He obtained his M.S. in Physics from MIT in the same year and in 1977, earned his Ph.D. in Education from University of North Carolina, Chapel Hill . In 1992, he undertook advanced studies in Medical Information Science at Stanford University . [ 1 ]
Friedman began his academic career in 1971 as a staff scientist at MIT and visiting lecturer at the Department of Physics at the University of Massachusetts , Boston where he remained until 1974. In 1977, he joined the Department of Family Medicine at the University of North Carolina, first as an assistant professor and later as an associate and full professor, and remained there until 1996. He was professor at the University of Pittsburgh between 1996 and 2006 and then joined the University of Michigan in 2011 where he was appointed as professor at the Schools of Information and Public Health. From 2014 to 2024, he was the Josiah Macy Jr. Professor of Medical Education and the founding chair of the Department of Learning Health Sciences. [ 1 ]
From 2007 to 2009, he was deputy national coordinator for Health Information Technology, a division of the US Department of Health and Human Services . In 2009, he was appointed the chief scientific officer of the division and remained at the position until 2011. [ 2 ]
Since 2015, he has been editor-in-chief of the journal Learning Health Systems . [ 3 ]
Friedman's work on learning health systems (LHS) emphasized the potential of a dynamic, data-driven approach to health and health care improvement. He suggested that the effective use of electronic health records (EHRs) could transform raw medical data into structured, computable information and change patient care outcomes. He also highlighted that the achievement of a nation-wide LHS required an IT-enabled socio-technical infrastructure as well as active participation from multiple and diverse stakeholders. [ 2 ]
Friedman's research also focused on interactions between providers , patients, and information technology, exploring the degree to which information resources provide advice that is helpful in addition to being correct. [ 4 ] To clarify the goal of biomedical informatics, he presented a theorem which stated that biomedical informatics resources should strive to make people better than they would be without assistance from these resources. [ 5 ]
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Charles Gordon Heyd (27 August 1884 – 4 February 1970) was an American surgeon and president of the American Medical Association in 1936–1937.
Heyd obtained a B.A. from the University of Toronto in 1905 and M.D. from University of Buffalo in 1909. [ 1 ] [ 2 ] During World War I he served as a Major in France. [ 1 ] Heyd was an opponent of compulsory health insurance and socialized medicine . Instead, he favoured voluntary medical insurance and public health testing. [ 1 ]
Heyd was Director of Surgery at New York Post-Graduate Medical School and Hospital and Professor of Clinical Surgery at Columbia University . [ 1 ] He was President of the United Medical Service (1948–1951). In 1932, he received the Legion of Honour of France. [ 1 ] He wrote the Preface for Lloyd Paul Stryker 's Courts and Doctors , published in 1932. [ 3 ]
He was President of the American Medical Association (1936–1937). [ 1 ] In 1937, Heyd was awarded honorary degree of doctor of science by Temple University . [ 4 ] In 1940, Heyd noted that most infections of the neck have their origin in the oral cavity. [ 5 ]
Heyd died on 4 February 1970. [ 6 ]
Heyd was an opponent of water fluoridation . [ 7 ] He has been quoted as saying "I am appalled at the prospect of using water as a vehicle for drugs. Fluoride is a corrosive poison which will produce harm on a long-term basis". [ 8 ]
Heyd's comment has been widely cited in anti-fluoridation literature as an argument from authority because he was a former President of the AMA. [ 7 ] However, Heyd was President of the AMA for two years in the 1930s long before evidence of the effectiveness from fluoridation was available to examine. Since Heyd, no other AMA President has opposed fluoridation. [ 7 ]
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Cheek teeth or postcanines comprise the molar and premolar teeth in mammals . Cheek teeth are multicuspidate (having many folds or tubercles ). Mammals have multicuspidate molars (three in placentals, four in marsupials, in each jaw quadrant) and premolars situated between canines and molars whose shape and number varies considerably among particular groups. For example, many modern Carnivora possess carnassials , or secodont teeth. This scissor-like pairing of the last upper premolar and first lower molar is adapted for shearing meat. In contrast, the cheek teeth of deer and cattle are selenodont . [ 1 ] Viewed from the side, these teeth have a series of triangular cusps or ridges, enabling the ruminants' sideways jaw motions to break down tough vegetable matter. Cheek teeth are sometimes separated from the incisors by a gap called a diastema . [ 2 ]
Cheek teeth in reptiles are much simpler as compared to mammals . [ 3 ]
Apart from helping grind the food to properly reduce the size of substrates for stomach enzymes, their minor role is in giving shape and definition to the animals' jaws. The shape of cheek teeth are directly related to their function, and morphological differences between species can be attributed to their dietary variations. Additionally, the shape a cheek tooth can be mechanically worn down based on diet, which is used to provide insights into the consumption habits of fossilized animals. [ 4 ] Proper cleaning of cheek teeth is vital for all species of organisms and many species including humans and ruminants keep it on top of their crucial priority list. Dental caries may result from improper care of cheek teeth which is a prominent problem across the globe. [ 5 ]
Mammalian, multicusped cheek teeth probably evolved from single-cusped teeth in synapsids, although the diversity of therapsid molar patterns and the complexity in the molars of the earliest mammals make determining how this happened impossible. According to the widely accepted "differentiation theory", additional cusps have arisen by budding or outgrowth from the crown, while the rivalling "concrescence theory" instead proposes that complex teeth evolved by the clustering of originally separate conical teeth. Therian mammals (placentals and marsupials) are generally agreed to have evolved from an ancestor with tribosphenic cheek teeth, with three main cusps arranged in a triangle. [ 6 ]
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In medicine, the term cheesewiring or cheesewire effect (used interchangeably) describes any process in which cells or intercellular matrix are dissected or extruded either by the material being pressed through a taut element, or by the tension of a taut element pulling through tissue. The procedure is typically conducted in a surgical setting.
Cheesewiring or the cheesewire effect can also describe the process of suture material cutting or tearing through viscera at the time of suture anastomosis and tension.
Cheesewiring can be a complication or part of a negative outcome of a procedure. Examples include tumor growth penetrating the openings in a bowel stent that was placed to open an obstructed bowel , [ 1 ] sutures used to hold a transplanted cornea in place, [ 2 ] and treatment of tendon rupture , when sutures pull through the tendon. [ 3 ]
Evidence that the cheesewire effect has occurred is most clearly seen after surgery has been completed. Postoperatively as wound margins begin to swell, a suture can drag through the thin portion of tissue present near the surface. This suture drag is most often the result of tension being reduced in tying or placing the suture. It is apparent that cheesewiring has occurred if the suture has moved a little closer to the insertion site. A tell tale Y-shaped scar is evidence that cheesewiring has taken place. Cheesewiring that causes drag can lead to damage to tissue and make a surgeon tug on the material, leading to suture pullout. This causes an increased procedure time for the surgeon as well as a prolonged recovery period for the patient. [ 4 ]
Cheesewire complications are most often seen in cornea surgeries due to the soft tissue present in the eye. One of the most common occurrences is cheese wiring of the puncta occurring during intubation . This can occur for many different reasons. One cause is excessive tension on the tubing. Cheesewiring can also occur late as scar tissue forms around the tubing. The scar tissue fixes the tube in place and prevents the movement in the canalicular system with each blink creating problems. The tubing must be removed if cheesewiring is greater than 3 mm. [ 5 ]
Whether intentional or non-intentionally occurring, a cheesewire suture can be removed in surgery. A cheesewire suture is removed by a small incision made in the conjunctiva overlying the two ends of the suture. Fine removal suture forceps are used to grasp both ends of the suture. Tangential traction is then used to cheesewire through the scar tissue [ 5 ]
There are many complications that can arise from the removal of the cheesewire suture. In the eye specifically, suture breaking can result in significant tissue scarring. This results in a large amount of traction force required to remove the suture. Occular Hypotony and hyphema following the removal of cheesewire sutures are also common occurrences. [ 5 ]
Surgeons can take several precautions to help decrease the probability of cheesewiring occurring. One technique determined to decrease suture drag is placement of the needle perpendicularly through the entire corneal thickness encompassed by the suture bite on each side of the incision. Certain sutures are also more prone to cheesewiring. 3-0 Vicryl is one of the least likely sutures to experience cheesewiring. Sutures may also be coated in materials to reduce tissue drag. Monofilament sutures create less drag while passing through tissue, but may decrease tensile strength and cause crimping. Therefore, multifilament sutures are more commonly used to prevent the occurrence of cheesewiring despite a decrease in mechanical properties [ 6 ]
Factors such as the type and size of the needle, suture type and thickness, and suture placement should all be considered as all factors have a significant effect on the surgical result. For instance, having a suture that is too short can lead to inflammation in tissue, while a suture that is too tight can cause necrosis, especially in association with significant edema. [ 7 ]
The term cheesewiring can also be used to name the process of using a guidewire or suture intentionally to cut through tissue during a surgical procedure or allowing a suture to slowly cut through tissue over time. Examples of cheesewiring used intentionally include treating fistulas, use in trabeculectomies, and to aid in endovascular aortic repair. [ 8 ] [ 9 ] [ 5 ]
Treatment of fistulas often involves placing a suture and allowing it to cut off the fistula over time. [ 9 ]
Cheesewiring is used as an intentional procedure in a trabeculectomy . In a trabecuiectomy, a loop of 8-0 nylon sutures is placed under the scleral flap. The cheesewiring suture allows rescuing failing or failed bleb , by mechanically breaking down the subscleral flap. [ 5 ]
In this procedure, a triangular partial thickness scleral flap is created using a diamond knife. The scleral flap is then extended to the limbus that is hinged anteriorly. A sclerotomy is then made with a punch followed by a peripheral iridectomy . An 8-0 nylon suture is then passed through the conjunctiva from the external aspect into the subconjunctival space. This process creates the cheesewiring effect. The needle is entered 3 mm (0.12 in) from the lateral edge of the future bleb site and 3–4 mm (0.12–0.16 in) away from the limbus. The 8-0 nylon suture is taken under the scleral flap. Once this happens, the suture is reversed and the needle is passed through the conjunctiva from the inside towards the outside position. A singular 10-0 vicryl suture can secure the scleral flap and then the cheesewire suture can then be cut flush to the conjunctiva. The conjunctiva flap can be then secured with 26 10-0 vicryl sutures at either end of the limbus. A single 10-0 vicryl mattress suture can be placed in the middle. This entire process allows for blebs to be rescued. [ 5 ]
Cheesewiring is commonly used in the endovascular repair. The cheesewire technique can be used to fenestrate an intimal flap, alleviating malperfusion in aortic dissection. Pulling both ends of a guide wire in a caudally sawing motion down through the infrarenal neck and into the aneurysm sac completes the technique. This process shears the flap with minimal damage. [ 8 ]
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A cheilectomy is a surgical procedure that removes bone spurs from the base of the big toe. [ 1 ]
Patients with a condition called hallux rigidus, or arthritis of the big toe, have pain and stiffness in the big toe.
The word cheilectomy comes from the Greek word Cheilos, meaning "lip." A cheilectomy removes the bone spurs, or lip of bone, that forms as a result of arthritis of the joint. Removing the bone spurs, eases pain and lessens stiffness of the big toe. [ citation needed ]
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Cheiloplasty or surgical lip restoration (from Greek : χείλος kheilos – "lip") is the technical term for surgery of the lip usually performed by a plastic surgeon or oral and maxillofacial surgeon . Among other procedures it includes lip reduction, the process of surgically reducing the size of the lip or lips to reduce the appearance of abnormally large or protruding lips, as well as the process of forming an artificial tip or part of the lips by using a piece of healthy tissue from some neighboring part. The procedure can also larger. [ clarification needed ]
Cheiloplasty can be performed to treat tight lip syndrome in Shar Pei dogs by repositioning the lower lip and allowing it to heal in a normal position. [ 1 ]
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Cheiralgia paraesthetica ( Wartenberg's syndrome ) is a neuropathy of the hand generally caused by compression or trauma to the superficial branch of the radial nerve . [ 1 ] [ 2 ] The area affected is typically on the back or side of the hand at the base of the thumb, near the anatomical snuffbox , but may extend up the back of the thumb and index finger and across the back of the hand. [ 1 ] [ 3 ] Symptoms include numbness, tingling, burning or pain. Since the nerve branch is sensory there is no motor impairment. [ 3 ] It may be distinguished from de Quervain syndrome because it is not dependent on motion of the hand or fingers. [ 4 ]
The most common cause is thought to be constriction of the wrist, as with a bracelet or watchband (hence reference to "wristwatch neuropathy"). It is especially associated with the use of handcuffs and is therefore commonly referred to as handcuff neuropathy . Other injuries or surgery in the wrist area can also lead to symptoms, including surgery for other syndromes such as de Quervain's. [ 5 ] The exact etiology is unknown, as it is unclear whether direct pressure by the constricting item is alone responsible, or whether edema associated with the constriction also contributes. [ 3 ]
Symptoms commonly resolve on their own within several months when the constriction is removed; NSAIDs are commonly prescribed. [ 4 ] In some cases a nerve decompression is required. [ 4 ] The efficacy of cortisone and laser treatment is disputed. [ 4 ] Permanent damage is possible.
This neuropathy was first identified by Robert Wartenberg in a 1932 paper. [ 6 ] Recent studies have focused on handcuff injuries due to the legal liability implications, but these have been hampered by difficulties in followup, particularly as large percentages of the study participants have been inebriated when they were injured. [ 7 ] Diagnostically it is often subsumed into compression neuropathy of the radial nerve as a whole (e.g. ICD-9 354.3 ), but studies and papers continue to use the older term to distinguish it from more extensive neuropathies originating in the forearm. [ citation needed ]
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Chemoprevention or chemoprophylaxis refers to the administration of a medication for the purpose of preventing disease or infection . [ 1 ] [ 2 ] Antibiotics , for example, may be administered to patients with disorders of immune system function to prevent bacterial infections (particularly opportunistic infection ). [ 3 ] Antibiotics may also be administered to healthy individuals to limit the spread of an epidemic , or to patients who have repeated infections (such as urinary tract infections ) to prevent recurrence. It may also refer to the administration of heparin to prevent deep venous thrombosis in hospitalized patients.
In some cases, chemoprophylaxis is initiated to prevent the spread of an existing infection in an individual to a new organ system, as when intrathecal chemotherapy is administered in patients with malignancy to prevent further infection.
The use of chemoprophylaxis is limited primarily by two factors: risk and financial costs.
Using chemoprophylaxis as a treatment against early signs of tuberculosis has proven to be effective. [ citation needed ] In familial adenomatous polyposis physicians observed polyps regression with NSAIDs for anti-inflammatory therapy. [ citation needed ] Chemoprophylaxis is also used to treat several different varieties of meningococcal infections for close contact exposure to Neisseria meningitidis . [ citation needed ]
The World Health Organization recommends chemoprevention to prevent Malaria in the Sahel region of Sub-Saharan Africa through the use of the drugs sulfadoxine/pyrimethamine and amodiaquine . [ 4 ] This technique is called Seasonal Malaria Chemoprevention (SMC). The charity evaluator GiveWell lists the Malaria Consortium's SMC program as one of its priority programs due to its high level of cost-effectiveness and ability to absorbe additional funding. [ 5 ]
Chemoprevention in cancer, was first proposed by Michael Sporn , seeks to identify ‘agents to reverse, suppress or prevent the carcinogenic process,’ from premalignancy to invasive and or metastatic cancer, by ‘using physiological mechanisms that do not kill healthy cells. [ 6 ] Anand Reddi proposed a role for the antidiabetes drug metformin as a chemoprevention agent for skin cancer . [ 7 ]
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A chemo-protective agent [ 1 ] is any drug that helps to reduce the side- effects of chemotherapy . These agents protect specific body parts from harmful anti-cancer treatments that could potentially cause permanent damage to important bodily tissues. Chemo-protective agents have only recently been introduced as a factor involved with chemotherapy with the intent to assist those cancer patients that require treatment, which as an result, improves the patients' quality of life.
Examples [ 2 ] include:
Chemo-protective agents are common drugs and like many other drugs, may have side effects of their own. Each agent has different side effects though the most common consist of dizziness, sleepiness, nausea, fever, etc. [ 3 ] It is important to discuss the side effects of these drugs with a doctor before using them to combat any type of chemotherapy to insure the drug will benefit each and every patient.
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
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Chemoradiotherapy ( CRT , CRTx , CT-RT ) is the combination of chemotherapy and radiotherapy to treat cancer . [ 1 ] Synonyms include radiochemotherapy ( RCT , RCTx , RT-CT ) and chemoradiation . It is a type of multimodal cancer therapy .
Chemoradiation can be concurrent [ 2 ] (together) or sequential (one after the other). [ 3 ]
The chemotherapy component can be or include a radiosensitizing agent . [ 2 ]
Chemoradiotherapy as neoadjuvant therapy before surgery has been shown to be effective in esophageal cancer . [ 4 ]
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A chemosensitivity assay is a laboratory test that measures the number of tumor cells that are killed by chemotherapy . The test is done after the tumor cells are removed from the body. A chemosensitivity assay may help in choosing the best drug or drugs for the cancer being treated.
With dozens of chemotherapy agents and hundreds of combinations available for treatment, oncologists often select a regimen from standard protocols developed in clinical trials.
Chemosensitivity assay entry in the public domain NCI Dictionary of Cancer Terms
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A chemosensitizer is a drug that makes tumor cells more sensitive to the effects of chemotherapy .
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
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Chemotherapy (often abbreviated chemo , sometimes CTX and CTx ) is the type of cancer treatment that uses one or more anti-cancer drugs ( chemotherapeutic agents or alkylating agents ) in a standard regimen . Chemotherapy may be given with a curative intent (which almost always involves combinations of drugs), or it may aim only to prolong life or to reduce symptoms ( palliative chemotherapy). Chemotherapy is one of the major categories of the medical discipline specifically devoted to pharmacotherapy for cancer , which is called medical oncology . [ 1 ] [ 2 ]
The term chemotherapy now means the non-specific use of intracellular poisons to inhibit mitosis (cell division) or to induce DNA damage (so that DNA repair can augment chemotherapy). [ 3 ] This meaning excludes the more-selective agents that block extracellular signals ( signal transduction ). Therapies with specific molecular or genetic targets, which inhibit growth-promoting signals from classic endocrine hormones (primarily estrogens for breast cancer and androgens for prostate cancer), are now called hormonal therapies . Other inhibitions of growth-signals, such as those associated with receptor tyrosine kinases , are targeted therapy .
The use of drugs (whether chemotherapy, hormonal therapy, or targeted therapy) is systemic therapy for cancer: they are introduced into the blood stream (the system) and therefore can treat cancer anywhere in the body. Systemic therapy is often used with other, local therapy (treatments that work only where they are applied), such as radiation , surgery , and hyperthermia .
Traditional chemotherapeutic agents are cytotoxic by means of interfering with cell division ( mitosis ) but cancer cells vary widely in their susceptibility to these agents. To a large extent, chemotherapy can be thought of as a way to damage or stress cells, which may then lead to cell death if apoptosis is initiated. Many of the side effects of chemotherapy can be traced to damage to normal cells that divide rapidly and are thus sensitive to anti-mitotic drugs: cells in the bone marrow , digestive tract and hair follicles . This results in the most common side-effects of chemotherapy: myelosuppression (decreased production of blood cells, hence that also immunosuppression ), mucositis (inflammation of the lining of the digestive tract), and alopecia (hair loss). Because of the effect on immune cells (especially lymphocytes), chemotherapy drugs often find use in a host of diseases that result from harmful overactivity of the immune system against self (so-called autoimmunity ). These include rheumatoid arthritis , systemic lupus erythematosus , multiple sclerosis , vasculitis and many others.
There are a number of strategies in the administration of chemotherapeutic drugs used today. Chemotherapy may be given with a curative intent or it may aim to prolong life or to palliate symptoms .
All chemotherapy regimens require that the recipient be capable of undergoing the treatment. Performance status is often used as a measure to determine whether a person can receive chemotherapy, or whether dose reduction is required. Because only a fraction of the cells in a tumor die with each treatment ( fractional kill ), repeated doses must be administered to continue to reduce the size of the tumor. [ 10 ] Current chemotherapy regimens apply drug treatment in cycles, with the frequency and duration of treatments limited by toxicity. [ 11 ]
The effectiveness of chemotherapy depends on the type of cancer and the stage. The overall effectiveness ranges from being curative for some cancers, such as some leukemias , [ 12 ] [ 13 ] to being ineffective, such as in some brain tumors , [ 14 ] to being needless in others, like most non-melanoma skin cancers . [ 15 ]
Dosage of chemotherapy can be difficult: If the dose is too low, it will be ineffective against the tumor, whereas, at excessive doses, the toxicity ( side-effects ) will be intolerable to the person receiving it. [ 4 ] The standard method of determining chemotherapy dosage is based on calculated body surface area (BSA). The BSA is usually calculated with a mathematical formula or a nomogram , using the recipient's weight and height, rather than by direct measurement of body area. This formula was originally derived in a 1916 study and attempted to translate medicinal doses established with laboratory animals to equivalent doses for humans. [ 16 ] The study only included nine human subjects. [ 17 ] When chemotherapy was introduced in the 1950s, the BSA formula was adopted as the official standard for chemotherapy dosing for lack of a better option. [ 18 ] [ 19 ]
The validity of this method in calculating uniform doses has been questioned because the formula only takes into account the individual's weight and height. Drug absorption and clearance are influenced by multiple factors, including age, sex, metabolism, disease state, organ function, drug-to-drug interactions, genetics, and obesity, which have major impacts on the actual concentration of the drug in the person's bloodstream. [ 18 ] [ 20 ] [ 21 ] As a result, there is high variability in the systemic chemotherapy drug concentration in people dosed by BSA, and this variability has been demonstrated to be more than ten-fold for many drugs. [ 17 ] [ 22 ] In other words, if two people receive the same dose of a given drug based on BSA, the concentration of that drug in the bloodstream of one person may be 10 times higher or lower compared to that of the other person. [ 22 ] This variability is typical with many chemotherapy drugs dosed by BSA, and, as shown below, was demonstrated in a study of 14 common chemotherapy drugs. [ 17 ]
The result of this pharmacokinetic variability among people is that many people do not receive the right dose to achieve optimal treatment effectiveness with minimized toxic side effects. Some people are overdosed while others are underdosed. [ 18 ] [ 20 ] [ 21 ] [ 23 ] [ 24 ] [ 25 ] [ 26 ] For example, in a randomized clinical trial, investigators found 85% of metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) did not receive the optimal therapeutic dose when dosed by the BSA standard—68% were underdosed and 17% were overdosed. [ 23 ]
There has been controversy over the use of BSA to calculate chemotherapy doses for people who are obese . [ 27 ] Because of their higher BSA, clinicians often arbitrarily reduce the dose prescribed by the BSA formula for fear of overdosing . [ 27 ] In many cases, this can result in sub-optimal treatment. [ 27 ]
Several clinical studies have demonstrated that when chemotherapy dosing is individualized to achieve optimal systemic drug exposure, treatment outcomes are improved and toxic side effects are reduced. [ 23 ] [ 25 ] In the 5-FU clinical study cited above, people whose dose was adjusted to achieve a pre-determined target exposure realized an 84% improvement in treatment response rate and a six-month improvement in overall survival (OS) compared with those dosed by BSA. [ 23 ]
In the same study, investigators compared the incidence of common 5-FU-associated grade 3/4 toxicities between the dose-adjusted people and people dosed per BSA. [ 23 ] The incidence of debilitating grades of diarrhea was reduced from 18% in the BSA-dosed group to 4% in the dose-adjusted group and serious hematologic side effects were eliminated. [ 23 ] Because of the reduced toxicity, dose-adjusted patients were able to be treated for longer periods of time. [ 23 ] BSA-dosed people were treated for a total of 680 months while people in the dose-adjusted group were treated for a total of 791 months. [ 23 ] Completing the course of treatment is an important factor in achieving better treatment outcomes.
Similar results were found in a study involving people with colorectal cancer who have been treated with the popular FOLFOX regimen. [ 25 ] The incidence of serious diarrhea was reduced from 12% in the BSA-dosed group of patients to 1.7% in the dose-adjusted group, and the incidence of severe mucositis was reduced from 15% to 0.8%. [ 25 ]
The FOLFOX study also demonstrated an improvement in treatment outcomes. [ 25 ] Positive response increased from 46% in the BSA-dosed group to 70% in the dose-adjusted group. Median progression free survival (PFS) and overall survival (OS) both improved by six months in the dose adjusted group. [ 25 ]
One approach that can help clinicians individualize chemotherapy dosing is to measure the drug levels in blood plasma over time and adjust dose according to a formula or algorithm to achieve optimal exposure. With an established target exposure for optimized treatment effectiveness with minimized toxicities, dosing can be personalized to achieve target exposure and optimal results for each person. Such an algorithm was used in the clinical trials cited above and resulted in significantly improved treatment outcomes. [ 28 ]
Oncologists are already individualizing dosing of some cancer drugs based on exposure. Carboplatin [ 29 ] : 4 and busulfan [ 30 ] [ 31 ] dosing rely upon results from blood tests to calculate the optimal dose for each person. Simple blood tests are also available for dose optimization of methotrexate , [ 32 ] 5-FU, paclitaxel , and docetaxel . [ 33 ] [ 34 ]
The serum albumin level immediately prior to chemotherapy administration is an independent prognostic predictor of survival in various cancer types. [ 35 ]
Alkylating agents are the oldest group of chemotherapeutics in use today. Originally derived from mustard gas used in World War I , there are now many types of alkylating agents in use. [ 4 ] They are so named because of their ability to alkylate many molecules, including proteins , RNA and DNA . This ability to bind covalently to DNA via their alkyl group is the primary cause for their anti-cancer effects. [ 37 ] DNA is made of two strands and the molecules may either bind twice to one strand of DNA (intrastrand crosslink) or may bind once to both strands (interstrand crosslink). If the cell tries to replicate crosslinked DNA during cell division , or tries to repair it, the DNA strands can break. This leads to a form of programmed cell death called apoptosis . [ 36 ] [ 38 ] Alkylating agents will work at any point in the cell cycle and thus are known as cell cycle-independent drugs. For this reason, the effect on the cell is dose dependent; the fraction of cells that die is directly proportional to the dose of drug. [ 39 ]
The subtypes of alkylating agents are the nitrogen mustards , nitrosoureas , tetrazines , aziridines , [ 40 ] cisplatins and derivatives, and non-classical alkylating agents. Nitrogen mustards include mechlorethamine , cyclophosphamide , melphalan , chlorambucil , ifosfamide and busulfan . Nitrosoureas include N-Nitroso-N-methylurea (MNU), carmustine (BCNU), lomustine (CCNU) and semustine (MeCCNU), fotemustine and streptozotocin . Tetrazines include dacarbazine , mitozolomide and temozolomide . Aziridines include thiotepa , mytomycin and diaziquone (AZQ). Cisplatin and derivatives include cisplatin , carboplatin and oxaliplatin . [ 37 ] [ 38 ] They impair cell function by forming covalent bonds with the amino , carboxyl , sulfhydryl , and phosphate groups in biologically important molecules. [ 41 ] Non-classical alkylating agents include procarbazine and hexamethylmelamine. [ 37 ] [ 38 ]
Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a similar structure to the building blocks of DNA and RNA. The building blocks are nucleotides ; a molecule comprising a nucleobase , a sugar and a phosphate group . The nucleobases are divided into purines ( guanine and adenine ) and pyrimidines ( cytosine , thymine and uracil ). Anti-metabolites resemble either nucleobases or nucleosides (a nucleotide without the phosphate group), but have altered chemical groups . [ 42 ] These drugs exert their effect by either blocking the enzymes required for DNA synthesis or becoming incorporated into DNA or RNA. By inhibiting the enzymes involved in DNA synthesis, they prevent mitosis because the DNA cannot duplicate itself. Also, after misincorporation of the molecules into DNA, DNA damage can occur and programmed cell death ( apoptosis ) is induced. Unlike alkylating agents, anti-metabolites are cell cycle dependent. This means that they only work during a specific part of the cell cycle, in this case S-phase (the DNA synthesis phase). For this reason, at a certain dose, the effect plateaus and proportionally no more cell death occurs with increased doses. Subtypes of the anti-metabolites are the anti-folates , fluoropyrimidines, deoxynucleoside analogues and thiopurines . [ 37 ] [ 42 ]
The anti-folates include methotrexate and pemetrexed . Methotrexate inhibits dihydrofolate reductase (DHFR), an enzyme that regenerates tetrahydrofolate from dihydrofolate . When the enzyme is inhibited by methotrexate, the cellular levels of folate coenzymes diminish. These are required for thymidylate and purine production, which are both essential for DNA synthesis and cell division. [ 6 ] : 55–59 [ 7 ] : 11 Pemetrexed is another anti-metabolite that affects purine and pyrimidine production, and therefore also inhibits DNA synthesis. It primarily inhibits the enzyme thymidylate synthase , but also has effects on DHFR, aminoimidazole carboxamide ribonucleotide formyltransferase and glycinamide ribonucleotide formyltransferase . [ 43 ] The fluoropyrimidines include fluorouracil and capecitabine . Fluorouracil is a nucleobase analogue that is metabolised in cells to form at least two active products; 5-fluourouridine monophosphate (FUMP) and 5-fluoro-2'-deoxyuridine 5'-phosphate (fdUMP). FUMP becomes incorporated into RNA and fdUMP inhibits the enzyme thymidylate synthase; both of which lead to cell death. [ 7 ] : 11 Capecitabine is a prodrug of 5-fluorouracil that is broken down in cells to produce the active drug. [ 44 ] The deoxynucleoside analogues include cytarabine , gemcitabine , decitabine , azacitidine , fludarabine , nelarabine , cladribine , clofarabine , and pentostatin . The thiopurines include thioguanine and mercaptopurine . [ 37 ] [ 42 ]
Anti-microtubule agents are plant -derived chemicals that block cell division by preventing microtubule function. Microtubules are an important cellular structure composed of two proteins, α-tubulin and β-tubulin . They are hollow, rod-shaped structures that are required for cell division, among other cellular functions. [ 45 ] Microtubules are dynamic structures, which means that they are permanently in a state of assembly and disassembly. Vinca alkaloids and taxanes are the two main groups of anti-microtubule agents, and although both of these groups of drugs cause microtubule dysfunction, their mechanisms of action are completely opposite: Vinca alkaloids prevent the assembly of microtubules, whereas taxanes prevent their disassembly. By doing so, they can induce mitotic catastrophe in the cancer cells. [ 46 ] Following this, cell cycle arrest occurs, which induces programmed cell death ( apoptosis ). [ 37 ] [ 47 ] These drugs can also affect blood vessel growth , an essential process that tumours utilise in order to grow and metastasise. [ 47 ]
Vinca alkaloids are derived from the Madagascar periwinkle , Catharanthus roseus , [ 48 ] [ 49 ] formerly known as Vinca rosea . They bind to specific sites on tubulin, inhibiting the assembly of tubulin into microtubules. The original vinca alkaloids are natural products that include vincristine and vinblastine . [ 50 ] [ 51 ] [ 52 ] [ 53 ] Following the success of these drugs, semi-synthetic vinca alkaloids were produced: vinorelbine (used in the treatment of non-small-cell lung cancer [ 52 ] [ 54 ] [ 55 ] ), vindesine , and vinflunine . [ 47 ] These drugs are cell cycle -specific. They bind to the tubulin molecules in S-phase and prevent proper microtubule formation required for M-phase . [ 39 ]
Taxanes are natural and semi-synthetic drugs. The first drug of their class, paclitaxel , was originally extracted from Taxus brevifolia , the Pacific yew. Now this drug and another in this class, docetaxel , are produced semi-synthetically from a chemical found in the bark of another yew tree, Taxus baccata . [ 56 ]
Podophyllotoxin is an antineoplastic lignan obtained primarily from the American mayapple ( Podophyllum peltatum ) and Himalayan mayapple ( Sinopodophyllum hexandrum ). It has anti-microtubule activity, and its mechanism is similar to that of vinca alkaloids in that they bind to tubulin, inhibiting microtubule formation. Podophyllotoxin is used to produce two other drugs with different mechanisms of action: etoposide and teniposide . [ 57 ] [ 58 ]
Topoisomerase inhibitors are drugs that affect the activity of two enzymes: topoisomerase I and topoisomerase II . When the DNA double-strand helix is unwound, during DNA replication or transcription , for example, the adjacent unopened DNA winds tighter (supercoils), like opening the middle of a twisted rope. The stress caused by this effect is in part aided by the topoisomerase enzymes. They produce single- or double-strand breaks into DNA, reducing the tension in the DNA strand. This allows the normal unwinding of DNA to occur during replication or transcription. Inhibition of topoisomerase I or II interferes with both of these processes. [ 59 ] [ 60 ]
Two topoisomerase I inhibitors, irinotecan and topotecan , are semi-synthetically derived from camptothecin , which is obtained from the Chinese ornamental tree Camptotheca acuminata . [ 39 ] Drugs that target topoisomerase II can be divided into two groups. The topoisomerase II poisons cause increased levels enzymes bound to DNA. This prevents DNA replication and transcription, causes DNA strand breaks, and leads to programmed cell death ( apoptosis ). These agents include etoposide , doxorubicin , mitoxantrone and teniposide . The second group, catalytic inhibitors, are drugs that block the activity of topoisomerase II, and therefore prevent DNA synthesis and translation because the DNA cannot unwind properly. This group includes novobiocin , merbarone, and aclarubicin , which also have other significant mechanisms of action. [ 61 ]
The cytotoxic antibiotics are a varied group of drugs that have various mechanisms of action. The common theme that they share in their chemotherapy indication is that they interrupt cell division . The most important subgroup is the anthracyclines and the bleomycins ; other prominent examples include mitomycin C and actinomycin . [ 62 ]
Among the anthracyclines, doxorubicin and daunorubicin were the first, and were obtained from the bacterium Streptomyces peucetius . [ 63 ] Derivatives of these compounds include epirubicin and idarubicin . Other clinically used drugs in the anthracycline group are pirarubicin , aclarubicin , and mitoxantrone . [ 64 ] The mechanisms of anthracyclines include DNA intercalation (molecules insert between the two strands of DNA), generation of highly reactive free radicals that damage intercellular molecules and topoisomerase inhibition. [ 65 ]
Actinomycin is a complex molecule that intercalates DNA and prevents RNA synthesis . [ 66 ]
Bleomycin, a glycopeptide isolated from Streptomyces verticillus , also intercalates DNA, but produces free radicals that damage DNA. This occurs when bleomycin binds to a metal ion , becomes chemically reduced and reacts with oxygen . [ 67 ] [ 6 ] : 87
Mitomycin is a cytotoxic antibiotic with the ability to alkylate DNA. [ 68 ]
Most chemotherapy is delivered intravenously , although a number of agents can be administered orally (e.g., melphalan , busulfan , capecitabine ). According to a recent (2016) systematic review, oral therapies present additional challenges for patients and care teams to maintain and support adherence to treatment plans. [ 69 ]
There are many intravenous methods of drug delivery, known as vascular access devices. These include the winged infusion device , peripheral venous catheter , midline catheter, peripherally inserted central catheter (PICC), central venous catheter and implantable port . The devices have different applications regarding duration of chemotherapy treatment, method of delivery and types of chemotherapeutic agent. [ 7 ] : 94–95
Depending on the person, the cancer, the stage of cancer, the type of chemotherapy, and the dosage, intravenous chemotherapy may be given on either an inpatient or an outpatient basis. For continuous, frequent or prolonged intravenous chemotherapy administration, various systems may be surgically inserted into the vasculature to maintain access. [ 7 ] : 113–118 Commonly used systems are the Hickman line , the Port-a-Cath , and the PICC line . These have a lower infection risk, are much less prone to phlebitis or extravasation , and eliminate the need for repeated insertion of peripheral cannulae. [ 70 ]
Isolated limb perfusion (often used in melanoma ), [ 71 ] or isolated infusion of chemotherapy into the liver [ 72 ] or the lung have been used to treat some tumors. The main purpose of these approaches is to deliver a very high dose of chemotherapy to tumor sites without causing overwhelming systemic damage. [ 73 ] These approaches can help control solitary or limited metastases, but they are by definition not systemic, and, therefore, do not treat distributed metastases or micrometastases . [ citation needed ]
Topical chemotherapies, such as 5-fluorouracil , are used to treat some cases of non-melanoma skin cancer . [ 74 ]
If the cancer has central nervous system involvement, or with meningeal disease, intrathecal chemotherapy may be administered. [ 4 ]
Chemotherapeutic techniques have a range of side effects that depend on the type of medications used. The most common medications affect mainly the fast-dividing cells of the body, such as blood cells and the cells lining the mouth, stomach, and intestines. Chemotherapy-related iatrogenic toxicities can occur acutely after administration, within hours or days, or chronically, from weeks to years. [ 6 ] : 265
Virtually all chemotherapeutic regimens can cause depression of the immune system , often by paralysing the bone marrow and leading to a decrease of white blood cells , red blood cells , and platelets . Anemia and thrombocytopenia may require blood transfusion . Neutropenia (a decrease of the neutrophil granulocyte count below 0.5 x 10 9 / litre ) can be improved with synthetic G-CSF ( granulocyte -colony-stimulating factor, e.g., filgrastim , lenograstim , efbemalenograstim alfa ). [ 75 ]
In very severe myelosuppression , which occurs in some regimens, almost all the bone marrow stem cells (cells that produce white and red blood cells ) are destroyed, meaning allogenic or autologous bone marrow cell transplants are necessary. (In autologous BMTs, cells are removed from the person before the treatment, multiplied and then re-injected afterward; in allogenic BMTs, the source is a donor.) However, some people still develop diseases because of this interference with bone marrow. [ 76 ]
Although people receiving chemotherapy are encouraged to wash their hands, avoid sick people, and take other infection-reducing steps, about 85% of infections are due to naturally occurring microorganisms in the person's own gastrointestinal tract (including oral cavity ) and skin. [ 77 ] : 130 This may manifest as systemic infections, such as sepsis , or as localized outbreaks, such as Herpes simplex , shingles , or other members of the Herpesviridea . [ 78 ] The risk of illness and death can be reduced by taking common antibiotics such as quinolones or trimethoprim/sulfamethoxazole before any fever or sign of infection appears. [ 79 ] Quinolones show effective prophylaxis mainly with hematological cancer. [ 79 ] However, in general, for every five people who are immunosuppressed following chemotherapy who take an antibiotic, one fever can be prevented; for every 34 who take an antibiotic, one death can be prevented. [ 79 ] Sometimes, chemotherapy treatments are postponed because the immune system is suppressed to a critically low level. [ citation needed ]
In Japan , the government has approved the use of some medicinal mushrooms like Trametes versicolor , to counteract depression of the immune system in people undergoing chemotherapy. [ 80 ]
Trilaciclib is an inhibitor of cyclin-dependent kinase 4/6 approved for the prevention of myelosuppression caused by chemotherapy. The drug is given before chemotherapy to protect bone marrow function. [ 81 ]
Due to immune system suppression, neutropenic enterocolitis (typhlitis) is a "life-threatening gastrointestinal complication of chemotherapy." [ 82 ] Typhlitis is an intestinal infection which may manifest itself through symptoms including nausea , vomiting , diarrhea , a distended abdomen , fever , chills , or abdominal pain and tenderness. [ 83 ]
Typhlitis is a medical emergency . It has a very poor prognosis and is often fatal unless promptly recognized and aggressively treated. [ 84 ] Successful treatment hinges on early diagnosis provided by a high index of suspicion and the use of CT scanning, nonoperative treatment for uncomplicated cases, and sometimes elective right hemicolectomy to prevent recurrence. [ 84 ]
Nausea , vomiting , anorexia , diarrhea , abdominal cramps, and constipation are common side-effects of chemotherapeutic medications that kill fast-dividing cells. [ 85 ] Malnutrition and dehydration can result when the recipient does not eat or drink enough, or when the person vomits frequently, because of gastrointestinal damage. This can result in rapid weight loss, or occasionally in weight gain, if the person eats too much in an effort to allay nausea or heartburn. Weight gain can also be caused by some steroid medications. These side-effects can frequently be reduced or eliminated with antiemetic drugs. Low-certainty evidence also suggests that probiotics may have a preventative and treatment effect of diarrhoea related to chemotherapy alone and with radiotherapy. [ 86 ] However, a high index of suspicion is appropriate, since diarrhoea and bloating are also symptoms of typhlitis , a very serious and potentially life-threatening medical emergency that requires immediate treatment. [ 87 ]
Anemia can be a combined outcome caused by myelosuppressive chemotherapy, and possible cancer-related causes such as bleeding , blood cell destruction ( hemolysis ), hereditary disease, kidney dysfunction, nutritional deficiencies or anemia of chronic disease . Treatments to mitigate anemia include hormones to boost blood production ( erythropoietin ), iron supplements , and blood transfusions . [ 88 ] [ 89 ] [ 90 ] Myelosuppressive therapy can cause a tendency to bleed easily, leading to anemia. Medications that kill rapidly dividing cells or blood cells can reduce the number of platelets in the blood, which can result in bruises and bleeding . Extremely low platelet counts may be temporarily boosted through platelet transfusions and new drugs to increase platelet counts during chemotherapy are being developed. [ 91 ] [ 92 ] [ 93 ] [ 94 ] Sometimes, chemotherapy treatments are postponed to allow platelet counts to recover.
Fatigue may be a consequence of the cancer or its treatment, and can last for months to years after treatment. One physiological cause of fatigue is anemia, which can be caused by chemotherapy, surgery , radiotherapy , primary and metastatic disease or nutritional depletion. [ 95 ] [ 96 ] Aerobic exercise has been found to be beneficial in reducing fatigue in people with solid tumours . [ 97 ]
Nausea and vomiting are two of the most feared cancer treatment-related side-effects for people with cancer and their families. In 1983, Coates et al. found that people receiving chemotherapy ranked nausea and vomiting as the first and second most severe side-effects, respectively. [ 98 ] Up to 20% of people receiving highly emetogenic agents in this era postponed, or even refused potentially curative treatments. [ 99 ] Chemotherapy-induced nausea and vomiting (CINV) are common with many treatments and some forms of cancer. Since the 1990s, several novel classes of antiemetics have been developed and commercialized, becoming a nearly universal standard in chemotherapy regimens, and helping to successfully manage these symptoms in many people. Effective mediation of these unpleasant and sometimes debilitating symptoms results in increased quality of life for the recipient and more efficient treatment cycles, as patients are less likely to avoid or refuse treatment. [ 100 ]
Hair loss (alopecia) can be caused by chemotherapy that kills rapidly dividing cells; other medications may cause hair to thin. These are most often temporary effects: hair usually starts to regrow a few weeks after the last treatment, but sometimes with a change in color, texture, thickness or style. Sometimes hair has a tendency to curl after regrowth, resulting in "chemo curls." Severe hair loss occurs most often with drugs such as doxorubicin , daunorubicin , paclitaxel , docetaxel , cyclophosphamide , ifosfamide and etoposide . Permanent thinning or hair loss can result from some standard chemotherapy regimens. [ 101 ]
Chemotherapy induced hair loss occurs by a non-androgenic mechanism, and can manifest as alopecia totalis , telogen effluvium , or less often alopecia areata . [ 102 ] It is usually associated with systemic treatment due to the high mitotic rate of hair follicles, and more reversible than androgenic hair loss, [ 103 ] [ 104 ] although permanent cases can occur. [ 105 ] Chemotherapy induces hair loss in women more often than men. [ 106 ]
Scalp cooling offers a means of preventing both permanent and temporary hair loss; however, concerns about this method have been raised. [ 107 ] [ 108 ]
Development of secondary neoplasia after successful chemotherapy or radiotherapy treatment can occur. The most common secondary neoplasm is secondary acute myeloid leukemia, which develops primarily after treatment with alkylating agents or topoisomerase inhibitors. [ 109 ] Survivors of childhood cancer are more than 13 times as likely to get a secondary neoplasm during the 30 years after treatment than the general population. [ 110 ] Not all of this increase can be attributed to chemotherapy.
Some types of chemotherapy are gonadotoxic and may cause infertility . [ 111 ] Chemotherapies with high risk include procarbazine and other alkylating drugs such as cyclophosphamide, ifosfamide, busulfan, melphalan, chlorambucil, and chlormethine. [ 111 ] Drugs with medium risk include doxorubicin and platinum analogs such as cisplatin and carboplatin. [ 111 ] On the other hand, therapies with low risk of gonadotoxicity include plant derivatives such as vincristine and vinblastine, antibiotics such as bleomycin and dactinomycin, and antimetabolites such as methotrexate, mercaptopurine, and 5-fluorouracil. [ 111 ]
Female infertility by chemotherapy appears to be secondary to premature ovarian failure by loss of primordial follicles . [ 112 ] This loss is not necessarily a direct effect of the chemotherapeutic agents, but could be due to an increased rate of growth initiation to replace damaged developing follicles. [ 112 ]
People may choose between several methods of fertility preservation prior to chemotherapy, including cryopreservation of semen, ovarian tissue, oocytes, or embryos. [ 113 ] As more than half of cancer patients are elderly, this adverse effect is only relevant for a minority of patients. A study in France between 1999 and 2011 came to the result that embryo freezing before administration of gonadotoxic agents to females caused a delay of treatment in 34% of cases, and a live birth in 27% of surviving cases who wanted to become pregnant, with the follow-up time varying between 1 and 13 years. [ 114 ]
Potential protective or attenuating agents include GnRH analogs , where several studies have shown a protective effect in vivo in humans, but some studies show no such effect. Sphingosine-1-phosphate (S1P) has shown similar effect, but its mechanism of inhibiting the sphingomyelin apoptotic pathway may also interfere with the apoptosis action of chemotherapy drugs. [ 115 ]
In chemotherapy as a conditioning regimen in hematopoietic stem cell transplantation, a study of people conditioned with cyclophosphamide alone for severe aplastic anemia came to the result that ovarian recovery occurred in all women younger than 26 years at time of transplantation, but only in five of 16 women older than 26 years. [ 116 ]
Chemotherapy is teratogenic during pregnancy , especially during the first trimester , to the extent that abortion usually is recommended if pregnancy in this period is found during chemotherapy. [ 117 ] Second- and third-trimester exposure does not usually increase the teratogenic risk and adverse effects on cognitive development, but it may increase the risk of various complications of pregnancy and fetal myelosuppression. [ 117 ]
Female patients of reproductive potential should use effective contraception during chemotherapy and for a few months after the last dose (e.g. 6 month for doxorubicin [ 118 ] ).
In males previously having undergone chemotherapy or radiotherapy, there appears to be no increase in genetic defects or congenital malformations in their children conceived after therapy. [ 117 ] The use of assisted reproductive technologies and micromanipulation techniques might increase this risk. [ 117 ] In females previously having undergone chemotherapy, miscarriage and congenital malformations are not increased in subsequent conceptions. [ 117 ] However, when in vitro fertilization and embryo cryopreservation is practised between or shortly after treatment, possible genetic risks to the growing oocytes exist, and hence it has been recommended that the babies be screened. [ 117 ]
Between 30 and 40 percent of people undergoing chemotherapy experience chemotherapy-induced peripheral neuropathy (CIPN), a progressive, enduring, and often irreversible condition, causing pain, tingling, numbness and sensitivity to cold, beginning in the hands and feet and sometimes progressing to the arms and legs. [ 119 ] Chemotherapy drugs associated with CIPN include thalidomide , epothilones , vinca alkaloids, taxanes, proteasome inhibitors , and the platinum-based drugs. [ 119 ] [ 120 ] Whether CIPN arises, and to what degree, is determined by the choice of drug, duration of use, the total amount consumed and whether the person already has peripheral neuropathy . Though the symptoms are mainly sensory, in some cases motor nerves and the autonomic nervous system are affected. [ 121 ] CIPN often follows the first chemotherapy dose and increases in severity as treatment continues, but this progression usually levels off at completion of treatment. The platinum-based drugs are the exception; with these drugs, sensation may continue to deteriorate for several months after the end of treatment. [ 122 ] Some CIPN appears to be irreversible. [ 122 ] Pain can often be managed with drug or other treatment but the numbness is usually resistant to treatment. [ 123 ]
Some people receiving chemotherapy report fatigue or non-specific neurocognitive problems, such as an inability to concentrate; this is sometimes called post-chemotherapy cognitive impairment , referred to as "chemo brain" in popular and social media. [ 124 ]
In particularly large tumors and cancers with high white cell counts , such as lymphomas , teratomas , and some leukemias , some people develop tumor lysis syndrome . The rapid breakdown of cancer cells causes the release of chemicals from the inside of the cells. Following this, high levels of uric acid , potassium and phosphate are found in the blood. High levels of phosphate induce secondary hypoparathyroidism, resulting in low levels of calcium in the blood. [ 125 ] This causes kidney damage and the high levels of potassium can cause cardiac arrhythmia . Although prophylaxis is available and is often initiated in people with large tumors, this is a dangerous side-effect that can lead to death if left untreated. [ 7 ] : 202
Cardiotoxicity (heart damage) is especially prominent with the use of anthracycline drugs ( doxorubicin , epirubicin , idarubicin , and liposomal doxorubicin ). The cause of this is most likely due to the production of free radicals in the cell and subsequent DNA damage . Other chemotherapeutic agents that cause cardiotoxicity, but at a lower incidence, are cyclophosphamide , docetaxel and clofarabine . [ 126 ]
Hepatotoxicity (liver damage) can be caused by many cytotoxic drugs. The susceptibility of an individual to liver damage can be altered by other factors such as the cancer itself, viral hepatitis , immunosuppression and nutritional deficiency . The liver damage can consist of damage to liver cells, hepatic sinusoidal syndrome (obstruction of the veins in the liver), cholestasis (where bile does not flow from the liver to the intestine) and liver fibrosis . [ 127 ] [ 128 ]
Nephrotoxicity (kidney damage) can be caused by tumor lysis syndrome and also due direct effects of drug clearance by the kidneys. Different drugs will affect different parts of the kidney and the toxicity may be asymptomatic (only seen on blood or urine tests) or may cause acute kidney injury . [ 129 ] [ 130 ]
Ototoxicity (damage to the inner ear) is a common side effect of platinum based drugs that can produce symptoms such as dizziness and vertigo . [ 131 ] [ 132 ] Children treated with platinum analogues have been found to be at risk for developing hearing loss. [ 133 ] [ 134 ] [ 135 ]
Less common side-effects include red skin ( erythema ), dry skin, damaged fingernails, a dry mouth ( xerostomia ), water retention , and sexual impotence . Some medications can trigger allergic or pseudoallergic reactions.
Specific chemotherapeutic agents are associated with organ-specific toxicities, including cardiovascular disease (e.g., doxorubicin ), interstitial lung disease (e.g., bleomycin ) and occasionally secondary neoplasm (e.g., MOPP therapy for Hodgkin's disease). [ 136 ]
Hand-foot syndrome is another side effect to cytotoxic chemotherapy. [ 137 ]
Nutritional problems are also frequently seen in cancer patients at diagnosis and through chemotherapy treatment. Research suggests that in children and young people undergoing cancer treatment, parenteral nutrition may help with this leading to weight gain and increased calorie and protein intake, when compared to enteral nutrition. [ 138 ]
Chemotherapy does not always work, and even when it is useful, it may not completely destroy the cancer. People frequently fail to understand its limitations. In one study of people who had been newly diagnosed with incurable, stage 4 cancer , more than two-thirds of people with lung cancer and more than four-fifths of people with colorectal cancer still believed that chemotherapy was likely to cure their cancer. [ 139 ]
The blood–brain barrier poses an obstacle to delivery of chemotherapy to the brain . This is because the brain has an extensive system in place to protect it from harmful chemicals. Drug transporters can pump out drugs from the brain and brain's blood vessel cells into the cerebrospinal fluid and blood circulation. These transporters pump out most chemotherapy drugs, which reduces their efficacy for treatment of brain tumors. Only small lipophilic alkylating agents such as lomustine or temozolomide are able to cross this blood–brain barrier. [ 140 ] [ 141 ] [ 142 ]
Blood vessels in tumors are very different from those seen in normal tissues. As a tumor grows, tumor cells furthest away from the blood vessels become low in oxygen ( hypoxic ). To counteract this they then signal for new blood vessels to grow. The newly formed tumor vasculature is poorly formed and does not deliver an adequate blood supply to all areas of the tumor. This leads to issues with drug delivery because many drugs will be delivered to the tumor by the circulatory system . [ 143 ]
Resistance is a major cause of treatment failure in chemotherapeutic drugs. There are a few possible causes of resistance in cancer, one of which is the presence of small pumps on the surface of cancer cells that actively move chemotherapy from inside the cell to the outside. Cancer cells produce high amounts of these pumps, known as p-glycoprotein , in order to protect themselves from chemotherapeutics. Research on p-glycoprotein and other such chemotherapy efflux pumps is currently ongoing. Medications to inhibit the function of p-glycoprotein are undergoing investigation, but due to toxicities and interactions with anti-cancer drugs their development has been difficult. [ 144 ] [ 145 ] Another mechanism of resistance is gene amplification , a process in which multiple copies of a gene are produced by cancer cells. This overcomes the effect of drugs that reduce the expression of genes involved in replication. With more copies of the gene, the drug can not prevent all expression of the gene and therefore the cell can restore its proliferative ability. Cancer cells can also cause defects in the cellular pathways of apoptosis (programmed cell death). As most chemotherapy drugs kill cancer cells in this manner, defective apoptosis allows survival of these cells, making them resistant. Many chemotherapy drugs also cause DNA damage, which can be repaired by enzymes in the cell that carry out DNA repair . Upregulation of these genes can overcome the DNA damage and prevent the induction of apoptosis. Mutations in genes that produce drug target proteins, such as tubulin , can occur which prevent the drugs from binding to the protein, leading to resistance to these types of drugs. [ 146 ] Drugs used in chemotherapy can induce cell stress, which can kill a cancer cell; however, under certain conditions, cells stress can induce changes in gene expression that enables resistance to several types of drugs. [ 147 ] In lung cancer , the transcription factor NFκB is thought to play a role in resistance to chemotherapy, via inflammatory pathways. [ 148 ] [ 149 ] [ 150 ]
Targeted therapies are a relatively new class of cancer drugs that can overcome many of the issues seen with the use of cytotoxics. They are divided into two groups: small molecule and antibodies. The massive toxicity seen with the use of cytotoxics is due to the lack of cell specificity of the drugs. They will kill any rapidly dividing cell, tumor or normal. Targeted therapies are designed to affect cellular proteins or processes that are utilised by the cancer cells. [ 151 ] This allows a high dose to cancer tissues with a relatively low dose to other tissues. Although the side effects are often less severe than that seen of cytotoxic chemotherapeutics, life-threatening effects can occur. Initially, the targeted therapeutics were supposed to be solely selective for one protein. Now it is clear that there is often a range of protein targets that the drug can bind. An example target for targeted therapy is the BCR-ABL1 protein produced from the Philadelphia chromosome , a genetic lesion found commonly in chronic myelogenous leukemia and in some patients with acute lymphoblastic leukemia . This fusion protein has enzyme activity that can be inhibited by imatinib , a small molecule drug. [ 152 ] [ 153 ] [ 154 ] [ 155 ]
Cancer is the uncontrolled growth of cells coupled with malignant behaviour: invasion and metastasis (among other features). [ 156 ] It is caused by the interaction between genetic susceptibility and environmental factors. [ 157 ] [ 158 ] These factors lead to accumulations of genetic mutations in oncogenes (genes that control the growth rate of cells) and tumor suppressor genes (genes that help to prevent cancer), which gives cancer cells their malignant characteristics, such as uncontrolled growth. [ 159 ] : 93–94
In the broad sense, most chemotherapeutic drugs work by impairing mitosis ( cell division ), effectively targeting fast-dividing cells . As these drugs cause damage to cells, they are termed cytotoxic . They prevent mitosis by various mechanisms including damaging DNA and inhibition of the cellular machinery involved in cell division. [ 39 ] [ 160 ] One theory as to why these drugs kill cancer cells is that they induce a programmed form of cell death known as apoptosis . [ 161 ]
As chemotherapy affects cell division, tumors with high growth rates (such as acute myelogenous leukemia and the aggressive lymphomas , including Hodgkin's disease ) are more sensitive to chemotherapy, as a larger proportion of the targeted cells are undergoing cell division at any time. Malignancies with slower growth rates, such as indolent lymphomas, tend to respond to chemotherapy much more modestly. [ 4 ] Heterogeneic tumours may also display varying sensitivities to chemotherapy agents, depending on the subclonal populations within the tumor. [ 162 ]
Cells from the immune system also make crucial contributions to the antitumor effects of chemotherapy. [ 163 ] For example, the chemotherapeutic drugs oxaliplatin and cyclophosphamide can cause tumor cells to die in a way that is detectable by the immune system (called immunogenic cell death ), which mobilizes immune cells with antitumor functions. [ 164 ] Chemotherapeutic drugs that cause cancer immunogenic tumor cell death can make unresponsive tumors sensitive to immune checkpoint therapy. [ 165 ]
Some chemotherapy drugs are used in diseases other than cancer, such as in autoimmune disorders, [ 166 ] and noncancerous plasma cell dyscrasia . In some cases they are often used at lower doses, which means that the side effects are minimized, [ 166 ] while in other cases doses similar to ones used to treat cancer are used. Methotrexate is used in the treatment of rheumatoid arthritis (RA), [ 167 ] psoriasis , [ 168 ] ankylosing spondylitis [ 169 ] and multiple sclerosis . [ 170 ] [ 171 ] The anti-inflammatory response seen in RA is thought to be due to increases in adenosine , which causes immunosuppression ; effects on immuno-regulatory cyclooxygenase -2 enzyme pathways; reduction in pro-inflammatory cytokines ; and anti-proliferative properties. [ 167 ] Although methotrexate is used to treat both multiple sclerosis and ankylosing spondylitis, its efficacy in these diseases is still uncertain. [ 169 ] [ 170 ] [ 171 ] Cyclophosphamide is sometimes used to treat lupus nephritis , a common symptom of systemic lupus erythematosus . [ 172 ] Dexamethasone along with either bortezomib or melphalan is commonly used as a treatment for AL amyloidosis . Recently, bortezomid in combination with cyclophosphamide and dexamethasone has also shown promise as a treatment for AL amyloidosis. Other drugs used to treat myeloma such as lenalidomide have shown promise in treating AL amyloidosis. [ 173 ]
Chemotherapy drugs are also used in conditioning regimens prior to bone marrow transplant ( hematopoietic stem cell transplant ). Conditioning regimens are used to suppress the recipient's immune system in order to allow a transplant to engraft. Cyclophosphamide is a common cytotoxic drug used in this manner and is often used in conjunction with total body irradiation . Chemotherapeutic drugs may be used at high doses to permanently remove the recipient's bone marrow cells (myeloablative conditioning) or at lower doses that will prevent permanent bone marrow loss (non-myeloablative and reduced intensity conditioning). [ 174 ] When used in non-cancer setting, the treatment is still called "chemotherapy", and is often done in the same treatment centers used for people with cancer.
In the 1970s, antineoplastic (chemotherapy) drugs were identified as hazardous, and the American Society of Health-System Pharmacists (ASHP) has since then introduced the concept of hazardous drugs after publishing a recommendation in 1983 regarding handling hazardous drugs. The adaptation of federal regulations came when the U.S. Occupational Safety and Health Administration (OSHA) first released its guidelines in 1986 and then updated them in 1996, 1999, and, most recently, 2006. [ 175 ]
The National Institute for Occupational Safety and Health (NIOSH) has been conducting an assessment in the workplace since then regarding these drugs. Occupational exposure to antineoplastic drugs has been linked to multiple health effects, including infertility and possible carcinogenic effects. A few cases have been reported by the NIOSH alert report, such as one in which a female pharmacist was diagnosed with papillary transitional cell carcinoma. Twelve years before the pharmacist was diagnosed with the condition, she had worked for 20 months in a hospital where she was responsible for preparing multiple antineoplastic drugs. [ 176 ] The pharmacist did not have any other risk factor for cancer, and therefore, her cancer was attributed to the exposure to the antineoplastic drugs, although a cause-and-effect relationship has not been established in the literature. Another case happened when a malfunction in biosafety cabinetry is believed to have exposed nursing personnel to antineoplastic drugs. Investigations revealed evidence of genotoxic biomarkers two and nine months after that exposure.
Antineoplastic drugs are usually given through intravenous , intramuscular , intrathecal , or subcutaneous administration. In most cases, before the medication is administered to the patient, it needs to be prepared and handled by several workers. Any worker who is involved in handling, preparing, or administering the drugs, or with cleaning objects that have come into contact with antineoplastic drugs, is potentially exposed to hazardous drugs. [ 177 ] Health care workers are exposed to drugs in different circumstances, such as when pharmacists and pharmacy technicians prepare and handle antineoplastic drugs and when nurses and physicians administer the drugs to patients. Additionally, those who are responsible for disposing antineoplastic drugs in health care facilities are also at risk of exposure. [ 178 ]
Dermal exposure is thought to be the main route of exposure due to the fact that significant amounts of the antineoplastic agents have been found in the gloves worn by healthcare workers who prepare, handle, and administer the agents. Another noteworthy route of exposure is inhalation of the drugs' vapors. Multiple studies have investigated inhalation as a route of exposure, and although air sampling has not shown any dangerous levels, it is still a potential route of exposure. Ingestion by hand to mouth is a route of exposure that is less likely compared to others because of the enforced hygienic standard in the health institutions. However, it is still a potential route, especially in the workplace, outside of a health institute. One can also be exposed to these hazardous drugs through injection by needle sticks . Research conducted in this area has established that occupational exposure occurs by examining evidence in multiple urine samples from health care workers. [ 179 ]
Hazardous drugs expose health care workers to serious health risks. Many studies show that antineoplastic drugs could have many side effects on the reproductive system, such as fetal loss, congenital malformation, and infertility. Health care workers who are exposed to antineoplastic drugs on many occasions have adverse reproductive outcomes such as spontaneous abortions, stillbirths, and congenital malformations. Moreover, studies have shown that exposure to these drugs leads to menstrual cycle irregularities. Antineoplastic drugs may also increase the risk of learning disabilities among children of health care workers who are exposed to these hazardous substances. [ 180 ]
Moreover, these drugs have carcinogenic effects. In the past five decades, multiple studies have shown the carcinogenic effects of exposure to antineoplastic drugs. Similarly, there have been research studies that linked alkylating agents with humans developing leukemias. Studies have reported elevated risk of breast cancer, nonmelanoma skin cancer, and cancer of the rectum among nurses who are exposed to these drugs. Other investigations revealed that there is a potential genotoxic effect from anti-neoplastic drugs to workers in health care settings. [ 176 ]
As of 2018, there were no occupational exposure limits set for antineoplastic drugs, i.e., OSHA or the American Conference of Governmental Industrial Hygienists (ACGIH) have not set workplace safety guidelines. [ 181 ]
NIOSH recommends using a ventilated cabinet that is designed to decrease worker exposure. Additionally, it recommends training of all staff, the use of cabinets, implementing an initial evaluation of the technique of the safety program, and wearing protective gloves and gowns when opening drug packaging, handling vials, or labeling. When wearing personal protective equipment , one should inspect gloves for physical defects before use and always wear double gloves and protective gowns. Health care workers are also required to wash their hands with water and soap before and after working with antineoplastic drugs, change gloves every 30 minutes or whenever punctured, and discard them immediately in a chemotherapy waste container. [ 182 ]
The gowns used should be disposable gowns made of polyethylene-coated polypropylene. When wearing gowns, individuals should make sure that the gowns are closed and have long sleeves. When preparation is done, the final product should be completely sealed in a plastic bag. [ 183 ]
The health care worker should also wipe all waste containers inside the ventilated cabinet before removing them from the cabinet. Finally, workers should remove all protective wear and put them in a bag for their disposal inside the ventilated cabinet. [ 178 ]
Drugs should only be administered using protective medical devices such as needle lists and closed systems and techniques such as priming of IV tubing by pharmacy personnel inside a ventilated cabinet. Workers should always wear personal protective equipment such as double gloves, goggles, and protective gowns when opening the outer bag and assembling the delivery system to deliver the drug to the patient, and when disposing of all material used in the administration of the drugs. [ 181 ]
Hospital workers should never remove tubing from an IV bag that contains an antineoplastic drug, and when disconnecting the tubing in the system, they should make sure the tubing has been thoroughly flushed. After removing the IV bag, the workers should place it together with other disposable items directly in the yellow chemotherapy waste container with the lid closed. Protective equipment should be removed and put into a disposable chemotherapy waste container. After this has been done, one should double bag the chemotherapy waste before or after removing one's inner gloves. Moreover, one must always wash one's hands with soap and water before leaving the drug administration site. [ 184 ]
All employees whose jobs in health care facilities expose them to hazardous drugs must receive training. Training should include shipping and receiving personnel, housekeepers, pharmacists, assistants, and all individuals involved in the transportation and storage of antineoplastic drugs. These individuals should receive information and training to inform them of the hazards of the drugs present in their areas of work. They should be informed and trained on operations and procedures in their work areas where they can encounter hazards, different methods used to detect the presence of hazardous drugs and how the hazards are released, and the physical and health hazards of the drugs, including their reproductive and carcinogenic hazard potential. Additionally, they should be informed and trained on the measures they should take to avoid and protect themselves from these hazards. This information ought to be provided when health care workers come into contact with the drugs, that is, perform the initial assignment in a work area with hazardous drugs. Moreover, training should also be provided when new hazards emerge as well as when new drugs, procedures, or equipment are introduced. [ 181 ]
When performing cleaning and decontaminating the work area where antineoplastic drugs are used, one should make sure that there is sufficient ventilation to prevent the buildup of airborne drug concentrations. When cleaning the work surface, hospital workers should use deactivation and cleaning agents before and after each activity as well as at the end of their shifts. Cleaning should always be done using double protective gloves and disposable gowns. After employees finish up cleaning, they should dispose of the items used in the activity in a yellow chemotherapy waste container while still wearing protective gloves. After removing the gloves, they should thoroughly wash their hands with soap and water. Anything that comes into contact or has a trace of the antineoplastic drugs, such as needles, empty vials, syringes, gowns, and gloves, should be put in the chemotherapy waste container. [ 185 ]
A written policy needs to be in place in case of a spill of antineoplastic products. The policy should address the possibility of various sizes of spills as well as the procedure and personal protective equipment required for each size. A trained worker should handle a large spill and always dispose of all cleanup materials in the chemical waste container according to EPA regulations, not in a yellow chemotherapy waste container. [ 186 ]
A medical surveillance program must be established. In case of exposure, occupational health professionals need to ask for a detailed history and do a thorough physical exam. They should test the urine of the potentially exposed worker by doing a urine dipstick or microscopic examination, mainly looking for blood, as several antineoplastic drugs are known to cause bladder damage. [ 176 ]
Urinary mutagenicity is a marker of exposure to antineoplastic drugs that was first used by Falck and colleagues in 1979 and uses bacterial mutagenicity assays. Apart from being nonspecific, the test can be influenced by extraneous factors such as dietary intake and smoking and is, therefore, used sparingly. However, the test played a significant role in changing the use of horizontal flow cabinets to vertical flow biological safety cabinets during the preparation of antineoplastic drugs because the former exposed health care workers to high levels of drugs. This changed the handling of drugs and effectively reduced workers' exposure to antineoplastic drugs. [ 176 ]
Biomarkers of exposure to antineoplastic drugs commonly include urinary platinum , methotrexate , urinary cyclophosphamide and ifosfamide , and urinary metabolite of 5-fluorouracil . In addition to this, there are other drugs used to measure the drugs directly in the urine, although they are rarely used. A measurement of these drugs directly in one's urine is a sign of high exposure levels and that an uptake of the drugs is happening either through inhalation or dermally. [ 176 ]
There is an extensive list of antineoplastic agents . Several classification schemes have been used to subdivide the medicines used for cancer into several different types. [ 187 ] [ 188 ]
The first use of small-molecule drugs to treat cancer was in the early 20th century, although the specific chemicals first used were not originally intended for that purpose. Mustard gas was used as a chemical warfare agent during World War I and was discovered to be a potent suppressor of hematopoiesis (blood production). [ 189 ] A similar family of compounds known as nitrogen mustards were studied further during World War II at the Yale School of Medicine . [ 190 ] It was reasoned that an agent that damaged the rapidly growing white blood cells might have a similar effect on cancer. [ 190 ] Therefore, in December 1942, several people with advanced lymphomas (cancers of the lymphatic system and lymph nodes) were given the drug by vein, rather than by breathing the irritating gas. [ 190 ] Their improvement, although temporary, was remarkable. [ 191 ] Concurrently, during a military operation in World War II, following a German air raid on the Italian harbour of Bari , several hundred people were accidentally exposed to mustard gas, which had been transported there by the Allied forces to prepare for possible retaliation in the event of German use of chemical warfare. The survivors were later found to have very low white blood cell counts. [ 192 ] After WWII was over and the reports declassified, the experiences converged and led researchers to look for other substances that might have similar effects against cancer. The first chemotherapy drug to be developed from this line of research was mustine . Since then, many other drugs have been developed to treat cancer, and drug development has exploded into a multibillion-dollar industry, although the principles and limitations of chemotherapy discovered by the early researchers still apply. [ 193 ]
The word chemotherapy without a modifier usually refers to cancer treatment, but its historical meaning was broader. The term was coined in the early 1900s by Paul Ehrlich as meaning any use of chemicals to treat any disease ( chemo - + -therapy ), such as the use of antibiotics ( antibacterial chemotherapy ). [ 194 ] Ehrlich was not optimistic that effective chemotherapy drugs would be found for the treatment of cancer. [ 194 ] The first modern chemotherapeutic agent was arsphenamine , an arsenic compound discovered in 1907 and used to treat syphilis . [ 195 ] This was later followed by sulfonamides (sulfa drugs) and penicillin . In today's usage , the sense "any treatment of disease with drugs" is often expressed with the word pharmacotherapy .
Specially targeted delivery vehicles aim to increase effective levels of chemotherapy for tumor cells while reducing effective levels for other cells. This should result in an increased tumor kill or reduced toxicity or both. [ 196 ]
Antibody-drug conjugates (ADCs) comprise an antibody , drug and a linker between them. The antibody will be targeted at a preferentially expressed protein in the tumour cells (known as a tumor antigen ) or on cells that the tumor can utilise, such as blood vessel endothelial cells . They bind to the tumor antigen and are internalised, where the linker releases the drug into the cell. These specially targeted delivery vehicles vary in their stability, selectivity, and choice of target, but, in essence, they all aim to increase the maximum effective dose that can be delivered to the tumor cells. [ 197 ] Reduced systemic toxicity means that they can also be used in people who are sicker and that they can carry new chemotherapeutic agents that would have been far too toxic to deliver via traditional systemic approaches. [ 198 ]
The first approved drug of this type was gemtuzumab ozogamicin (Mylotarg), released by Wyeth (now Pfizer ). The drug was approved to treat acute myeloid leukemia . [ 199 ] Two other drugs, trastuzumab emtansine and brentuximab vedotin , are both in late clinical trials, and the latter has been granted accelerated approval for the treatment of refractory Hodgkin's lymphoma and systemic anaplastic large cell lymphoma . [ 197 ]
Nanoparticles are 1–1000 nanometer (nm) sized particles that can promote tumor selectivity and aid in delivering low- solubility drugs. Nanoparticles can be targeted passively or actively. Passive targeting exploits the difference between tumor blood vessels and normal blood vessels. Blood vessels in tumors are "leaky" because they have gaps from 200 to 2000 nm, which allow nanoparticles to escape into the tumor. Active targeting uses biological molecules ( antibodies , proteins , DNA and receptor ligands ) to preferentially target the nanoparticles to the tumor cells. There are many types of nanoparticle delivery systems, such as silica , polymers , liposomes [ 200 ] and magnetic particles. Nanoparticles made of magnetic material can also be used to concentrate agents at tumor sites using an externally applied magnetic field. [ 196 ] They have emerged as a useful vehicle in magnetic drug delivery for poorly soluble agents such as paclitaxel . [ 201 ]
Electrochemotherapy is the combined treatment in which injection of a chemotherapeutic drug is followed by application of high-voltage electric pulses locally to the tumor. The treatment enables the chemotherapeutic drugs, which otherwise cannot or hardly go through the membrane of cells (such as bleomycin and cisplatin), to enter the cancer cells. Hence, greater effectiveness of antitumor treatment is achieved. [ 202 ]
Clinical electrochemotherapy has been successfully used for treatment of cutaneous and subcutaneous tumors irrespective of their histological origin. [ 202 ] [ 203 ] The method has been reported as safe, simple and highly effective in all reports on clinical use of electrochemotherapy. According to the ESOPE project (European Standard Operating Procedures of Electrochemotherapy), the Standard Operating Procedures (SOP) for electrochemotherapy were prepared, based on the experience of the leading European cancer centres on electrochemotherapy. [ 204 ] [ 205 ] Recently, new electrochemotherapy modalities have been developed for treatment of internal tumors using surgical procedures, endoscopic routes or percutaneous approaches to gain access to the treatment area. [ 206 ] [ 207 ]
Hyperthermia therapy is heat treatment for cancer that can be a powerful tool when used in combination with chemotherapy (thermochemotherapy) or radiation for the control of a variety of cancers. The heat can be applied locally to the tumor site, which will dilate blood vessels to the tumor, allowing more chemotherapeutic medication to enter the tumor. Additionally, the tumor cell membrane will become more porous, further allowing more of the chemotherapeutic medicine to enter the tumor cell.
Hyperthermia has also been shown to help prevent or reverse "chemo-resistance." Chemotherapy resistance sometimes develops over time as the tumors adapt and can overcome the toxicity of the chemo medication. "Overcoming chemoresistance has been extensively studied within the past, especially using CDDP-resistant cells. In regard to the potential benefit that drug-resistant cells can be recruited for effective therapy by combining chemotherapy with hyperthermia, it was important to show that chemoresistance against several anticancer drugs (e.g. mitomycin C, anthracyclines, BCNU, melphalan) including CDDP could be reversed at least partially by the addition of heat. [ 208 ]
Chemotherapy is used in veterinary medicine similar to how it is used in human medicine. [ 209 ]
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Chemotherapy-induced acral erythema , also known as palmar-plantar erythrodysesthesia or hand-foot syndrome is reddening , swelling , numbness and desquamation (skin sloughing or peeling) on palms of the hands and soles of the feet (and, occasionally, on the knees, elbows, and elsewhere) that can occur after chemotherapy in patients with cancer . Hand-foot syndrome is also rarely seen in sickle-cell disease . These skin changes usually are well demarcated. Acral erythema typically disappears within a few weeks after discontinuation of the offending drug. [ 1 ] [ 2 ]
The symptoms can occur anywhere between days to months after administration of the offending medication, depending on the dose and speed of administration. [ 3 ] [ 4 ] The patient first experiences tingling and/or numbness of the palms and soles. This is followed 2–4 days later by bright redness, which is symmetrical and sharply defined. [ 5 ]
In severe cases this may be followed by burning pain and swelling, blistering and ulceration, peeling of the skin. [ 6 ] Healing occurs without scarring unless there has been skin ulceration or necrosis (skin loss/death). With each subsequent cycle of chemotherapy, the reaction will appear more quickly, be more severe and will take longer to heal. [ 5 ]
Acral erythema is a common adverse reaction to cytotoxic chemotherapy drugs, particularly cabozantinib , cytarabine , doxorubicin (including pegylated liposomal doxorubicin, PLD), and fluorouracil and its prodrug capecitabine . [ 3 ]
Targeted cancer therapies , especially the tyrosine kinase inhibitors sorafenib and sunitinib , have also been associated with a high incidence of acral erythema. However, acral erythema due to tyrosine kinase inhibitors seems to differ somewhat from acral erythema due to classic chemotherapy drugs. [ 7 ]
The cause of palmar-plantar erythrodysesthesia (PPE) is unknown. Existing hypotheses are based on the fact that only the hands and feet are involved and posit the role of temperature differences, vascular anatomy, differences in the types of cells (rapidly dividing epidermal cells and eccrine glands ). [ 8 ]
In the case of PPE caused by pegylated liposomal doxorubicin ( PLD ), the following mechanism has been demonstrated: sweat deposits and spreads the drug on the skin surface; then the drug penetrates into the stratum corneum like an external agent; palms and soles have high density of sweat glands, and their stratum corneum is approximately 10 times thicker than the rest of the body, and becomes an efficient long-term reservoir for the penetrating PLD, which was deposited on the skin before. [ 9 ]
Painful red swelling of the hands and feet in a patient receiving chemotherapy is usually enough to make the diagnosis. The problem can also arise in patients after bone marrow transplants , as the clinical and histologic features of PPE can be similar to cutaneous manifestations of acute (first three weeks) graft-versus-host disease . It is important to differentiate PPE, which is benign, from the more dangerous graft-versus-host disease. As time progresses, patients with graft-versus-host disease progress to have other body parts affected, while PPE is limited to hands and feet. Serial biopsies every 3 to 5 days can also be helpful in differentiating the two disorders. [ 10 ]
The cooling of hands and feet during chemotherapy may help prevent PPE. [ 3 ] [ 11 ] Support for this and a variety of other approaches to treat or prevent acral erythema comes from small clinical studies, although none has been proven in a randomised controlled clinical trial of sufficient size. [ 12 ]
Modifying some daily activities to reduce friction and heat exposure to your hands and feet for a period of time following treatment (approximately one week after IV medication, much as possible during the time you are taking oral medication such as capecitabine). [ 13 ] [ 14 ]
The main treatment for acral erythema is discontinuation of the offending drug, and symptomatic treatment to provide analgesia , lessen edema , and prevent superinfection . However, the treatment for the underlying cancer of the patient must not be neglected. Often, the discontinued drug can be substituted with another cancer drug or cancer treatment. [ 15 ] [ 16 ]
Symptomatic treatment can include wound care, elevation, and pain medication. Various emollients (creams) are recommended to keep skin moist. Corticosteroids and pyridoxine have also been used to relieve symptoms. [ 17 ] Other studies do not support the conclusion. A number of additional remedies are listed in recent medical literature. [ 18 ] Among them henna and 10% uridine ointment which went through clinical trial. [ 19 ]
Hand-foot invariably recurs with the resumption of chemotherapy. Long-term chemotherapy may also result in reversible palmoplantar keratoderma . Symptoms resolve 1–2 weeks after cessation of chemotherapy. [ 6 ] The range is 1–5 weeks, so it has recovered by the time the next cycle is due. Healing occurs without scarring unless there has been skin ulceration or necrosis . With each subsequent cycle of chemotherapy, the reaction will appear more quickly, be more severe and will take longer to heal. [ 5 ]
Hand-foot syndrome was first reported in association with chemotherapy by Zuehlke in 1974. [ 20 ] Synonyms for acral erythema (AE) include: hand-foot syndrome, palmar-plantar erythrodysesthesia, peculiar AE, chemotherapy-induced AE, toxic erythema of the palms and soles, palmar-plantar erythema, and Burgdorf's reaction. Common abbreviations are HFS and PPE.
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Chemotherapy-induced nausea and vomiting ( CINV ) is a common side-effect of many cancer treatments. Nausea and vomiting are two of the most feared cancer treatment -related side effects for cancer patients and their families. In 1983, Coates et al. found that patients receiving chemotherapy ranked nausea and vomiting as the first and second most severe side effects, respectively. Up to 20% of patients receiving highly emetogenic agents in this era postponed, or even refused, potentially curative treatments. [ 1 ] Since the 1990s, several novel classes of antiemetics have been developed and commercialized, becoming a nearly universal standard in chemotherapy regimens, and helping to better manage these symptoms in a large portion of patients. Efficient mediation of these unpleasant and sometimes debilitating symptoms results in increased quality of life for the patient, and better overall health of the patient, and, due to better patient tolerance, more effective treatment cycles.
There are several subtypes of CINV. The classifications of nausea and vomiting are: [ 2 ]
Vomiting is a defense mechanism controlled by the area postrema of the medulla oblongata . There are various sources of input to the vomiting center. Receptors on the floor of the fourth ventricle of the brain represent the chemoreceptor trigger zone . The chemoreceptor trigger zone contains dopamine D2 receptors , serotonin 5-HT 3 receptors , opioid receptors , acetylcholine receptors , and receptors for substance P . Stimulation of different receptors are involved in different pathways leading to emesis. In the final common pathway, substance P, which activates the neurokinin-1 receptor , appears to be involved. [ 3 ] Additionally, the vagal and enteric nervous system inputs transmit information regarding the state of the gastrointestinal system.
Chemotherapy interferes with cell division, which particularly affects rapidly dividing cells like those of the gastrointestinal mucosa and immune cells. Irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the 5-HT 3 receptors of these inputs. [ 4 ] It is now widely known that cytotoxic chemotherapeutic agents cause enterochromaffin cells to produce more serotonin in response to free radical damage , leading to a detectable increase in blood levels of serotonin (5-HT) and its major metabolite, 5-Hydroxyindoleacetic acid (5-HIAA). [ 5 ] The presence of these chemicals in the blood activate 5-HT 3 receptors in the chemoreceptor trigger zone, in turn releasing substance P, which activates NK 1 receptors to cause an emetic response (vomiting).
The risk of chemotherapy-induced nausea and vomiting varies based on the type of treatment received as well as several outside factors. Some types of chemotherapy are more prone to causing nausea and vomiting than others. Some chemotherapeutic agents may not cause nausea and vomiting on their own, but may when used in combination with other agents. [ 6 ] Regimens that are linked to a high incidence (90% or higher) of nausea and vomiting are referred to as "highly emetogenic chemotherapy", and those causing a moderate incidence (30–90%) of nausea and vomiting are referred to as "moderately emetogenic chemotherapy". [ 7 ]
Some highly emetogenic agents and chemotherapy regimens include: [ 6 ] [ 8 ]
Some moderately emetogenic agents and regimens include: [ 8 ]
Besides the type of treatment, personal factors may put a patient at greater risk for CINV. Other risk factors include: [ 2 ] [ 6 ] [ 9 ]
Several treatment methods are available to help prevent CINV. Pharmaceutical treatment is generally separated into two types: prophylactic (preventative) treatment, given before the dose of chemotherapy agents, and rescue treatment, given to treat breakthrough nausea and vomiting.
5-HT 3 receptor antagonists are very effective antiemetics and constitute a great advance in the management of CINV. These drugs block one or more of the nerve signals that cause nausea and vomiting. During the first 24 hours after chemotherapy, the most effective approach appears to be blocking the 5-HT 3 nerve signal. [ 10 ] Approved 5-HT 3 inhibitors include dolasetron (Anzemet), granisetron (Kytril, Sancuso), and ondansetron (Zofran). Their antiemetic effect due to blockade of 5HT3 receptor on vagal afferent in the gut. in addition they also block 5-HT3 receptors in CTZ and STN. The newest 5-HT 3 inhibitor, palonosetron (Aloxi), also prevents delayed nausea and vomiting, which can occur during the 2–5 days after treatment. Since some patients have trouble swallowing pills, these drugs are often available by injection , as orally disintegrating tablets , or as transdermal patches .
A newer class of drugs known as the NK 1 antagonists are a recently developed class of very efficacious drugs for controlling CINV. These drugs are often used alongside 5HT 3 inhibitors and corticosteroids to form a very potent cocktail of antiemetics that verge on achieving a nearly complete patient response (that is, completely stopping CINV). [ 11 ] The substance P inhibitor aprepitant (Emend), which became available in 2005, is highly effective in controlling nausea and vomiting associated with cancer chemotherapy. [ 11 ] Aprepitant has been shown to inhibit both the acute and delayed emesis induced by cytotoxic chemotherapeutic drugs by blocking substance P landing on receptors in the brains neurons. Indeed, positron emission tomography (PET) studies have shown that aprepitant can penetrate the brain and NK 1 receptors in the brain. [ 12 ] Aprepitant has also been shown to increase the activity of the 5-HT 3 receptor antagonists ondansetron and the corticosteroid dexamethasone , which are also used to prevent nausea and vomiting caused by chemotherapy. [ 11 ] Netupitant has recently been approved by USFDA. It has also been marketed in combination with palonosetron. Rolapitant is the newest addition in the approved NK1 antagonist list. It has advantage of a very long half life, duration of action is around 150 hours. Rolapitant got its approval by USFDA in 2015.
Olanzapine , as well as several other neuroleptic drugs , have also has been investigated for the control of CINV. [ 13 ] A 2007 study demonstrated Olanzapine's successful potential for this use, achieving a complete response in the acute prevention of nausea and vomiting in 100% of patients treated with moderately and highly emetogenic chemotherapy, when used in combination with palonosetron and dexamethasone . [ 14 ] Neuroleptic agents are now indicated for rescue treatment and the control of breakthrough nausea and vomiting. [ 13 ]
Some studies [ 15 ] and patient groups say that the use of cannabinoids derived from cannabis during chemotherapy greatly reduces the associated nausea and vomiting, and enables the patient to eat. Synthesized tetrahydrocannabinol (also one of the main active substances in marijuana) is marketed as Marinol and may be practical for this application. Natural medical cannabis is also used and recommended by some oncologists, though its use is regulated and it is not legal in all jurisdictions. [ 16 ] However, Marinol was less effective than megestrol acetate in helping cancer patients regain lost appetites. [ 17 ] A phase III study found no difference in effects of an oral cannabis extract or THC on appetite and quality of life (QOL) in patients with cancer-related anorexia - cachexia syndrome (CACS) to placebo . [ 18 ] [ independent source needed ]
Dexamethasone , a corticosteroid, is often used alongside other antiemetic drugs, as it has synergistic action with many of them, although its specific antiemetic mechanism of action is not fully understood. Metoclopramide , a dopamine D 2 receptor antagonist with possible other mechanisms, is an older drug that is sometimes used, either on its own or in combination with others. Histamine blockers such as diphenhydramine or meclozine may be used in rescue treatment. Lorazepam and diazepam may sometimes be used to relieve anxiety associated with CINV before administration of chemotherapy, and are also often used in the case of rescue treatment. [ 13 ]
There are several compounds that have been identified within ginger that have been shown to possess properties that are likely to be beneficial in the treatment of CINV. This includes 5-HT3 and substance P antagonism, modulation of gastrointestinal motility, and antioxidant properties. [ 19 ] [ 20 ] There have been multiple clinical trials that have investigated the use of ginger supplementation as a treatment for CINV. However, due to conflicting results and methodological issues, a 2013 systematic review of seven clinical trials summarized the current evidence as stating that "Despite the widespread use of ginger in the treatment of nausea in other contexts such as gestational nausea, the current literature provides mixed support for the use of ginger as a standard part of anti-CINV control for patients undergoing chemotherapy." [ 21 ]
Non-pharmacological approaches to remedy CINV typically involve small lifestyle alterations, such as using unscented deodorants and soaps, avoiding strong scents altogether, and dietary modifications such as eating several small meals throughout the day, eating high-protein, high-calorie food, drinking many clear liquids, and removing spicy, fatty, fried, or acidic foods from the diet. [ 22 ] Patients may also participate in alternative practices such as self-hypnosis , relaxation and imagery therapy, distraction, music therapy , biofeedback , desensitization , or acupressure . [ 2 ]
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Chemotherapy: International Journal of Experimental and Clinical Chemotherapy is a peer-reviewed medical journal covering antimicrobial chemotherapy , published by Karger Publishers . The journal was established in 1960 and was originally named Chemotherapia , obtaining its current name in 1968. According to the Journal Citation Reports , the journal has a 2014 impact factor of 1.288. [ 1 ]
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See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
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https://en.wikipedia.org/wiki/Chemotherapy_(journal)
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The Chemturion is a multi-use, positive pressure totally encapsulating protective suit, manufactured by ILC Dover . It is currently used by Public Health Canada , Boston University , USAMRIID and AI Signal Research , the Center for Disease Control in Atlanta, and many industrial companies such as DuPont , Dow , and Georgia Pacific . [ 1 ]
The Chemturion is based on technology developed by ILC Dover as part of the development of the Demilitarization Protective Ensemble , a one-piece disposable suit used in chemical weapons disposal. [ 2 ]
The Chemturion is commonly used in biohazard environments, including BSL4 environments, and is sometimes known as the "blue suit" because of its colour. Other suits used in BSL4 environments include Honeywell Safety's Delta suits , and HVO suits manufactured by HVO-ISSI-Deutschland GmbH . [ 3 ]
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https://en.wikipedia.org/wiki/Chemturion
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Chen Haozhu ( Chinese : 陈灏珠 ; 6 November 1924 – 30 October 2020) was a Chinese cardiologist.
Chen was born on 6 November 1924 and attended National Zhongzheng Medical College [ zh ] , where he completed a bachelor's degree in 1949. He was responsible for introducing the term " myocardial infarction " to Chinese medical professionals, and is credited with pioneering modern cardiology in China by using newer methods of treatment and diagnosis. Chen was the director of the Shanghai Institute of Cardiovascular Diseases and served as vice chair of the Chinese Society of Cardiology, as well as the Chinese Medical Association. [ 1 ] He taught as a professor at Zhongshan Hospital , affiliated to Fudan University , and was elected a member of the Chinese Academy of Engineering in 1997. [ 2 ]
Chen died on 30 October 2020, aged 95. [ 1 ]
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https://en.wikipedia.org/wiki/Chen_Haozhu
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The Cherney incision is an incision used in gynecologic surgery. It is similar to the Pfannenstiel incision but allows access to the space of Retzius and gives a larger area in which to operate. [ 1 ]
The Cherney incision begins when the skin is cut 2-3 centimeters above the pubic symphysis and the surgeon dissects down to the rectus abdominis muscle . The surgeon then uses blunt dissection with the fingers to separate the tendons from the overlying fascia before cutting the tendons 1-2 centimeters above the pubic symphysis. The muscles are then lifted away, toward the patient's head (cephalad). Then, the peritoneum can be cut and the surgery can proceed. [ 1 ]
Complications can ensue. If surgical retractors are not placed carefully under the edges of the incision, they can damage the femoral nerve or other nerves in the area. If during wound closure, tendons are sewn directly to the pubic symphysis, osteitis pubis or osteomyelitis can result. [ 1 ]
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https://en.wikipedia.org/wiki/Cherney_incision
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This is a list of plants documented to have been traditionally used by the Cherokee , and how they are used.
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https://en.wikipedia.org/wiki/Cherokee_ethnobotany
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Tanya Denise Jackson (October 22, 1970 – c. June 25, 1997), formerly known as " Peaches ", " The Girl with the Peach Tattoo " or as Jane Doe No. 3, was a formerly-unidentified murder victim whose torso was discovered on June 28, 1997, in Lakeview, New York , near Hempstead Lake State Park . She remained unidentified until 2025, and her skull has yet to be found. [ 1 ] [ 2 ] Jackson had a tattoo on her left breast depicting a heart-shaped peach with a bite taken out of it and two drops falling from its core, which resulted in her nickname. [ 3 ] By December 2016, additional skeletal remains found on Long Island in 2011 had been positively identified as belonging to Jackson, along with the remains of her daughter, identified in 2025 as Tatiana Marie Dykes . [ 4 ] Due to the location of her remains, the murders of Jackson and Dykes have been linked to the Long Island serial killer as potential victims. [ 5 ]
On June 28, 1997, a dismembered body was discovered by a man and his daughter out for a stroll in a wooded area of Hempstead Lake State Park , Lakeview, New York . [ 6 ] The head, both arms, and both legs (below the knee) were severed and have yet to be found. The torso was found on the west side of Lake Drive, about 200 yards north of Peninsula Boulevard by the McDonald Pond. She was found in a Rubbermaid container along with a red towel and a floral pillowcase. With no leads to the woman's identity, the police published a picture of the approximately two-inch-wide tattoo in a national tattoo magazine, in the hopes of finding the artist who did the work. They received a call from Steve Cullen, a tattoo artist in Connecticut who claimed he remembered giving the tattoo to a woman. Cullen said he remembered the customer as a young black woman, about 18 or 19 years old, who was accompanied by two women, an aunt and a cousin. During the session, he also claimed she told him she was from either the Bronx or Long Island and that she was in Connecticut because she was having trouble with her boyfriend at the time. It is possible the woman had other tattoos on her arms or lower legs that the killer did not want found. [ 7 ]
On December 13, 2016, Long Island Press reported that local authorities had positively identified skeletal remains (formerly referred to as "Jane Doe 3") found at Jones Beach State Park in 2011 as belonging to "Peaches". Remains of a child were also found in 2011, east of Cedar Beach, with DNA testing identifying Jane Doe 3—or "Peaches"—as its mother. As a result of these findings, Peaches has now been linked to the Long Island serial killer as a potential early victim. [ 8 ]
On October 8, 2022, the Mobile Police Department announced on its official Facebook page that the FBI was seeking relatives and friends of Elijah "Lige" Howell/Howard (1927–1963). Howard lived in Prichard, Alabama , with his wife Carrie and died in Mobile, Alabama , in 1963 while living with a Ms. Lillie Mae Wiggins Packer. The FBI believed his relatives may be able to assist in identifying Peaches and her child. [ 9 ]
On April 23, 2025, Nassau County police announced that they had identified Peaches as Tanya Denise Jackson, who was born on October 22, 1970, in Alabama . [ 10 ] Jackson had served in the United States Army from 1993 to 1995. Her daughter, Tatiana Marie Dykes, formerly known as "Baby Doe", was born on March 17, 1995, in Texas. [ 11 ] [ 12 ] At the time of their deaths, they lived in Brooklyn , where Jackson may have been working as a medical assistant. [ 13 ] Jackson was estranged from her family, and the two were never reported missing. Tatiana's father has been identified and is cooperating with the investigation. [ 14 ] Police did not specify whether their murders were linked to the ongoing Gilgo Beach serial killings investigation. [ 15 ]
On March 3, 2007, a dismembered torso was found in a suitcase in Harbor Island Park in Mamaroneck , Westchester County , New York . [ 16 ] Investigators believe the victim was a heavy-set Hispanic or light-skinned African-American woman, about five feet seven inches tall, and 180 to 200 pounds. She had a tattoo of two red cherries on a green stem located on her right breast. [ 17 ] "Cherries" (as she is referred to by law enforcement) was also decapitated and dismembered, although her original cause of death was a stab wound to the torso. [ 18 ] Unlike Peaches, investigators found both of Cherries' legs, which washed up on the shore of Cablevision owner James Dolan 's beachfront estate in Oyster Bay, New York . Inside the suitcase investigators found a pair of gray Champion sweat pants, a tan or cream-colored long-sleeved shirt by Voice and a red camisole bearing Spanish-language labels. The dark blue or black suitcase is sold exclusively at Walmart stores. Police also found small scraps of paper tucked away in the crevices of the suitcase. When pieced together, it looks like a calendar with the Spanish word "cinco" and the phrase "begin to live." Police claim that since the torso floated onto the beach as storm-fed floods hit the region, it could have originated from almost anywhere. [ 19 ] [ 20 ]
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https://en.wikipedia.org/wiki/Cherries_(murder_victim)
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Chest reconstruction , also known as top surgery , refers to any of various surgical procedures to reconstruct the chest by removing breast tissue or altering the nipples and areolae in order to mitigate gender dysphoria . Transgender men and non-binary people may pursue chest reconstruction as part of their transition , though it is also used to treat cases of gynecomastia in cisgender men.
The removal of breast tissue in chest reconstruction is a type of mastectomy called a subcutaneous (under the skin) mastectomy. This type of mastectomy removes tissue from inside the breast ( subcutaneous tissue ), as well as excess skin. The surgeon then contours the chest, altering the size and position of the areolae and nipples as needed or as indicated by the patient.
Those undergoing chest reconstruction may opt to forgo nipple grafts, with the intent of having a completely blank, flat chest, or, to have them tattooed on at a later date. Some patients may also request specific shapes for the nipples that will be reattached, such as hearts or stars; some surgeons may have no qualms with providing this service, while others may feel less skilled or experienced in creating 'non binary' top surgery chests. [ 1 ] [ 2 ] [ 3 ]
In 1942, [ 4 ] British physician and author Michael Dillon underwent a chest masculinizing mastectomy as part of his transition to male. This would be among the first of Dillon's 13 gender-affirming surgeries . All were performed by Harold Gillies , a New Zealand plastic surgeon, [ 5 ] who is sometimes referred to as "the father of modern plastic surgery." [ 6 ] It is possible this was the first top surgery performed.
In the mid-1970s, Chicago surgeon Dr. Michael Brownstein (having graduated from UCSF ) opened a plastic surgery practise in San Francisco. [ 7 ] In 1978, Dr. Michael Brownstein conducted his first chest reconstructive surgery under the request of a FTM (Female to Male) identified as "John L." [ 7 ] The surgery was successful, and shortly thereafter, "FTMs were 'flocking to him,' including some who had not had any so-called gender counseling." [ 7 ] Brownstein continued to provide the plastic surgery until healthcare misconduct defense attorney Paul Walker contacted him, stating that he was violating the Standards of Care. Following this, Brownstein requested referrals from trans patients and Brownstein became known for his "outstanding results." [ 7 ] Brownstein became a "world renowned" surgeon, [ 8 ] [ 9 ] with patients including Lou Sullivan [ 7 ] in 1980 [ 10 ] [ 11 ] and Chaz Bono in 2009. [ 12 ] Brownstein retired in 2013, "after 35 years of serving the transgender and gender-non-conforming communities." [ 9 ]
In 2017, German model Benjamin Melzer called top surgery "the most important surgery for all trans men". [ 13 ] It was one of the 11 surgeries he had during his own transition. Right after his healing process was over, Melzer went to a public pool and jumped into the water with just shorts on, which he described as "the best". [ 13 ]
Canadian actor Elliot Page underwent the surgery circa March 2021; he stated, "It has completely transformed my life... [It's] not only life-changing but lifesaving." [ 14 ]
Chest reconstruction surgery candidates desire a flat chest, which may or may not include masculinization. These candidates may include cisgender men with gynecomastia; transgender men who are medically transitioning and have chest dysphoria; and non-binary people with breasts. [ 15 ] All of the above listed may experience chest dysphoria and/or a desire to masculinize its size or shape. [ 16 ] [ 17 ]
Gynecomastia is a common breast deformity that can occur in cisgender men, which may require surgical intervention. Causes of gynecomastia may vary but may include drug side effects or genetics. [ 16 ]
People assigned female at birth with male, masculine, or non-binary genders may experience gender dysphoria caused by their chest and/or gender euphoria after the surgical recovery. [ 17 ]
A transverse inframammary incision with free nipple areolar grafts may be one approach. If there is too much blousing of the skin, the alternatives are to extend the incision laterally (chasing a dog ear) or to make a vertical midline incision (inverted T). [ citation needed ]
The areola is trimmed to a pre-agreed-upon diameter and the nipple sectioned with a pie-shaped excision and reconstituted. There may be varying sensory loss because of nerve disruption.
One of the most common chest reconstructive procedures, double incision involves an incision above and below the breast mass, the removal of the fatty and glandular tissue, and the closure of the skin. This method leaves scars under the pectoral muscles, stretching from the underarms to the medial pectoral. [ citation needed ]
Double incision is usually accompanied by free nipple grafts to make male-looking nipples. The areola and nipple is removed from the breast tissue, cutting away along the circumference and removing the top layer of flesh from the rest of the tissue. After the chest has been reconstructed, the nipples are grafted on in the appropriate male position. The areolae are often sized down as well as the nipples themselves, as female areolae are often larger in circumference and the nipples protrude farther.
Nipple grafts are generally associated with double incision style chest reconstruction, but may be used in any reconstruction procedure if necessary.
With nipple grafts comes the possibility of rejection. In such cases, the nipple is often tattooed back on cosmetically or further surgical procedures may be applied.
Sensation may return to the grafted nipples over time. However, the procedure severs the nerves that go into the nipple-areola and recipients may experience complete or partial loss of sensation. [ 18 ]
To remove the glandular and fatty tissue which constitute the breast mass and the added skin that drapes the mass, there are three basic approaches.
For petite breasts, such as an A or a small B, a peri-areolar incision can be done. That is
a circular incision around the areola, combined with an inner circular incision to remove some of the excess areola. Drawing the skin into the center will result in some puckering, but this often smooths out with time. There will be significant tension on the scar line, and to prevent spreading of the scar, a permanent fixation suture is needed. Leaving outer dermis (raw skin) underneath the marginalized areola helps in its survival.
The keyhole incision (i.e., skeleton key) augments the periareolar incision further by making a vertical closure underneath (lollipop), which results after the unwanted skin is pulled in from side to side and the excess is removed. [ 19 ]
An anchor incision adds to that a transverse incision usually in the infra mammary fold to further remove excessive skin. Draping or blousing is not desirable. This is reserved for much larger breasts or topographically a larger surface area as seen in women with postpartum breast atrophy.
The nipple areolar complex may be supported by a pedicle which has the advantage of leaving some sensation and blood supply intact, but can have the disadvantage when the pedicle has sufficient bulk not to provide the flat look most FTM patients desire.
Occasionally, the side limbs may be quite long, and the expression doctors use is "chasing a dog ear" into the axilla (or underarm). A dog ear may occur when the skin at the edge or corner of an incision 'flows over,' when there is too much gathering, usually at an angle greater than 30 degrees. This usually becomes more apparent after several months of healing, and can be caused by things like weight gain (excess skin or fat changing the shape in areas like torso, hips, stomach, or buttocks, may also occur along the incision line), or due to 'poor surgical planning and execution.' [ 20 ] Using a curved incision can reduce the chances of dog ears developing because it requires less gathering of skin to be done, but some patients dislike the appearance of the curved scar as it can mimic the appearance of breasts.
Not uncommonly, a surgeon may revise the incision lines after 3 or more months of settling shows some residual problem areas. Other revisions may include changing 'slight irregularities,' such as reshaping of the nipple that may have stretched 'out of shape' due to too much upper arm/over the head arm movement, or general 'overextension' during the healing process (which may also cause asymmetry), bulges or puckering (typically along incision lines), failed nipple grafts (which may result in one or both nipples 'failing' to 'take' to the patient's healing chest, or scarring patterns a patient may not be happy with. [ 21 ]
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Chewing or mastication is the process by which food is crushed and ground by the teeth . It is the first step in the process of digestion , allowing a greater surface area for digestive enzymes to break down the foods.
During the mastication process, the food is positioned by the cheek and tongue between the teeth for grinding. The muscles of mastication move the jaws to bring the teeth into intermittent contact, repeatedly occluding and opening. As chewing continues, the food is made softer and warmer, and the enzymes in saliva begin to break down carbohydrates in the food. After chewing, the food (now called a bolus ) is swallowed. It enters the esophagus and via peristalsis continues on to the stomach, where the next step of digestion occurs. [ 1 ] Increasing the number of chews per bite stimulates the production of digestive enzymes and peptides and has been shown to increase diet-induced thermogenesis (DIT) by activating the sympathetic nervous system . [ 2 ] Studies suggest that thorough chewing may facilitate digestion and nutrient absorption, improve insulin secretion and glucose homeostasis, and decrease food intake and levels of self-reported hunger. [ 2 ] Chewing gum has been around for many centuries; there is evidence that northern Europeans chewed birch bark tar 9,000 years ago.
Mastication, as it requires specialized teeth, is mostly a mammalian adaptation that appeared in early Synapsids , although some later herbivorous dinosaurs, now extinct, also developed chewing, too. Today only modern mammals chew in the strictest sense of the word, but some fish species exhibit a somewhat similar behavior. By contrast, mastication is not found in any living birds, amphibians, or reptiles.
Premastication is sometimes performed by human parents for infants who are unable to do so for themselves. The food is masticated in the mouth of the parent into a bolus and then transferred to the infant for consumption [ 3 ] (some other animals also premasticate).
Cattle and some other animals, called ruminants , chew food more than once to extract more nutrients. After the first round of chewing, this food is called cud .
Chewing is primarily an unconscious ( semi-autonomic ) act, but can be mediated by higher conscious input. The motor program for mastication is a hypothesized central nervous system function by which the complex patterns governing mastication are created and controlled.
It is thought that feedback from proprioceptive nerves in teeth and the temporomandibular joints govern the creation of neural pathways, which in turn determine duration and force of individual muscle activation (and in some cases muscle fiber groups as in the masseter and temporalis).
This motor program continuously adapts to changes in food type or occlusion. [ 4 ] This adaptation is a learned skill that may sometimes require relearning to adapt to loss of teeth or to dental appliances such as dentures .
It is thought that conscious mediation is important in the limitation of parafunctional habits as most commonly, the motor program can be excessively engaged during periods of sleep and times of stress. It is also theorized that excessive input to the motor program from myofascial pain or occlusal imbalance can contribute to parafunctional habits .
Chewing stimulates saliva production and increases sensory perception of the food being eaten, controlling when the food is swallowed. [ 5 ] Evidence from one study suggests that chewing almonds 25-40 times kept people fuller while also allowing them to get more nutrients out of the almonds. The researchers also suggest that this is likely to be the case in other foods. [ 6 ] A 2015 systemic review found evidence that chewing can decrease self-reported hunger and therefore food intake. [ 7 ] Eating food which does not require chewing, by choice or for medical reasons as tooth loss , is known as a soft diet . Such a diet may lead to inadequate nutrition due to a reduction in fruit and vegetable intake. [ 8 ]
Chewing also stimulates the hippocampus and is necessary to maintain its normal function. [ 9 ] Chewing stimulates hippocampal neurogenesis in both humans and mice. [ 10 ]
Chewing is largely an adaptation for mammalian herbivory . Carnivores generally chew very little or swallow their food whole or in chunks. [ 11 ] This act of gulping food (or medicine pills) without chewing has inspired the English idiom "wolfing it down". [ 12 ]
Other animals such as cows chew their food for long periods to allow for proper digestion in a process known as rumination. Rumination in cows has been shown by researchers to intensify during the night. They concluded that cows chewed more intently in the night time compared to the morning. [ 13 ]
Ornithopods , a group of dinosaurs including the Hadrosaurids ("duck-bills"), developed teeth analogous to mammalian molars and incisors during the Cretaceous period; this advanced, cow-like dentition allowed the creatures to obtain more nutrients from the tough plant life. This may have given them the advantage needed to compete with the formidable sauropods , who depended on their massive gastrointestinal tracts to digest food without grinding it. [ 14 ]
The process of chewing has, by analogy, been applied to machinery. The U.S. Forest Service uses a machine called a masticator (also called a forestry mulching machine ) to "chew" through brush and timber in order to clear firelines in advance of a wildfire. [ 15 ]
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RCSI , Royal College of Surgeons in Ireland , 2011
Chinyelu Uchechukwu Anne Menakaya (born 4 June 1980) is a Nigerian trauma and orthopedic surgeon based in the United Kingdom . She is the founder of Annomo Health concierge service, [ 1 ] [ 2 ] which brings together doctors and hospitals to the awareness of patients. [ 1 ] [ 3 ] [ 4 ]
Menakaya has held honorary lectures at Hull and York Medical Schools in Yorkshire , United kingdom and works as a surgical medical student tutor for the University College of London . [ 5 ] [ 3 ] She is also the founder of Okwuís_Frocentric, a fashion line with African ideas. [ 6 ]
She was born on 4 June 1980 to Dr. Tim Menakaya (Nigeria's former Minister of Health) and Chief Magistrate Ann Menakaya in Nigeria. She hails from Umunya in Anambra State of Nigeria. [ 3 ] [ 7 ] She attended the University of Ibadan from 1999 to 2006. While there, she served as Director of Finance, Federation of African Medical and Dental Students, and later earned a bachelor's degree in medicine and surgery. She then proceeded to the Imperial College, London , in 2009 and earned a master's degree in surgical technology with supplementary module in medico-legal diploma from that college in 2011. She attended the Royal College of Surgeons in Ireland (RCSI) in 2011 and she is a member of the Royal College of Surgeons of England (MRCS RCSEng). [ 3 ] [ 8 ]
Menakaya founded Annomo in 2013. [ 3 ] [ 4 ] [ 9 ] In 2020, the group donated boxes of masks to rural areas and hospitals in Nigeria. [ 10 ] Menakaya served as the development director (Europe) for RISE Global Health Initiative from July 2014 to September 2017. She served as clinical research fellow for Hull and East Yorkshire Hospitals from August 2011 to August 2013. She was orthopaedic trauma travelling and research fellow for Harvard medical school and Massachusetts General Hospital from 2013 to 2016. In 2023, she became a National Health Service (NHS) Clinical Entrepreneur Fellow. [ 3 ] [ 8 ] Menakaya, through a non-profit organisation, Okwuí Mask Scheme, based in the United Kingdom and Nigeria, empowers victims of domestic violence. [ 11 ] [ 4 ]
Menakaya served as the ice hockey doctor for the Hull Stingrays lce Hockey Club from September 2009 to August 2013. She has been a Foundation Board Member of Chelsea and Westminster Hospital NHS Foundation Trust since 2007. Menakaya was a mailroom and campaign volunteer for the Society for Protection of Unborn Children from July 2006 to August 2007 and director of CareConnect Incorporated since September 2015. She was an academic honorary clinical tutor for Hull York Medical School (HYMS) from August 2011 to August 2013. [ 3 ]
Menakaya was awarded the Marcela Uribe Zamudio Award for Women Researchers (issued by SICOT. Société Internationale de Chirurgie Orthopédique et de Traumatologie ) in November 2014; [ 12 ] Travelling Fellow and Research Collaborator (issued by Harvard Orthopedics Combined Residency Program) in September 2013; [ 3 ] and Year of the African Child Essay Award for Eastern Nigeria (issued by UNICEF ) in June 1997. [ 3 ]
Menakaya is a cousin of Lorenzo Menakaya . The name of her company, Annomo, is derived from the names of her mother, "Ann Okwuchukwu Menakaya Orakwue." [ 10 ]
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The chief complaint , formally known as CC in the medical field, or termed presenting complaint ( PC ) in Europe and Canada, forms the second step of medical history taking. It is sometimes also referred to as reason for encounter ( RFE ), presenting problem , problem on admission or reason for presenting . [ citation needed ] [ 1 ] The chief complaint is a concise statement describing the symptom , problem, condition , diagnosis , physician -recommended return, or other reason for a medical
encounter. [ 2 ] In some instances, the nature of a patient's chief complaint may determine if services are covered by health insurance . [ 3 ]
When obtaining the chief complaint, medical students are advised to use open-ended questions. [ 4 ] [ 5 ] Once the presenting problem is elucidated, a history of present illness can be done using acronyms such as SOCRATES or OPQRST to further analyze the severity, onset and nature of the presenting problem. The patient's initial comments to a physician, nurse , or other health care professionals are important for formulating differential diagnoses . [ citation needed ]
The collection of chief complaint data may be useful in addressing public health issues. [ 6 ] Certain complaints are more common in certain settings and among certain populations. Fatigue has been reported as one of the ten most common reasons for seeing a physician. [ 7 ] In acute care settings, such as emergency rooms , reports of chest pain are among the most common chief complaints. [ 8 ] The most common complaint in ERs has been reported to be abdominal pain . [ 9 ] Among nursing home residents seeking treatment at ERs, respiratory symptoms, altered mental status, gastrointestinal symptoms , and falls are the most commonly reported. [ 10 ]
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The Child Cancer Foundation is a New Zealand -based charity that offers support to children with cancer and their families. [ 1 ]
It has a high profile through public fundraising events. [ 2 ] [ 3 ]
As of 2011, it had an income of NZ$ 4.8 million, of which NZ$1.9 million was fundraising income, with most of the rest being from donations and bequests. [ 4 ]
This article about an organisation in New Zealand is a stub . You can help Wikipedia by expanding it .
This pediatrics article is a stub . You can help Wikipedia by expanding it .
This oncology article is a stub . You can help Wikipedia by expanding it .
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The Child Mania Rating Scales ( CMRS ) is a 21-item diagnostic screening measure designed to identify symptoms of mania in children and adolescents aged 9–17 using diagnostic criteria from the DSM-IV , developed by Pavuluri and colleagues. [ 1 ] There is also a 10-item short form. [ 2 ] The measure assesses the child's mood and behavior symptoms, asking parents or teachers to rate how often the symptoms have caused a problem for the youth in the past month. Clinical studies have found the CMRS to be reliable and valid when completed by parents in the assessment of children's bipolar symptoms. [ 1 ] [ 3 ] The CMRS also can differentiate cases of pediatric bipolar disorder from those with ADHD or no disorder, as well as delineating bipolar subtypes. [ 2 ] A meta-analysis comparing the different rating scales available found that the CMRS was one of the best performing scales in terms of telling cases with bipolar disorder apart from other clinical diagnoses. [ 4 ] The CMRS has also been found to provide a reliable and valid assessment of symptoms longitudinally over the course of treatment. [ 3 ] The combination of showing good reliability and validity across multiple samples and clinical settings, along with being free and brief to score, make the CMRS a promising tool, especially since most other checklists available for youths do not assess manic symptoms.
The Child Mania Rating Scale (CMRS) was created as a complement already existing measures like the Altman Self-Rating Mania Scale and the Young Mania Rating Scale , which were formulated for adults. The purpose of the CMRS is to both assess the symptoms of mania in pediatric bipolar disorder, and to accurately discriminate the symptoms of mania from symptoms of ADHD . [ 1 ] It is important that the CMRS accurately discriminate from symptoms of ADHD because core symptoms of adolescent Bipolar Disorder and ADHD are shared between the two disorders: hyperactivity, impulsivity, and distractibility. [ 5 ] The CMRS was designed specifically for younger children who may or may not have the ability to accurately answer questions about their behavior. As a result, the questionnaire is filled out by parents are/or caregivers who work with the children on a daily basis. Previous mania scales were designed for use by either the clinician or the patient. Therefore, the CMRS is unique in that it allows parents and caregivers to contribute information about their child's symptoms. This is especially important in cases where the child may be too young to fill out the questionnaires themselves.
Historically, effective rating and diagnosis of mania has been limited. Though many mania scales have been tested on adult populations, the Young Mania Rating Scale (YMRS) – which was tested against the child version (CMRS) as standard measure for screening mania- is the only adult scale that has also been studied for validity and reliability in prepubertal children. [ 6 ] [ 7 ] Previous attempts include the Beigel Scale/Manic State Rating Scale (MSRS) [ 8 ] and the Patterson Scale, which used nurse and clinician reports to rate levels of mania. Neither scale effectively and consistently captured levels of mania in patients. [ 9 ] Other measures of pediatric mania are generally limited because they are completed by the clinician, introducing potential for bias, and because they lack the depth necessary to differentiate between patient-specific ways in which symptoms are presented. [ 3 ] The CMRS Parent and Teacher versions attempt to address some of the limitations by including a checklist that can gather information about behavior at home, school, and other settings, rather than focusing only on what a clinician could directly observe. [ 10 ] One study examined the accuracy of a shortened version of the CMRS-P, which included only 10 items, and found that its accuracy was similar to the full scale. [ 2 ]
Typically, the CMRS takes only 10–15 minutes to administer. [ 1 ] The questions ask about behavior-specific actions and tendencies the child may have exhibited within the past month. The parent rates the behavior on a scale from 1 to 4, where 1=never/rarely, 2=sometimes, 3=often, and 4=very often. A clinician examines the total score and determines if the child has ADHD or Bipolar Disorder. If a diagnosis Bipolar Disorder is deemed to be appropriate, the clinician will also determine the sub-type.
There is a short version (10 items) of the CMRS called the Brief CMRS/Brief CMRS-P. [ 2 ] The shorter version was created because a shorter version is preferred to longer assessments if the shorter gives similar accuracy, which it does. [ 2 ] Additionally, there is a teacher's version of the CMRS called the CMRS-Teacher (CMRS-T).
Construct validity analyses (Exploratory Factor Analysis and Confirmatory Factor Analysis) for the CMRS-P indicated that the scale is unidimensional. Internal consistency measured by Cronbach's alpha was .96 in a sample consisting of ADHD, Bipolar, and healthy control participants. [ 1 ] In a sample of participants with bipolar disorder, the cronbach's alpha was 91. [ 1 ] Additionally, it has the ability to accurately differentiate pediatric bipolar disorder from ADHD and healthy controls greater than 90% of the time.
The teacher version (CMRS-T) also has 21 items. The internal consistency, measured by Cronbach's alpha, was .86. [ 3 ] Correlations between the parent and teacher versions of the CMRS range from .23 [ 11 ] to .27. [ 12 ] The CMRS teacher version has not been shown to discriminate bipolar from nonbipolar cases at better than chance levels and is not recommended for use in clinical practice for diagnosing bipolar disorder in children. [ 11 ]
The CMRS was developed as a shorter, reliable, and valid parent-report screening instrument for mania. [ 1 ] [ 15 ] The short form was derived from the CMRS 21 item scale which is the first original mania rating scale developed for children and adolescents. It was not developed from the Young Mania Rating Scale (YMRS) that was originally designed for adults, 'Young' being the name of the author than the fact that it was a scale for 'young' population. The YMRS was derived from the Parent-Young Mania Rating Scale (P-YMRS). [ 16 ] This scale, developed from the YMRS , was created for use with adult inpatients. The items of the P-YMRS did not include the updated DSM-IV criteria for adolescent Bipolar Disorder, and it includes several items with poor factor loadings. [ 16 ] Furthermore, the content is not developmentally appropriate for children, as many of the items require insight or appearance, which are irrelevant to young children. [ 16 ] Another promising measure is the GBI as it has good psychometric properties. However, the GBI is lengthy and complicated and requires the child to have at least a 7th-grade reading ability. [ 16 ] One of the most widely used measures of mania symptoms is the Kiddie Schedule for Affective Disorders and Schizophrenia mania section. [ 17 ] However, this measure is extremely extensive and requires much clinical training to administer.
During the development of the CMRS, researchers found that reliable and more accurate diagnostic accuracy is found in parent reports in comparison to teacher reports or self-reports and that these other reports rarely added new information to the parent report. [ 18 ] Furthermore, the areas under the curve (AUC) of parent-rated instruments reported modest to excellent validity. [ 18 ] Based on the evidence, the developers of the CMRS chose to create a measure that relied mainly on parent report.
Other parent report measures have been used to screen for Pediatric Bipolar Disorder, but these measures were not developed to look specifically for mania. One such measure is the Child Behavior Checklist (CBCL). The CBCL, in addition to providing markers of psychopathology, has been used to detect mania in children. [ 19 ] [ 20 ] [ 21 ] However, on the CBCL, researchers saw a consistent pattern of elevated scores, especially on the following symptoms: aggressive behavior, attention problems, delinquency, anxiety, and depression. [ 22 ] [ 23 ] [ 24 ] This pattern may be due to the high comorbidity of ADHD, oppositional defiant disorder, conduct disorder, and anxiety disorders in children with pediatric Bipolar Disorder. And although the CBCL is a reliable and validated measure, low scores on the CBCL may only rule out mania—conversely, it would be erroneous to rule in mania using CBCL scores alone. [ 24 ]
For these reasons, the CMRS was developed to accurately and reliably assess mania in pediatric Bipolar Disorder, and differentiate its symptoms from other disorders with high comorbidity with pediatric Bipolar Disorder.
Though there is no gold-standard screening tool for Pediatric Bipolar Disorder, the CMRS has been described as a promising and useful tool for such a purpose. [ 25 ] For example, institutional protocols for diagnosing and evaluating Bipolar Disorder in children may use the CMRS as an initial screening tool to establish the need to further evaluation of mania symptoms. [ 26 ] In addition, the parent version of the CMRS (the CMRS-P) has been used in research studies to detect changes in children's mania symptoms due to pharmacotherapy or psychotherapy . [ 3 ] [ 27 ] The CMRS is the first measure specifically developed for the purpose of screening for Bipolar Disorder in children. [ 28 ] As such, it offers an alternative to broadband rating scales like the Child Behavior Checklist , which has been used as a screening tool for Bipolar Disorder in children with mixed findings regarding its reliability . [ 28 ] [ 29 ]
Furthermore, the CMRS-P (both the brief and full versions) have shown to be effective in distinguishing between mania and ADHD. The brief version effectively retains characteristics of the original CMRS, allowing for wider application and longitudinal use. [ 2 ] Psychometric studies of the CMRS has demonstrated that the measure has excellent reliability and validity. Internal consistency is excellent and the measure correlates with clinician-administered interview measures for diagnosing pediatric mania. The measure is also accurately able to differentiate symptoms of pediatric Bipolar Disorder from ADHD and healthy control groups more than 90% of the time. [ 1 ] Furthermore, the use of the CMRS in pharmacological research suggests that this measure is sensitive to treatment over time, which means that you can use this measure to assess treatment effectiveness. [ 3 ]
The CMRS suffers from the same problems as other self-report inventories , in that scores can be easily exaggerated or minimized by the person completing them - in this case, the parent or teacher—in a phenomenon called the social desirability bias . Like all questionnaires, the way the instrument is administered can also influence the final score. If a person is asked to fill out the form in front of other people in a clinical environment, for instance, social expectations have been shown to elicit a different response compared to administration via a postal survey. [ 30 ] The age of the youth also may matter. Although the Child Mania Rating Scale has been shown to be a valid and reliable measure of mania in children, one concern is that its validity might change as the youth becomes an adolescent, and parents or teachers have less influence and awareness about the youth's behavior outside of the home or school. [ 31 ] Additionally, it is also unclear of the CMRS's ability to assess the change in mania systems as a child cycles out of mania and into depression. [ 2 ]
While the CMRS has not been validated in other languages, the CBCL, YMRS, GBI, and KSADS all have. However, the CMRS has been tested and translated into Spanish. [ 32 ] The CMRS is available in fourteen languages with back translation through native/bilingual speakers, though not tested in all languages.
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Child development stages are the theoretical milestones of child development , some of which are asserted in nativist theories. This article discusses the most widely accepted developmental stages in children. There exists a wide variation in terms of what is considered "normal", caused by variations in genetic, cognitive, physical, family, cultural, nutritional, educational, and environmental factors. Many children reach some or most of these milestones at different times from the norm. [ 1 ]
Holistic development sees the child in the round, as a whole person – physically, emotionally, intellectually, socially, morally, culturally and spiritually. Learning about child development involves studying patterns of growth and development, from which guidelines for 'normal' development are construed. Developmental norms are sometimes called milestones – they define the recognized development pattern that children are expected to follow. Each child develops in a unique way; however, using norms helps in understanding these general patterns of development while recognizing the wide variation between individuals.
One way to identify pervasive developmental disorders is if infants fail to meet the development milestones in time or at all. [ 2 ]
Physical development
Motor development
Communication skills
Emotional development
Cognitive skills
Physical development
Motor development
Communication skills
Social development
Emotional development
Cognitive skills
Sensory development
Physical development
Motor development
Communication skills
Social development
Emotional development
Cognitive skills
Physical development
Social development
Physical development
Motor development
Communication skills
Social development
Language development
Emotional development
Cognitive skills
Physical development
Motor development
Communication skills
Social development
Language development
Emotional development
Cognitive skills
Physical development
Motor development
Sensory development
Language development
Cognitive skills
Physical
Motor development
Physical
Motor development
Cognitive development
Language
Social [ 37 ]
Walking development [ 38 ]
Physical
Motor development
Cognitive
Language
Social and emotional
Physical
Motor development
Cognitive development
Physical development
Motor development
Cognitive
Language
Social development
Physical
Motor development
Cognitive
Language development
Social development
Physical
Motor development
Language
Social and emotional
Motor development
Writing grips
Language
Social and emotional
Motor development
Language skills
Social and emotional
Motor skills
Language skills
Social skills
Motor skills
Language skills
Social skills
Motor skills
Language skills
Social and emotional development
Girls are developing breasts, filled out pubic hair, underarm hair, and may begin menstruation .
Changes in boys less dramatic, but enlargement of the testicles and penis typically occurs along with the growth of fine pubic hair and frequent, random erections . Their voice may begin to change as well.
Capable of categorizing information to make better sense of it. Reads adult books and magazines on subjects of interest. Capable of proofreading homework for spelling, grammar, and logic.
Overall disposition is pleasant and upbeat. Can become extremely excited over subjects of interest or accomplishments. Strongly prone to peer pressure and following trends. More stable friendships with fewer melodramatics than at 11.
May begin to have sexual attraction to/interest in peers.
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Child psychopathology refers to the scientific study of mental disorders in children and adolescents. Oppositional defiant disorder , attention-deficit hyperactivity disorder , and autism spectrum disorder are examples of psychopathology that are typically first diagnosed during childhood. [ 1 ] Mental health providers who work with children and adolescents are informed by research in developmental psychology , clinical child psychology, and family systems. Lists of child and adult mental disorders can be found in the International Statistical Classification of Diseases and Related Health Problems, 10th Edition (ICD-10), published by the World Health Organization (WHO) and in the Diagnostic and Statistical Manual of Mental Disorders , Fifth Edition (DSM-5), published by the American Psychiatric Association (APA). In addition, the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC: 0-3R) is used in assessing mental health and developmental disorders in children up to age five. [ 2 ]
The etiology of child psychopathology has many explanations which differ from case to case. Many psychopathological disorders in children involve genetic and physiological mechanisms, though there are still many without any physical grounds. It is absolutely imperative that multiple sources of data be gathered. Diagnosing the psychopathology of children is daunting. It is influenced by development and contest, in addition to the traditional sources. Interviews with parents about school, etc., are inadequate. Either reports from teachers or direct observation by the professional are critical. (author, Robert B. Bloom, Ph.D.) The disorders with physical or biological mechanisms are easier to diagnose in children and are often diagnosed earlier in childhood. As psychopathy exists on a spectrum, the initial indications of the disorder can differ greatly. Certain children may exhibit subtle indications as early as two or three years old, while in other children, symptoms may not come apparent unit later in life. It's also possible for signs to manifest before the age of two in some cases. [ 3 ] However, there are some disorders, no matter the mechanisms, that are not identified until adulthood. There is also reason to believe that there is co-morbidity of disorders, in that if one disorder is present, there is often another. [ 4 ]
Emotional stress or trauma in the parent-child relationship tends to be a cause of child psychopathology. First seen in infants, separation anxiety in root of parental-child stress may lay the foundations for future disorders in children. There is a direct correlation between maternal stress and child stress that is factored in both throughout adolescent development. [ 5 ] In a situation where the mother is absent, any primary caregiver to the child could be seen as the "maternal" relationship. Essentially, the child would bond with the primary caregiver, and may exude some personality traits of the caregiver. [ 6 ]
In studies of child in two age groups of pregnancy to five years, and fifteen years and twenty years, Raposa and colleagues (2011) studied the impact of psychopathology in the child-maternal relationship and how not only the mothers stress affected the child, but the child's stress affected the mother. Historically, it was believed that mothers who had post partum depression might be the reason their child has mental disorders both earlier and later in development. However this correlation was found to not only reflect maternal depression on child psychopathology, but also child psychopathology could reflect on maternal depression. [ 7 ]
Children with a predisposition to psychopathology may cause higher stress in the relationship with their mother, and mothers who have psychopathology may also cause higher stress in the relationship with their child. Child psychopathology creates stress in parenting which may increase the severity of the psychopathology within the child. [ 8 ] Together, these factors push and pull the relationship thus causing higher levels of depression, ADHD, defiant disorder, learning disabilities, and pervasive developmental disorder in both the mother and the child. The outline and summary of this study is found below:
""In looking at child-related stress, the number of past child mental health diagnoses significantly predicted a higher number of acute stressors for mothers as well as more chronic stress in the mother-child relationship at age 15. These increased levels of maternal stress and mother-child relationship stress at age 15 then predicted higher levels of maternal depression when the youth were 20 years old. [ 7 ]
Looking more closely at the data, the authors found that it was the chronic stress in the mother-child relationship and the child-related acute stressors that were the linchpins between child psychopathology and maternal depression. The stress is what fueled the fires between mother and child mental health. Going one step further, the researchers found that youth with a history of more than one diagnosis as well as youth that had externalizing disorders (e.g., conduct disorder) had the highest number of child-related stressors and the highest levels of mother-child stress. Again, all of the findings held up when other potentially stressful variables, such as economic worries and past maternal depression, were controlled for. [ 8 ]
Additionally, siblings- both older and younger and of both genders, can be factored into the etiology and development of child psychopathology. In a longitudinal study of maternal depression and older male child depression and antisocial behaviors on younger siblings adolescent mental health outcome. The study factored in ineffective parenting and sibling conflicts such as sibling rivalry . Younger female siblings were more directly affected by maternal depression and older brother depression and anti social behaviors when the indirect effects were not place, in comparison to younger male siblings who showed no such comparison. However, if an older brother were anti-social, the younger child- female or male would exude higher anti-social behaviors. In the presence of a sibling conflict, anti social behavior was more influential on younger male children than younger female children. Female children were more sensitive to pathological familial environments, thus showing that in a high- stress environment with both maternal depression and older- male sibling depression and anti social behavior, there is a higher risk of female children developing psychopathological disorders. [ 9 ] This was a small study, and more research needs to be done especially with older female children, paternal relationships, maternal-paternal-child stress relationships, and/or caregiver-child stress relationships if the child is orphaned or not being raised by the biological parent to reach a conclusive child-parent stress model on the effects of familial and environmental pathology on the child's development. [ citation needed ]
The child-parent stress and development is only one hypothesis for the etiology of child psychopathology. Other experts believe that child temperament is a large factor in the development of child psychopathology. High susceptibility to child psychopathology is marked by low levels of effortful control and high levels of emotionality and neuroticism . Parental divorce is often a large factor in childhood depression and other psychopathological disorders. [ 10 ] This is more so when the divorce involves a long-drawn separation and one parent bad-mouthing the other. [ 11 ] That is not to say that divorce will lead to psychopathological disorders, there are also other factors such as temperament, trauma, and other negative life events (e.g. death, sudden moving of home, physical or sexual abuse), genetics, environment, and nurture that correlate to the onset of a disorder. Research has also shown that child maltreatment may increase risk for various forms of psychopathology as it increases threat sensitivity, decreases responsivity to reward, and causes deficits in emotion recognition and understanding. [ 12 ] Psychopaths states that up to 30% of the population exhibits varying levels of diminished empathy, a tendency towards taking risks, and an excessive sense of self importance. [ 13 ]
Found in "The Role of Temperament in the Etiology of Child Psychopathology", a model for the etiology of child psychopathology by Vasey and Dadds (2001) proposed that the four things that are important to the development of psychopathological disorders is: 1) biological factors: hormones, genetics, neurotransmitters 2) psychological: self-esteem, coping skills, cognitive issues 3) social factors: family rearing, negative learning experiences, and stress 4) child's temperament. Using an array of neurological scans and exams, psychological evaluations , family medical history, and observing the child in daily factors can help the physician find the etiology of the psychopathological disorder to help release the child of the symptoms through therapy, medication use, social skills training, and life style changes. [ 10 ]
Child psychopathology can cause separation anxiety from parents, [ 14 ] attention deficit disorders in children, [ 15 ] sleep disorders in children, [ 16 ] aggression with both peers and adults, [ 17 ] night terrors, [ 18 ] extreme anxiety, [ 19 ] anti social behavior, [ 20 ] depression symptoms, [ 21 ] aloof attitude, [ 22 ] sensitive emotions, [ 23 ] and rebellious behavior [ 24 ] that are not in line of typical childhood development. Aggression is found to manifest in children before five years of age, and early stress and aggression in the parental-child relationship correlates with the manifestation of aggression. [ 25 ] [ 26 ] Aggression in children causes problematic peer relationships, difficulty adjusting, and coping problems. [ 27 ] Children who fail to overcome acceptable ways of coping and emotion expression are put on tract for psychopathological disorders and violent and anti social behaviors into adolescence and adulthood. [ 28 ] There is a higher rate of substance abuse in these children with coping and aggression issues, and causes a cycle of emotional instability and manifestation psychopathological disorders. [ 29 ] [ 30 ]
Borderline personality disorder (BPD) is one of many psychopathology disorders a child can develop. In the neurobiological scheme, borderline personality disorder may have effects on the left amygdala . In a 2003 study of BPD patients versus control patients, when faced with expressions that were happy, sad, or fearful BPD patients showed significantly more activation versus control patients. In neutral faces, BPD patients attributed negative qualities to these faces. [ 31 ] As stated by Gabbard, an experimenter in this study:
"A hyperactive amygdala may be involved in the predisposition to be hyper vigilant and over reactive to relatively benign emotional expressions. Misreading neutral faces is clearly related to transference misreadings that occur in psychotherapy and the creation of bad object experiences linked with projective identification." [ 31 ]
Also linked to BPD, is the presence of serotonin transporter (5-HTT) in a short allele demonstrated larger amygdala neuronal activity when presented with fearful stimuli as in comparison to individuals with a long allele of 5-HTT. As found in the Dunedin Longitudinal Study a short allele of 5-HTT predisposes the person to have hyperactivity in the amygdala in response to trauma, and thus moderated the impact of stressful life events leading to a higher risk of depression and suicidal idealities. These same qualities were not observed in individuals with long alleles of 5-HTT. However, the environment the child is in can change in impact of this gene, proving that correct treatment, intensive social support, and a healthy and nurturing environment can modify genetic vulnerability. [ 31 ]
Possibly the most studied or documented of the child psychopathologies is attention deficit hyperactivity disorder (ADHD) which is marked with learning disabilities, mood disorders, or aggression. [ 32 ] Though believed to be over diagnosed, ADHD is highly comorbid for other disorders such as depression and obsessive compulsive disorder . [ 32 ] In studies of the prefrontal cortex in ADHD children, which is responsible for the regulation of behavior, cognition, and attention; and in the dopamine system there has been identified a hidden genetic polymorphisms. [ 33 ] More specifically, the 7-repeat allele of the dopamine D4 receptor gene, responsible for inhibited prefrontal cortex cognition and less efficient receptors, causes more externalized behaviors such as aggression since the child has trouble "thinking through" seemingly ordinary and at level childhood tasks. [ 34 ]
Agenesis of the corpus callosum (ACC) is used to determine the frequency of social and behavioral problems in children with a prevalence rate of about 2-3%. ACC is described as a defect in the brain where the 200 million axons that make the corpus callosum are either completely absent, or partially gone. In many cases, the anterior commissure is still present to allow for the passing of information from one cerebral hemisphere to the other. The children are of normal intelligence level. For younger children, ages two to five, Agenesis of the corpus callosum causes problems in sleep. Sleep is critical for development in children, and lack of sleep can set the grounds for a manifestation of psychopathological disorders. [ 35 ] In children ages six to eleven, ACC showed manifestation in problems with social function, thought, attention, and somatic grievances. In comparison, of children with autism, children with ACC showed less impairment on almost all scales such as anxiety and depression, attention, abnormal thoughts, and social function versus autistic children. However, a small percentage of children with ACC showed traits that may lead to the diagnosis of autism in the areas of social communications and social interactions but do not show the same symptoms of autism in the repetitive and restricted behaviors category. [ 36 ] The difficulties from ACC may lead to the etiology of child psychopathological disorders, such as depression or ADHD and manifest many autistic-like disorders that can cause future psychological disorders in later adolescence.
The etiology of child psychopathology is a multi-factor path. A slew of factors must be taken into account before diagnosis of a disorder. [ 37 ]
The child's genetics, environment, temperament, past medical history, family medical history, prevalence of symptoms and neuro-anatomical structures are all factors that should be considered when diagnosing a child with a psychopathological disorder. [ 36 ] Thousands of children each year are misdiagnosed [ 38 ] [ 39 ] and put on the wrong treatment, which may result in the manifestation of other disorders the child would have not have gotten else wise. There are hundreds of causes of psychopathological disorders, and each one manifests at different ages and stages in child development and can come out due to trauma and stress. Some disorders may "disappear" and reappear in the presence of a trauma, depression, or stress similar to the one that brought the disorder out in the child in the beginning. [ citation needed ]
In the United States , It is estimated that 1 in 6 children from ages two to eight have a psychopathology disorder. Boys of this age are more likely to be diagnosed with a disorder than girls. [ 40 ] From age 9-17, at least 1 in 5 children have a diagnosed disorder, but only about a third of these children receive treatment for their disorder. [ 41 ] Anxiety and depression disorders in children- whether noted or unnoted, are found to be a precursor for similar episodes in adulthood. [ 42 ] Usually a large stressor similar to the one the person experienced in childhood brings out the anxiety or depression in adulthood. [ citation needed ]
Multifinality refers to the idea that two children can react to same stressful event quite differently, and may display divergent types of problem behavior. Psychopathological disorders are extremely situational- having to take into account the child, the genetics, the environment, the stressor, and many other factors to tailor the best type of treatment to relieve the child of the psychopathology symptoms. [ 43 ]
Many child psychopathology disorders are treated with control medications prescribed by a pediatrician or psychiatrist. After extensive evaluation of the child through school visits, by psychologists and physicians, a medication can be prescribed. [ 44 ] A patient may need to go through several trials of medicines to find the best fit, as many cause uncomfortable and undesired side effects- such as dry mouth or suicidal thoughts can occur. [ 45 ] There are many classes of drugs a physician can choose from and they are: psychostimulants , beta blockers , atypical antipsychotics , lithium , alpha-2 agonists , traditional antipsychotics , SSRIs , and anticonvulsant mood- stabilizers. [ 44 ] Given the multifinality of psychopathological disorders, two children may be on the same medication for two completely different disorders, or have the same disorder and be taking two completely different medications.
ADHD is the most commonly diagnosed disorder of child psychopathology; [ 46 ] however, the medications used to treat it have a high abuse rate, especially among college-aged student. [ 47 ] Psycho stimulants such as Ritalin , amphetamine- related stimulant drugs: e.g., Adderall , and antidepressants such as Wellbutrin have been successfully used to treat ADHD. [ 48 ] Many of these drug treatment options are paired with behavioral treatment such as therapy or social skills lessons. [ 46 ] Counter-intuitively, patients whose ADHD is given therapeutic treatment with psychostimulants actually have significantly lower rates of drug abuse and addiction than their untreated peers; psychostimulants are widely abused drugs, but in those treated for ADHD, psychostimulant treatment actually reduces the patient's risk of acquiring an addiction. [ 49 ]
Lithium has shown to be extremely effective in treating bipolar disorder, as it is affective for both mania and depression, and with chronic treatment it helps to prevent relapse. Additionally, lithium treatment produces notable reductions in suicide in all exposed populations, including general populations whose drinking water has naturally high levels of lithium salts. Lithium is the only known intervention that is generically effective in reducing suicidal ideation and behavior, and is additionally the only agent known to affect suicide directly and specifically; this treatment effect is independent from the resolution of any other possible underlying cause, and so it is still observed even in, e.g., patients who continue to experience severe depression that is resistant to treatment. This effect on suicide is especially remarkable in BPD patients, who are especially high risk; in BPD patients that successfully comply with lithium treatment, suicide rates begin to more closely resemble the non-BPD population, and do so for as long as these BPD patients continue to take use lithium as directed. Additionally, lithium is effective in reducing aggressive and/or antisocial behavior; as in suicide, this effect is generic and occurs in all exposed populations, but the effect is larger in patients with predisposing illness, such as ADHD. Consequently, lithium appears to be highly effective in treating antisocial behaviors in BPD patients that also have ADHD (which is highly co-morbid with BPD, and thus frequently co-occurs in BPD patients). However, there is some uncertainty as to whether this observed treatment effect may be an indirect result of inadequate initial treatment of ADHD in those with BPD. Psychostimulant medications, such as methylphenidate and mixed amphetamine salts , are the only known gold standard treatment for ADHD, being both safe and highly effective for most patients with ADHD; however, unfortunately, psychostimulant use (or abuse) is a known risk factor for the occurrence of (hypo)manic episodes in BPD patients. (Indeed, even in those without BPD, these medications can produce states resembling mania, even in those who do not experience them otherwise, though such occurrences are extremely rare at the therapeutic dosages used to treat ADHD.) As a result, clinicians are reluctant to prescribe these medications for patients with BPD, and where do choose to prescribe them, they may be reluctant to titrate the patient's dosage upward as they normally would, as a precaution against any possible risk of inducing (hypo)mania. Thus, ADHD-associated antisocial behaviors that persist despite the patient receiving ADHD treatment, which are resolved by subsequent treatment with lithium, may simply indicate inadequate control of ADHD symptoms, and not that lithium is a uniquely effective frontline treatment for "treatment-resistant" antisocial behavior in BPD patients with co-morbid ADHD. In any case, there is no evidence that lithium is effective as a primary treatment for ADHD; its only observed utility is a reduction in aggressive/antisocial behavior, which is observed generically in anyone taking lithium, and is not specific to ADHD, and those symptoms may be better controlled by simply ensuring that gold standard treatments for ADHD are being titrated adequately. [ 50 ] The mechanism of lithium include the inhibition of GSK-3, it is a glutamate antagonism at NMDA receptors that together make lithium a neuroprotective medicine. The drug relieves bipolar symptoms, aggressiveness and irritability. Lithium has many, many side effects and requires weekly blood tests to tests for toxicity of the drug. [ citation needed ] [ 51 ]
Medications that act on cell membrane ion channels, enhance GABA inhibitory neurotransmission, and inhibit excitatory glutamate transmission have shown to be extremely effective in treating an array of child psychopathological disorders. [ citation needed ] [ 52 ] Pharmaceutical companies are in the process of creating new drugs and improving those on the market to help avoid negative and possibly life altering short term and long term side effects, making drugs more safe to use in younger children and over long periods of time during adolescent development. [ citation needed ]
A 2025 systematic review by AHRQ and PCORI emphasized the effectiveness of psychosocial interventions, especially those involving parental participation, in reducing disruptive behaviors in children and adolescents. These approaches outperformed usual care in preschool and school-aged children. While medications such as stimulants and antipsychotics offered modest improvements in select cases, they carried a higher risk of side effects, and long-term comparative effectiveness remains unclear. [ 53 ]
Some psychological disorders commonly found in children include depression , anxiety , and conduct disorder . [ 54 ] [ 55 ] For adolescents with depression, a combination of antidepressants and cognitive-behavioral or interpersonal psychotherapy is recommended, in contrast there is not much evidence for the efficacy of antidepressants in children under 12 years of age, therefore a combination of parent training and cognitive-behavioral psychotherapy is recommended. [ 56 ] [ 57 ] For children and adolescents with anxiety disorders, cognitive-behavioral therapy in combination with exposure-based techniques is a highly recommended and evidence-based treatment. [ 58 ] [ 59 ] Research suggests that children and adolescents with conduct disorder or disruptive behavior may benefit from psychotherapy that includes both a behavioral component and parental involvement. [ 60 ] [ 61 ]
The future of child psychopathology- etiology and treatment has a two-way path. While many professionals agree that many children who have a disorder do not receive proper treatment, at the rate of 5-15% that receive treatment leaving many children in the dark. In the same boat are the physicians who also say that not only do more of these disorders need to be recognized in children and treated properly, but also even those children who show some qualifying symptoms of a disorder but not to the degree of diagnosis should also receive treatment and therapy to avoid the manifestation of the disorder. By treating children even with slight degrees of a psychopathological disorder, children can show improvements in their relationships with peers, family, and teachers and also improvements in school, mental health, and personal development. [ 62 ] Many physicians believe the best prevention and help starts in the home and the school of the child, before physicians and psychologists are contacted.
The current trend in the U.S. is to understand child psychopathology from a systems based perspective called developmental psychopathology . Recent emphasis has also been on understanding psychological disorders from a relational perspective with attention also given to neurobiology . Practitioners who follow attachment theory believe that early attachment experiences of children can promote adaptive strategies or lay the groundwork for maladaptive ways of coping which can later lead to mental health disorders. [ 63 ] [ 64 ]
Research and clinical work on child psychopathology tends to fall under several main areas: etiology , epidemiology , diagnosis, assessment , and treatment.
Parents are considered a reliable source of information because they spend more time with children than any other adult. A child's psychopathology can be connected to parental behaviors. Clinicians and researchers have experienced problems with children's self-reports and rely on adults to provide the information. [ 65 ]
Detecting signs of psychopathology in children during their formative years is crucial for timely intervention. Early intervention programs focus on mitigating risk factors and strengthening protective factors to prevent the onset or progression of mental health disorders. These preventative measures can range from cognitive-behavioral therapy to social skills training for the children. Recognizing and addressing symptoms early can significantly improve long-term outcomes, potentially reducing the severity or even preventing certain disorders from developing fully. [ 66 ]
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https://en.wikipedia.org/wiki/Child_psychopathology
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The Children's Cardiomyopathy Foundation ( CCF ) is a national 501(c)(3) nonprofit organization focused on the pediatric forms of cardiomyopathy , a rare and chronic heart condition. [ 1 ] Founded in New Jersey , CCF has grown into a global community of families, physicians, and scientists focused on accelerating the search for causes and cures for pediatric cardiomyopathy through increased research, education, awareness, and advocacy. The organization also provides support and resources to affected children and their families. [ 2 ]
CCF was founded in 2002 by Eddie Yu and Lisa Yue, who lost two children to cardiomyopathy. At the time, cardiomyopathy was a poorly understood disease in young children, and it had low public awareness. [ 3 ] Due to the lack of research being conducted on pediatric cardiomyopathy, the Foundation established a research grant program and formed research partnerships with the American Heart Association , American Academy of Pediatrics , and National Heart, Lung, and Blood Institute -funded Pediatric Cardiomyopathy Registry. [ 1 ] The Foundation also organizes international scientific conferences to encourage collaboration among researchers across medical centers. [ 4 ]
CCF's investment into research and education has led to more than 420 medical presentations and peer-reviewed publications on pediatric cardiomyopathy and a four-fold increase in the number and dollar amount of pediatric cardiomyopathy studies funded by the National Institutes of Health . [ 3 ]
In a 2017 paper published in the Journal of the American College of Cardiology , “Survival Without Cardiac Transplantation Among Children with Dilated Cardiomyopathy,” it was shown that there was a 50% reduction in diagnosed children dying and needing a heart transplant because of better care guidelines and collaborative research efforts made possible by CCF's support of the Pediatric Cardiomyopathy Registry. [ 5 ]
Through CCF's advocacy work, the Cardiomyopathy Health Education Awareness Risk Assessment and Training in the Schools Act was the first bill on cardiomyopathy to be introduced in the United States House of Representatives and United States Senate . [ 6 ] [ 7 ] In 2020, it was reintroduced as a bipartisan bill in the House of Representatives.
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https://en.wikipedia.org/wiki/Children's_Cardiomyopathy_Foundation
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Children with Special Healthcare Needs (CSHCN) are defined by the Maternal and Child Health Bureau as:
There are a wide variety of physical, mental, and psychological health conditions considered to be special healthcare needs in the United States. They range from relatively mild to chronic and severe. The functional impairments of CSHCN include problems with one or more of the following criteria: breathing, swallowing/digestion/metabolism, blood circulation, chronic pain, hearing even with corrective devices, seeing even with corrective devices, taking care of self, coordination/moving around, learning/understanding/paying attention, speaking/communicating, making/keeping friends, and behavior. [ 2 ] The list below states health conditions considered to be special healthcare needs.
As of 2009, 15.1% of all children in the US are considered to have special healthcare needs, [ 2 ] [ 3 ]
The prevalence of children with special healthcare needs in the population depends on several factors, including gender, age, socioeconomic level and family household education. [ 4 ] In the National Survey of Children's Health Data in 2007, gender is the strongest predictor of special health care needs—about 60% of children with special health care needs are boys and 30% are girls. [ 2 ] A study by Newacheck et al. found that age is also a strong predictor, as school-age children are found to be twice as likely as toddlers to require special needs care, and this prevalence continues to increase as children grow older. [ 4 ] Families with income below the federal poverty level are 1/3 more likely to have children with special health care needs, and families with 12 or fewer years of education have increased prevalence of a child with SHCN as well. [ 4 ] Family structure also correlates with this prevalence—for single-mother families are 40% more likely to have a CSHCN than two-parent households. [ 4 ]
In a comprehensive study by the U.S. Health Resources and Services Administration (HRSA), using the 2007 National Survey of Children's Health data, it was found that children with SHCN when compared to those children without SHCN, face more inadequacies in healthcare, education, health of family, and maintaining a healthy lifestyle. [ 3 ] CSHCN face more difficulties with accessing mental health care [ 3 ] as well as having a medical home . A medical home is one of the standards of administering healthcare recommended by the Maternal and Child Health Bureau. [ 5 ] In school, these children have an increased risk of missing class, being disengaged in the classroom, and repeating a grade. [ 3 ] They also have more cases of inadequate sleep every night in comparison to their peers. [ 3 ] CSHCN are more likely to not exercise the recommended four times a week, and they have higher chance of being overweight/obese. [ 3 ] They also face increased challenges in making friends. [ 3 ] The parents of CSHCN have challenges as well. The study by HRSA, found that the parents of special needs children experience more stress, decreased health, and more questioning of their parenting skills. [ 3 ]
Despite these challenges, children with SHCN fare better than non-affected children in preventative health care and preventative dental care. [ 3 ] They have a higher rate of having health insurance than normal children. [ 2 ] They more frequently complete the recommended annual primary care visit, and bi-annual dentist visit. [ 2 ] They also have a tendency to use more Developmental Screening, especially those with public healthcare. [ 3 ] Developmental screening is used by doctors to check and evaluate for proper child development over time on a physical and cognitive level. The American Academy of Pediatrics recommends visits for developmental screening at ages 9,18 and at 24–30 months. [ 6 ]
Emotional and behavioral disorders (EBD) are disorders that include ADD/ADHD, anxiety, ASD, depression, OCD/conduct disorder, developmental delay and Tourette's Syndrome, and they increase the challenges CSHCN face. [ 3 ] 40% of CSHCN have an EBD and 80% of these children also experience another health problem along with their EBD, according to the 2007 National Survey of Children's Health. [ 2 ] The Health Resources and Services Administration found that these disorders are associated with an even greater decrease in quality of family-life, education and healthcare. [ 3 ] Parent's health worsens and stress increases when they have children with an EBD. [ 3 ] These EBD children miss more classes and are more disengaged in class than non-EBD CSHCN. [ 3 ] EBD-CSHCN experience reduced family center-care and effective care-coordination. [ 3 ] They also face greater difficulty in their ability to make friends than non-EBD CSHCN. [ 3 ]
A systematic review of randomized controlled trials found evidence that
The United States governments employs several different programs in order to provide insurance and care for CSHCN. These include Title V grants, Medicaid and Children's Health Insurance Program (CHIP). These three programs vary in their definition and eligibility of care for CSHCN. [ 1 ]
Medicaid is the program implemented under Title XIX of the Social Security Act. [ 8 ] It is a public insurance program that provides mandatory services for patients such as:
Medicaid requires no co-payment or deductibles. To be eligible for the program one must be in one of four categories. The first is income level, the second is disability criteria, the third is eligibility for institutional level of care, and the fourth is out of home placement. Many CSHCN qualify for Medicaid based on low income level, but some children qualify independently of income level due to their disabilities. Medicaid has a more restrictive definition of disabilities and special healthcare needs than the Maternal and Children's Health Bureau (MCHB), and defines special needs as needs that must impede daily functioning. Medicaid accepts children who need to receive Supplemental Security Income program money, and children who are defined as medically needy. [ 8 ] [ 9 ] Medically needy children are those whose families have above the maximum income to receive Medicaid, but due to health expenditures their income is lowered to the level required. 40 states currently offer this program. [ 10 ] Medicaid programs in each state are administered differently, and federal dollars go to each state based on per capita income levels. As of 2010, the Medicaid program had 405 billion dollars for the entire program. With the new Patient Protection and Affordable Care Act , by 2014 state Medicaid levels will rise to 138% of the Federal Poverty Line, increasing the number of CSHCN receiving Medicaid. [ 8 ] [ 9 ]
This program, the Children's Health Insurance Program (CHIP), was created with Title XXI of the Social Security Act, [ 11 ] and is meant to cover the gap between children who qualify for Medicaid and those who can afford private insurance. [ 9 ] It covers children up to nineteen years of age and many states also choose to help insure pregnant women. 46 of the states and the District of Columbia insure up to 200% of the Federal Poverty Line. CHIP receives its funding from the federal government but it is capped, unlike Medicaid. CSHCN who use CHIP receive all of the same federally mandated programs that Medicaid must offer. The program also requires that mental health services be offered as equally as physical health services. [ 9 ] [ 11 ]
This Social Security Act, Title V, states that $850,000,000 in grant money is to be allotted starting in 2001 and every year after to the states in order to accomplish health goals of the Public Health Service Act as well as the goals of Title V. The Title V grant money is set out to specifically affect CSHCN in several ways. First, it requires states to provide rehabilitation services for blind or disabled individuals under the age of 16. It also allocates money to projects of both national and state importance that help maternal and child health as well as children with special healthcare needs. The act requires that there are community-based programs such as daycare that help provide for CSHCN. Another requirement is the creation of family-to-family health information centers that assist families with CSHCN to make informed decisions regarding healthcare and resources. [ 12 ]
This program works with the Maternal and Child Health Bureau , and employs their definition of CSHCN as stated earlier. Title V does not provide as much money as CHIP or Medicaid, but is used to fill the gaps where these programs do not cover. The Title V money is used to help with the Early Periodic Screening Diagnosis and Treatment Program (EPSDT) that is employed by Medicaid to test children. Title V shares the data collection responsibility of these three programs as well as develops educational materials. The Title V programs also have the goal to promote community-based services for all children as well as to promote coordinated care for families. [ 9 ] [ 12 ]
Children with special healthcare needs require more healthcare for their various health conditions as well as more types of therapies and treatments. [ 2 ] Therapies include occupational therapy , physical therapy , and speech-language pathology among others.
The American Academy of Pediatrics (AAP) medical home model is the suggested form of healthcare administration for children with special health care needs due to their increased healthcare needs. [ 5 ] In a study by Judith Palfrey et al. it was found to indicate improved health and increase patient satisfaction. [ 13 ] This model as defined by the AAP is a total coordination of care for infants, children and adolescents. It consists of a primary physician, preferably a pediatrician, that a child and their family know well and who is a medical advocate for the care of the child. All medical care in the medical home is accessible, continuous, comprehensive, family-centered, compassionate and coordinated. [ 5 ] This model requires several elements:
The pediatrician assumes the ultimate responsibility for all care that is provided for the child even though other medical professionals are involved. [ 5 ] Currently, 48.9% of CSHCN have access to a medical home while 59.6% of non-affected children have access to a medical home. [ 2 ]
Therapies for children with special healthcare needs can be accessed via public schools or private therapists. The Individuals with Disabilities Education Act (IDEA) includes occupational and physical therapy as well as other therapies, as part of the special education that should be offered in all public schools to CSHCN. This act states that all children with disabilities should have access to education that suits their SHCN, including needed therapies. [ 14 ] [ 15 ] Out of school therapies can also be used be employed by children with SHCN but only 3.2% of CSHCN qualify for uses of special therapy under their insurance programs. [ 2 ]
One type of therapy for children with SHCN is occupational therapy. Occupational therapists work with CSHCN by supporting them and their families to learn how to participate in everyday routines and daily activities. They encourage children with physical, cognitive, communication and behavior challenges to develop ways to live, play, learn and make friends despite their special needs. [ 16 ] Occupational therapists can work with these children and their schools to create more accommodating learning environments. Another skill these professionals teach to children with SHCN is how to use adaptive equipment such as wheelchairs, eating aids and braces in daily life. Some occupational therapists try to work with very young children at risk for SHCN in order to try and prevent future disability through occupational therapy. [ 17 ]
The types of insurance vary for children with special healthcare needs, 9.3% of CSHCN have no insurance at all, 52.4% have private insurance, 35.9% have public insurance and 8.2% have some combination of both public and private. [ 2 ] Insurance gaps and other health costs affect 21.6% of families with CSHCN, who state that they face financial problems due to their CSHCN. In total, 34.3% of these families believe that their current insurance is not adequate in providing for all of their additional healthcare costs. [ 2 ]
The Maternal and Child Health Bureau requires services to be available that are necessary for CSHCN to transition to all aspects of adult life. [ 18 ] 90% of Adolescents with SHCN (ASHCN) are expected to live into adulthood, and access to healthcare decreases as ASHCN grow older according to the Maternal and Child Health Bureau. [ 19 ] Youth lose health coverage they received in the past from programs like CHIP as well as Supplemental Security Income once they reach the ages of 18–21. Adult healthcare providers are not as familiar with childhood onset conditions as pediatricians. [ 19 ] A study by Jane Park et al. found that mental health conditions increase in prevalence as children get older and age into adulthood, and ASHCN who have mental health conditions (with or without physical conditions) fare worse on their transition to adult healthcare. [ 20 ] [ 21 ] The MCHB recommends that children should have their transition to adult healthcare be mediated and provided for by their doctors. The Bureau requires that doctors need to have discussed with the adolescents with SHCN and their families three points: how to transition to adult primary care doctors as opposed to pediatricians, how health needs will change as the youth become adults, and how to maintain health insurance as an adult. The doctor is also supposed to encourage youth to take responsibility for their own health needs. [ 19 ] Currently 60% of doctors of adolescents with SHCN do not meet these criteria. [ 2 ]
Another recommendation for healthcare providers by the Maternal and Child Health Bureau is the creation of a written Healthcare Transition (HCT) plan. [ 19 ] According to a study by Peter Scal and Marjorie Ireland, 30.08% of ASHCN had discussed such a plan. It was also found that adolescents who were older and who had more complicated needs were more likely to have an HCT. [ 22 ]
The Patient Protection and Affordable Care Act passed by the Obama administration in 2010 sets forth new requirements for ability of adolescents with SHCN to transition healthcare services from pediatric services. The Act also expands their ability to pay for and access these services. [ 23 ] It states three criteria that must be met for adolescents. First, adolescents need to have access to a comprehensive healthcare system that they can find a way to pay for, as well as be able to navigate the system. Second, preventable health problems need to be successfully prevented. Third, chronic conditions need to be managed and the transition to adult healthcare needs to be assured. Skills that ASHCN are recommended to possess to accomplish these goals include the ability to describe their own illness, know their own medication and dosages, know how to contact a clinician, and the ability to schedule appointments and call in for refills. [ 20 ] [ 21 ] [ 23 ]
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A chimney sweep is a person who inspects then clears soot and creosote from chimneys . The chimney uses the pressure difference caused by a hot column of gas to create a draught and draw air over the hot coals or wood enabling continued combustion. Chimneys may be straight or contain many changes of direction. During normal operation, a layer of creosote builds up on the inside of the chimney, restricting the flow. The creosote can also catch fire, setting the chimney (and potentially the entire building) alight . The chimney must be swept to remove the soot.
In Great Britain , master sweeps took apprentices, typically workhouse or orphan boys, and trained them to climb chimneys. In the German States , master sweeps belonged to trade guilds [ 1 ] and did not use climbing boys. In Italy , Belgium , and France , climbing boys were used.
The occupation requires some dexterity, and carries health risks. [ 2 ]
The Tudors in England had established the risk of chimneys and an ordinance was created in 1582 both controlling materials (brick and stone rather than plastered timber) and requiring chimneys to be swept four times per year to prevent the build-up of soot (which is highly flammable). Any chimney fire could result in the owner being fined 3 shillings and 4 pence. [ 3 ]
With the increased urban population that came with the age of industrialisation , the number of houses with chimneys grew apace and the services of the chimney sweep became much sought-after.
Buildings were higher than before and the new chimneys' tops were grouped together. [ 4 ] The routes of flues from individual grates could involve two or more right angles and horizontal angled and vertical sections. The flues were made narrow to create a better draught, 14in by 9in (36 × 23 cm) being a common standard. Buckingham Palace had one flue with 15 angles, with the flue narrowing to 9in by 9in (23 × 23 cm). [ 5 ] Chimney sweeping was one of the more difficult, hazardous, and low-paying occupations of the era, and consequently has been derided in verse, ballad, and pantomime.
The first mechanical sweeper was invented by George Smart in 1803 but was resisted in the UK and the US . Joseph Glass marketed an improved sweeping machine in 1828; he is credited with being the inventor of the modern chimney sweep's brush. [ 6 ] In the northern US, whites gave up the trade and employed black sweep-boys from the South. [ 7 ] After regulation finally took hold in 1875 in the UK and the turn of the century in the US, the occupation became romanticized in popular media.
Boys as young as four climbed hot flues that could be as narrow as 81 square inches (9 × 9 inches or 23 × 23 cm). Work was dangerous and they could get jammed in the flue, suffocate or burn to death. As soot is carcinogenic , and as the boys slept under the soot sacks and were rarely washed, they were prone to chimney sweeps' carcinoma . From 1775 onward, there was increasing concern for the welfare of the boys, and Acts of Parliament were passed to restrict, and in 1875 to stop this usage. [ 8 ] Lord Shaftesbury , the philanthropist, led the later campaign.
Chimneys started to appear in Britain around 1200 (with the oldest extant example of a chimney in Britain being in the keep of Conisbrough Castle in Yorkshire , dating from 1185 AD [ 9 ] ), when they replaced the open fire burning in the middle of the one room house. At first there would be one heated room in the building and chimneys would be large. Over the next four hundred years, rooms became specialized and smaller and many were heated. Sea coal started to replace wood, and it deposited a layer of flammable creosote in the inside surface of the flue, and caked it with soot. Whereas before, the chimney was a vent for the smoke, now the plume of hot gas was used to suck air into the fire, and this required narrower flues. [ 10 ] Even so, boys rarely climbed chimneys before the Great Fire of London , when building regulations were put in place and the design of chimneys was altered. The new chimneys were often angular and narrow, and the usual dimension of the flue in domestic properties was 9 inches (23 cm) by 14 inches (36 cm). The master sweep was unable to climb into such small spaces himself and employed climbing boys to go up the chimneys to dislodge the soot. The boys often 'buffed it', that is, climbed naked, [ 11 ] propelling themselves by their knees and elbows which were scraped raw. They were often put up hot chimneys, and sometimes up chimneys that were alight in order to extinguish the fire. Chimneys with sharp angles posed a particular hazard. [ 12 ] These boys were apprenticed to the sweep, and from 1778 until 1875 a series of laws attempted to regulate their working conditions, and many firsthand accounts were documented and published in parliamentary reports. From about 1803, there was an alternative method of brushing chimneys, but sweeps and their clients resisted the change, preferring climbing boys to the new humane sweeping machines. [ 13 ] Compulsory education was established in 1870 by the Elementary Education Act 1870 but it was a further five years before legislation was put in place to license chimney sweeps and finally prevent boys being sent up chimneys. [ 14 ]
The climbing boys, and sometimes girls, [ 15 ] [ 16 ] were technically called chimney sweeps' apprentices , and were apprenticed to a master sweep , who, being an adult, was too large to fit into a chimney or flue. He would be paid by the parish to teach orphans or paupers the craft. They were totally reliant on him: they or their guardians had signed papers of indenture , in front of a magistrate, which bound them to him until they were adults. It was the duty of the Poor Law guardians to apprentice as many children of the workhouse in their care as possible, so as to reduce costs to the parish. The master sweep had duties: to teach the craft and its mysteries, to provide the apprentice with a second suit of clothes, to have him cleaned once a week, allow him to attend church, and not send him up chimneys that were on fire. An apprentice agreed to obey his master. [ 17 ] Once his seven-year-long apprenticeship was completed he would become a journeyman sweep, and would continue to work for a master sweep of his choice. Other apprentices were sold on to the sweep, or sold by their parents. Prices ranged from 7 shillings [ 18 ] to 4 guineas .
It was generally agreed that six was a good age to train a boy. [ 19 ] Though Lord Shaftesbury once encountered one of the age of four, they were considered to be too weak. [ 19 ] A master sweep would have many apprentices, who would start the morning by roaming the streets calling out " Soot -Oh, Sweep " or another cry to let the house-owners know they were around; this would remind the owners of the dangers of un-swept chimneys. When engaged, the master sweep would fix a cloth over the fireplace , and the climbing boy would take off his boots and any excess clothes, then get behind it. The flue would be as tall as the house and twist several times, and its dimensions would be 14in by 9in. He would pull his cap down over his face and hold a large flat brush over his head, and wedge his body diagonally in the flue. [ 20 ] Using his back, elbows, and knees, he would shimmy up the flue in the manner of a caterpillar [ 19 ] and use the brush to dislodge loose soot, which would fall over him and down to the bottom, and a scraper to chip away the solid bits, as a smooth chimney was a safe chimney. Having reached the top he would slide back down at speed back to the floor and the soot pile. It was now his job to bag up the soot and carry it back to the master sweep's cart or yard.
Soot was valuable and could be sold for 9d a bushel in 1840. [ 21 ] An apprentice would do four or five chimneys a day. When they first started they scraped their knees and elbows, so the master would harden up their skin by standing them close to a hot fire and rubbing in strong brine using a brush. This was done each evening until the skin hardened. [ 19 ] The boys got no wages but lived with the master, who fed them. They slept together on the floor or in the cellar under the sacks and the cloth used during the day to catch the soot. This was known as "sleeping black". [ 20 ] The boy would be washed by the mistress in a tub in the yard; this might happen as often as once a week, but rarely. One sweep used to wash down his boys in the Serpentine . [ 22 ] Another Nottingham sweep insisted they washed three times a year, for Christmas, Whitsun , and the Goose Fair . Sometimes, a boy would need to be persuaded to climb faster or higher up the chimney, and the master sweep would light either a small fire of straw or a brimstone candle, to encourage him to try harder. One method to stop him from "going off" ( asphyxiating ) was to send another boy up behind him to prick pins into his buttocks or the soles of his feet. [ 23 ]
Chimneys varied in size. The common flue was designed to be one and a half bricks long by one brick wide, though they often narrowed to one brick square, that is 9 inches (230 mm) by 9 inches (230 mm) or less. [ 24 ] Often the chimney would still be hot from the fire, and occasionally it would actually be on fire. [ 18 ] [ 25 ] Climbing boys risked getting stuck with their knees jammed against their chins. The harder they struggled the tighter they became wedged. They could remain in this position for many hours until they were pushed out from below or pulled out with a rope. If their struggling caused a fall of soot they would suffocate. Dead or alive, the boy had to be removed and this would be done by removing bricks from the side of the chimney. [ 26 ] If the chimney was particularly narrow the boys would be told to "buff it", that is to do it naked; [ 27 ] otherwise they just wore trousers and a shirt made from thick rough cotton cloth.
The conditions to which these children were subjected caused concern and societies were set up to promote mechanical means for sweeping chimneys and it is through their pamphlets that we have a better idea of what the job could entail. Here a sweep describes the fate of one boy:
After passing through the chimney and descending to the second angle of the fireplace the Boy finds it completely filled with soot, which he has dislodged from the sides of the upright part. He endeavours to get through, and succeeds in doing so, after much struggling as far as his shoulders; but finding that the soot is compressed hard all around him, by his exertions, that he can recede no farther; he then endeavours to move forward, but his attempts in this respect are quite abortive; for the covering of the horizontal part of the Flue being stone, the sharp angle of which bears hard on his shoulders, and the back part of his head prevents him from moving in the least either one way or the other. His face, already covered with a climbing cap, and being pressed hard in the soot beneath him, stops his breath. In this dreadful condition he strives violently to extricate himself, but his strength fails him; he cries and groans, and in a few minutes he is suffocated. An alarm is then given, a brick-layer is sent for, an aperture is perforated in the Flue, and the boy is extracted, but found lifeless. In a short time an inquest is held, and a Coroner's Jury returns a verdict of "Accidental Death". [ 28 ]
These however were not the only occupational hazards that chimney sweeps suffered. In the 1817 report to Parliament, witnesses reported that climbing boys suffered from general neglect, and exhibited stunted growth and deformity of the spine, legs, and arms, which were thought to be caused by being required to remain in abnormal positions for long periods of time before their bones had hardened. The knees and ankle joints were the most affected. Sores and inflammation of the eyelids that could lead to loss of sight, were slow in healing because the boy kept rubbing them. Bruises and burns were obvious hazards of having to work in an overheated environment. Cancer of the scrotum was found only in chimney sweeps so was referred to as Chimney Sweep Cancer in the teaching hospitals. Asthma and inflammation of the chest were attributed to the fact that the boys were out in all weathers. [ 29 ]
Chimney sweeps' carcinoma , which the sweeps called soot wart , did not occur until the sweep was in his late teens or twenties. It has now been identified as a manifestation of scrotal squamous cell carcinoma . It was reported in 1775 by Sir Percival Pott in climbing boys or chimney sweepers. It is the first industrially related cancer to be found. Potts described it:
It is a disease which always makes it first attack on the inferior part of the scrotum where it produces a superficial, painful ragged ill-looking sore with hard rising edges ... in no great length of time it pervades the skin, dartos and the membranes of the scrotum, and seizes the testicle , which it inlarges [ sic ], hardens and renders truly and thoroughly distempered. Whence it makes its way up the spermatic process into the abdomen .
He also comments on the life of the boys:
The fate of these people seems peculiarly hard ... they are treated with great brutality ... they are thrust up narrow and sometimes hot chimnies, [ sic ] where they are bruised burned and almost suffocated; and when they get to puberty they become ... liable to a most noisome, painful and fatal disease.
The carcinogen was thought to be coal tar , possibly containing some arsenic . [ 28 ] [ 30 ]
There were many deaths caused by accidents, frequently caused by the boy becoming jammed in the flue of a heated chimney, where he could suffocate or be burned to death. Sometimes a second boy would be sent to help and, on occasions would suffer the same fate. [ 31 ]
In 1788, the Chimney Sweepers Act 1788 (long title: An Act for the Better Regulation of Chimney Sweepers and their Apprentices) was passed, to limit a sweeper to six apprentices, at least 8 years old, but lacked enforcement. [ 32 ] It introduced the Apprenticeship Cap badge. The Act had been partially inspired by the interest in climbing boys shown by Jonas Hanway , and his two publications The State of Chimney Sweepers' Young Apprentices (1773) and later Sentimental History of Chimney Sweeps in London and Westminster (1785). He asserted that while Parliament was exercised with the abolition of slavery in the new world it was ignoring the slavery imposed on climbing boys. He looked to Edinburgh , Scotland , where sweeps were regulated by the police, climbing was not allowed and chimneys were swept by the Master Sweep himself pulling bundles of rags up and down the chimney. He did not see how climbing chimneys could be considered a valid apprenticeship, as the only skill obtained was that of climbing chimneys, which did not lead to future employment. [ 33 ] Hanway advocated that Christianity should be brought into the boys' lives and lobbied for Sunday Schools for the boys. The Lords removed the proposed clause that Master Sweeps should be licensed, and before civil registration , there was no way that anyone could check if a child was actually eight.
In the same year, David Porter, a humane master sweep, sent a petition to Parliament, and in 1792 published Considerations of the Present State of Chimney Sweepers with some Observations on the Act of Parliament intended for their Relief and Regulation . Though concerned for the boys' welfare he believed that boys were more efficient than any of the new mechanical cleaning machines. In 1796 a society was formed for Bettering the Conditions of the Poor , and they encouraged the reading of Hanway's and Porter's tracts. They had influential members and royal patronage from George III . [ 34 ] A Friendly Society for the Protection and Education of Chimney-Sweepers' Boys had been established in 1800. [ 35 ]
In 1803, it was thought by some that a mechanical brush could replace a climbing boy (the Human brush), and members of the 1796 society formed The London Society for Superseding the Necessity for Employing Climbing Boys ; [ 34 ] they ascertained that children had now cleaned flues as small as 7in by 7in, and promoted a competition for a mechanical brush. The prize was claimed by George Smart for what, in effect, was a brush head on a long segmented cane, made rigid by an adjustable cord that passed through the canes. [ 36 ]
The Chimney Sweepers Act 1834 contained many of the needed regulations. It stated that an apprentice must express himself in front of a magistrate that he was "willing and desirous". Masters must not take on boys under the age of fourteen. The master could only have six apprentices and an apprentice could not be lent to another master. Boys under fourteen who were already apprenticed must wear brass cap badges on a leather cap. Apprentices were not allowed to climb flues to extinguish fires. Street cries were regulated. [ 37 ] The act was resisted by the master sweeps, and the general public believed that property would be at risk if the flues were not cleaned by a climbing boy.
Also that year building regulations relating to the construction of chimneys were changed.
The Chimney Sweepers and Chimneys Regulation Act 1840 made it illegal for anyone under the age of 21 to sweep chimneys. It was widely ignored. Attempts were made in 1852 and 1853 to reopen the issue, another enquiry was convened and more evidence was taken. There was no bill . The Chimney Sweepers Regulation Act 1864, c. 37, tightened controls significantly, by authorizing fines and imprisonment for master sweeps who were ignoring the law, giving the police the power of arrest on suspicion and authorizing Board of Trade inspections of new and remodelled chimneys. Lord Shaftesbury was a main proponent of the Act.
In February 1875 a twelve-year-old boy, George Brewster, was sent up the Fulbourn Hospital chimneys by his master, William Wyer. He stuck and smothered. The entire wall had to be pulled down to get him out and although he was still alive, he died shortly afterward. There was a coroner's inquest which returned a verdict of manslaughter . Wyer was sentenced to six months' imprisonment with hard labour. Lord Shaftesbury seized on the incident to press his campaign again. He wrote a series of letters to The Times and in September 1875 pushed another bill through Parliament which finally stopped the practice of sending boys up chimneys. [ 38 ] [ 39 ]
The Chimney Sweepers Act 1875 required chimney sweepers "to be authorized by the police to carry on their businesses in the district", thus providing the legal means to enforce all previous legislation. [ 32 ]
The history of sweeping in the United States varies little from that in the United Kingdom. Differences arise from the nature of housing and the political pressures. Early settler houses were built close together out of wood, so when one burnt it spread quickly to neighbouring properties. This caused the authorities to regulate the design of flues. From an early date, fire wardens and inspectors were appointed.
Sweeping of the wide flues of these low buildings was often done by the householder himself, using a ladder to pass a wide brush down the chimney. In a narrow flue, a bag of bricks and brushwood would be dropped down the chimney. But in longer flues climbing boys were used, complete with the tradition of coercion and persuasion using burning straw and pins in the feet and the buttocks. [ 7 ] Sweeping was not a popular trade. During the eighteenth century the employment of African-American chimney sweeps spread from the south to the north. African-American sweeps faced discrimination and were accused of being inefficient and starting fires. It was claimed that there were fewer fires in London where chimneys were swept by white boys than in New York City. As in the UK, Smart's sweeping machine was available in the US shortly after 1803, but few were used. Unlike the UK, there were no societies formed to advocate for the climbing boys. In fact, the contemporary novel Tit for Tat went so far as to deny the black slave chimney sweeps' hardships by claiming that they had it easier than the London chimney sweeps. [ 40 ]
The London boys had one day's holiday a year, the first of May (Mayday). They celebrated by parading through the streets, dancing and twisting with Jack in the Green , merging several folk traditions. [ 41 ] There is also a Sweeps' Festival in Santa Maria Maggiore in Italy, [ 42 ] and in Rochester in Kent [ 43 ] where the tradition was revived in 1980.
Today, chimney sweeps are still operating, as venting systems for coal, heating oil , natural gas, and wood- and pellet -burning appliances need to be maintained. There is a greater understanding of the dangers of flue deposits and carbon monoxide and gases from combustion. The standard chimney brush is still used, along with more modern tools (such as vacuum cleaners, cameras, and special chimney cleaning tools). [ example needed ] Most sweeps are done from the bottom of the chimney, rather than the top, to prevent the dispersion of dust and debris and because it is safer for the chimney sweep to do the sweeping from this position. Inspection may be done from the bottom or top, or both if accessible. Chimney sweeps often encounter a range of unexpected objects [ 47 ] in chimneys ranging from dead birds to tools, notes, love letters , and other pieces of ephemera .
Most modern chimney sweeps are professionals, and are usually trained to diagnose and repair hazards along with maintenance such as removal of flammable creosote , firebox and damper repair, and smoke chamber repair. Some sweeps also offer more complicated repairs such as flue repair and relining, crown repair, and tuckpointing or rebuilding of masonry chimneys and cement crowns.
In the United States, the two trade organizations that help to regulate the industry are the Chimney Safety Institute of America and The National Chimney Sweep Guild . Certification for chimney sweeps are issued by two organizations: Certified Chimney Professionals and The Chimney Safety Institute of America, which was first to establish certification and requires sweeps to re-test every three years or demonstrate the commitment to education by earning CEUs through CSIA or the National Fireplace Institute to bypass the test. Certification for chimney sweeps who reline chimneys are issued by Certified Chimney Professionals and the Chimney Safety Institute of America. CEU credits may be obtained from these organizations and regional associations as well as private trainers.
In the United Kingdom Chimney Sweeping is unregulated however many sweeps have organised themselves into trade associations including the Association of Professional Independent Chimney Sweeps, [ 48 ] the Guild of Master Chimney Sweeps, [ 49 ] and The National Association of Chimney Sweeps. [ 50 ] As well as offering support to members they provide training and representation to DEFRA and other interested parties.
Modern trade associations:
United States:
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Chin augmentation using surgical implants alter the underlying structure of the face , intended to balance the facial features. The specific medical terms mentoplasty and genioplasty are used to refer to the reduction and addition of material to a patient's chin . This can take the form of chin height reduction or chin rounding by osteotomy , or chin augmentation using implants. Altering the facial balance is commonly performed by modifying the chin using an implant inserted through the mouth. The intent is to provide a suitable projection of the chin as well as the correct height of the chin which is in balance with the other facial features. [ 1 ]
This operation is often, but not always, performed at the time of rhinoplasty to help balance the facial proportions. Chin augmentation may be achieved by manipulation of the jaw bone (mandible) and augmentation utilizing this technique usually provides a more dramatic correction than with the use of prosthetic implants.
Chin implants are used in the cosmetic industry to alter one's profile [ 2 ] to resolve confidence and self-esteem issues by the physical augmentation of an individual's jawline and neck. [ 3 ] Patients' own bone is donated from ribs and from part of the pelvis (the ilium). Use of donated bone implants in chin augmentation, even the patient's own, appears to be associated with a higher rate of infection , even after the implant has been in place for decades.
Chin augmentation is still popular because it is a relatively easy operation for the patient while producing noticeable changes in the silhouette of the face. This type of surgery is usually performed by an oral and maxillofacial surgeon, otolaryngologist, or plastic surgeon.
T-osteotomy method (or mini V-line) [ 4 ] is used to narrow and lengthen the chin using an osteotomy technique formulated by Korean surgeons. The surgery is performed under general anesthesia (orotracheal intubation) using an intraoral approach. [ 5 ] Using a double-bladed reciprocating saw, [ 6 ] a horizontal osteotomy is performed, leaving a small portion of bone in the middle. Then two vertical osteotomies are performed in an upside-down trapezoidal shape which is excised. The bones remaining from the horizontal osteotomy are then attached and adjusted to lengthen the chin, and advanced forward for an additional frontal chin projection if required. [ 5 ] Pre-bent titanium plates and screws are used to fixate the bone to its new position. [ 6 ] The chin can be lengthened 2 to 3 mm on average. [ 7 ]
The mentalis muscles controls the elevation functions of the lower lip and chin, so extra caution should be taken to carefully attach the mentalis muscle back after the surgery. [ 8 ] [ 9 ]
The usual complications are relatively minor and include swelling, hematoma (blood pooling), weakness or numbness of the lower lip, which usually does not last long. Other, less common risks include infection, bony changes, displacement of the implant, and nerve damage. [ 10 ] Surgeon experience can help reduce risks of complications. [ 11 ]
Chewing should be kept at a minimum immediately after this procedure, and patients are recommended to eat only soft food and drink for a time after the surgery.
Silicone - Silicone chin Implants are one of the most commonly used implants for chin augmentation. They are soft, smooth, flexible and come in different shapes and sizes. They do not incorporate (stick) to the surrounding tissues, so the pocket must be made precisely. They usually stay in place, but may move, buckle and cause bone resorption where they contact the mandible in some cases. Since they are smooth, they can also be removed easily.
Polyethylene - Polyethylene chin implants, brand name Medpor, are hard, porous, slightly flexible and come in various shapes and sizes. They do incorporate, as the surrounding tissues can grow into the pores of the material. This fixes the polyethylene chin implants in place, and provides a blood supply to help prevent infection. It also makes these implants much more difficult to remove.
Polytetrafluoroethylene - Polytetrafluoroethylene, brand name Gore-Tex , is used in plastic surgery and other operations is known by an abbreviation of its chemical name, ePTFE (expanded polytetrafluoroethylene ) or Gore S.A.M. (subcutaneous augmentation material). [ 12 ] Because ePTFE is flexible and soft but very strong, it is inserted during operations in trimmed sheets and carved blocks and held to the bone by titanium screws. But because the material is porous , the force that really holds the implant in place is soft tissue and bone growing through and into the implant.
The above artificial materials are used in medicine because they are biocompatible and have a low incidence of causing problems inside the human body. They are abundant, FDA cleared and can be used "off-the-shelf", without a donor site injury to the recipient.
Acellular dermal matrix - ADMs are another chin augmentation implant material. Commercially known as AlloDerm and known to physicians as acellular human cadaveric dermis, AlloDerm comes from tissue donors Just after death, technicians remove a layer of skin, remove the epidermis, and treat the remaining dermis with antibiotics and other substances to remove the donor's cells and DNA that would cause rejection. The graft that emerges is often used to cover chin implants.
Other implant materials include Supramid, a braided nonabsorbable synthetic suture material in polymer shell and Mersiline, a mesh-like material that provides a scaffold on the bone. [ 13 ]
Surgical chin augmentation - The most common type of surgical chin augmentation uses a chin implant. There are many types of chin implants, and many are described in the previous section. Chin augmentation with a chin implant is usually a cosmetic procedure. An incision is made either under the chin or inside the lower lip, a pocket is made and the implant placed into the pocket. Some chin implants are fixed to the mandible, while others are held in place by the pocket itself.
Another surgical chin augmentation uses the lower prominence of the mandible as the "implant." Known as a sliding genioplasty, the procedure involves cutting a horseshoe-shaped piece of bone from the lower border of the mandible known as an osteotomy. For chin augmentation, the piece of bone is advanced forward to increase to projection of the chin. The piece can also be recessed backward for a chin reduction. The new position is held in place with a titanium step plate using titanium screws. The bone segment can also be fixated with 26 or 27 gauge wires and IMF (wiring the jaw shut) for 3-4weeks. This type of surgery is usually performed by an oral and maxillofacial surgeon or a plastic surgeon .
More involved Orthognathic Surgery may be required in cases where the chin is small and a significant overbite co-exist. While the procedures above may improve the cosmetic appearance of the chin, they will not improve dental occlusion. Mandibular advancement surgery can be used to correct the alignment of the teeth and improve the projection of the chin.
Non-surgical chin augmentation - Another method of chin augmentation uses an injectable filler. Most fillers are temporary, with results lasting months to years. Common temporary fillers include hyaluronic acid and calcium hydroxyapatite preparations. Permanent fillers, like "free" silicone , have fallen out of favor due to the risk of migration, chronic inflammation and infection, which can permanently disfigure the chin.
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The China Tribunal was a non-governmental tribunal to inquire into forced organ harvesting in China . [ 1 ] It was headquartered in London .
The chair of the China Tribunal was Sir Geoffrey Nice KC , [ 1 ] who had also been lead prosecutor at the trial of Slobodan Milošević in the International Criminal Tribunal for the Former Yugoslavia . [ 2 ] Its other members were Professor of Paediatric Cardiothoracic Surgery at University College London Martin Elliott , Malaysian lawyer Andrew Khoo, Iranian lawyer, Shadi Sadr, US lawyer Ragina Paulose, businessman Nick Vetch and historian Arthur Waldron . [ 1 ] All members of the Tribunal provided their time pro bono publico. The Judgment states: "All members of the Tribunal, Counsel to the Tribunal, volunteer lawyers and the editor of this Judgment have worked entirely pro bono publico (for the public good) which for those unfamiliar with the term or practice means completely without financial return of any kind." [ 3 ]
The Tribunal was initiated by the International Coalition to End Transplant Abuse in China (ETAC). [ 4 ]
The China Tribunal was initiated by the charity ETAC, of which "a minority of [the] committee members are Falun Gong practitioners". [ 3 ] The Tribunal states that it itself is independent from ETAC, [ 4 ] "none of the members of the Tribunal, Counsel to the Tribunal, the editor or the volunteer lawyers working with Counsel to the Tribunal is a Falun Gong practitioner or has any special interest in Falun Gong." [ 3 ]
In 2016, ETAC asked Geoffrey Nice to write an opinion about the issues that the tribunal was later to consider; Nice advised that a body of several people would be better able to consider the facts and law, which eventually led to ETAC forming the China Tribunal. [ 5 ]
The China Tribunal held 5 days of public hearings in December 2018 and April 2019, in which over 50 fact witnesses, experts, and investigators testified. [ 6 ] [ 7 ]
On 17 June 2019, the China Tribunal pronounced its "final judgment" on organ harvesting in China, concluding that the Chinese Communist Party was, beyond reasonable doubt, guilty of committing crimes against humanity against China's Uyghur Muslim and Falun Gong populations, and that removing hearts and other organs from living victims constituted one of the worst mass atrocities of this century. [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ] [ 14 ]
The China Tribunal Judgment stated: "In the long-term practice in the PRC of forced organ harvesting it was indeed Falun Gong practitioners who were used as a source – probably the principal source – of organs for forced organ harvesting." [ 15 ] Adding that there was no evidence of the practice having been stopped and that the Tribunal was satisfied that it continued. [ 15 ]
The judgment was published on 1 March 2020. [ 5 ]
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The Chinese Journal of Cancer ( Chinese : 《癌症》 ) is a monthly peer-reviewed open access medical journal covering oncology . The editor-in-chief is Rui-Hua Xu of the Sun Yat-sen University Cancer Center. It is published by BioMed Central and sponsored by the Sun Yat-sen University Cancer Center. The journal was established in 1982.
The journal is abstracted and indexed in:
According to the Journal Citation Reports , the journal has a 2017 impact factor of 4.11. [ 3 ]
This article about an oncology journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
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The Chinese Society of Psychiatry ( CSP ; Chinese : 中华医学会精神病学分会 ; lit. ' Chinese Medical Association Psychiatry Branch') is the largest organization for psychiatrists in China . It publishes the Chinese Classification of Mental Disorders ("CCMD"), first published in 1985. [ 1 ] The CSP also publishes clinical practice guidelines; promotes psychiatric practice, research and communication; trains new professionals; and holds academic conferences.
The organization developed out of the Chinese Society of Neuro-Psychiatry, which was founded in 1951. This separated into the Chinese Society of Psychiatry and Chinese Society of Neurology in 1994. Since then, successive committees have run the organisation, currently the 3rd Committee, which started in 2003, whose president is Dongfeng Zhou. The CCMD is now on its third revision.
The official journal of the CSP is the Chinese Journal of Psychiatry ( 中华精神科杂志 ). [ 2 ] The Society held its seventh annual academic conference in 2006. [ 3 ] The Society is a member of the World Psychiatric Association .
As of 2005, the CSP had 800 members. [ 4 ]
In 2001, the CSP declassified homosexuality and bisexuality as a mental disorder. [ 5 ] [ 6 ] [ 7 ] However, the organization specified that, "although homosexuality was not a disease, a person could be conflicted or suffering from mental illness because of their sexuality, and that condition could be treated", according to Damien Lu, founder of the Information Clearing House for Chinese Gays and Lesbians . Reportedly, this loophole is used to promote conversion therapy in China. [ 8 ]
Beginning in 2014, the CSP began collaborating with the McLean Hospital . [ 9 ] The purpose of the program is to share research cross-culturally between specialists in psychotic and mood disorders . [ 10 ]
The Chinese Society of Psychiatrists (CSP) has been criticised for alleged complicity in the government's political abuse of psychiatry towards Falun Gong practitioners—including by detaining individuals via diagnosing adherents as "political maniacs" or with " Qi Gong psychosis". [ 11 ] [ 4 ] Antipsychotic drugs were wrongly prescribed to practitioners. [ 12 ]
In 2004, the CSP agreed on a joint response with the World Psychiatric Association to the allegations. According to the CSP, certain psychiatrists had "failed to distinguish between spiritual-cultural beliefs and delusions" due to "lack of training and professional skills", and this led to misdiagnoses. However, they claimed this was not a systematic issue and invited the WPA to correct the problem. [ 12 ] [ 13 ]
The WPA stated, "What has become clear... has been the need to assist Chinese colleagues in matters concerning forensic psychiatry, medical ethics, patients' rights, mental health legislation, diagnosis and classification, to help them improve the care of mentally ill in China and prevent future abuses." [ 12 ] Arthur Kleinman , a psychiatrist at Harvard University , said he believed the claims about systematic abuse of psychiatry were exaggerated, while acknowledging that it did occur in some cases. Abraham Halpern , a psychiatrist at New York Medical College and board member of the Friends of Falun Gong, USA , criticized the WPA for not demanding an investigative mission in China. [ 13 ] [ 14 ]
A follow-up review of the controversy was written by Alan A. Stone , a professor of psychiatry and president of the American Psychiatric Association , and published in the Psychiatric Times . Stone determined that psychiatrists in China were generally poorly trained and did not receive the sort of medical training which was standard in the West . Stone said this was cause for the misdiagnoses. [ 4 ]
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Chinese herbology ( traditional Chinese : 中藥學 ; simplified Chinese : 中药学 ; pinyin : zhōngyào xué ) is the theory of traditional Chinese herbal therapy, which accounts for the majority of treatments in traditional Chinese medicine (TCM). A Nature editorial described TCM as "fraught with pseudoscience ", and said that the most obvious reason why it has not delivered many cures is that the majority of its treatments have no logical mechanism of action . [ 1 ]
The term herbology is misleading in the sense that, while plant elements are by far the most commonly used substances, animal, human, and mineral products are also used, some of which are poisonous. In the Huangdi Neijing they are referred to as 毒藥 (pinyin: dúyào ) which means "poison-medicine". Paul U. Unschuld points out that this is similar etymology to the Greek pharmakon and so he uses the term pharmaceutic . [ 2 ] Thus, the term medicinal (instead of herb ) is usually preferred as a translation for 藥 (pinyin: yào ). [ 3 ]
Research into the effectiveness of traditional Chinese herbal therapy is of poor quality and often tainted by bias, [ 4 ] with little or no rigorous evidence of efficacy. [ 5 ] There are concerns over a number of potentially toxic Chinese herbs, [ 6 ] including Aristolochia which is thought to cause cancer. [ 7 ]
Chinese herbs have been used for centuries. Among the earliest literature are lists of prescriptions for specific ailments, exemplified by the manuscript Recipes for 52 Ailments , found in the Mawangdui which were sealed in 168 BCE.
The first traditionally recognized herbalist is Shénnóng ( 神農 , lit. ' Divine Farmer ' ), a mythical god-like figure, who is said to have lived around 2800 BCE. [ 8 ] He allegedly tasted hundreds of herbs and imparted his knowledge of medicinal and poisonous plants to farmers. His Shénnóng Běn Cǎo Jīng ( 神農本草經 , Shennong's Materia Medica ) is considered as the oldest book on Chinese herbal medicine. It classifies 365 species of roots, grass, woods, furs, animals and stones into three categories of herbal medicine: [ 9 ]
The original text of Shennong's Materia Medica has been lost; however, there are extant translations. [ 10 ] The true date of origin is believed to fall into the late Western Han dynasty [ 8 ] (i.e., the first century BCE).
The Treatise on Cold Damage Disorders and Miscellaneous Illnesses was collated by Zhang Zhongjing , also sometime at the end of the Han dynasty , between 196 and 220 CE. Focusing on drug prescriptions, [ 11 ] it was the first medical work to combine Yinyang and the Five Phases with drug therapy. [ 12 ] This formulary was also the earliest Chinese medical text to group symptoms into clinically useful "patterns" ( zheng , 證 ) that could serve as targets for therapy. Having gone through numerous changes over time, it now circulates as two distinct books: the Treatise on Cold Damage Disorders and the Essential Prescriptions of the Golden Casket , which were edited separately in the eleventh century, under the Song dynasty . [ 13 ]
Succeeding generations augmented these works, as in the Yaoxing Lun ( 藥性論 ; 药性论 ; 'Treatise on the Nature of Medicinal Herbs'), a 7th-century Tang dynasty Chinese treatise on herbal medicine.
There was a shift in emphasis in treatment over several centuries. A section of the Huangdi Neijing Suwen including Chapter 74 was added by Wang Bing in his 765 edition. In which it says: 主病之謂君，佐君之謂臣，應臣之謂使，非上下三品之謂也。 "Ruler of disease it called Sovereign, aid to Sovereign it called Minister, comply with Minister it called Envoy (Assistant), not upper lower three classes (qualities) it called." The last part is interpreted as stating that these three rulers are not the three classes of Shénnóng mentioned previously. This chapter in particular outlines a more forceful approach. Later on Zhang Zihe ( a.k.a. Zhang Cong-zhen, 1156–1228) is credited with founding the 'Attacking School' which criticized the overuse of tonics.
Arguably the most important of these later works is the Compendium of Materia Medica ( Bencao Gangmu , 本草綱目 ) compiled during the Ming dynasty by Li Shizhen , which is still used today for consultation and reference.
The use of Chinese herbs was popular during the medieval age in western Asian and Islamic countries. They were traded through the Silk Road from the East to the West. Cinnamon , ginger , rhubarb , nutmeg and cubeb are mentioned as Chinese herbs by medieval Islamic medical scholars Such as Rhazes (854–925 CE), Haly Abbas (930–994 CE) and Avicenna (980–1037 CE). There were also multiple similarities between the clinical uses of these herbs in Chinese and Islamic medicine. [ 14 ]
There are roughly 13,000 medicinals used in China and over 100,000 medicinal recipes recorded in the ancient literature. [ 15 ] Plant elements and extracts are by far the most common elements used. [ 16 ] In the classic Handbook of Traditional Drugs from 1941, 517 drugs were listed – out of these, only 45 were animal parts, and 30 were minerals. [ 16 ] For many plants used as medicinals, detailed instructions have been handed down not only regarding the locations and areas where they grow best, but also regarding the best timing of planting and harvesting them. [ 17 ]
Some animal parts used as medicinals can be considered rather strange such as cows' gallstones. [ 18 ]
Furthermore, the classic materia medica Bencao Gangmu describes the use of 35 traditional Chinese medicines derived from the human body , including bones, fingernail, hairs, dandruff, earwax, impurities on the teeth, feces, urine, sweat, and organs, but most are no longer in use. [ 19 ] [ 20 ] [ 21 ]
Typically, one batch of medicinals is prepared as a decoction of about 9 to 18 substances. [ 22 ] Some of these are considered as main herbs, some as ancillary herbs; within the ancillary herbs, up to three categories can be distinguished. [ 23 ] Some ingredients are added to cancel out toxicity or side-effects of the main ingredients; on top of that, some medicinals require the use of other substances as catalysts .
Chinese patent medicine ( 中成藥 ; 中成药 ; zhōngchéng yào ) is a kind of traditional Chinese medicine . They are standardized herbal formulas. From ancient times, pills were formed by combining several herbs and other ingredients, which were dried and ground into a powder. They were then mixed with a binder and formed into pills by hand. The binder was traditionally honey. Modern teapills, however, are extracted in stainless steel extractors to create either a water decoction or water-alcohol decoction, depending on the herbs used. They are extracted at a low temperature (below 100 °C (212 °F)) to preserve essential ingredients. The extracted liquid is then further condensed, and some raw herb powder from one of the herbal ingredients is mixed in to form a herbal dough. This dough is then machine cut into tiny pieces, a small amount of excipients are added for a smooth and consistent exterior, and they are spun into pills. [ citation needed ]
These medicines are not patented in the traditional sense of the word. No one has exclusive rights to the formula. Instead, "patent" refers to the standardization of the formula. In China, all Chinese patent medicines of the same name will have the same proportions of ingredients, and manufactured in accordance with the PRC Pharmacopoeia, which is mandated by law. However, in western countries there may be variations in the proportions of ingredients in patent medicines of the same name, and even different ingredients altogether. [ citation needed ]
Several producers of Chinese herbal medicines are pursuing FDA clinical trials to market their products as drugs in U.S. and European markets. [ 24 ]
Chinese herbal extracts are herbal decoctions that have been condensed into a granular or powdered form. Herbal extracts, similar to patent medicines, are easier and more convenient for patients to take. The industry extraction standard is 5:1, meaning for every five pounds of raw materials, one pound of herbal extract is derived. [ 25 ] [ better source needed ]
There are several different methods to classify traditional Chinese medicinals:
The Four Natures are: hot ( 熱 ; 热 ), warm ( 溫 ; 温 ), cool ( 涼 ), cold ( 寒 ) or neutral ( 平 ). [ 26 ] Hot and warm herbs are used to treat cold diseases, while cool and cold herbs are used to treat hot diseases. [ 26 ]
The Five Flavors, sometimes also translated as Five Tastes , are: acrid/pungent ( 辛 ), sweet ( 甘 ), bitter ( 苦 ), sour ( 酸 ), and salty ( 鹹 ; 咸 ). [ 26 ] Substances may also have more than one flavor, or none (i.e., a bland ( 淡 ) flavor). [ 26 ] Each of the Five Flavors corresponds to one of the zàng organs , which in turn corresponds to one of the Five Phases : [ 27 ] A flavor implies certain properties and presumed therapeutic "actions" of a substance: saltiness "drains downward and softens hard masses"; [ 26 ] sweetness is "supplementing, harmonizing, and moistening"; [ 26 ] pungent substances are thought to induce sweat and act on qi and blood ; sourness tends to be astringent ( 澀 ; 涩 ) in nature; bitterness "drains heat , purges the bowels, and eliminates dampness".
These categories mainly include:
Many herbs earn their names from their unique physical appearance. Examples of such names include Niu Xi ( Radix cyathulae seu achyranthis ), 'cow's knees,' which has big joints that might look like cow knees; Bai Mu Er ( Fructificatio tremellae fuciformis ), 'white wood ear', which is white and resembles an ear; Gou Ji ( Rhizoma cibotii ), 'dog spine,' which resembles the spine of a dog. [ 31 ]
Color is not only a valuable means of identifying herbs, but in many cases also provides information about the therapeutic attributes of the herb. For example, yellow herbs are referred to as huang (yellow) or jin (gold). Huang Bai ( Cortex Phellodendri ) means 'yellow fir," and Jin Yin Hua ( Flos Lonicerae ) has the label 'golden silver flower." [ 31 ]
Unique flavors define specific names for some substances. Gan means 'sweet,' so Gan Cao ( Radix glycyrrhizae ) is 'sweet herb,' an adequate description for the licorice root. Ku means 'bitter', thus Ku Shen ( Sophorae flavescentis ) translates as 'bitter herb.' [ 31 ]
The locations or provinces in which herbs are grown often figure into herb names. For example, Bei Sha Shen ( Radix glehniae ) is grown and harvested in northern China, whereas Nan Sha Shen ( Radix adenophorae ) originated in southern China. And the Chinese words for north and south are respectively bei and nan . [ 31 ]
Chuan Bei Mu ( Bulbus fritillariae cirrhosae ) and Chuan Niu Xi ( Radix cyathulae ) are both found in Sichuan province, as the character chuan indicates in their names. [ 31 ]
Some herbs, like Fang Feng ( Radix Saposhnikoviae ), literally 'prevent wind,' preventing or treating wind-related illnesses. Xu Duan ( Radix Dipsaci ), literally 'restore the broken,' treating torn soft tissues and broken bones. [ 31 ]
Many herbs indigenous to other countries have been incorporated into the Chinese materia medica. Xi Yang Shen ( Radix panacis quinquefolii ), imported from North American crops, translates as 'western ginseng,' while Dong Yang Shen ( Radix ginseng Japonica ), grown in and imported from North Asian countries, is 'eastern ginseng.' [ 31 ]
From the earliest records regarding the use of medicinals to today, the toxicity of certain substances has been described in all Chinese materia medica. [ 32 ] Since TCM has become more popular in the Western world, there are increasing concerns about the potential toxicity of many traditional Chinese medicinals including plants, animal parts and minerals. [ 6 ] For most medicinals, efficacy and toxicity testing are based on traditional knowledge rather than laboratory analysis. [ 6 ] The toxicity in some cases could be confirmed by modern research (i.e., in scorpion ); in some cases it could not (i.e., in Curculigo ). [ 33 ] Further, ingredients may have different names in different locales or in historical texts, and different preparations may have similar names for the same reason, which can create inconsistencies and confusion in the creation of medicinals, [ 34 ] with the possible danger of poisoning. [ 35 ] [ 36 ] [ 37 ] [ unreliable source? ] Edzard Ernst "concluded that adverse effects of herbal medicines are an important albeit neglected subject in dermatology, which deserves further systematic investigation." [ 38 ] Research suggests that the toxic heavy metals and undeclared drugs found in Chinese herbal medicines might be a serious health issue. [ 39 ]
Substances known to be potentially dangerous include aconite , [ 33 ] secretions from the Asiatic toad , [ 40 ] powdered centipede, [ 41 ] the Chinese beetle ( Mylabris phalerata , Ban mao), [ 42 ] and certain fungi. [ 43 ] There are health problems associated with Aristolochia . [ 6 ] Toxic effects are also frequent with Aconitum . [ 6 ] To avoid its toxic adverse effects Xanthium sibiricum must be processed. [ 6 ] Hepatotoxicity has been reported with products containing Reynoutria multiflora ( synonym Polygonum multiflorum ), glycyrrhizin , Senecio and Symphytum . [ 6 ] The evidence suggests that hepatotoxic herbs also include Dictamnus dasycarpus , Astragalus membranaceus , and Paeonia lactiflora ; although there is no evidence that they cause liver damage. [ 6 ] [ clarification needed ] Contrary to popular belief, Ganoderma lucidum mushroom extract, as an adjuvant for cancer immunotherapy, appears to have the potential for toxicity. [ 44 ]
Also, adulteration of some herbal medicine preparations with conventional drugs which may cause serious adverse effects, such as corticosteroids , phenylbutazone , phenytoin , and glibenclamide , has been reported. [ 45 ] [ 46 ]
However, many adverse reactions are due to misuse or abuse of Chinese medicine. [ 6 ] For example, the misuse of the dietary supplement Ephedra (containing ephedrine ) can lead to adverse events including gastrointestinal problems as well as sudden death from cardiomyopathy . [ 6 ] Products adulterated with pharmaceuticals for weight loss or erectile dysfunction are one of the main concerns. [ 6 ] Chinese herbal medicine has been a major cause of acute liver failure in China. [ 47 ]
Most Chinese herbs are safe but some have shown not to be. Reports have shown products being contaminated with drugs, toxins, or false reporting of ingredients. Some herbs used in TCM may also react with drugs, have side effects, or be dangerous to people with certain medical conditions. [ 48 ]
Only a few trials exist that are considered to have adequate methodology by scientific standards. Proof of effectiveness is poorly documented or absent. [ 4 ] A 2016 Cochrane review found "insufficient evidence that Chinese Herbal Medicines were any more or less effective than placebo or hormonal therapy" for the relief of menopause related symptoms. [ 49 ] A 2012 Cochrane review found no difference in decreased mortality for SARS patients when Chinese herbs were used alongside Western medicine versus Western medicine exclusively. [ 50 ] A 2010 Cochrane review found there is not enough robust evidence to support the effectiveness of traditional Chinese medicine herbs to stop the bleeding from haemorrhoids . [ 51 ] A 2008 Cochrane review found promising evidence for the use of Chinese herbal medicine in relieving painful menstruation , compared to conventional medicine such as NSAIDs and the oral contraceptive pill, but the findings are of low methodological quality. [ 52 ] A 2012 Cochrane review found weak evidence suggesting that some Chinese medicinal herbs have a similar effect at preventing and treating influenza as antiviral medication. [ 53 ] Due to the poor quality of these medical studies, there is insufficient evidence to support or dismiss the use of Chinese medicinal herbs for the treatment of influenza. [ 53 ] There is a need for larger and higher quality randomized clinical trials to determine how effective Chinese herbal medicine is for treating people with influenza. [ 53 ] A 2005 Cochrane review found that although the evidence was weak for the use of any single herb, there was low quality evidence that some Chinese medicinal herbs may be effective for the treatment of acute pancreatitis . [ 54 ]
The traditional practice of using now- endangered species is controversial within TCM. Modern Materia Medicas such as Bensky, Clavey and Stoger's comprehensive Chinese herbal text discuss substances derived from endangered species in an appendix, emphasizing alternatives. [ 55 ]
Parts of endangered species used as TCM drugs include tiger bones [ 56 ] and rhinoceros horn . [ 57 ] Poachers supply the black market with such substances, [ 58 ] [ 59 ] and the black market in rhinoceros horn, for example, has reduced the world's rhino population by more than 90 percent over the past 40 years. [ 60 ] Concerns have also arisen over the use of turtle plastron [ 61 ] and seahorses . [ 62 ]
TCM recognizes bear bile as a medicinal. In 1988, the Chinese Ministry of Health started controlling bile production, which previously used bears killed before winter. Now bears are fitted with a sort of permanent catheter , which is more profitable than killing the bears. [ 63 ] [ verification needed ] More than 12,000 asiatic black bears are held in "bear farms", where they suffer cruel conditions while being held in tiny cages. The catheter leads through a permanent hole in the abdomen directly to the gall bladder , which can cause severe pain.
Increased international attention has mostly stopped the use of bile outside of China; gallbladders from butchered cattle ( 牛胆 ; 牛膽 ; niú dǎn ) are recommended as a substitute for this ingredient. [ citation needed ]
Collecting American ginseng to assist the Asian traditional medicine trade has made ginseng the most harvested wild plant in North America for the last two centuries, which eventually led to a listing on CITES Appendix II . [ 64 ]
Chinese medicinal plant materials (CMPMs) release chemicals that attracts the Drugstore beetle , leading to the accumulation of this pest and further infestation and damage to these plants. [ 65 ]
Chinese herbology is a pseudoscientific practice with potentially unreliable product quality, safety hazards or misleading health advice. [ 66 ] [ 67 ] [ 68 ] There are regulatory bodies, such as China GMP (Good Manufacturing Process) of herbal products. [ 69 ] There is a lack of high-quality scientific research on herbology practices and product effectiveness for anti-disease activity. [ 66 ] [ 67 ] In the herbal sources listed below, there is little or no evidence for efficacy or proof of safety across consumer age groups and disease conditions for which they are intended. [ 66 ] [ 67 ]
There are over 300 herbs in common use. Some of the most commonly used herbs are Ginseng ( 人参 ; 人參 ; rénshēn ), wolfberry ( 枸杞子 ; gǒuqǐzǐ), dong quai ( Angelica sinensis , 当归 ; 當歸 ; dāngguī ), astragalus ( 黄耆 ; 黃耆 ; huángqí ), atractylodes ( 白术 ; 白朮 ; báizhú ), bupleurum ( 柴胡 ; cháihú ), cinnamon (cinnamon twigs ( 桂枝 ; guìzhī ) and cinnamon bark ( 肉桂 ; ròuguì )), coptis ( 黄连 ; 黃連 ; huánglián ), ginger ( 姜 ; 薑 ; jiāng ), hoelen ( 茯苓 ; fúlíng ), licorice ( 甘草 ; gāncǎo ), ephedra sinica ( 麻黄 ; 麻黃 ; máhuáng ), peony (white: 白芍 ; báisháo and reddish: 赤芍 ; chìsháo ), rehmannia ( 地黄 ; 地黃 ; dìhuáng ), rhubarb ( 大黄 ; 大黃 ; dàhuáng ), and salvia ( 丹参 ; 丹參 ; dānshēn ).
In Chinese herbology, there are 50 "fundamental" herbs, as given in the reference text, [ 70 ] although these herbs are not universally recognized as such in other texts. The herbs are:
In addition to the above, many other Chinese herbs and other substances are in common use, and these include:
Traditional Chinese herbs are used either standalone, or in a grouping, jointly with other herbs. When several herbs are used together, this amalgamation is called a 'herbal formula'. [ medical citation needed ]
There are, generally speaking, three types of herbal formulas used in TCM:
1. Classic Formulas - these are formulas which TCM practitioners believe have withstood the test of time over the centuries, and are mentioned in classical texts, such as the Shanghan Lun .
2. Patent Formulas - these are either classic formulas, or newer commonly-used formulas created in recent decades. The patent formulas stand out in that their usage is common enough, that they are frequently mass-produced by large companies, in China, the United States, and elsewhere.
3. Custom-Made Formulas - these formulas are composed by a TCM Practitioner, to match the specific diagnosis and medical condition of a patient. These formulas are often partially-based on the older, classic formulas.
The prescription of TCM formulas, is based on 4-tier system of hierarchy. [ 90 ] The 4-tiers are: Jun (君), Chen (臣), Zuo (佐) and Shi (使). [ 91 ] [ 92 ] These four tiers are often translated as: Sovereign, Minister, Assistant, Courier; or Monarch, Minister, Assistant, Envoy (also: 'Guide'). [ 93 ]
This feudal-like hierarchy denotes the power and role of each herb in a given formula. [ 94 ] [ 95 ] The Jun is the herb which is usually of the highest relative dosage, and leads the main action of the formula. In the majority of formulas, there is only one Jun (Monarch) herb. Sometimes, a formula may feature 2-3 Jun herbs, or lack a dominant Jun herb altogether. The Chen support the Jun in its actions, and provide additional uses for the medical purpose of the formula. The Zuo assist the Jun and Chen, but are given at a much lower dosage (relative to themselves), to deemphasize their influence, for various reasons. The Shi's main role is to help guide the formula to the correct bodily areas or organ systems inside of which it is meant to act. [ 96 ] [ 97 ] [ 98 ] The Shi are also sometimes used "to harmonize the properties of other herbs in the formula". [ 99 ] [ 100 ]
Most herbs can serve as either Jun (Monarch), Chen (Minister) or Zuo (Assistant) - the first three tiers in the herbal hierarchy. But only certain herbs, are considered fit to serve as Shi. This is because only some herbs are believed to have the ability, to guide other herbs into a given bodily area or organ system. [ 101 ]
Within TCM formulas, there are also strict rules about which herbs pair well together (Dui Yao), and which are either contradictory, incompatible, or may cause a reaction amongst themselves, or with Western Medicine Drugs. [ 102 ] For example: Gan Cao (Licorice) is incompatible with the herbs Yuan hua, Jing Da Ji, Hai Zao and Gan Sui. It may also alter the therapeutic effects of corticosteroids. [ 103 ] [ 104 ]
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https://en.wikipedia.org/wiki/Chinese_herbology
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