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Biotheology is the synthetic application of understanding of biology to the understanding of God, synthesizing modern biology and traditional religious doctrines . [ 1 ]
Scripturally, Biotheology is motivated by, amongst other things, Saint Paul 's exposition of the Church as the Body of Christ , likening its form and functions to the form and functions of the human body ( 1 Cor . 12:12-17), his remarks in Romans (Ro. 1:20), and Jesus ' many parables concerning nature.
A key concept is the thought that the Kingdom of God may be understood as an integral part of evolution . Areas of research include questions of the establishment and maintenance of order, of the relationship between spirit and emergence , and of the relationship between sin and natural selection .
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Biothesiometry is a noninvasive medical test used to quantify the perception of vibration by measuring its threshold . [ 1 ] It is used in neurology and electrophysiology to diagnose a number of conditions, like diabetic neuropathy and erectile dysfunction , where the vibration perception threshold (VPT) would be higher than average. [ 1 ] [ 2 ] The numerical nature of the test can help stage the progression of disease or complications.
The test is done through a biothesiometer , which is composed of a handheld probe wired to a display unit. Both digital and analog types are commercially available, giving the reading on either a dial or a screen .
In a systematic review of screening methods for pediatric diabetic peripheral neuropathies , biothesiometry and fine microfilaments were shown to be the only diagnostic methods with high sensitivity and specificity . [ 3 ]
A systematic review showed that there is a strong co-relation between HbA1c values and Vibration Perception Test and could be a predictor for complications in the foot following Diabetic Peripheral Neuropathy . [ 4 ]
In a systemic review of modern devices available for the assessment and screening of peripheral neuropathy , digital devices were evaluated to measure tactile sensation , vibration perception, thermal perception and foot skin temperature. [ 5 ]
This article related to medical equipment is a stub . You can help Wikipedia by expanding it .
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Although the term has occasionally been used in other ways, in medical literature biotrauma is usually defined as a severe inflammatory response produced in the lungs of patients who breathe by means of a mechanical ventilator for a long period of time. [ 1 ] The term was coined in a 1998 paper by L. N. Tremblay and A. S. Slutsky, titled Ventilator-induced injury: from barotrauma to biotrauma . [ 2 ] The message of that paper was that barotrauma caused by pressure differentials is only one of several types of lung damage that a ventilator can produce.
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Biotronik (BIOTRONIK SE & Co. KG ; [ 1 ] [ 2 ] Biotronik Worldwide) is a limited partnership [ 1 ] multi-national cardiovascular biomedical research and technology company, headquartered in Berlin , Germany.
The company offers equipment for diagnosis, treatment, and therapy support in the areas of cardiac rhythm management, electrophysiology , and vascular intervention. [ 3 ] In the area of cardiac rhythm management, Biotronik Home Monitoring uses tele-monitoring technology to provide doctors with up-to-date information for implant patients. [ 4 ]
Biotronik employs more than 9,000 people worldwide in over 100 countries, with research and development activities in Europe, North America, and Singapore. It produces all critical components of its products in-house. One in every five employees at its Berlin headquarters works in research and development (R&D). [ citation needed ]
BIOTRONIK began with the development of the first German implantable pacemaker (Biotronik IP-03) in 1963. The pacemaker was developed at Technische Universität Berlin by physicist Professor. Dr. Max Schaldach (1936–2001 [ 5 ] ), [ 6 ] [ 7 ] a professor of biomedical technology at the Friedrich-Alexander- University of Erlangen-Nuremberg (FAU), [ 8 ] and electrical engineer Otto Franke. In the early years, the company worked to improve pacemakers' capacity and battery life, and secure the connections among electrodes, pacemakers, and the heart. Since its start, more than 19 million BIOTRONIK devices in over 100 countries have been implanted. [ citation needed ]
In 1976, the company moved to Sieversufer 8 in Berlin-Neukölln . In 1979, a US production site in Lake Oswego, Oregon was built. This subsidiary resulted from the acquisition of the American pacemaker producer Stimulation Technology, Inc. At the same time, with the development and production of advanced hybrid circuitry and structural components for the medical technology industry, the company also began to develop circuits for pacemakers. In the 1980s, the dual-chamber stimulation method (DDD) was developed, leading to the manufacturing of a pacemaker that could read and react to spontaneous contractions of the atrium, and better respond to them of its own accord. To this end, BIOTRONIK developed the Diplos 03, a multi-programme DDD pacemaker with bilateral telemetry, which made it a European market leader and increased its presence in South America and Asia.
In 1987, the firm moved its headquarters to Woermannkehre 1, next door to its previous location. In 1993, BIOTRONIK produced the first German implantable cardioverter defibrillator (ICD), among them the Phylax 06. Closed loop stimulation (CLS), which integrates the pacemaker into the body's own regulatory system, thereby allowing it to react to patients’ changing physical and emotional activity, was introduced in the 1990s. Also in 1993, BIOTRONIK developed fractal coating for implantable electrodes. This coating optimises the electrically active surface of the electrode, thereby improving its perception and stimulation properties. BIOTRONIK remains the only manufacturer of fractal-coated electrodes.
In 1994 and 1995 respectively, BIOTRONIK began offering a full spectrum of electrophysiology products and vascular intervention products. BIOTRONIK also develops and produces balloon catheters and stents for the treatment of coronary artery disease . With Philos, the company has offered a complete pacemaker family with telemetry since 2000, when it received CE Mark approval for the product, and also successfully implanted the first pacemaker with Home Monitoring ( remote patient monitoring ). Home Monitoring has shown significant clinical benefits, including over a 50% reduction in mortality of heart failure patients. [ 9 ]
With the Lumax 540 VR-T DX in 2010, BIOTRONIK launched the first and only single-chamber defibrillator with comprehensive atrial diagnostics worldwide. Additionally, the company entered into an exclusive international distribution partnership with the Swiss medical technology company Endosense to distribute their ablation catheter TactiCath with optical contact force. The following year, BIOTRONIK released Orsiro to the market, the world's first hybrid drug-eluting stent with a bio-absorbable coating, adding to innovative treatment options combatting coronary artery disease. [ citation needed ]
In 2011, BIOTRONIK was the subject of an investigation by the United States Department of Justice (US DoJ) into payments made to doctors in Nevada , United States, who use the company's products in their practices. [ 10 ] The case was settled in 2014. [ 11 ] In 2013, a similar investigation began and was settled involving payments to physicians in Oregon . [ 12 ] [ 13 ]
In 2012, the company acquired the old Postfuhramt , a historical brick postal building on Berlin's Oranienburger Strasse in the sub-neighbourhood of Spandauer Vorstadt , in the district of Mitte . [ 14 ]
The following year, BIOTRONIK launched BioMonitor, a type of mini ECG device that offers continuous monitoring and daily remote data collection. In addition, BIOTRONIK also developed the world's first series of implantable defibrillators that enable patients, including those suffering heart failure, to undergo MRI scans under certain conditions. BIOTRONIK's ProMRI® technology includes systems approved for 1.5 T and 3.0 T MR scanning, as well as full-body scanning. The company offers the broadest portfolio of pacemakers, defibrillators, and therapies approved to undergo MRIs, with more than 1,000,000 ProMRI® devices and leads implanted worldwide. [ 15 ] To navigate through this portfolio, BIOTRONIK invented two online tools in 2016 and 2017; the ProMRI®SystemCheck and ProMRI®Configurator , correspondingly.
For radiation protection, BIOTRONIK distributes the Zero-Gravity Radiation Protection System, which consists of a movable suspended body and head shield. The shield material has a significantly higher lead equivalency than traditional radiation apparel, thereby reducing radiation exposure by 87–100%. [ 16 ]
Indicated to treat peripheral artery disease in the lower limbs, BIOTRONIK released the Passeo-18 Lux in 2014 as the first peripheral drug-coated balloon. The year following, CardioMessenger Smart was launched, its new patient device for Home Monitoring, [ 17 ] and BioMonitor 2, the second-generation insertable cardiac monitor. [ 18 ]
In February 2016, BIOTRONIK Inc. opened an Education and Innovation Center, a training facility and meeting location in New York City. [ 19 ]
In 2007, BIOTRONIK was given the EuroPCR 2007 Novelty Award for its innovative absorbable metal stents (AMS) by the European Association of Percutaneous Cardiovascular Interventions (EAPCI). In 2009, it was nominated for the German Future Prize for its Home Monitoring system by the German Federal Ministry of Education and Research. In 2010, BIOTRONIK endowed the Berlin-Brandenburg Academy of Sciences and Humanities ' Technical Science Prize, first awarded to Till Schlösser. The CARDIOSTIM Innovation Award for Practice Improvement was granted to BIOTRONIK for its MRI AutoDetect. [ 20 ]
BIOTRONIK collaborates with the EPIC Alliance, a global network of female electrophysiologists. The alliance aims to enhance collaboration and support for women in the field of electrophysiology.
In 2014, Biotronik faced allegations regarding kickback payments to cardiologists, leading to a settlement of nearly five million dollars. [ 21 ] [ 22 ] [ 23 ] [ 24 ] Currently, another case is ongoing in the California Central District Court. Additionally,
In a landmark case from New Mexico in 2016, a jury found Biotronik negligent for unnecessarily implanting a pacemaker in Tommy Sowards due to an alleged conspiracy involving the company, a salesman, a hospital, and a cardiologist. The lawsuit exposed a scheme where Biotronik paid kickbacks to the cardiologist, significantly inflating his earnings per procedure. Despite later advice from medical professionals that the pacemaker was not needed, it could not be removed without risking heart damage. As a result, the jury awarded Sowards $2.3 million in compensatory damages and $65 million in punitive damages. [ 25 ]
Biotronik is under investigation in the Netherlands, with inquiries initiated in autumn 2020. This investigation, reported by Der Spiegel and the Dutch newspaper NRC Handelsblad, focuses on suspicions that medical specialists received millions of euros to promote Biotronik products. [ 26 ] Over ten residences have been searched, and assets worth 3.1 million euros belonging to medical specialists have been confiscated. Biotronik has not provided comments on these allegations.
In July 2022, Biotronik resolved a prolonged legal dispute in the USA by agreeing to a multimillion dollar settlement. The case involved allegations from two whistleblowers, who were former independent sales representatives, concerning a kick-back scheme. According to the whistleblowers the scheme entailed treating cardiologists to lavish dinners, winery tours, baseball games, strip club visits, and golf outings, sometimes including their spouses or employees. [ 27 ] Additionally, cardiologists were allegedly compensated for making brief appearances at international conferences or provided with business class flights. Another aspect of the scheme involved a trainee program where Biotronik employees observed cardiologists during the implantation of ICDs, for which the cardiologists were paid $400. [ 28 ] [ 27 ] Despite concerns raised by the compliance department, the payments continued. The alleged kick-back system, intended to encouraged the use of Biotronik products, occurred between 2013 and 2021. Although Biotronik denied the allegations, they settled with the US authorities without admitting guilt, paying nearly $13 million. [ 29 ] [ 30 ] [ 31 ] [ 32 ]
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Biphenotypic acute leukaemia ( BAL ) is an uncommon type of leukemia which arises in multipotent progenitor cells which have the ability to differentiate into both myeloid and lymphoid lineages. [ 1 ] [ 2 ] [ 3 ] It is a subtype of "leukemia of ambiguous lineage". [ 4 ]
The direct reasons leading to BAL are still not clear. BAL can be de novo or secondary to previous cytotoxic therapy. Many factors, such viruses, hereditary factors, and radiation , might have a relationship with BAL.
BAL is hard to treat. Usually the chemotherapy is chosen according to the morphology of the blast ( ALL or AML ). A blood-forming stem-cell transplantation is highly recommended.
About 5% of acute leukaemia cases are BAL. BAL can occur in all ages of people but occurs more in adults than in children. [ 5 ]
BAL has similar symptoms to other types of leukemia, but they are usually more serious.
Symptoms caused by bone marrow damage
Bruising , spotting: the reason is lack of platelets. it is very common in BAL patients, most of patients die due to the
A low level of red blood cells in the bloodstream : Because the decline of hematopoietic function, need blood transfusion therapy
Persistent fever, infection prolonged healing:
Diffuse hemorrhage: which is dangerous and might lead to death.
Symptoms caused by blood cancer cells infiltration into tissues:
Swollen lymph nodes
Joint pain
Swelling of the gums
Enlargement of the liver and spleen
Headache and vomiting : blood cancer infiltration into the wear performance of the central nervous system .
Skin lumps: Because look was slightly green, also known as the "Green tumor."
Pericardial or pleural effusion
The cause that directly leads to BAL is unclear. Exposure to radiation , chemical exposure, virus and genetics are the primary reasons proposed by researchers.
The mechanism of BAL is related to several mutations. The most common abnormalities are t(9;22) and MLL gene rearrangement at 11q23.
T(9;22) affect the ABL gene at 9q34 and BCR at 22q11. The hybrid gene product ABL/BCR is an oncogene which could lead several types of leukemia including BAL.
ABL/BCR could active several molecular pathways:
MLL gene encode Histone-lysine N-methyltransferase (HRX), which is a histone methyltransferase. It is a positive regulator for gene transcription. It has been shown that associates with Host cell factor C1, CREB binding protein, WDR5 , CTBP , MEN1 , etc. The rearrangement of MLL are related with different kinds of aggressive acute leukemias. Most of biphenotypic leukemia in children is due to the rearrangement of MLL [ 7 ]
Besides them, other gene abnormalities has been reported. Such as t(8;21), t(15;17), del(6q), del(12p), t(x;12) and t(14;19). [ 8 ] In BAL patients, it is prone to bruising , spotting , which is due to megakaryocytes that could produce platelets decrease, resulting in a lack of platelets.
Anemia: reduction metrocytes that could produce red blood cells, resulting in a lack of red blood cells. Patients are prone to asthma and dizziness in walking or exercise.
Persistent fever, infection prolonged healing: Most of the white blood cells are leukemia cells, no normal function, leading to decreased immunity, susceptible to infection.
Following observation of the symptoms, the patients need to get complete blood counts and a bone marrow examination . If the patient has leukemia, the morphology and immunophenotype check is needed to make sure the type of leukemia.
The morphology of the blast in BAL is not certain. The cells could display both myeloid lineage and lymphoid or undifferentiated morphology. Therefore, the diagnosis cannot based on the morphology result. The immunophenotype check is the most important basis of the diagnosis of BAL.
Before 2008, the diagnosis of BAL was based on a score system proposed by the European Group for the Immunological Classification of Leukemias (EGIL) which could differentiate from other kinds of acute leukemia. The table shows this method. [ 9 ] If the score of only one lineage is higher than 2, the acute leukemia could be acute myeloid leukemia (AML) or acute lymphoblastic leukemia (ALL). According to the original EGIL scoring system BAL is defined when scores are over two points for both myeloid and T- or B- lymphoid lineages.
In 2008, WHO established a new and strict criteria standard for diagnosis of BAL. The presence of specific T-lymphoid antigens, cytoplasmic CD3 (cCD3), MPO and CD 19 became the most important standard for recognizing the lineage. Other B-lineage markers (CD22, CD79a, CD 10) and monocytic markers are also needed. Table 2 shows the method.
Compared with the EGIL scoring system, the current 2008 WHO criteria applied less but more specific markers to define the lineage of the blasts, and incorporated the intensity of markers expression into the diagnostic algorithm. [ 10 ] The diagnosis of BAL is so difficult that sometimes is misdiagnosed with AML or ALL because the morphology thus the therapy would not have a good effect.
BAL is difficult to treat, most patients receive treatment based on the morphology of blasts and get AML or ALL induction chemotherapy. The induction drug for AML such as cytarabine and anthracycline , drug for ALL such as prednisolone , dexamethasone , vincristine , asparaginase or daunorubicin is common for BAL remission induction therapy. Recently, researches showed that using both myeloid and lymphoid induction therapy may be better for prognosis. [ 11 ] Chemotherapy has strong side effects such as typhlitis , gastrointestinal distress , anemia, fatigue, hair loss , nausea and vomiting, etc. Thus, the different dose and times of chemotherapy for different individuals is important.
If the patients enter fully remission , the consolidation with stem cell transplantation is highly recommended.
The prognosis for BAL patients is not good which is worse than ALL and AML. Medical Blood Institute reported cases of CR rate was 31.6%, with a median remission are less than 6 months
The median survival time is only 7.5 months. [ 12 ] The life quality is also low because the immune function of patient is damaged seriously. They have to stay in hospital and need 24h care.
In another study, the results showed that young age, normal karyotype and ALL induction therapy will have a better prognosis than Ph+, adult patients. The study shows median survival of children is 139 months versus 11 months of adults, 139 months for normal karyotype patients versus 8 months for ph+ patients. [ 13 ] [ 14 ]
Research on the mechanisms of BAL does not show a great progress in terms of the causes, molecular processes and therapy. Some new translocate case of BAL has been reported, such as t(15,17) [ 15 ] and t(12,13). [ 16 ] For t(15;17), the blasts with morphology of acute lymphoblastic leukemia co-expressed in B-lymphoid and myeloid lineages, and the cytogenetic study showed that the 4q21 abnormalities and t(15;17). However, promyelocytic-retinoid acid receptor rearrangement was not found by fluorescence in situ hybridization on interphase nuclei. Researchers also found some new chemotherapy method for specific cases. For example, The chemotherapy for ALL and gemtuzuab ozogamicin without all-trans-retinoic acid remain complete remission of the BAL patients with t(15,17) for more than 3.7 years. [ 17 ] The detection of BCR-ABL1 chimeric gene neutrophils was also found a good method for diagnosis some cases of BAL. [ 18 ]
aggressive: Sézary disease
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Bipolar I disorder (BD-I; pronounced "type one bipolar disorder") is a type of bipolar spectrum disorder characterized by the occurrence of at least one manic episode , with or without mixed or psychotic features. [ 1 ] Most people also, at other times, have one or more depressive episodes. [ 2 ] Typically, these manic episodes can last at least 7 days for most of each day to the extent that the individual may need medical attention, while the depressive episodes last at least 2 weeks. [ 3 ]
It is a type of bipolar disorder and conforms to the classic concept of manic-depressive illness, which can include psychosis during mood episodes. [ 4 ]
The essential feature of bipolar I disorder is a clinical course characterized by the occurrence of one or more manic episodes or mixed episodes. [ 5 ] Often, individuals have had one or more major depressive episodes . [ 6 ] One episode of mania is sufficient to make the diagnosis of bipolar disorder; the person may or may not have a history of major depressive disorder . [ 6 ] Episodes of substance-induced mood disorder due to the direct effects of a medication , or other somatic treatments for depression, substance use disorder , or toxin exposure, or of mood disorder due to a general medical condition need to be excluded before a diagnosis of bipolar I disorder can be made. Bipolar I disorder requires confirmation of only 1 full manic episode for diagnosis, but may be associated with hypomanic and depressive episodes as well. [ 7 ] Diagnosis for bipolar II disorder does not include a full manic episode; instead, it requires the occurrence of both a hypomanic episode and a major depressive episode. [ 7 ] Serious aggression has been reported to occur in one out of every ten major, first-episode, BD-I patients with psychotic features, the prevalence in this group being particularly high in association with a recent suicide attempt, alcohol use disorder , learning disability, or manic polarity in the first episode. [ 8 ]
Bipolar I disorder often coexists with other disorders including PTSD , substance use disorders, and a variety of mood disorders. [ 9 ] [ 10 ] Studies suggest that psychiatric comorbidities correlate with further impairment of day-to-day life. [ 11 ] Up to 40% of people with bipolar disorder also present with PTSD, with higher rates occurring in women and individuals with bipolar I disorder. [ 9 ] A diagnosis of bipolar 1 disorder is only given if bipolar episodes are not better accounted for by schizoaffective disorder or superimposed on schizophrenia , schizophreniform disorder , delusional disorder , or a psychotic disorder not otherwise specified. [ 12 ]
Regular medical assessments are performed to rule-out secondary causes of mania and depression. [ 13 ] These tests include complete blood count , glucose , serum chemistry/electrolyte panel, thyroid function test , liver function test , renal function test , urinalysis , vitamin B12 and folate levels, HIV screening , syphilis screening , and pregnancy test , and when clinically indicated, an electrocardiogram (ECG), an electroencephalogram (EEG), a computed tomography (CT scan), and/or a magnetic resonance imagining (MRI) may be ordered. [ 13 ] Drug screening includes recreational drugs , particularly synthetic cannabinoids , and exposure to toxins.
In May 2013, American Psychiatric Association released the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders ( DSM-5 ). There are several proposed revisions to occur in the diagnostic criteria of Bipolar I Disorder and its subtypes. For Bipolar I Disorder 296.40 (most recent episode hypomanic) and 296.4x (most recent episode manic), the proposed revision includes the following specifiers: with psychotic features, with mixed features, with catatonic features, with rapid cycling, with anxiety (mild to severe), with suicide risk severity , with seasonal pattern , and with postpartum onset. [ 14 ] Bipolar I Disorder 296.5x (most recent episode depressed) will include all of the above specifiers plus the following: with melancholic features and with atypical features. [ 14 ] The categories for specifiers will be removed in DSM-5 and criterion A will add or there are at least 3 symptoms of major depression of which one of the symptoms is depressed mood or anhedonia . [ 14 ] For Bipolar I Disorder 296.7 (most recent episode unspecified), the listed specifiers will be removed. [ 14 ]
The criteria for manic and hypomanic episodes in criteria A & B will be edited. Criterion A will include "and present most of the day, nearly every day", and criterion B will include "and represent a noticeable change from usual behavior". These criteria as defined in the DSM-IV-TR have created confusion for clinicians and need to be more clearly defined. [ 15 ] [ 16 ]
There have also been proposed revisions to criterion B of the diagnostic criteria for a Hypomanic Episode, which is used to diagnose For Bipolar I Disorder 296.40, Most Recent Episode Hypomanic. Criterion B lists "inflated self-esteem, flight of ideas, distractibility, and decreased need for sleep" as symptoms of a Hypomanic Episode. This has been confusing in the field of child psychiatry because these symptoms closely overlap with symptoms of attention deficit hyperactivity disorder (ADHD). [ 15 ]
Mood stabilizers are often used as part of the treatment process. [ 17 ]
Antidepressant -induced mania occurs in 20–40% of people with bipolar disorder. Mood stabilizers, especially lithium, may protect against this effect, but some research contradicts this. [ 22 ]
A frequent problem in these individuals is non-adherence to pharmacological treatment; long-acting injectable antipsychotics may contribute to solving this issue in some patients. [ 23 ]
A review of validated treatment guidelines for bipolar disorder by international bodies was published in 2020. [ 24 ]
Bipolar I usually has a poor prognosis, which is associated with substance abuse, psychotic features, depressive symptoms, and inter-episode depression. [ 25 ] A manic episode can be so severe that it requires hospitalization. An estimated 63% of all BP-I related mania results in hospitalization. [ 26 ] The natural course of BP-I, if left untreated, leads to episodes becoming more frequent or severe over time. [ 27 ] The absolute risk of suicide is highest for BP-I than all other mood and mental disorders. [ 28 ] Up to a quarter of individuals with BP-I die by suicide. [ 29 ] Individuals with BP-I typically have a shorter life expectancy compared to the general population, with estimates suggesting a reduction of 11 to 20 years. [ 30 ] With proper treatment, individuals with BP-I can, however, lead a healthy lifestyle. [ 31 ]
Psychosocial interventions can be used for managing acute depressive episodes and for maintenance treatment to aid in relapse prevention. [ 32 ] This includes psychoeducation , cognitive behavioural therapy (CBT), family-focused therapy (FFT), interpersonal and social rhythm therapy (IPSRT), and peer support . [ 32 ]
Information on the condition, importance of regular sleep patterns, routines and eating habits and the importance of compliance with medication as prescribed . Behavior modification through counseling can have positive influence to help reduce the effects of risky behavior during the manic phase. Additionally, the lifetime prevalence for bipolar I disorder is estimated to be 1%. [ 33 ]
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Bipolar disorder in children , or pediatric bipolar disorder ( PBD ), is a rare mental disorder in children and adolescents . The diagnosis of bipolar disorder in children has been heavily debated for many reasons including the potential harmful effects of adult bipolar medication use for children. PBD is similar to bipolar disorder (BD) in adults , and has been proposed as an explanation for periods of extreme shifts in mood called mood episodes. [ 1 ] [ 2 ] These shifts alternate between periods of depressed or irritable moods and periods of abnormally elevated moods called manic or hypomanic episodes. [ 1 ] Mixed mood episodes can occur when a child or adolescent with PBD experiences depressive and manic symptoms simultaneously. [ 2 ] Mood episodes of children and adolescents with PBD are different from general shifts in mood experienced by children and adolescents because mood episodes last for long periods of time (i.e. days, weeks, or years) and cause severe disruptions to an individual's life. [ 2 ] There are three known forms of PBD: Bipolar I , Bipolar II , and Bipolar Not Otherwise Specified (NOS). [ 2 ] The average age of onset of PBD remains unclear, but reported age of onset ranges from 5 years of age to 19 years of age. [ 3 ] PBD is typically more severe and has a poorer prognosis than bipolar disorder with onset in late-adolescence or adulthood. [ 4 ]
Since 1980, the DSM Tooltip Diagnostic and Statistical Manual of Mental Disorders has specified that the criteria for bipolar disorder in adults can also be applied to children with some adjustments based on developmental differences. [ 5 ] Genetics and environment are considered risk factors for the development of bipolar disorder with the exact cause unknown at this time. Therefore, diagnosis of bipolar disorder requires evaluation by a professional and diagnosis of PBD typically requires more in depth observation due to children's inability to properly report symptoms.
While there is limited understanding regarding the development of bipolar disorder, research shows that there are many environmental and biological risk factors. [ 2 ] Family history is a strong predictor of childhood development of bipolar disorder, with genetics contributing to risk by up to 50%. [ 2 ] [ 6 ] [ 7 ] With this in mind, it is important to understand that family history does not lead to absolute diagnosis of PBD in the child. Only 6% of children with parents diagnosed with bipolar disorder also have bipolar disorder. [ 2 ] Still, children of parents with bipolar disorder should be monitored for possible development of bipolar disorder especially if they exhibit sleep disturbances and symptoms of anxiety disorders early on. [ 6 ] Other factors that can contribute to pediatric bipolar disorder include substance use disorder and childhood adversity such as abuse or school trauma. [ 8 ] [ 9 ]
Diagnosis is made based on a clinical interview by a licensed mental health professional. There are no blood tests or imaging to diagnose bipolar disorder. [ 10 ] Pediatric bipolar disorder can be difficult to diagnose, especially in children under 11–12 years as they may be unable to properly self-assess and communicate any possible symptoms. [ 11 ] Therefore, it is helpful to obtain information from multiple sources, such as family members and teachers, and use questionnaires and checklists for a more accurate diagnosis. [ 6 ] Commonly used assessment tools include the K-SADS (Kiddie Schedule for Affective Disorders and Schizophrenia), the Diagnostic Interview Schedule for Children (DISC), and the Child Mania Rating Scale (CMRS). [ 5 ] It is important to assess the child's baseline mood and behavior and determine if the symptoms present episodically. Often, parents are encouraged to keep mood logs to assist with this. [ 5 ] Family history is also important to obtain as bipolar disorder is heritable. Medication, substance use, or other medical problems should be ruled out to appropriately diagnose bipolar disorder. [ 6 ]
Early diagnosis is important for children to start treatment soon and leads to better outcomes. Often, anxiety disorders and sleep disturbances precede the mood symptoms of PBD. [ 6 ] [ 7 ] If a child presents with symptoms of anxiety and changes in sleep pattern with major changes in energy and deterioration of function, especially in school, this may warrant evaluation for PBD. [ 8 ]
It can be difficult to distinguish pediatric bipolar disorder due to overlapping symptoms with other conditions such as ADHD, OCD, autism spectrum disorder, depression, anxiety, or conduct disorders. [ 12 ] [ 13 ] For example, irritability, distractibility, and poor judgment are symptoms commonly seen in pediatric bipolar disorder and ADHD. Elated mood and decreased need for sleep can be specifically diagnostic of PBD. [ 6 ]
The American Psychiatric Association's DSM-5 Tooltip Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and the World Health Organization's ICD-10 Tooltip International Classification of Diseases (ICD-10) , use the same criteria to diagnose bipolar disorder in adults and children with some adjustments to account for differences in age and developmental stage, particularly with depressive episodes . [ 5 ] [ 14 ] For example, the DSM-5 specifies that children may exhibit persistently irritable moods instead of a depressed mood. [ 1 ] Additionally, children will more than likely fail to meet their expected body weight instead of presenting with weight loss. [ 8 ]
In diagnosing manic episodes , it is important to compare the changes in mood and behavior to the child's normal mood and behaviors at baseline instead of to other children or adults. [ 6 ] For example, grandiosity (i.e., unrealistic overestimation of one's intelligence, talent, or abilities) is normal at varying degrees during childhood and adolescence. Therefore, grandiosity is only considered symptomatic of mania in children when the beliefs are held despite being presented with concrete evidence otherwise or when they lead to a child attempting activities that are clearly dangerous, and most importantly, when the grandiose beliefs are an obvious change from that particular child's normal self-view in between episodes. [ 1 ]
It is important to distinguish if irritability is related to bipolar disorder or another condition as it is commonly in other childhood disorders. [ 5 ] If irritability is persistent, it is important to differentiate from chronic irritability seen in disruptive mood dysregulation disorder (DMDD). [ 8 ]
In particular, PBD and ADHD have many overlapping symptoms at the surface, such as the hyperactivity characteristic of the manic episodes that occur in PBD. [ 15 ] As a result, many children and adolescents with PBD are instead diagnosed with ADHD. [ 15 ] Misdiagnosis of PBD can lead to complications in youth and adolescents as different disorders require different types of medications that may make symptoms of PBD more severe. [ 16 ]
According to the DSM-5 there are 3 major categories of bipolar disorder: Bipolar I , Bipolar II , and Bipolar Not Otherwise Specified (NOS). [ 1 ] [ 2 ] Just as in adults, bipolar I is the most severe form of PBD in children and adolescents, and can impair sleep, general function, and lead to hospitalization. [ 2 ] Bipolar NOS is the mildest form of PBD in children and adolescents. [ 2 ] The criteria for distinguishing is the same as that of bipolar disorder (BD) in adults .
The diagnosis of childhood bipolar disorder has been heavily debated. [ 5 ] It is recognized that the typical symptoms of bipolar disorder are dysfunctional and have negative consequences for minors with the condition. [ 17 ] The main discussion is centered on whether what is called bipolar disorder in children refers to the same disorder in adults, [ 18 ] and the related question on whether the criteria for adult diagnosis is useful and accurate when applied to children. [ 5 ] More specifically, regarding the symptomatology of mania and its differences between children and adults. [ 12 ]
There are significant differences in how commonly PBD is diagnosed across clinics and in different countries. In the United States, there were concerns about over diagnosis and misdiagnosis of PBD. [ 5 ] [ 19 ] More understanding and research lead to a decrease in PBD diagnosis from mid-2000s to 2010. [ 20 ] This is likely due to the various challenges that come with identifying bipolar disorder in youth. PBD has many overlapping symptoms with other childhood conditions.
A combination of medication and psychosocial intervention is recommended for most pediatric populations with PBD and has been proven to lead to improved prognosis. [ 13 ] [ 7 ] [ 9 ] In order to choose the best medication and therapy, it is important to consider the child's age, their psychosocial environment, presentation and severity of symptoms, and their family history. [ 7 ]
Mood stabilizers , which help manage manic episodes, and atypical antipsychotics , which help manage both manic and depressive episodes, have been demonstrated to be the safest and most effective in pediatric populations for the treatment of PBD. [ 8 ] [ 13 ] Mood stabilizers used for the treatment of PBD include: lithium , valproic acid , divalproex sodium , carbamazepine , and lamotrigine . [ 21 ] Lithium is FDA approved for those 12 years and older appears to be particularly effective in children with a family history of mood disorders especially if the family members have been successfully treated with lithium. [ 5 ] [ 9 ] Atypical antipsychotics that have been approved for use by the FDA for treatment of PBD include risperidone, cariprazine , lurasidone , olanzapine-fluoxetine combination, and quetiapine . [ 21 ] Risperidone has been approved for use in children 10 and older. [ 5 ] Medications have also been proven effective when used in combination whether that is multiple mood stabilizers or a mood stabilizer with an atypical antipsychotic. [ 5 ]
Medications for the treatment of PBD can produce significant side effects, so it is recommended that families of patients be informed of the different possible issues that can arise. [ 18 ] Although atypical antipsychotics are more effective in treating PBD than mood stabilizers, they can lead to more side effects. [ 17 ] [ 22 ] Typical antipsychotics may produce weight gains as well as other metabolic problems, including diabetes mellitus type 2 and hyperlipidemia . Extrapyramidal secondary effects may occur with the use of these medications, including tardive dyskinesia , a difficult-to-treat movement disorder. [ 23 ] Liver and kidney damage may occur as a result of the use of mood stabilizers. [ 18 ] Lithium overdose can also occur in individuals with low sodium levels. [ 21 ] Pediatric populations often struggle with medication adherence for PBD, which can be improved with motivational interviewing techniques. [ 13 ]
Psychological treatment for PBD can take on several different forms such as psychoeducation, psychotherapy, and alternative treatments. [ 24 ] One form of psychotherapy is psychoeducation , in which children with bipolar disorder and their families are informed, in ways accordingly to their age and family role, about the different aspects of bipolar disorder and its management including causes, signs and symptoms and treatments. [ 21 ] Similarly, family-focused therapy (FFT) is therapy for both individuals with PBD and their caregivers, in which families take part in communication improvement training and problem-solving skills training. [ 21 ] Group therapy aims to improve social skills and manage group conflicts, with role-playing as a critical tool. Another type of therapy used in individuals with PBD is chronotherapy , which helps children and adolescents form a healthy sleep pattern, as sleep is often disrupted by PBD symptoms. [ 21 ] Finally, cognitive-behavioral therapy (CBT) aims to make participants have a better understanding and control over their emotions and behaviors. [ 12 ]
Psychotherapy can be tailored to each individual and address needs that medication alone cannot to help improve lifestyle and functionality. Additionally, psychotherapy improves medication adherence. [ 7 ]
Alternative treatments are currently being developed for pediatric populations with PBD in which medication and psychotherapy has proven to be ineffective. Currently, interventions involving dialectical behavioral therapy (DBT) are being explored due to the focus on mindfulness and distress tolerance skill building. According to the APA, studies have shown that DBT may lead to decreased suicidal ideation compared to typical psychosocial treatments. Nutritional interventions are also currently undergoing further research along with other lifestyle modifications including exercise and proper sleep habits. [ 13 ] [ 9 ]
Bipolar disorder is a chronic condition that requires lifelong care and treatment. [ 2 ] Without proper treatment, PBD oftentimes has a poor prognosis in children and adolescents. [ 21 ] Chronic adherence to medication is often needed, with relapses of individuals reaching rates over 90% in those not following medication indications and almost 40% in those complying with medication regimens in some studies. [ 12 ] Other risk factors for poor outcomes of PBD and increased severity of symptoms are comorbid pathologies and early onset of disease. [ 6 ] [ 8 ] [ 18 ] [ 9 ]
Children with PBD, especially early onset, are more likely to commit suicide than other children, as well as misuse alcohol and/or other drugs. [ 5 ] [ 6 ] [ 8 ] [ 21 ] Studies have shown that among adolescents with PBD, 44% report a lifetime suicide rate, twice as much compared to teens diagnosed major depressive disorder. [ 25 ] Children and adolescents with PBD are also at an increased risk for behavior that can result in incarceration. [ 21 ]
Hypomanic episodes in adolescents have been shown to not always progress into adult bipolar disorder. [ 26 ] However, research surrounding PBD emphasizes the importance of early diagnosis of PBD for improved prognosis. [ 26 ]
The most common comorbidities seen with PBD is ADHD (80%) and oppositional defiant disorder (47%). [ 27 ] Anywhere between 13.2% and 29% of patients with bipolar disorder are diagnosed with conduct disorder, substance use disorders, anxiety disorders, or borderline personality disorder. [ 6 ] [ 8 ] [ 27 ]
Comorbid ADHD can be diagnosed if symptoms such as hyperactivity and distractibility are present persistently. If they are purely related to mood episodes, this is likely a symptom of PBD. [ 6 ] Therefore, it is important to carefully evaluate onset of symptoms and course of time present. While difficulty with sleep can be present in both, patients with bipolar disorder will typically have a decreased need for sleep during manic episodes while children with ADHD will have sleep problems with increased fatigue. Grandiosity is also a distinguishing factor as mania typically presents with increased self-esteem and in ADHD children may actually have lower self esteem. [ 15 ]
Globally, the prevalence of PBD in children and adolescents under the age of 18 is estimated at 3.9% as of 2019. [ 21 ] [ 26 ] However, 5 surveys (from Brazil, England, Turkey, and the United States) have reported pre-adolescence rates of PBD as zero or close to zero. [ 26 ]
The increase in PBD in children in the United States is attributed to the cohort effect (shared circumstances of more recently born children) as well as the anticipation effect (the earlier onset of genetic conditions in later generations). [ 28 ]
Descriptions of children with symptoms similar to contemporary concepts of mania date back to the 18th century. In 1898, a detailed psychiatric case history was published about a 13-year-old that met Jean-Pierre Falret and Jules Baillarger 's criteria for folie circulaire , which is congruent to the modern conception of bipolar I disorder . [ 29 ]
In Emil Kraepelin 's descriptions of bipolar disorder in the 1920s, which he called "manic depressive insanity", he noted the rare possibility that it could occur in children. In addition to Kraepelin, Adolf Meyer , Karl Abraham , and Melanie Klein were some of the first to document bipolar disorder symptoms in children in the first half of the 20th century. [ 30 ] It was not mentioned much in English literature until the 1970s when interest in researching the subject increased. It became more accepted as a diagnosis in children in the 1980s after the DSM-III (1980) specified that the same criteria for diagnosing bipolar disorder in adults could also be applied to children. [ 5 ]
Recognition came twenty years after, with epidemiological studies showing that approximately 20% of adults with bipolar disorder already had symptoms in childhood or adolescence. Nevertheless, onset before age 10 was thought to be rare, below 0.5% of the cases. During the second half of the century misdiagnosis with schizophrenia was not rare in the non-adult population due to common co-occurrence of psychosis and mania, this issue diminishing with an increased following of the DSM criteria in the last part of the 20th century. [ 18 ] [ 31 ]
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Birte Melsen (born 9 June 1939) is an orthodontist from Denmark. She was the past President of European Orthodontic Society in 2004 and has made significant contributions in the field of orthodontics with her research, publishing about 350 papers in scientific journals on topics related to Anchorage (orthodontics) and adult orthodontics. [ 1 ]
Birthe Melsen was born in Aabenraa , Denmark in 1939. She received her dental degree in 1964 from Aarhus University in Aarhus, Denmark. Melsen specialized in orthodontics in the year of 1971 and received her orthodontic certificate in 1974 from Royal Dental College. She became Head of Department of Orthodontics at the same college in 1975 and is currently serving at that position. Melsen also works as part-time at a private practice in Lübeck , Germany . She has published a textbook called Adult Orthodontics in 2012. [ 2 ] Melsen and co-workers in Denmark, designed the Aarhus Mini-Implant (Medicon eG, Tuttlingen, Germany. ScanOrto A/S, Charlottenlund, Denmark) and furnished scientific evidence for the possibility of immediate loading of mini-screw implants. [ 3 ]
This dentistry article is a stub . You can help Wikipedia by expanding it .
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Bispectral index ( BIS ) is one of several technologies used to monitor depth of anesthesia . BIS monitors are used to supplement Guedel's classification system for determining depth of anesthesia. Titrating anesthetic agents to a specific bispectral index during general anesthesia in adults (and children over 1 year old) allows the anesthetist to adjust the amount of anesthetic agent to the needs of the patient, possibly resulting in a more rapid emergence from anesthesia. Use of the BIS monitor could reduce the incidence of intraoperative awareness during anaesthesia. [ 1 ] The exact details of the algorithm used to create the BIS index have not been disclosed by the company that developed it.
BIS cannot be used as the sole monitor of anaesthesia, as it is affected by several other factors, including the anaesthetic drugs used (BIS is relatively insensitive to agents such as ketamine and nitrous oxide ), and muscle movement or artefact from surgical equipment. BIS is used as an adjunct to monitoring under anaesthesia - its use has been shown to reduce overall dose of anaesthetic agent used and therefore may improve recovery time from anaesthesia. [ 2 ]
The BIS was introduced by Aspect Medical Systems, Inc. in 1994 [ 3 ] as a novel measure of the level of consciousness by algorithmic analysis of a patient's electroencephalogram during general anesthesia . This is used in conjunction with other physiologic monitoring such as electromyography to estimate the depth of anesthesia in order to minimize the possibility of intraoperative awareness. The US Food and Drug Administration (FDA) cleared BIS monitoring in 1996 for assessing the hypnotic effects of general anesthetics and sedatives . The FDA further stated in 2003 that "...A reduction in awareness provides a public health benefit, in that BIS technology can now provide anesthestists with a way to reduce this often debilitating, yet preventable medical error". Aspect Medical was acquired by Covidien in 2009. [ 4 ]
The bispectral index is a statistically based, empirically derived complex parameter. It is a weighted sum of several electroencephalographic subparameters, including a time domain , frequency domain , and high order spectral subparameters. [ 5 ] The BIS monitor provides a single dimensionless number, which ranges from 0 (equivalent to EEG silence) to 100. A BIS value between 40 and 60 indicates an appropriate level for general anesthesia , as recommended by the manufacturer. The BIS monitor thus gives the anesthetist an indication of how "deep" under anesthesia the patient is. [ 6 ] Additionally, BIS values less than 40 for greater than 5 minutes have been associated with increased risk of stroke ( hazard ratio of 3.23), MI (1.94) and death (1.41). [ 7 ]
The essence of BIS is to take a complex signal (the EEG), analyse it, and process the result into a single number. Several other systems claim to be able to perform the same thing. The recent availability of cheap, fast computer processors has enabled great advances in this field. When a subject is awake, the cerebral cortex is very active, and the EEG reflects vigorous activity. When asleep or under general anesthesia, the pattern of activity changes. Overall, there is a change from higher-frequency signals to lower-frequency signals (which can be shown by Fourier analysis ), and there is a tendency for signal correlation from different parts of the cortex to become more random.
As with other types of EEG analysis, the calculation algorithm that the BIS monitor uses is proprietary, although it has been successfully reverse engineered. [ 8 ]
Some of the limitations of this form of processed EEG monitoring are:
BIS monitoring is widely used in operating rooms and ICUs, as well as in emergency departments. Some of the benefits that have been attributed to it include: [ 9 ]
The BIS is an electroencephalogram-derived multivariant scale that, when a drug such as propofol is used, correlates with the metabolic rate of glucose. [ 15 ] Both loss of consciousness and awakening from anesthesia are correlated with this scale. [ 16 ] The efficacy of BIS index monitoring is not without controversy. [ 17 ]
Some controlled studies have found that using the BIS reduced the incidence of memory but this was not confirmed in several very large multicenter studies on awareness. [ 14 ] [ 18 ] A Cochrane review in 2014 [ 19 ] found that "Four studies (7761 patients) that used clinical signs as a guide to anaesthetic administration in standard practice, as the control group, demonstrated a significant reduction in the risk of awareness with BIS monitoring. Four studies (26,530 patients) compared BIS monitoring with end tidal anaesthetic gas (ETAG) monitoring as a guide to management of anaesthesia and they did not demonstrate any difference in terms of intraoperative awareness". The Sociedad de Anestesiología Reanimación y Terapéutica del Dolor de Madrid recommends monitoring of anesthetic depth in accordance with literature-based evidence. BIS, however, is not explicitly endorsed. In fact, they cite an American Society of Anesthesiologists (ASA) statement saying that the decision for cerebral function monitoring should be made on an individual basis. [ 20 ]
The bispectral index has not been proven to measure the level of consciousness, independently of the cause of reduced consciousness (whether this be drugs, metabolic disease, hypothermia , head trauma , hypovolemia , natural sleep and so on). [ citation needed ] Not all unconscious patients will have a low BIS value, although the general clinical state may be very different from one to the other, and the prognosis may also differ. [ citation needed ] Furthermore, not all conscious patients will have a high BIS value. [ 21 ]
The bispectral index is prone to artifacts. Some conscious patients who are administered neuromuscular blocking agents such as succinylcholine may have low bispectral index scores; thus, the BIS may fail to detect consciousness in such patients. [ 22 ] Its numbers cannot be relied upon in all situations, including brain death, circulatory arrest or hypothermia. [ 23 ] [ 24 ] [ 25 ] [ 26 ] A monitor of the Autonomic Nervous System (the first commercial monitor was the ANEMON-I monitor developed by former Swiss company Medical System SA based on the patent WO1997037586 [ 27 ] ) may be more appropriate for purposely assessing the reaction to noxious stimuli during surgery. However, a monitor of the central nervous system may be more appropriate for monitoring consciousness. After the publication of the B-Aware Trial [ 28 ] ensuring that the BIS index was below 60 was suggested to reduce the risk of anesthesia awareness during surgery for a 'high risk' group, when using a conventional anaesthetic technique. [ 29 ] However, this result was not reproduced by a recently published randomized control trial, the "B-Unaware Trial". [ 18 ] In it, the use of BIS monitoring was not associated with a lower incidence of anesthesia awareness. In some cases, the BIS may underestimate the depth of anesthesia, leading the anesthetist to administer a higher than necessary dose of anesthetic agent(s). In such cases, the patient may be anesthetized to a lower BIS level than is necessary for the surgery or procedure—this is called "treating the BIS", and may result in a deeper level of anesthesia than required). [ citation needed ]
The monitoring of EEG in ICU patients has been employed in one form or other for more than two decades. BIS monitoring is also being used during transport of critically ill patients in ambulances , helicopters and other vehicles.
Some studies show a greater incidence of intra-operative awareness in children, when compared to adults. [ 30 ] The correlation between bispectral index in children over one year and state of consciousness has already been proven, although in younger patients the monitor is unreliable because of the differences between immature infant EEG patterns and the adult EEG patterns that the BIS algorithm utilises. [ 31 ] [ 32 ]
Specifically for intraoperative awareness, according to a 2013 article in The Atlantic , "Today, the BIS monitor has become the most controversial medical device in anesthesiology, if not all of surgery." [ 33 ]
(Commercial interest publications)
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The Bisset Hawkins Medal is a triennial award made by the Royal College of Physicians of London to acknowledge work done in the preceding ten years in advancing sanitary science or promoting public health. It is named after Francis Bisset Hawkins (1796–1884), a distinguished London physician and is presented after the Harveian Oration . [ 1 ]
The medal, made of gold, was endowed by Captain Edward Wilmot Williams in 1896. [ 2 ]
Medallists have been: [ 3 ]
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" Biting the bullet " is a metaphor which is used to describe a situation, often a debate , where one accepts an inevitable impending hardship or hard-to-refute point, and then endures the resulting pain with fortitude.
It has been suggested that it is derived historically from the practice of having a patient clench a bullet in their teeth as a way to cope with the pain of a surgical procedure without anesthetic. Evidence for biting a bullet rather than a leather strap during surgery is sparse, [ 1 ] although Harriet Tubman related having once assisted in a Civil War amputation in which the patient was given a bullet to bite down on. [ 2 ] It has been speculated to have evolved from the British expression "to bite the cartridge", which dates to the Indian Rebellion of 1857 , but the phrase "chew a bullet", with a similar meaning, dates to at least 1796. [ 1 ] It may be helpful for modern audiences to recall that in the era of the origin of this phrase bullets were typically made of lead , a very soft metal, and would have been independent of any charge or cartridge.
The phrase was used in a literal sense in the 1975 film Bite the Bullet . One of the characters has a broken, aching tooth and cannot get treatment. He uses a shell casing to cover the exposed nerve; the slug was removed from the cartridge, the cap was hit to expend the charge, and the casing was cut down to allow it to sit level with his other teeth. [ 3 ] [ better source needed ]
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The Björk–Shiley valve is a mechanical artificial heart valve . The valve was co-invented by American engineer Donald Shiley and Swedish heart surgeon Viking Björk .
Beginning in 1971, it has been used to replace aortic valves and mitral valves . It was the first successful tilting-disc valve. It was manufactured first by Shiley Laboratories, then later by Pfizer after that company purchased Shiley. One model of the Bjork–Shiley valve became the subject of a famous lawsuit and recall after it was shown to malfunction.
The Björk–Shiley valve consists of a single carbon-coated disc in a metal housing. The disc is held in place by two metal struts, an inflow and an outflow strut. The housing is made from the alloy Haynes 25, [ 1 ] which is composed of 51% cobalt , 20% chromium , 15% tungsten , and 10% nickel . [ 2 ] The Björk–Shiley valve was considered very durable and was widely used in the 1970s. [ 3 ] However, later research indicated it was susceptible to long-term wear problems, and could shed microscopic metal fragments. [ 4 ]
Attempts to improve the design of the valve and speed manufacturing, however, led to a weaker structure, with serious consequences. Beginning in 1979, Björk–Shiley valves with the convexo-concave design had a tendency to develop fractures in the outflow strut which could result in catastrophic valve failure and possibly sudden cardiac death. Later analysis revealed that the strut was fracturing at the place where it was welded onto the metal valve ring. One end of the strut would fracture first, followed by the second strut some months later. Eventually, 619 of the 80,000 convexo-concave valves implanted fractured in this way, with the patient dying in two-thirds of those cases. The FDA withdrew approval of the convexo-concave valve in 1986. [ 5 ] [ 6 ] Valves welded by specific welders were at greater risk of fracture.
The convexo-concave valve was withdrawn from the market and multiple lawsuits were filed.
In 1992, Pfizer (Shiley's parent company) and patients with defective valves agreed to a settlement, with Pfizer proposing a fund of $80 million to $130 million in compensation, and to set aside $75 million for research to identify recipients of heart valves with a significant risk of fracture. [ 7 ] The eventual settlement totaled $215 million. A separate part of the agreement required Pfizer to provide up to $300 million for patient or survivor claims in the event of valve fractures. [ 8 ]
Not all of these valves have been removed and replaced. The risk of valve fracture has been balanced against the risk of the surgery to replace the valve. Decision tools have been published and are available from a trust set up for this purpose during the litigation surrounding the valve "recall". The tools take into account patient age, the size and location of the valve (aortic or mitral) and other factors to come up with a recommendation as to whether surgery to replace the valve is worthwhile. In some patients the risk of surgery to replace the valve is higher than the risk of the valve fracturing. A fund was also established for patient compensation and to pay for the costs of heart surgery to replace the valve.
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The Black Report was a 1980 document published by the Department of Health and Social Security (now the Department of Health and Social Care ) in the United Kingdom , which was the report of the expert committee into health inequality chaired by Sir Douglas Black . It was demonstrated that although, in general, health had improved since the introduction of the welfare state , there were widespread health inequalities . It also found that the main cause of these inequalities was economic inequality . The report showed that the death rate for men in social class V was twice that for men in social class I and that gap between the two was increasing, not reducing as was expected.
The Black report was commissioned in March 1977 by David Ennals , Labour Secretary of State, following publication of a two-page article by Richard G. Wilkinson in New Society , on 16 December 1976, entitled Dear David Ennals . The report was nearly ready for publication in early 1979.
In the General Election on 3 May 1979 , the Conservatives were elected. The Black Report was not issued until 1980 by the Conservative Government . The Black report was published on August Bank Holiday with only 260 copies made available on the day for the media. The foreword, by Patrick Jenkin rejected "the view that the causes of health inequalities are so deep rooted that only a major and wide-ranging programme of public expenditure is capable of altering the pattern." He made "it clear that additional expenditure on the scale which could result from the report’s recommendations – the amount involved could be upwards of £2 billion a year – is quite unrealistic in present or any foreseeable economic circumstances, quite apart from any judgement that may be formed of the effectiveness of such expenditure in dealing with the problems identified." [ 1 ]
The report had a huge impact on political thought in the United Kingdom and overseas. It led to an assessment by the Office for Economic Co-Operation and Development and the World Health Organization of health inequalities in 13 countries. [ 2 ]
Professor Clare Bambra in 2016 compared the report with the later Acheson Report and the subsequent report by Michael Marmot . The Acheson report was released into a more favourable climate than either. She said that at least between 1997 and 2003, health policy across the UK reflected some of the ideas set out in the Black and Acheson Reports. There was a consistent emphasis on the need to tackle the social and economic determinants of health inequalities as well as a commitment to employing cross-cutting government policies to tackle health inequality. Most importantly, by 2004, national targets to reduce health inequalities were also introduced with a focus on life expectancy and Infant Mortality Rate. A series of initiatives were introduced - Health Action Zones , Healthy Living Centres, Health Improvement Programmes and the New Deal for Communities . But, perhaps because of these initiatives, from 2004 to 2007, public health policy moved away from social and economic determinants and instead focused more on health services and lifestyle behaviours. The health inequalities targets were abandoned across the UK in 2011. The effect of policy in reducing health inequality was modest. [ 3 ]
Penguin Books published a shortened version of the Black Report in 1982, making it widely available [ 4 ]
The Whitehall Report published in 1987 [ 5 ] came to the same conclusions as the Black report, as did the Acheson Report later in 1998, and the Marmot Review [ 6 ] in 2010.
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Black salve , also known by the brand name Cansema , is an ineffective and unsafe alternative cancer treatment . The product is commonly classified as an escharotic—a topical paste which destroys skin tissue and leaves behind a scar called an eschar . [ 1 ] Escharotics were widely used to treat skin lesions in the early 1900s, but have since been replaced by safer and more effective treatments. [ 2 ] Escharotics, such as black salves, are currently advertised by some alternative medicine marketers as treatments for skin cancer , often with unsubstantiated testimonials and unsupported claims of effectiveness. [ 3 ]
The U.S. Food and Drug Administration has listed Cansema as a "fake cancer cure" and warns consumers to avoid it. [ 4 ]
Cancer salves were first utilized during the Victorian period. As the medical profession started to gain a better understanding, many home remedies, black salve as one example, started to be criticized by medical professionals. An example of this is documented and labeled as a form of quackery in a 1955 Time magazine article: [ 5 ]
A 37-year-old housewife had a skin condition that later (at Duke) proved not to be a cancer. Convinced that it was, she had gone to a backwoods healer, who applied a salve. Soon, a quarter-sized hole disfigured her nose, opening up the nasal cavity. Duke's plastic surgeons had to build her a new nose.
They are not recommended as treatments for skin lesions or skin cancer by medical authorities, but are marketed as such by some alternative medicine practitioners. [ 3 ] [ 6 ] Use of escharotics, particularly when used instead of proven treatments, can be dangerous. [ 3 ] [ 6 ] The escharotic may not remove all of the cancerous cells, and frequently removes healthy tissue. [ 3 ] [ 6 ] Practitioners who use or sell escharotics frequently provide testimonials , in place of scientific evidence, to convince others of effectiveness and safety, which does not exist. [ 3 ] Safer and more effective treatments exist for skin cancers, such as: cryotherapy ; topical agents such as imiquimod , fluorouracil and ingenol mebutate ; radiation therapy ; and surgical excision, including Mohs surgery (microscopically controlled surgery used to remove and test cancerous tissue). [ 3 ]
Escharotics can cause serious scarring and damage to normal skin. Their manufacture is largely unregulated, so the strength and purity of marketed products are unknown and unverified. [ 3 ] Numerous reports in the medical literature describe serious consequences of using escharotics in place of standard treatments for skin cancer, ranging from disfigurement to preventable cancer recurrences. [ 1 ] [ 6 ] [ 7 ] [ 8 ] The website Quackwatch warned against the use of escharotics in 2008, with a collection of sourced documents compiling issues of patient injury from their use. [ 9 ] A more recent study revealed that many individuals who have used black salve were unaware of its potential dangers. [ 10 ] In 2016, the American Academy of Dermatology urged patients to consult a dermatologist before using home remedies for skin cancers. [ 11 ]
It was reported in 2018 that the use of black salve had been expanded to include pets. In a Facebook group, people described the use of black salve on cats, dogs, and horses. [ 12 ]
In 2018, black salve was strongly linked to the death of Helen Lawson in Australia . Lawson covered her abdomen in black salve under the direction of Dennis Wayne Jensen , a self-proclaimed healer, who advised her that it would draw out her ovarian cancer. The black salve left Lawson with a mass of wounds on her abdomen, which became so large within a few weeks that surgeons could not operate on it. Lawson's sister-in-law described the wounds as extending from "above her pubic bone, all across her abdomen almost up to her rib cage", and as "raw, mutilated bubbling flesh". Lawson died in April 2018. [ 13 ]
In 2019, Jensen was issued a prohibition order by the Health Complaints Commissioner of Victoria, forbidding him permanently from providing substances which "he (or anyone else) claims can cure or treat cancer or other serious disease or illness". [ 14 ] This includes black salve. [ 14 ]
Common ingredients of black salves include zinc chloride , chaparral (also known as creosote bush), [ 15 ] and often bloodroot , a plant frequently used in herbal medicine . [ 16 ] The extract of bloodroot is called sanguinarine , a quaternary benzophenanthridine alkaloid which attacks and destroys living tissue and is also classified as an escharotic. [ 17 ]
The Therapeutic Goods Administration (TGA) of Australia is advising consumers against purchasing or using black salve, red salve, or Cansema products. [ 13 ] [ 18 ] The TGA has found the Australian Vaccination-Skeptics Network (AVN) in breach of advertising regulations, [ 19 ] and in a separate finding the AVN's former president Meryl Dorey together with Leon Pittard of Fair Dinkum Radio were found to be in breach. [ 20 ]
Cansema is listed by the U.S. Food and Drug Administration (FDA) as one of 187 fake cancer cures. [ 4 ] Cansema continues to be marketed by numerous individuals, as evidenced by recent FDA Warning Letters . [ 21 ] The FDA has taken enforcement action against illegal marketing of Cansema as a cancer cure, as in the 2004 arrest and conviction of Greg Caton . [ 22 ]
The FDA has taken an active role in the banning of these chemicals for use as a cancer cure. [ 23 ] Typical warning letters detail the dangers of this product while also admonishing the purveyors of their obligation to comply with federal law. [ 24 ] Summaries of recent letters are cataloged on the FDA website. [ 25 ]
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Bladder augmentation is a surgical alteration of the urinary bladder . It involves removing strips of tissue from the intestinal tract and adding this to the tissue of the bladder. This has two intended results: increased bladder volume; and a reduced percentage of the bladder involved in contraction, that in turn results in lower internal pressures in the bladder during urination. Risks of bladder augmentation include incomplete voiding of the bladder post-surgery (resulting in the patient having to undergo intermittent catheterisation or receive an indwelling catheter), acute intestinal obstruction due to adhesions some years after surgery, and, in extremely rare cases, cancers of the intestinal tissue within the bladder.
This surgery has been popular since the 1980s and 90s.
This surgery article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Bladder_augmentation
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Blastic phase chronic myelogenous leukemia is a phase of chronic myelogenous leukemia in which more than 30% of the cells in the blood or bone marrow are blast cells (immature blood cells ). When tiredness , fever , and an enlarged spleen occur during the blastic phase, it is called blast crisis .
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
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In medicine , a bleb is a blister -like protrusion (often hemispherical) or vesicle filled with serous fluid . Blebs can form in a number of tissues by different pathologies, including frostbite and can "appear and disappear within a short time interval".
In pathology, pulmonary blebs are small subpleural thin-walled air-containing spaces, not larger than 1-2 cm in diameter, found by the upper lobe of the lung, between the lung and the visceral pleura . Their walls are thin, being less than 1 mm thick. If they rupture, they allow air to escape into pleural space, resulting in a spontaneous pneumothorax and possibly a collapsed lung. [ 1 ] [ 2 ] Blebs can grow larger or join together to create a larger cyst, or bulla. There are usually no symptoms unless a pneumothorax occurs or the bulla grows very large. Blebs are usually associated with emphysema. [ 3 ]
In ophthalmology , blebs may be formed intentionally in the treatment of glaucoma . In such treatments, functional blebs facilitate the circulation of aqueous humor , the blockage of which will lead to increase in eye pressure. Use of collagen matrix wound modulation device such as ologen during glaucoma surgery is known to produce vascular and functional blebs, which are positively correlated with treatment success rate. [ 4 ] [ 5 ] [ 6 ] [ 7 ]
In the lungs, a bleb is a collection of air within the layers of the visceral pleura .
In breasts , a bleb is a milk blister (also known as blocked nipple pore, nipple blister, or "milk under the skin"). [ 8 ]
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Blebbishield emergency program is a process which acts as a last line of defense for cancer stem cells after induction of apoptosis where the apoptotic blebs fuse to shield the cells/nucleus from the destructive force of apoptosis by forming blebbishields. Blebbishields in turn fuse to each other and generate cancer stem cell spheres/cellular transformation, essentially shifting the balance of dying cells back towards survival.
Blebbishields were first identified in human bladder cancer cell line RT4 (HTB-2: ATCC), referred to as RT4P (RT4 parent) in the initial report. [ 1 ]
Every cell type, especially cancer cells, are capable of undergoing apoptosis, a process in which the plasma membrane undergoes blebbing followed by orderly deconstruction of cells into apoptotic bodies. Cancer stem cells have the extraordinary ability to construct blebbishields from these apoptotic bodies by bleb-bleb fusion and form stem cell spheres/cellular transformation by sub-sequent blebbishield-blebbishield fusion. [ 1 ] [ 2 ] Endocytosis and endocytosis-driven serpentine filopodia are necessary to tether and tie apoptotic bodies to facilitate fusion. [ 3 ] The involvement of membrane fusion was confirmed by inhibiting cholesterol using the cholesterol antagonist Filipin-III. [ 1 ]
Sphere forming cells widely display characteristics of tumorigenesis . Cells from blebbishield derived spheres are tumorigenic in nature, providing an important clue for tumorigenesis. Blebbishield emergency program is postulated to have the strong rationale for bladder cancer recurrence as it is a potential cause for multifocal/satellite bladder tumors. [ 4 ] The blebbishield derived cells exhibit strong drug resistance behavior and exhibit high sensitivity to Hoechst-33342 similar to side-population cells. [ 1 ]
Caspases ( Caspase-3 , caspase-8 , caspase-9 ) are found to have important roles in contributing the formation of blebbishields as well as sub-sequent cancer stem cell spheres. [ 1 ] Caspase-3 plays a dual role where it is needed for induction of proper apoptosis: [ 1 ] to activate Bax and Bak by cleavage to kill the cells and also needed for transformation from blebbishields. [ 5 ]
VEGF signaling, especially VEGF-A to VEGFR2 signaling plays a commanding role during the transformation from blebbishields. [ 3 ] VEGF signaling leads to IRES translation of N-Myc , which in concert with mitochondrial oligomers to boost glycolysis to power blebbishield formation and transformation from blebbishields. [ 5 ] Lactic acid , a tumor derived metabolite, altering pH of tumor microenvironment enhances sphere formation from blebbishields positively regulating VEGF bioavailability. [ 1 ]
Reactive oxygen species plays a role in cellular transformation. Various PKC isoforms were implicated in p47phox/Nox1 axis mediated ROS generation during cellular transformation. PKC-ζ isoform interaction with p47phox was found to be critical for ROS production and transformation from blebbishields. [ 6 ]
Protection of mitochondria from outer membrane permeabilization is important to retain the transforming potential of blebbishields. [ 7 ] Functional mitochondria lead to uninterrupted glycolysis which in turn protects the blebbishields from secondary necrosis. K-Ras , BAD (phosphorylated at Ser-112), p27 , Bax and Bak forms oligomers to boost glycolysis , which in turn overrides secondary necrosis and offer energy required to proceed with the reconstruction process during cellular transformation from blebbishields. [ 5 ]
N-linked glycosylation and v-ATPase were implicated to have survival roles in blebbishield emergency program. [ 1 ]
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Blendax GmbH , founded in 1932 in Mainz , was a German manufacturer of personal hygiene products and toothpaste between 1936 and 2002. With an annual production of 43 million tubes of toothpaste, it was at one time Europe's largest toothpaste producer.
The company's best known brand, introduced in 1951, [ 1 ] was called blend-a-med. [ 2 ] Since 1987, the company has belonged to Procter & Gamble . [ 3 ]
The wordmark "Blendax" for toothpaste was registered in Germany on 4 January 1910, [ 4 ] and the Blendax factory was founded in 1932 by the brothers Rudolf und Hermann Schneider in Mainz; production started in 1936. The goal was to produce a brand of toothpaste that would be affordable by everyone. By the end of the 1930s, Blendax had become Europe's largest producer of toothpaste with 43 million tubes per year. The product portfolio was expanded to include other personal hygiene products like shampoo , soap , skin cream and Mouthwash .
The main and original factory in Mainz on the Ingelheimer Aue (an island in the Rhine ) was almost completely destroyed during World War II . The undamaged branch in Gera was appropriated after the war. At first it was known as VEB Blendax, later as VEB Gerana and after German reunification, as Gerana Cosmetic GmbH, before finally being closed in 2007 as a result of bankruptcy. The original buildings in Gera by the city moat are still extant.
The Mainz work was rebuilt in 1946, with toothpaste production resuming in 1949. In 1956, the production was expanded to include shampoo and bath foam . A special toothpaste for milk teeth was introduced in 1956 under the name Blendi , and in 1957 the production of toothbrushes was started. In the 1970s, the toothpaste Strahler 70 was introduced.
In 1949 the Mainz pharmacist Hertha Hafer offered Blendax her original toothpaste recipe, and In 1951 they started production of blend-a-med , Germany's first medicated toothpaste, at first only available from pharmacies and dentists.
As a result of this new product, a research and development division was founded in the same year under the name blend-a-med Forschung , with the goal to develop products for the prevention of dental and oral diseases.
Dental care
Haircare
Skincare
In 1987 the family business was taken over by the American company Procter & Gamble . At first the takeover led to a strengthening of the site, as P&G moved their British toothpaste production to Mainz in 1989, making the site their main European dental hygiene centre. In 1993, however, the production of skincare products in Mainz was stopped. The production of toothpaste and toothbrushes was continued until 2002, when it was moved to the previous Richardson Wicks site in nearby Groß-Gerau .
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Abdominal bloating (or simply bloating ) is a short-term disease that affects the gastrointestinal tract . [ 1 ] [ 2 ] Bloating is generally characterized by an excess buildup of gas, air or fluids in the stomach . A person may have feelings of tightness, pressure or fullness in the stomach; it may or may not be accompanied by a visibly distended abdomen . [ 3 ] Bloating can affect anyone of any age range and is usually self-diagnosed. In most cases it does not require serious medical attention or treatment. [ 4 ] [ 5 ] Although this term is usually used interchangeably with abdominal distension, these symptoms probably have different pathophysiological processes, which are not fully understood. [ 6 ]
The first step for management is to find a treatment for the underlying causes that produce it through a detailed medical history and a physical examination. The discomfort can be alleviated by the use of certain drugs and dietary modifications. [ 4 ]
Bloating can also be caused by chronic conditions and in rare cases can be a reoccurring life-threatening problem. [ 7 ]
The most common symptom associated with bloating is a sensation that the abdomen is full or distended. Rarely, bloating may be painful or cause shortness of breath. [ citation needed ]
Pains that are due to bloating will feel sharp and cause the stomach to cramp . These pains may occur anywhere in the body and can change locations quickly. [ 8 ] They are so painful that they are sometimes mistaken for heart pains when they develop on the upper left side of the chest. Pains on the right side are often confused with problems in the appendix or the gallbladder .
One symptom of gas that is not normally associated with it is the hiccup . Hiccups are harmless and will diminish on their own; they also help to release gas that is in the digestive tract before it moves down to the intestines and causes bloating. Important but uncommon causes of abdominal bloating include ascites and tumors. [ 9 ]
There are many causes of bloating, including: diet, irritable bowel syndrome , lactose intolerance , reflux , and constipation . [ 10 ] [ 11 ] [ 12 ] [ 13 ] Specific medical conditions like Crohn's disease or bowel obstruction can also contribute to the amount of stomach bloating experienced.
Common causes of abdominal bloating are:
Important but uncommon causes of abdominal bloating include:
In animals, causes of abdominal bloating include:
All the factors mentioned contribute to bloated stomach abdominal pain.
Every person produces gases in their body during the digestion of food, such as methane, hydrogen, carbon dioxide, and nitrogen. And some of them are released outside the body, sometimes in small quantities that one does not notice and sometimes in larger quantities that may affect the normal course of life.
Most cases of stomach bloating are due to improper diet . [ medical citation needed ] Gas occurs because of the bacteria in the colon and is a by-product of soluble fiber digestion. Inadequate or irregular intake of fiber and water will cause a person to experience bloating or constipation. The most common natural sources of fiber include fruits and vegetables as well as wheat or oat bran. These fibers are most likely to cause flatulence . [ 29 ] Fiber is made by plants and is not easily digested by the human gastrointestinal tract . There are two main types of dietary fiber : soluble and insoluble fiber. Soluble fiber is prebiotic and readily fermented in the colon into gases, while insoluble fiber is metabolically inert and absorbs water as it moves through the digestive system, aiding in defecation. Most types of fiber (insoluble) are attached to body water in the intestine and increase the volume of stools. [ citation needed ]
Gas in the gastrointestinal tract has only two sources. It is either swallowed air or is produced by bacteria that normally inhabit the intestines, primarily the colon. [ 30 ]
Belching or burping is a universal ability that works by removing gas from the stomach through the mouth. The stomach can become bloated when too much air is swallowed during eating and drinking too quickly. As the stomach swells, belching removes the gas and alleviates the pain associated with it. Burping can also be used as a form of relief from abdominal discomfort other than too much gas in the stomach. [ citation needed ]
Flatulence , or farting, provides relief of much the same kind as burping, but involves the passage of gas from the body via the anus , not the mouth. Bacteria present in the intestinal tract cause gas that is expelled from the anus. They produce the gas as food is digested and moved from the small intestine . This gas builds up and causes swelling or bloating in the abdominal area before it is released.
A common gastrointestinal problem is constipation —infrequent bowel movements, hard stools, or strain during the movements—which causes serious cases of bloating. Since most cases of constipation are temporary, simple lifestyle changes, such as getting more exercise and increasing one's intake of fiber, can contribute to alleviating constipation. [ 31 ] Some cases of constipation will continue to worsen and require unconventional methods to release the feces and reduce the amount of stomach bloating. Blood in the stool, intense pain in the abdomen, rectal pain, unexplained weight loss, and continued bloating and constipation not relieved by the above lifestyle changes should be reported to a doctor. Bloating consistently accompanies constipation, and they will not develop without an underlying cause. [ 22 ]
Painful burning sensations in the chest that are caused by gastroesophageal reflux is known as heartburn . Reflux is the backflow of gastric acid juices from the stomach into the oesophagus . [ 32 ] Heartburn has different triggers, including certain foods, medications, obesity , and stress. These triggers are different for each individual. Gastroesophageal reflux disease or GERD is a chronic condition that can lead to more serious complications like esophageal cancer . [ 33 ] Treatment options are available to treat the symptoms and the condition, but there is no cure for the disease. Symptoms include burping, abdominal and stomach bloating, along with pain and discomfort. Heavy meals, lying down or bending over after eating should be avoided to help prevent reflux from occurring. The stomach bloating experienced with reflux is intense and will remain until the food is digested all the way.
Postmortem bloating occurs in cadavers, due to the formation of gases by bacterial action and putrefaction of the internal tissues of the abdomen and the inside of the intestines. [ 34 ]
Conditions that are related to bloating include constipation, lactose intolerance, and acid reflux disease. [ 32 ] All of these conditions share the same symptoms and can share the same causative agents. These causes include unhealthy diet, smoking, alcohol consumption, low amount of exercise, and overall health. Each of these conditions can be experienced as a symptom of the others and is also a cause for each of them. In most cases where one of the conditions is present, there is at least one if not two of the others. Treatment for each condition is performed using the same medications and recommended dietary changes like increased fiber intake and reduced fat intake. If the conditions develop into diseases such as gastroesophageal reflux disease or chronic constipation, additional medications will be required. Bloating and flatulence are sometimes related to constipation, and treating the underlying condition may be helpful. [ 35 ]
Promising evidence on the potential efficacy of the low-FODMAP diet in functional abdominal bloating is provided by the reduction of the bloating which has been observed in some studies on patients with irritable bowel syndrome . Regarding the gluten-free diet , there is insufficient scientific evidence to recommend it to reduce bloating and abdominal distension. [ 36 ] As regards the FODMAP diet, this should be provided by experts in nutrition to reduce the risks associated with elimination diets. [ 37 ]
There are many over-the-counter (OTC) medications that can be used to treat bloating.
Food enzymes can be found in some products that will help break down the sugars found in grains, vegetables and dairy products . They can be taken before food is consumed or added to the food that causes the gas and bloating. [ 38 ] The most common treatment is antacids . These medications have no effect on the gas that is present in the intestines but enable gas build-up to be belched away more easily, reducing the amount of bloating that develops. Another treatment is simethicone , an oral anti-foaming agent that helps the body to expel the gas more quickly.
Combinations of prokinetics , such as domperidone + metoclopramide + diphenhydramine (the latter for the prevention of extrapyramidal reactions, especially acute dystonic reactions) + proton pump inhibitors (PPIs), have dramatic effects on bloaters and belchers especially. [ citation needed ]
Notes
Bibliography
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The Blob Tree is a visual tool designed to allow individuals to express themselves and their emotions in a non-verbal way through the use of human figures known as Blobs who are genderless, ageless, and culture-less. [ 1 ]
The original Blob Tree was created in the early 1980s [ 2 ] by Pip Wilson and Ian Long as a way of communicating with young people and adults who found reading difficult. [ 3 ]
The Blob Tree collection consists of a set of illustrations of blob figures in various poses and expressions, each representing a different emotion or feeling . [ 4 ] These illustrations are intended to be used as prompts for individuals to identify and express their own emotions, or as a way to start a conversation about emotions and feelings. [ 5 ]
The Blob Tree has been adopted by professionals in a variety of fields, including counselling , therapy , education , and youth work , and in a variety of settings, including schools , hospitals , community centers , and prisons . [ 6 ] The tool's success came from its simplicity and universality where the blob figures were easily recognizable and relatable, making it easy for individuals to connect with the illustrations and express their own emotions. [ 7 ]
The Blob Tree was created by Pip Wilson & Ian Long. Recognising the need for a non-verbal, universally accessible tool for emotional expression and communication , they developed the Blob Tree as a way to bridge language and cultural barriers and make emotional expression more accessible to people of different ages and backgrounds. [ 8 ]
Pip Wilson (1939–2023) was born in St Helens, Merseyside. A trained youth worker [ 9 ] working with gangs, running community centres and training youth leaders. He was author of many books including Gutter Feelings & Pip Wisdom. With many years of experience working with young people, Pip branched out specialising in team leadership, workshops, teaching and practical training in the area of emotional intelligence . [ 10 ]
The intentions for the blobs according to Wilson was that they can "help facilitate and stimulate meaningful discussions about difficult issues or situations. Individuals or groups can start discussions by identifying themselves, or others, with an individual or group of blobs whose actions or feelings represent their own. " [ 11 ] Wilson died on 22 September 2023. On the BBC "pause for thought", it referenced Wilson's "You are a beautiful human person", phrase which inspired much of the Blob Tree content. [ 12 ]
Ian Charles Long, born in Birmingham in 1965 to Sidney and Doreen Long, is an author and artist and worked for 17 years as a primary school teacher. [ 13 ] Long's contribution to the Blob Tree originated in discussion with Wilson who shared his ideas for a non-verbal image to help with emotional expression. Wilson gave ideas to Long who would illustrate the ideas and turn them into pictures. [ citation needed ]
Through growing fame, the Blob Tree moved away from just visual tools and began to involve conferences and training workshops ran by Pip and then Ian Long at the request of schools, colleges and countries most popularly in the United Kingdom, Norway, Finland, Bulgaria, Germany and Czechia. [ 14 ]
Since Wilson's death in 2023, Long continues the Blobtree with the Wilson family, which by this time also involves daily inspirational quote images posted on social media, [ 15 ] and a new project called the 'Visual Bible' illustrating each verse of the Bible into Blob format. [ 16 ]
Their most notable works include:
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Blocq's disease was first considered by Paul Blocq (1860–1896), [ 1 ] who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra. [ 1 ]
In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.
One of the issues that neurobiologists are more concerned is related with the ability of learning and retaining motor skills controlled by the primary motor cortex . Through literature, they have found that primary motor cortex neurons may control skill acquisition and retention. One of the abilities of the motor cortex that allow this control is plasticity which occurs due to the everyday experience of movement repetition. A common substrate of plasticity are the internal system of connections that are located around these regions, creating motor maps. [ 2 ]
Vestibulospinal tracts: The importance is involved in the control of postural adjustments and head movements as well as balance maintenance. Any movement of the body is detected by the vestibular sensory neurons, and the sensory motor replies by counteracting the movements through the vestibulospinal tracts and exerting action on a group of muscles throughout the body. The lateral vestibulospinal tract excites antigravity muscles in order to exert control over postural changes necessary to compensate for tilts and movements of the body. The medial vestibulospinal tract innervates neck muscles in order to stabilize head position as one moves around the world. [ 3 ]
Reticulospinal tracts: It serves as a connector for the corticospinal system by which cortical neurons can control motor function. These tracts regulate the sensitivity of flexor responses to ensure that only noxious stimuli elicit the responses. The reticular formation also contains circuitry for many complex actions, such as orienting, stretching, and maintaining a complex posture. Commands that initiate locomotor circuits in the spinal cord are also transmitted through the medullary reticulospinal tract. Thus, the reticulospinal tracts are involved in many aspects of motor control, including the integration of sensory input to guide motor output. [ 4 ]
Balance between various interacting neuronal systems such as locomotion which includes initiation and maintenance of rhythmic stepping, balance, and ability to adapt to the environment. [ 7 ] Deficit appears to be localized in the putamen and globus pallidus resulting in a reduction in the muscle force produced at the initiation of the movement. Initiation of a movement starts by inducing stepping through reticulospinal and vestibulospinal projection in ventromedial descending brainstem pathways. The bulbospinal pathways are modulated with the support of and swing of the gait cycle, and this modulation is accomplished through the connections with the cerebral vermis. Diseases that affect the vestibular system such as gait disorders often impair the initiation of a movement. Most of the patients with blocq's syndrome suffer from hypokinetic gait disorder defined as slowness of movement due to the dysfunction of the circuitry controlled by the basal ganglia, frontal lobe and brainstem. Patients are limited to a wide-based or variable stance and truncal imbalance. [ 7 ]
Another region involved in the psychogenic tremor is the temporoparietal junction depicted by a hypo-activation in patients that were functional imaging recorded during an episode of functional tremor or when the same patients were voluntarily mimicking their tremor. This region is thought to be a comparator region, comparing actual with predicted sensory feedback. This experiment suggests that the hypoactivity might represent a failure to match the actual and predicted sensory feedback, resulting in an inhibition of the movement. [ 8 ] In addition, another functional imaging study in psychogenic movement disorder noted abnormally strong amygdala–supplementary motor area connectivity when patients were presented with emotionally stimuli and abnormally weak supplementary motor area– prefrontal cortex connectivity in a reaction time task. [ 9 ] Scientists thus speculated that the hypoactivity may be due to the lack of an appropriate prediction outcome signal of the conversion tremor. Thus, without the predicted outcome signal, there would be no comparison between the predicted versus the actual sensory outcome of the conversion movement and hence the temporoparietal junction hypoactivity and the sensation that the movement is not under one's control enabling the initiation of it.
Psychogenic disorder has been linked with basal ganglia dysfunction and dopamine deficiency observed by a decrease in neuronal density in substantia nigra in elderly patients. [ 10 ] On an in-vivo study, the absence of dopamine in the cultures perturbed the dynamics of the subthalamic nucleus (STN) and the GABAergic neurons of the globus pallidus (GP). It is believed that the activation of the indirect pathway (striatum-GP-STN-output nuclei) increases the firing rate of GP-STN neurons resulting in an excessive inhibition of basal ganglia targets. [ 11 ] In psychogenic disorder, the activity in the indirect pathway (inhibits movement, thoughts) predominates over that on the direct pathway (increases movement, thoughts, feelings), giving rise to an increase in the globus pallidus interior (GPi) inhibitory output, which results in decrease motor activity. Specifically, it begins on the cerebral cortex sending projections to neurons in striatum. These neurons will inhibit the external segment of the Globus Pallidus (GPe), which normally inhibits the subthalamic nucleus (STN). However, the GPe is inhibited and no longer inhibit the STN and the STN will excite the GPi which finally inhibits the thalamus and prevents from exciting to the cerebral cortex and command the spinal cord for initiation of a movement. [ 11 ] In addition, scientists have found that the degree of slowness of movement is characterized by the decrease of F-fluorodpa uptake in the striatum and nucleus accumbens complex.
Basal ganglia are a group of nuclei of varied origin in the brains of vertebrates that act as a cohesive functional unit. The basal ganglia are associated with a variety of functions, including voluntary motor control, procedural learning relating to routine behaviors. Nowadays, the basal ganglia is implicated primarily in action selection, meaning execution of a task at a given time. The main components of the basal ganglia are the striatum, the globus pallidus, the substantia nigra, and the subthalamic nucleus. The largest component, the striatum, receives input from many brain areas but sends output only to other components of the basal ganglia. The pallidum receives input from the striatum, and sends inhibitory output to a number of motor-related areas. The substantia nigra is the source of the striatal input of the neurotransmitter dopamine, which plays an important role in basal ganglia function. The subthalamic nucleus receives input mainly from the striatum and cerebral cortex, and projects to the globus pallidus. The basal ganglia have a limbic sector that involve the ventral tegmental area (VTA), its dysfunction has been related in some diseases such as Parkinson's disease and movement disorders.
Striatum is a subcortical part of the forebrain. It is the major input station of the basal ganglia system. The striatum, in turn, gets input from the cerebral cortex.
The putamen and caudate nucleus together form the dorsal striatum which contributes directly to decision-making, especially to action selection and initiation. It works under dopamine intake and sends its signal to the basal ganglia.
The putamen, together with the globus pallidus, makes up the lenticular nucleus. The important aspect of this interaction is that the globus pallidus sends the inhibitory output from the basal ganglia to the thalamus and sends a few projections to parts of the midbrain, which have been assumed to affect posture control.
Excitation of the globus pallidus interior (GPi) by the subthalamus facilitates movement suppression. When non-motor cerebral cortex excites the striate body, the caudate and putamen specifically inhibit neurons in the globus pallidus and subthalamus. This specific disinhibition enables movement initiation, by releasing excitatory thalamic neurons.
Functionally strongly associated with emotional and motivational aspects of behavior. Strongly innervated by dopaminergic fibers from the ventral tegmental area (VTA).
The projections of the basolateral nucleus to the dorsal or ventral striatum have been suggested to play a role in avoidance learning. The amygdala has also been implicated in conditioned approach behaviors. Scientists demonstrated surprising limbic-motor interactions in patients with motor conversion disorder that may underlie the influence of affect or arousal on motor function. The amygdala projects to the nucleus accumbens core and dorsal striatum, which have projections via the pallidum and thalamus to the supplementary motor area. The supplementary motor area is a major source of input to the corticospinal tract and is reciprocally connected to the primary motor cortex and basal ganglia. The supplementary motor complex is implicated in self-initiated action. [ 9 ] It is believed to be one source of a slowly increasing negative potential that precedes movement onset. The supplementary motor area has also been implicated in non-conscious motor inhibition. In a study on healthy individuals, masked stimuli that are briefly presented and not consciously observed can act as a prime to initially facilitate a response but the response is then inhibited. In the lesion patients, the responses were normally facilitated but not subsequently inhibited suggesting a potential role of the supplementary motor area in non-conscious motor response inhibition. Thus, they speculated that effect of arousal on amygdala activity may influence motor symptoms either through a general effect on initiation of the motor conversion symptom or possibly through a failure of inhibition of the motor conversion symptom. [ 9 ]
The doctor will review the person's medical history and perform a complete physical and neurological examination that will include an evaluation of the gait. The doctor may ask the patient to walk in a corridor or climb stairs to observe specific features including: [ 6 ]
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The Blood Pressure Association (or BPA) is a British charitable organisation , established in October 2000, that seeks to provide information and support to people with high blood pressure (also known as hypertension ) and to educate the general public about the importance of blood pressure to health.
It is based at St George's Hospital in Tooting , London .
Every September, the association runs a blood pressure testing week as part of its Know Your Numbers campaign, where doctors, nurses, pharmacists and trainers offer free blood pressure tests in hospitals , pharmacies , health centres and shopping centres throughout the UK. [ 1 ] [ 2 ]
The organization was founded in 2001 by Graham MacGregor . [ 3 ]
Sir David Attenborough was appointed patron of the Association in May 2005.
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Blood sugar regulation is the process by which the levels of blood sugar , the common name for glucose dissolved in blood plasma , are maintained by the body within a narrow range.
This tight regulation is referred to as glucose homeostasis . Insulin , which lowers blood sugar, and glucagon , which raises it, are the most well known of the hormones involved, but more recent discoveries of other glucoregulatory hormones have expanded the understanding of this process. The gland called pancreas secretes two hormones and they are primarily responsible to regulate glucose levels in blood. [ 1 ]
Blood sugar levels are regulated by negative feedback in order to keep the body in balance . [ 2 ] [ 3 ] [ 4 ] [ 5 ] The levels of glucose in the blood are monitored by many tissues, but the cells in the pancreatic islets are among the most well understood and important. [ citation needed ]
Granule docking is an important glucose-dependent step in human insulin secretion that does not work properly in type 2 diabetes . [ 6 ]
If the blood glucose level falls to dangerously low levels (as during very heavy exercise or lack of food for extended periods), the alpha cells of the pancreas release glucagon , a peptide hormone which travels through the blood to the liver, where it binds to glucagon receptors on the surface of liver cells and stimulates them to break down glycogen stored inside the cells into glucose (this process is called glycogenolysis ). The cells release the glucose into the bloodstream, increasing blood sugar levels. Hypoglycemia , the state of having low blood sugar, is treated by restoring the blood glucose level to normal by the ingestion or administration of dextrose or carbohydrate foods. It is often self-diagnosed and self-medicated orally by the ingestion of balanced meals. In more severe circumstances, it is treated by injection or infusion of glucagon. [ citation needed ]
When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from beta cells found in the islets of Langerhans in the pancreas. This hormone, insulin , causes the liver to convert more glucose into glycogen (this process is called glycogenesis ), and to force about 2/3 of body cells (primarily muscle and fat tissue cells) to take up glucose from the blood through the GLUT4 transporter, thus decreasing blood sugar. When insulin binds to the receptors on the cell surface, vesicles containing the GLUT4 transporters come to the plasma membrane and fuse together by the process of endocytosis , thus enabling a facilitated diffusion of glucose into the cell. As soon as the glucose enters the cell, it is phosphorylated into glucose-6-phosphate in order to preserve the concentration gradient so glucose will continue to enter the cell. [ 7 ] Insulin also provides signals to several other body systems, and is the chief regulator of metabolic control in humans. [ citation needed ]
There are also several other causes for an increase in blood sugar levels. Among them are the 'stress' hormones such as epinephrine (also known as adrenaline), several of the steroids, infections, trauma, and of course, the ingestion of food. [ citation needed ]
Diabetes mellitus type 1 is caused by insufficient or non-existent production of insulin, while type 2 is primarily due to a decreased response to insulin in the tissues of the body ( insulin resistance ). Both types of diabetes, if untreated, result in too much glucose remaining in the blood ( hyperglycemia ) and many of the same complications. Also, too much insulin and/or exercise without enough corresponding food intake in diabetics can result in low blood sugar ( hypoglycemia ). [ citation needed ]
Insects have two types of „blood sugar", the monosaccharide glucose and the disaccharide trehalose . Trehalose is the major carbohydrate used by insects for flight. [ 9 ]
The concentrations of the carbohydrates trehalose and glucose in the insect hemolymph are tightly controlled by multiple enzymes and hormones, including trehalase , insulin -like peptides (ILPs and DILPs), adipokinetic hormone (AKH), leucokinin (LK), octopamine and other mediators, thereby maintaining carbohydrate homeostasis by endocrine and metabolic feedback mechanisms. [ 10 ] [ 11 ] [ 12 ] [ 13 ]
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Bloodless surgery is a non-invasive surgical method developed by orthopedic surgeon Adolf Lorenz , who was known as "the bloodless surgeon of Vienna ". [ 1 ] [ 2 ] [ 3 ] [ 4 ] His medical practice was a consequence of his severe allergy to carbolic acid routinely used in operating rooms of the era. His condition forced him to become a "dry surgeon". [ 5 ] Contemporary usage of the term refers to both invasive and noninvasive medical techniques and protocols. [ 6 ] The expression does not mean surgery that makes no use of blood or blood transfusion . Rather, it refers to surgery performed without transfusion of allogeneic blood. [ 7 ] [ 8 ] Champions of bloodless surgery do, however, transfuse products made from allogeneic blood (blood from other people) and they also make use of pre-donated blood for autologous transfusion (blood pre-donated by the patient). [ 9 ] Interest in bloodless surgery has arisen for several reasons. Jehovah's Witnesses reject blood transfusions on religious grounds; others may be concerned about bloodborne diseases , such as hepatitis and AIDS.
During the early 1960s, American heart surgeon Denton Cooley successfully performed numerous bloodless open-heart surgeries on Jehovah's Witness patients. Fifteen years later, he and his associate published a report of more than 500 cardiac surgeries in this population, documenting that cardiac surgery could be safely performed without blood transfusion . [ 10 ]
Ron Lapin (1941–1995) was an American surgeon, who became interested in bloodless surgery in the mid-1970s. He was known as a "bloodless surgeon" due to his willingness to perform surgeries on severely anemic Jehovah's Witness patients without the use of blood transfusions .
Patricia A. Ford (born 1955) was the first surgeon to perform a bloodless bone marrow transplant. [ 11 ]
In 1988, Professor James Isbister, a haematologist from Australia, first proposed a paradigm shift back to a patient focus. In 2005, he penned an article in the journal, 'Updates in Blood Conservation and Transfusion alternatives'. In this article Prof. Isbister coined the term 'patient blood management', noting that the focus should be changed from the product to the patient.
Several principles of bloodless surgery have been published. [ 12 ]
Preoperative techniques such as erythropoietin (EPO) or iron administration are designed to stimulate the patient's own erythropoiesis .
In surgery, control of bleeding is achieved with the use of laser or sonic scalpels, minimally invasive surgical techniques, electrosurgery and electrocautery , low central venous pressure anesthesia (for select cases), or suture ligation of vessels. [ 13 ] Other methods include the use of blood substitutes , which at present do not carry oxygen but expand the volume of the blood to prevent shock . Blood substitutes which do carry oxygen, such as PolyHeme , are also under development. [ contradictory ] Many doctors view acute normovolemic hemodilution, a form of storage of a patient's own blood, as a pillar of "bloodless surgery" but the technique is not an option for patients who refuse autologous blood transfusions .
Intraoperative blood salvage is a technique which recycles and cleans blood from a patient during an operation and redirects it into the patient's body.
Postoperatively, surgeons seek to minimize further blood loss by continuing administration of medications to augment blood cell mass and minimizing the number of blood draws and the quantity of blood drawn for testing, for example, by using pediatric blood tubes for adult patients. [ 13 ] HBOC's such as Polyheme and Hemepure have been discontinued due to severe adverse reactions including death. South Africa was the only country where they were legally authorized as standard treatment but they are no longer available.
Bloodless medicine appeals to many doctors because it carries low risk of post-operative infection when compared with procedures requiring blood transfusion . Additionally, it may be economically beneficial in some countries. For example, the cost of blood in the US hovers around $500 a unit, including testing. [ 14 ] These costs are further increased as, according to Jan Hoffman (an administrator for the blood conservation program at Geisinger Medical Center in Danville, Pennsylvania ), hospitals must cover the cost of the first three units of blood infused per patient per calendar year. [ citation needed ] By contrast, hospitals may be reimbursed for drugs that boost a patient's red blood cell count, a treatment approach often used before and after surgery to reduce the need for a blood transfusion . [ citation needed ] However, such payments are highly contingent upon negotiations with insurance companies. Geisinger Medical Center began a blood conservation program in 2005 and reported a recorded savings of $273,000 in its first six months of operation. [ 15 ] The Cleveland Clinic lowered their direct costs from US$35.5 million in 2009 to $26.4 million in 2012—a savings of nearly $10 million over 3 years. [ 16 ]
Health risks appear to be another contributing factor in their appeal, especially in light of recent studies that suggest that blood transfusions can increase the risk of complications and reduce survival rates. [ 17 ] [ 18 ] Thus, patients who do not receive blood products during hospitalization often recover more quickly, experience fewer complications, and are able to be discharged home more quickly.
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Bloodstopping refers to an American folk practice once common in the Ozarks and the Appalachians , Canadian lumbercamps and the northern woods of the United States. It was believed (and still is) that certain persons, known as bloodstoppers , could halt bleeding in humans and animals by supernatural means. The most common method was to walk east and recite Ezekiel 16:6 . This is referred to as the blood verse.
Bloodstopping was used in areas of North American where modern medicine was not reachable. Many of these communities had one or two bloodstoppers in their community. Since they were able to help when doctors were unavailable they became very popular in their community and were well respected. Bloodstopping was used mostly in the Ozarks, in the states Illinois, Missouri, and Arkansas. Each bloodstopper used their own technique to fix wounds. [ 1 ] [ better source needed ] The person performing the bloodstopping must have been given the power to do so. The gift was mostly passed down through family (older to younger). It can only be passed down to the opposite sex. It can only be told to three people, with the third person gaining the power. [ 2 ] [ self-published source ] The person performing it does not need to believe in it fully or be sinless since the blood verse is so powerful. [ 3 ] [ unreliable source? ]
Throughout Europe Christianity was becoming the main religion. However those who lived in rural areas were not as quick to convert. They were more fond of polytheistic religions since they had been used to it for so many years. German settlers who ended up in the Appalachians had many folk beliefs about magic. At first they used stars to determine planting cycles and to predict weather. When medical treatment became scarce they turned to other forms of medicine. This is when bloodstopping became a practice. [ 4 ]
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The blood–brain barrier ( BBB ) is a highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and the central nervous system , thus protecting the brain from harmful or unwanted substances in the blood . [ 1 ] The blood–brain barrier is formed by endothelial cells of the capillary wall , astrocyte end-feet ensheathing the capillary, and pericytes embedded in the capillary basement membrane . [ 2 ] This system allows the passage of some small molecules by passive diffusion , as well as the selective and active transport of various nutrients, ions, organic anions, and macromolecules such as glucose and amino acids that are crucial to neural function. [ 3 ]
The blood–brain barrier restricts the passage of pathogens , the diffusion of solutes in the blood, and large or hydrophilic molecules into the cerebrospinal fluid , while allowing the diffusion of hydrophobic molecules (O 2 , CO 2 , hormones) and small non-polar molecules. [ 4 ] [ 5 ] Cells of the barrier actively transport metabolic products such as glucose across the barrier using specific transport proteins . [ 6 ] The barrier also restricts the passage of peripheral immune factors, like signaling molecules, antibodies, and immune cells, into the central nervous system, thus insulating the brain from damage due to peripheral immune events. [ 7 ]
Specialized brain structures participating in sensory and secretory integration within brain neural circuits —the circumventricular organs and choroid plexus —have in contrast highly permeable capillaries. [ 8 ]
The BBB results from the selectivity of the tight junctions between the endothelial cells of brain capillaries, restricting the passage of solutes. [ 1 ] At the interface between blood and the brain, endothelial cells are adjoined continuously by these tight junctions, which are composed of smaller subunits of transmembrane proteins , such as occludin , claudins (such as Claudin-5 ), junctional adhesion molecule (such as JAM-A). [ 6 ] Each of these tight junction proteins is stabilized to the endothelial cell membrane by another protein complex that includes scaffolding proteins such as tight junction protein 1 (ZO1) and associated proteins. [ 6 ]
The BBB is composed of endothelial cells restricting passage of substances from the blood more selectively than endothelial cells of capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as " glia limitans ") surround the endothelial cells of the BBB, providing biochemical support to those cells. [ 9 ] The BBB is distinct from the quite similar blood-cerebrospinal fluid barrier , which is a function of the choroidal cells of the choroid plexus , and from the blood-retinal barrier , which can be considered a part of the whole realm of such barriers. [ 10 ]
Not all vessels in the human brain exhibit BBB properties. Some examples of this include the circumventricular organs , the roof of the third and fourth ventricles , capillaries in the pineal gland on the roof of the diencephalon and the pineal gland . [ 11 ] [ 12 ]
The BBB appears to be functional by the time of birth. P-glycoprotein , a transporter , exists already in the embryonal endothelium. [ 13 ]
Measurement of brain uptake of various blood-borne solutes showed that newborn endothelial cells were functionally similar to those in adults, [ 14 ] indicating that a selective BBB is operative at birth.
The blood–brain barrier acts effectively to protect brain tissue from circulating pathogens and other potentially toxic substances. [ 15 ] Accordingly, blood-borne infections of the brain are rare. [ 1 ] Infections of the brain that do occur are often difficult to treat. Antibodies are too large to cross the blood–brain barrier, and only certain antibiotics are able to pass. [ 16 ] In some cases, a drug has to be administered directly into the cerebrospinal fluid where it can enter the brain by crossing the blood-cerebrospinal fluid barrier . [ 17 ] [ 18 ]
Circumventricular organs (CVOs) are individual structures located adjacent to the fourth ventricle or third ventricle in the brain, and are characterized by dense capillary beds with permeable endothelial cells unlike those of the blood–brain barrier. [ 11 ] [ 12 ] Included among CVOs having highly permeable capillaries are the area postrema , subfornical organ , vascular organ of the lamina terminalis , median eminence , pineal gland , and three lobes of the pituitary gland . [ 11 ] [ 19 ]
Permeable capillaries of the sensory CVOs (area postrema, subfornical organ, vascular organ of the lamina terminalis) enable rapid detection of circulating signals in systemic blood, while those of the secretory CVOs (median eminence, pineal gland, pituitary lobes) facilitate transport of brain-derived signals into the circulating blood. [ 11 ] [ 12 ] Consequently, the CVO permeable capillaries are the point of bidirectional blood–brain communication for neuroendocrine function. [ 11 ] [ 19 ] [ 20 ]
The border zones between brain tissue "behind" the blood–brain barrier and zones "open" to blood signals in certain CVOs contain specialized hybrid capillaries that are leakier than typical brain capillaries, but not as permeable as CVO capillaries. Such zones exist at the border of the area postrema— nucleus tractus solitarii (NTS), [ 21 ] and median eminence— hypothalamic arcuate nucleus . [ 20 ] [ 22 ] These zones appear to function as rapid transit regions for brain structures involved in diverse neural circuits—like the NTS and arcuate nucleus—to receive blood signals which are then transmitted into neural output. [ 20 ] [ 21 ] The permeable capillary zone shared between the median eminence and hypothalamic arcuate nucleus is augmented by wide pericapillary spaces, facilitating bidirectional flow of solutes between the two structures, and indicating that the median eminence is not only a secretory organ, but may also be a sensory organ. [ 20 ] [ 22 ]
The blood–brain barrier is formed by the brain capillary endothelium and excludes from the brain 100% of large-molecule neurotherapeutics and more than 98% of all small-molecule drugs. [ 23 ] Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders. [ 24 ] [ 25 ] In its neuroprotective role, the blood–brain barrier functions to hinder the delivery of many potentially important diagnostic and therapeutic agents to the brain. Therapeutic molecules and antibodies that might otherwise be effective in diagnosis and therapy do not cross the BBB in adequate amounts to be clinically effective. [ 24 ] To overcome this problem some peptides able to naturally cross the BBB have been widely investigated as a drug delivery system. [ 26 ]
Mechanisms for drug targeting in the brain involve going either "through" or "behind" the BBB. Modalities for drug delivery to the brain in unit doses through the BBB entail its disruption by osmotic means, or biochemically by the use of vasoactive substances, such as bradykinin , [ 27 ] or even by localized exposure to high-intensity focused ultrasound (HIFU) . [ 28 ]
Other methods used to get through the BBB may entail the use of endogenous transport systems, including carrier-mediated transporters, such as glucose and amino acid carriers, receptor-mediated transcytosis for insulin or transferrin , and the blocking of active efflux transporters such as p-glycoprotein . [ 24 ] Some studies have shown that vectors targeting BBB transporters, such as the transferrin receptor , have been found to remain entrapped in brain endothelial cells of capillaries, instead of being ferried across the BBB into the targeted area. [ 24 ] [ 29 ]
The brain can be targeted non-invasively via the nasal passage. The drugs that remain in the passage after mucociliary clearance, enter the brain via three pathways: (1) Olfactory nerve-olfactory bulb-brain; (2) Trigeminal nerve-brain; and (3) Lungs/ Gastrointestinal tract-blood–brain [ 30 ] The first and second methods involve the nerves, so they use the neuronal pathway and the third is via systemic circulation. However, these methods are less efficient to deliver drugs as they are indirect methods.
Nanotechnology is under preliminary research for its potential to facilitate the transfer of drugs across the BBB. [ 24 ] [ 31 ] [ 32 ] Capillary endothelial cells and associated pericytes may be abnormal in tumors and the blood–brain barrier may not always be intact in brain tumors. [ 32 ] Other factors, such as astrocytes , may contribute to the resistance of brain tumors to therapy using nanoparticles. [ 33 ] Fat soluble molecules less than 400 daltons in mass can freely diffuse past the BBB through lipid mediated passive diffusion. [ 34 ]
The blood–brain barrier may become damaged in certain neurological diseases , as indicated by neuroimaging studies of Alzheimer's disease , amyotrophic lateral sclerosis , epilepsy , ischemic stroke, [ 15 ] [ 35 ] [ 36 ] [ 37 ] and brain trauma , [ 24 ] and in systemic diseases , such as liver failure . [ 1 ] Effects such as impaired glucose transport and endothelial degeneration may lead to metabolic dysfunction within the brain, and an increased permeability of the BBB to proinflammatory factors, potentially allowing antibiotics and phagocytes to move across the BBB. [ 1 ] [ 24 ] However, in many neurodegenerative diseases, the exact cause and pathology remains unknown. It is still unclear whether the BBB dysfunction in the disease is a causative agent, a result of the disease, or somewhere in the middle.
A 1898 study observed that low-concentration " bile salts " failed to affect behavior when injected into the blood of animals. Thus, in theory, the salts failed to enter the brain. [ 38 ]
Two years later, Max Lewandowsky may have been the first to coin the term "blood–brain barrier" in 1900, referring to the hypothesized semipermeable membrane. [ 39 ] There is some debate over the creation of the term blood–brain barrier as it is often attributed to Lewandowsky, but it does not appear in his papers. The creator of the term may have been Lina Stern . [ 40 ] Stern was a Russian scientist who published her work in Russian and French. Due to the language barrier between her publications and English-speaking scientists, this could have made her work a lesser-known origin of the term.
All the while, bacteriologist Paul Ehrlich was studying staining , a procedure that is used in many microscopy studies to make fine biological structures visible using chemical dyes. [ 41 ] As Ehrlich injected some of these dyes (notably the aniline dyes that were then widely used), the dye stained all of the organs of some kinds of animals except for their brains. [ 41 ] At that time, Ehrlich attributed this lack of staining to the brain simply not picking up as much of the dye. [ 39 ]
However, in a later experiment in 1913, Edwin Goldmann (one of Ehrlich's students) injected the dye directly into the cerebrospinal fluid of animal brains. He found then the brains did become dyed, but the rest of the body did not, demonstrating the existence of a compartmentalization between the two. At that time, it was thought that the blood vessels themselves were responsible for the barrier, since no obvious membrane could be found.
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Blood–gas partition coefficient , also known as Ostwald coefficient for blood–gas , [ 1 ] is a term used in pharmacology to describe the solubility of inhaled general anesthetics in blood. [ 2 ] According to Henry's law , the ratio of the concentration in blood to the concentration in gas that is in contact with that blood, when the partial pressure in both compartments is equal, is nearly constant at sufficiently low concentrations. The partition coefficient is defined as this ratio and, therefore, has no units. The concentration of the anesthetic in blood includes the portion that is undissolved in plasma and the portion that is dissolved (bound to plasma proteins ). The more soluble the inhaled anesthetic is in blood compared to in air, the more it binds to plasma proteins in the blood and the higher the blood–gas partition coefficient .
It is inversely related to induction rate . Induction rate is defined as the speed at which an agent produces anesthesia. The higher the blood:gas partition coefficient , the slower the rate of induction.
Newer anesthetics (such as desflurane ) typically have smaller blood–gas partition coefficients than older ones (such as ether ); this leads to faster onset of anesthesia and faster emergence from anesthesia once application of the anesthetic is stopped, which may be preferable in certain clinical scenarios. [ 3 ] [ 4 ] If an anesthetic has a high coefficient, then a large amount of it will have to be taken up in the body's blood before being passed on to the fatty (lipid) tissues of the brain where it can exert its effect.
The potency of an anesthetic is associated with its lipid solubility, which is measured by its oil/gas partition coefficient. [ 5 ]
Minimum alveolar concentration (MAC) is defined as the alveolar concentration of anesthetic gas that prevents a movement response in half of subjects undergoing a painful (surgical) stimulus; simplified, it is the exhaled gas concentration required to produce anaesthetic effects – an inverse indicator of anesthetic gas potency.
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Bloomage , also known as Bloomage Biotech , is a biomaterial company based in China. [ 7 ] [ 8 ] Bloomage primarily specializes in hyaluronic acid and other bioactive substances products. It is listed on the Shanghai Stock Exchange . [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ]
In 2000, Bloomage was established and began to mass-produce hyaluronic acid using microbial fermentation . [ 8 ] [ 14 ]
Bloomage's first plant in Jinan was completed and put into production in 2005.
Bloomage was licensed by the US FDA and established a US subsidiary in 2012. [ 15 ] [ 16 ] [ 17 ]
Bloomage specializes in hyaluronic acid microbial fermentation production. It also focuses on pharmaceutical, cosmetic, and food-grade application products. [ 18 ]
Other than hyaluronic acid, Bloomage also manufactures recombinant collagen , ergothioneine , ectoine , GABA , PDRN, among others. [ 19 ] The company also produces skin fillers and various cosmetic products. [ 20 ] [ 21 ] [ 22 ]
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Blue stain fungi (also known as sap stain fungi ) is a vague term including various fungi that cause dark staining in sapwood. [ 1 ] The staining is most often blue, but could also be grey or black. Because the grouping is based solely on symptomatics, it is not a monophyletic grouping.
Depending on the author, the group can include between 100 and 250 species of ascomycetes and so-called deuteromycetes . They are usually divided into three different groups: [ 1 ]
Importance of the symbiotic relationship between blue stain fungi and bark beetles.
Symbiotic association between bark beetles and species of blue stain fungi is a well-known and studied phenomenon in the forestry pathology. Some bark beetle species like Mountain Pine Beetle ( Dendroctonus ponderosae) feed on phloem layer just underneath the bark of a lodgepole pines when they are developing from larval to adult stage. Mountain Pine Beetle carry the spores of at least 2 known blue stain fungi species, Ophiostoma clavigerum and Ophiostoma montium. [ 2 ] These spores are carried on the exoskeleton of the beetles from one tree to another and aid the insects in overcoming defence mechanisms of different pine species. After the beetles initiate their attack and bore through the bark spores are released. These spores immediately start to multiply and block important conductive vessels within the tree tissues. The tree loses its ability to produce resin and to defend itself. [ 3 ]
Trade and pulp production problems associated with blue stain fungi
Developing spores of the blue stain fungi are a concern in packaging materials used for shipping from Canada to Australia due to the potential risk of introducing invasive species of fungi. [ 4 ]
According to Pulp and Paper Research Institute of Canada the wood infected with the blue stain fungus have a high proportion of fines that are not suitable for pulp production. [ 2 ]
The major economic damage caused by the blue stain fungi is aesthetic because of the usually undesirable discoloration of wood. Blue stain fungi do not affect the strength of wood. [ 5 ] In some cases the staining is desirable in fine wood crafting applications where it is called spalting .
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Blumer's shelf , or the rectal shelf , is a finding palpable (felt) in rectal or vaginal examination that indicates that a tumor has metastasized to the pouch of Douglas .
It is usually a site of metastasis of cancers of the lung , pancreas and stomach , [ 1 ] due to metastatic tumor cells gravitating from an abdominal cancer and growing in the rectovesical [ 2 ] or rectouterine pouch .
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Blunt dissection describes the careful separation of tissues along tissue planes by either fingers or convenient blunt instruments during many diverse surgical procedures . Blunt dissection consumes a large proportion of time in most surgeries and has not changed significantly in centuries. Blunt dissection is contrasted to sharp dissection , the practice of slicing through tissues with scalpels, scissors, electrosurgical instruments, or other technologies.
Blunt dissection is one method employed prior to the insertion of a chest drain following a pneumothorax . Following incision above the rib (to avoid the neurovascular bundle ), blunt dissection of the subcutaneous tissue , external, internal and innermost intercostal muscles allows access to the pleura. [ 1 ] Blunt dissection is considered the favoured approach for the insertion of large bore chest tubes since it results in fewer complications . [ 2 ]
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A body broker (also non-transplant tissue banks ) is a firm or an individual that buys and sells cadavers or human body parts.
Whereas the market for organ transplantation is heavily regulated in the United States, the use of cadaver parts for research, training, and other uses is not. Trade in these body parts is performed in a manner akin to raw materials , though many brokers say they charge fees as opposed to selling body parts. [ 1 ]
Whereas body snatching was a common way of acquiring bodies for research up until the 20th century, modern body brokers usually receive cadavers via body donation . [ 2 ] Body brokers often offer free cremation as a means to induce donation from families who are unable to pay funeral costs, returning ashes of part of the body to the next of kin. [ 3 ] In some cases body brokers obtain bodies fraudulently by stating use of the donation for research, subsequently reselling the body for profit. [ 4 ]
Body brokers also obtain cadavers and body parts from institutions who receive donations and have a surplus. In some cases, this is done illegally against the donor's wishes or by employees who act independently of the institution. In 2004, the UCLA Willed Body Program was suspended for a year after a scheme for the sale of body parts for profit involving its director at the time Henry Reid and body broker named Ernest Nelson was uncovered. [ 5 ] [ 6 ] The scheme yielded some 1.5 million dollars in profits. Reid and Nelson were subsequently convicted for theft and related tax offenses and were sentenced to 4 and 10 years respectively. [ 7 ] [ 8 ] [ 9 ]
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Body donation , anatomical donation, or body bequest is the donation of a whole body after death for research and education. There is usually no cost to donate a body to science; donation programs will often provide a stipend and/or cover the cost of cremation or burial once a donated cadaver has served its purpose and is returned to the family for interment .
For years, only medical schools accepted bodies for donation, but starting in the early 2000 [ when? ] private programs (either for- or non-profits) also accept donors. [ 1 ] Depending on the program's need for body donation, some programs accept donors with different specifications. [ clarification needed ]
Any person wishing to donate their body may do so through a willed body program. The donor may be required, but not always, to make prior arrangements with the local medical school, university, or body donation program before death. Individuals may request a consent form, and will be supplied information about policies and procedures that will take place after the potential donor is deceased.
The practice is still relatively rare, and in attempts to increase these donations, many countries have instituted programs and regulations surrounding the donation of cadavers or body parts. For example, in some states within the United States and for academic-based programs, a person must make the decision to donate their remains themselves prior to death; the decision cannot be made by a power of attorney . If a person decides not to donate their whole body, or they are unable to, there are other forms of donation via which one can contribute their body to science after death, such as organ donation and tissue donation .
Hinduism, [ 2 ] Buddhism, [ 3 ] Islam, [ 4 ] Christianity [ 5 ] and Sikhism all support the idea of body donation and/or organ donation for the betterment of the world. [ citation needed ]
The decision to become a body donor is influenced by factors such as: social awareness, cultural attitudes and perceptions of body donation, cultural attitudes and perceptions of death, religion, and perceptions of the body-mind relationship. [ 6 ] Studies indicate most donors are primarily driven by altruism and their desire to aid the advancement of medical knowledge and to be useful after death. [ 7 ] Other reasons include helping future generations, expressing gratitude for life and good health or for the medical field, to avoid a funeral or to avoid waste. [ 7 ]
The offering of financial incentives as a way to increase donor numbers or as an acknowledgement for donors is generally considered to detract from the act of donation and serve as a deterrent. [ 8 ] However, a US study showing a positive correlation between body donation numbers and funeral cover cost savings offered as compensation suggests that, in reality, the added incentive could be a persuasive factor for donors. [ 9 ]
Bodies donated to any organization are used for scientific research and medical training. Bodies are used to teach medical students anatomy, but they are also used to improve and create new medical technologies. Many programs that accept body donations have specific research affiliations, these can be viewed by looking at each programs website. These can include cancer research, Alzheimer's research, and research into improving surgeries. [ 10 ]
Some programs accept whole bodies but distribute different body parts based on need. This ensures a maximum benefit from each donation. These programs can assist with research as shown above, technical training, or improvement/research of medical devices. [ 11 ]
After bodies are accepted for donation, a timeframe of six months to three years is expected before the donor's body will be returned to the family. This takes into account embalming, research, and the number of bodies the program has access to at the time. [ 12 ]
Body disposal and donation are regulated by the Bestattungsgesetze (funeral laws) of the states. In Germany, the right to autonomy extends beyond death, as a result of which the instructions given by a deceased during their lifetime must be respected when dealing with their body. A body donation can only take place if the deceased signed a declaration of last will in their lifetime, stating the intention of donating their body to an anatomical institute. Relatives of the deceased can neither give permission nor deny body donation against said declaration, the institute however may deny the body. Denial of the body may occur if it carries infectious diseases, has had organs or body parts removed for donation or surgery, is gravely injured or otherwise unfit for teaching, if the body is located too far away from the institute or for reasons of storage capacity. Most institutes require an advance fee to be deposited to pay for funeral costs. [ 13 ]
In 1948, the Anatomy Act was passed in all of India's states. This allows bodies to be donated by the donor and bodies to be claimed for medical and research use if there is no claim to one's body within a 48-hour timeframe. [ 14 ] Similar to the US, India also has specific guidelines for accepting bodies for donations. Donations that are not deemed suitable include bodies with HIV/AIDS, hepatitis (A, B, and C), donated organs, extreme BMI, or skin diseases.
Some leaders have donated their bodies for medical research, such as communist leader Jyoti Basu [ 15 ] and Jana Sangh leader Nanaji Deshmukh . [ 16 ] Nowadays, many people in India donate their bodies after death by signing a pledge form with two accompanying witness signatures. [ 17 ]
Only the legal next-of-kin of the deceased can provide the necessary consent for donation if the donor did not provide it to the specific accepting program prior to death. [ citation needed ] Body donation is not regulated through licensure and inspection by the federal government and most states. [ citation needed ]
Body brokers (or non-transplant tissue banks) engage in the acquisition of cadavers , often via offers of free cremation, and then subsequently process the cadaver and resell body parts in a largely unregulated national market. [ 18 ] [ 19 ]
The legal right for an individual to choose body donation is governed by the Uniform Anatomical Gift Act , which has been largely adopted by most states. Laws relating to the transportation and disposition of human bodies currently apply, regardless of the recent House Bill introduced. [ citation needed ]
The American Association of Tissue Banks (AATB) provides accreditation to non-transplant tissue bank research and education programs to establish that the level of medical, technical, and administrative performance meets or exceeds the standards set by the AATB. Whole body donation and non-transplant tissue banking remains an industry with limited regulation, and while it is not a legal requirement, accreditation allows for individuals choosing to donate their body to medical research or education programs to choose a program with the highest quality standards. [ citation needed ]
The American Medical Education and Research Association (AMERA) is a peer-recognized national accrediting body in the United States that provides accreditation to organizations using standards developed solely for non-transplant organizations. This includes whole body donor organizations, university anatomical programs, bio-repository programs, and end users of human tissue. AMERA encourages the industry to become accredited and involved in establishing standards that are relevant to non-clinical tissue organizations. [ citation needed ]
Many medical programs in the United States now hold student-led memorial services for the donated bodies. This is to show respect for the donors and their families, and to shine a positive light on the process of body donation. [ 20 ]
There are many private body donation programs in the US. Each of these private programs accepts bodies from certain surrounding areas. Most programs also have guidelines for bodies they will and will not accept. Generally, programs will not accept bodies that are positive for hepatitis (A, B, and C), HIV/AIDS, history of illegal drug use, or fall within an extreme category for their BMI . The embalming process adds even more weight to a donor's body, so if they have a high BMI the programs may not take them because they cannot handle the weight of the donor after embalming. [ 21 ] If a donor has a specific disease prior to death, which is not contagious, and would like to be a part of a program's study, they may contact that research program specifically. [ citation needed ]
Body donation in the UK is governed by the Human Tissue Authority (HTA) under the auspices of the Human Tissue Act 2004 . The HTA licenses and inspects establishments, such as medical schools, which teach anatomy using donated bodies. Under the Human Tissue Act, written consent must be given prior to death; consent cannot be given by anyone else after death. [ 22 ] The minimum age to consent to donate one's body in the UK is 17. [ citation needed ]
The Human Tissue Authority provides information to donors about where they can donate and answers many prevalent questions related to tissue donation on their website. The HTA provides the links to each establishment's information, but each establishment has its own guidelines for body donation. The HTA also provides the tools to find donation sites local to the person wishing to donate their body or tissues. [ citation needed ]
Although most establishments accept most donations, donors who have had an autopsy may be declined from a program. Certain programs also may decline bodies of donors who have died abroad. [ 23 ]
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Body fluids , bodily fluids , or biofluids , sometimes body liquids , are liquids within the body of an organism. [ 1 ] In lean healthy adult men, the total body water is about 60% (60–67%) of the total body weight ; it is usually slightly lower in women (52–55%). [ 2 ] [ 3 ] The exact percentage of fluid relative to body weight is inversely proportional to the percentage of body fat. A lean 70 kg (150 lb) man, for example, has about 42 (42–47) liters of water in his body.
The total body of water is divided into fluid compartments , [ 1 ] between the intracellular fluid compartment (also called space, or volume) and the extracellular fluid (ECF) compartment (space, volume) in a two-to-one ratio: 28 (28–32) liters are inside cells and 14 (14–15) liters are outside cells.
The ECF compartment is divided into the interstitial fluid volume – the fluid outside both the cells and the blood vessels – and the intravascular volume (also called the vascular volume and blood plasma volume) – the fluid inside the blood vessels – in a three-to-one ratio: the interstitial fluid volume is about 12 liters; the vascular volume is about 4 liters.
The interstitial fluid compartment is divided into the lymphatic fluid compartment – about 2/3, or 8 (6–10) liters, and the transcellular fluid compartment (the remaining 1/3, or about 4 liters). [ 4 ]
The vascular volume is divided into the venous volume and the arterial volume; and the arterial volume has a conceptually useful but unmeasurable subcompartment called the effective arterial blood volume . [ 5 ]
Clinical samples are generally defined as non-infectious human or animal materials including blood , saliva , excreta , body tissue and tissue fluids , and also FDA-approved pharmaceuticals that are blood products . [ 7 ] In medical contexts, it is a specimen taken for diagnostic examination or evaluation, and for identification of disease or condition. [ 8 ]
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Body integrity dysphoria ( BID ), also referred to as body integrity identity disorder ( BIID ), amputee identity disorder or xenomelia , and formerly called apotemnophilia , is a rare mental disorder characterized by a desire to have a sensory or physical disability or feeling discomfort with being able-bodied , beginning in early adolescence and resulting in harmful consequences. [ 1 ] BID appears to be related to somatoparaphrenia . [ 2 ] People with this condition may refer to themselves as transabled , [ 3 ] [ 4 ] [ 5 ] but the term is controversial.
BID is a rare, infrequently studied condition in which there is a mismatch between the mental body image and the physical body, characterized by an intense desire for amputation or paralysis of a limb, usually a leg, or to become blind or deaf. [ 2 ] A 2017 survey by researchers at the University of Amsterdam of 80 individuals with BID found that 71.3% experienced sexual arousal related to their condition, with this group more likely to be male, religious, homosexual, and to have pursued self-amputation compared to those without such arousal. [ 6 ]
Some become somewhat more comfortable with their own bodies by using prostheses and other tools to help their dysphoria, such as using a wheelchair or by blocking their vision or hearing. Some people with BID have reported to the media or by interview with researchers that they have resorted to self-amputation of a "superfluous" limb by, for example, allowing a train to run over it or otherwise damaging it so severely that surgeons will have to amputate it. However, the medical literature records few cases of self-amputation [ 7 ] [ 8 ] apart from that of cricket historian Rowland Bowen , who self-amputated one of his legs below the knee in 1968. [ 9 ]
To the extent that generalizations can be made, people with BID appear to start to wish for amputation when they are young, between eight and twelve years of age, and often knew a person with an amputated limb when they were children; however, people with BID tend to seek treatment only when they are much older. [ 8 ] People with BID seem to be predominantly male, and while there is no evidence that sexual preference is relevant, there does seem to be a correlation with BID and a person having a paraphilia ; there appears to be a weak correlation with personality disorders . [ 8 ] Family psychiatric history does not appear to be relevant, and there does not appear to be any strong correlation with the site of the limb or limbs that the person wishes they did not have, nor with any past trauma to the undesired limb. [ 8 ]
As of 2014 the cause was not clear and was a subject of ongoing research. [ 10 ] However a small sample of people with body integrity dysphoria connected to their left leg have had MRI scans that showed less gray matter in the right side of their superior parietal lobule . The amount of gray matter missing was correlated to the strength of the patients' desire to remove their leg. [ 11 ]
In the ICD-11 , BID is included under the category "Disorders of bodily distress or bodily experience". It is "characterised by an intense and persistent desire to become physically disabled in a significant way (e.g. major limb amputee, paraplegic, blind), with onset by early adolescence accompanied by persistent discomfort, or intense feelings of inappropriateness concerning current non-disabled body configuration. The desire to become physically disabled results in harmful consequences, as manifested by either the preoccupation with the desire (including time spent pretending to be disabled) significantly interfering with productivity, with leisure activities, or with social functioning (e.g. person is unwilling to have close relationships because it would make it difficult to pretend) or by attempts to actually become disabled have resulted in the person putting their health or life in significant jeopardy. The disturbance is not better accounted for by another mental, behavioural or neurodevelopmental disorder, by a Disease of the Nervous System or by another medical condition, or by Malingering ." A diagnosis of gender dysphoria must be ruled out. [ 12 ]
Prior to the release of the ICD-11, the diagnosis of BID as a mental disorder was controversial. There was debate about including it in the DSM-5 , and it was not included; it was also not included in the ICD-10 . [ 2 ] [ 10 ] It has been included in the ICD-11, which reached a stable version in June 2018, as 'Body integrity dysphoria' with code 6C21. [ 1 ]
There is no evidence-based treatment for BID; there are reports of the use of cognitive behavioral therapy and antidepressants . [ 8 ]
The ethics of surgically amputating the undesired limb of a person with BID are difficult and controversial. [ 7 ] [ 13 ] [ 14 ]
There are numerous case reports that amputation permanently resolves the desire in affected individuals. [ 8 ] [ 15 ] For example, a 2024 case report described a patient diagnosed with BID whose distress persisted despite antidepressant treatment and cognitive-behavioral therapy; elective amputation of two fingers resolved all symptoms, with immediate relief and improved functionality. [ 16 ] A one-year follow-up confirmed sustained remission, with the patient reporting enhanced quality of life, full social and occupational adaptation, and no regrets. [ 17 ]
Longterm outcomes of treated and untreated BID are not known.
Apotemnophilia was first described in a 1977 article by psychologists Gregg Furth and John Money as primarily sexually oriented. In 1986 Money described a similar condition he called acrotomophilia ; namely, sexual arousal in response to a partner's amputation. Publications before 2004 were generally case studies . [ 18 ] The condition received public attention in the late 1990s after Scottish surgeon Robert Smith amputated limbs of two otherwise healthy people who were desperate to have this done. [ 18 ]
In 2004 Michael First published the first clinical research in which he surveyed fifty-two people with the condition, a quarter of whom had undergone an amputation. Based on that work, First coined the term "body integrity identity disorder" to express what he saw as more of an identity disorder than a paraphilia. [ 10 ] [ 19 ] After First's work, efforts to study BID as a neurological condition looked for possible causes in the brains of people with BID using neuroimaging and other techniques. [ 2 ] [ 18 ] Research provisionally found that people with BID were more likely to want removal of a left limb than right, consistent with damage to the right parietal lobe ; in addition, skin conductance response is significantly different above and below the line of desired amputation, and the line of desired amputation remains stable over time, with the desire often beginning in early childhood . [ 18 ] This work did not completely explain the condition, and psychosexual research has been ongoing as well. [ 18 ] [ 20 ] [ 21 ]
BID has been portrayed in various media formats. Representations in literature, film, and television. The following sections describe notable appearances of BID across different media.
Fictional literature specifically focusing on BID is rare. Career of Evil by Robert Galbraith (pseudonym of J.K. Rowling) references BID. [ 22 ] [ 23 ] Headcheese (2018) by Jess Hagemann includes themes related to BID and voluntary amputation. [ 24 ] [ 25 ]
The documentary Whole , directed by Melody Gilbert, follows individuals with BID, offering insight into their coping mechanisms and societal reactions. The comedy film Armless , directed by Habib Azar, follows John, a man with BID who leaves his wife and travels to New York City in search of a doctor willing to amputate his arms.
BID has been featured in fictional series on television. CSI: NY (Season 1, Episode 6, "Outside Man", 2004) featured an investigation about the death of a man who had his physically healthy leg amputated. Nip/Tuck (Season 3, Episode 7, "Ben White", 2005) included a character with BID who requests the amputation of his healthy leg. Casualty (Season 22, Episode 21, 2008) portrayed a woman who intentionally had her leg amputated by a train and was diagnosed with BID. Similarly, Mental (Season 1, Episode 12, "Life and Limb," 2009) depicts a factory worker who chopped off his fingers and refused reattachment surgery.
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https://en.wikipedia.org/wiki/Body_integrity_dysphoria
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The ongoing Bogalusa Heart Study is one of the first longitudinal studies to track individual's health outcomes from childhood to adulthood. [ 1 ] The study began in 1973, with the objective of investigating the early natural history of cardiovascular disease in a cohort of children and young adults from a biracial, semirural community in Bogalusa , Louisiana . [ 2 ] [ 3 ]
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Bogart–Bacall syndrome ( BBS ) is a voice disorder that is caused by abuse or overuse of the vocal cords. [ 1 ] [ 2 ]
People who speak or sing outside their normal vocal range can develop BBS; symptoms are chiefly an unusually deep or rough voice, or dysphonia , and vocal fatigue. [ 3 ] The people most commonly affected are those who speak in a low-pitched voice, particularly if they have poor breath and vocal control. [ 4 ] The syndrome can affect both men and women. [ 5 ]
In 1988, an article was published describing a discrete type of vocal dysfunction which results in men sounding like actor Humphrey Bogart and women sounding like actress Lauren Bacall ; [ 6 ] Bogart and Bacall were married to each other and made several films together. BBS is now the medical term for an ongoing hoarseness that often affects actors, singers or TV/radio voice workers who routinely speak in a very low pitch. [ 7 ]
Treatment usually involves voice therapy by a speech language pathologist . [ 8 ]
Signs and symptoms of Bogart–Bacall Syndrome can appear differently depending on the vocal use of the individual. In singers, symptoms may appear more subtly due to their extreme sensitivity to small changes in the laryngeal mechanism and being able to control their laryngeal muscles more than the average person. This vocal control can compensate for irritation, weakness, or change in vibration patterns for the vocal folds. Signs and symptoms will vary on a case-by-case basis and will depend on vocal strain and the degree of daily use. Women are also more susceptible than men to experience heightened symptoms due to their increased likelihood of speaking at a lower pitch in professional settings. [ 9 ]
Signs and symptoms of Bogart–Bacall include the following: [ 10 ]
The cause of Bogart–Bacall syndrome is most commonly identified as abuse or overuse of the vocal cords. Individuals who speak or sing outside of their normal range can develop BBS over a long period of misuse. Individuals who develop this syndrome tend to speak or perform with poor breath support and laryngeal muscle tension. Causes include speech and communication disorders, throat conditions, and work-related conditions.
Speech and communication disorders refers to issues involving language and related areas such as oral motor function. Some examples include expressive language disorder , receptive-expressive language disorder, phonologic disorder, and stuttering . [ 11 ]
Throat conditions can be any one of the following: [ 12 ]
Work-related conditions typically affect individuals whose professions require extensive use or overuse of their vocal cords. Some examples include news and television broadcasters, radio hosts, as well as singers or actors. Teachers may also be susceptible to BBS depending on their volume and how much they talk on a regular basis.
There are many plausible reasons for how Bogart–Bacall and other vocal disorders occur, but it can not be determined for certain due to the many factors that play a role in speech production. Voice production requires the coordination of many muscles and other structures in the larynx. Many factors can cause the larynx to become tensed which changes the position of larynx. This affects the cartilaginous structures within the larynx leading to abnormal phonation . Bogart–Bacall refers to an unnaturally deep voice, so when lowering their voice, individuals may continue to speak even when the air in their lungs has been almost entirely expelled. Due to the effort exerted in lowering the pitch range, the muscles involved in respiration become tensed and strained along with speech.
Bogart–Bacall syndrome is considered a secondary muscle tension dysphonia disorder, meaning that there is an abnormality in the voice box that causes the overuse of muscles to help produce your voice. This abnormality can be caused by an underlying medical reason or a physical exertion. By lowering vocal pitch, the larynx compresses the vocal folds which regulate air flow and production of the sounds used in speech which can cause damage to these muscles over time. Vocal fold lesions or nodules can cause changes in the vocal fold mucosa which leads to increased tension in the larynx, ultimately causing dysphonia. [ 13 ]
A speech-language pathology evaluation will need to be conducted to be conscious vocal use history as well examination of the throat and larynx. This evaluation potentially involves imaging to visualize the vocal cords. Imaging options can include a laryngoscope , videostroboscopy , or laryngeal electromyography . [ 14 ] Diagnosis of Bogart–Bacall can be difficult due to the variance in symptom presentation and vocal use.
Videostroboscopy provides a magnified, slow-motion view of the vocal cords and larynx in action which allows professionals to see any abnormal movement. Videostroboscopy can be used to visualize any swelling of the vocal folds, irritation, or polyps and growth. Occasionally, redness or bumps can be seen on vocal cords which is useful in making a correct diagnosis. [ 15 ]
Laryngeal electromyography is a test that measures the electrical signals from the voice box muscles (laryngeal muscles) during speaking, breathing, and swallowing. This evaluation is to check if vocal issues are related to any one of the following: partial paralysis resulting in muscle weakness, paralysis resulting in loss of muscle function, and the functionality of the motor unit of the laryngeal muscles. Laryngeal electromyography plays an important role in determining whether or not a nerve problem is the cause of a vocal disorder. [ 16 ]
Prevention of Bogart–Bacall syndrome aims to target the two main symptoms of this disorder, dysphonia and vocal fatigue. Having effective posture allows a person to shift the tension between the muscles allowing free movement of the larynx without blockage leading to effective voice production. Improvement of breath control with a professional vocal coach is also important for individuals who may have work-related conditions that require continuous strain on the vocal cords and larynx.
Speech therapy with a speech-language pathologist is a very common method of treatment to return speaking level to its normal pitch range. Consultation with a speech-language pathologist will determine what levels of rest, fluid, and performance corrections are needed for the vocal cords and larynx to sustain a healthy voice. If there is a particular underlying cause of the condition that can be treated with medication, this can be coupled with speech therapy as a form of treatment. [ 17 ]
Individuals with persistent symptoms after speech therapy may require more invasive treatment. Invasive treatment may require the removal of lesions, nodules, or masses on the vocal cords if visualized during diagnostic imaging. If the disorder is found to be nerve related through electromyography the nerve in question may need to be replaced or the vocal cords can be pushed together with a bulk injection or thyroplasty . A bulk injection involves adding a filler substance to the paralyzed vocal cord to have it vibrate closer to the functioning vocal cord. Thyroplasty involves the insertion of an implant against the paralyzed vocal cord moving it closer to the other vocal cord. [ 18 ]
Individuals with Bogart–Bacall syndrome that do not have an underlying condition are typically expected to make a vocal recovery through voice therapy. Having a form of muscle tension dysphonia go untreated, can cause further long-term disorders that require additional forms of treatment.
Bogart–Bacall syndrome can develop in individuals at any age. It is more likely to develop in individuals who work in voice performance which can range from singers, actors, teachers or radio and television broadcasters. Women are more likely than men to develop BBS due to the tendency of lowering their voices in a professional environment. This syndrome is also more prevalent in the 40–50-year-old-age group as their vocal cords thin. Vocal disorders are prevalent in roughly 10% of the population and can range from muscle tension dysphonia to speech and language disorders. [ 19 ]
Further studies need to be conducted to further examine the long-term effects of Bogart–Bacall syndrome if left untreated. Studies that are currently ongoing aim to understand what the best course of treatment may be for individuals with muscle tension dysphonia, which includes individuals with Bogart–Bacall. It is currently understood that an interdisciplinary approach to target the causes such as poor breath support, overuse, and inappropriate intensity is most effective. [ 20 ]
Vocal disorders and misuse are currently being researched depending on work conditions and professions. A study based on over 1,200 teachers has indicated that voice disorders play a significant role in their profession. The study found that a substantial number of teachers have needed to take time off work or seek medical attention due to voice issues or to seek treatment. The study also found that women are more likely to develop these disorders over their male counterparts. [ 21 ]
There is more research available on vocal disorders and how they may be effected by additional lifestyle factors. A study was conducted to understand how reflux effected vocal disorders such as dysphonia in singers with bulimia . Singers tend to overuse their vocal cords which makes them very susceptible to a variety of vocal disorders. Dysphonia associated with bulimia has been linked to vocal fold edema and polypoid changes. The aim was to understand if bulimia was linked to laryngopharyngeal reflux as a plausible cause of dysphonia. In preliminary results, it was understood that reflux was the case in every singer with bulimia and dysphonia, indicating it may be a contributing factor to their vocal disorder. [ 22 ]
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https://en.wikipedia.org/wiki/Bogart–Bacall_syndrome
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A Bogota bag is a sterile plastic bag used for closure of abdominal wounds. [ 2 ] It is generally a sterilized 3-liter (0.66 imp gal; 0.79 U.S. gal) genitourinary irrigation bag that is sewn to the skin or fascia of the anterior abdominal wall. Its use was first described by Oswaldo Borraez while he was a resident in Bogotá , Colombia .
These temporary abdominal closure techniques are most commonly used in cases of abdominal compartment syndrome in which decompressive laparotomy is necessary to reduce intra-abdominal pressure to restore blood flow. The Bogota bag is used to postpone definite closure until the underlying cause of the elevated intra-abdominal pressure can be resolved. Other techniques include the use of absorbable mesh, the Wittmann patch , negative pressure wound therapy and dynamic closure systems. [ 3 ] [ 1 ] These techniques are characterized by a tension-free closure. In addition, the Bogota bag acts as a hermetic barrier that prevents disembowelment and loss of fluids. Another advantage to the Bogota bag is that the abdominal contents can be visually inspected which is particularly useful in cases of ischemic bowel .
The Bogota bag can be used in cases of "burst abdomen" following laparotomies , especially those using a midline vertical incision. Burst abdomen is usually characterized by a serosanguinous pink discharge from the wound 6 to 8 days after surgery.
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https://en.wikipedia.org/wiki/Bogota_bag
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Bolton Analysis is a tooth analysis developed by Wayne A. Bolton to determine the discrepancy between size of maxillary and mandibular teeth. This analysis helps to determine the optimum interarch relationship. This analysis measures the Mesio-distal width of each tooth and is divided into two analyses. [ 1 ] [ 2 ]
Wayne A Bolton presented this analysis in the year 1958. In 1962, he published another paper which talked about clinical applications of using Bolton Analysis in Orthodontics . He graduated from The University Of Washington Dental School in 1950. A bole gauge is usually the instrument of choice to measure the widths of each teeth. However, in 1995, Shellhart et al. showed during their study that Vernier caliper can also be used as an alternative for Bolton Analysis. [ 3 ] Many other investigation models have been developed, such as measurement from photocopies and traveling microscope but the studies have produced no results. [ 4 ]
Recently, digital calipers from companies such as OrthoCad, are being used to measure the mesiodistal widths of the teeth.
An Overall Analysis measures the sum of mesio-distal width of all 12 (first molar to first molar) mandibular teeth and compares them to the 12 maxillary teeth. The overall ratio known to be 91.3%. [ 5 ] The anterior analysis measures the sum of Mesio-distal width of front 6 mandibular teeth and compares them to maxillary teeth. The anterior ratio is known to be 77.2%. An overall ratio of more than 91.3% means that the mandibular teeth are bigger when compared to normal. A ratio smaller than 91.3% would mean the mandibular teeth are smaller than normal. Anterior analysis follows the same principle. Having a different ratio than normal is referred to as Bolton Discrepancy. A standard deviation of more than 2 yields a significant discrepancy.
One of the drawbacks of this analysis, is that the sample that Bolton measured in his paper in 1958, consisted of only Caucasian population. Therefore, Bolton's Overall Ratio and Anterior Ratio Mean and Standard Deviations are not representative of samples from other race and population. In addition, because the samples that were measured had perfect malocclusion , any samples after performing Bolton Analysis, will yield a high discrepancy compared to Bolton ratios. It is seen that majority of the populations when studied and compared to Bolton's ratios, are usually not ideal compared to his ratios.
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https://en.wikipedia.org/wiki/Bolton_analysis
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In radiation therapy , bolus is a material which has properties equivalent to tissue when irradiated. It is widely used in practice to reduce or alter dosing for targeted radiation therapy.
It must be possible to mould the bolus to fill the tissue space. Lincolnshire and Spier's bolus, which is loosely packed in polyethylene bags, is suitable as the bolus bags take the shape of the skin surface these bags are easily smoothed to achieve a flat surface.
A specific thickness of bolus can be applied to the skin to alter the dose received at depth in the tissue and on the skin surface. A typical example of this is the application of a defined thickness of bolus to a chest wall for post-mastectomy chest wall treatment, to increase the skin dose. The thickness of bolus applied is dependent on the skin dose required and the angle of incidence of the treatment beams. For example, if oblique 6 MV beams are used for tangential pair, 1 cm of bolus effectively becomes 1.5 cm, i.e., "full bolus".
When a full bolus is applied, bolus thickness equal to the depth of the build-up region removes the skin-sparing effect of a megavoltage x-ray beam. On the other hand, there are boluses that do not require the selection of specific thicknesses to treat a certain depth. These types of boluses have densities higher than water but can be calculated from CT images by the Treatment Planning System (TPS). One of these boluses is commonly known as high-density and high-adaptation bolus (e.g., eXaSkin and eXaSkin Plus ).
Suitable material must be pliable and easily moulded to the skin surface, but retain a constant thickness. One example includes paraffin gauze.
For smaller areas which do not require the bolus to be moulded over the skin, Perspex can be used. The use of Perspex bolus is advantageous for electron set-ups because it is transparent. Since the f.s.d. for most electron fields is 95 cm, so that the movements of the couch are not isocentric, inaccuracies may arise for aligning angled fields when an opaque bolus is inserted.
To ensure that the patient receives the required dose, bolus of the right thickness must be placed correctly. Therefore, bolus requirements must be clearly documented in the setup sheets of the treatment card. When using bolus to compensate for missing tissue, the whole of the bolussed area must be level with the point on the patient where the f.s.d. is set, to ensure dose homogeneity.
When the bolus is used to reduce the skin-sparing effect, the bolus does not necessarily need to touch the skin all over the bolussed area as the scatter is of sufficiently high energy to be unaffected by an air gap. However, it is important that the bolus is uniform thickness. Some bolus materials are easily squashed and must be carefully measured at regular intervals.
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https://en.wikipedia.org/wiki/Bolus_(radiation_therapy)
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A bone-seeking radioisotope is a radioactive substance that is given through a vein , and collects in bone cells and in tumor cells that have spread to the bone . It kills cancer cells by giving off low-level radiation .
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
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Bone Marrow Transplantation is a peer-reviewed medical journal covering transplantation of bone marrow in humans. It is published monthly by Nature Research . The scope of the journal includes stem cell biology , transplantation immunology , translational research , and clinical results of specific transplant protocols. [ 1 ]
According to the Journal Citation Reports , Bone Marrow Transplantation has a 2020 impact factor of 5.483. [ 2 ]
Bone Marrow Transplantation is abstracted and indexed in BIOBASE /Current Awareness in Biological Sciences, BIOSIS , Current Contents /Clinical Medicine, Current Contents/Life Sciences, EMBASE/Excerpta Medica , MEDLINE / Index Medicus , and Science Citation Index .
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https://en.wikipedia.org/wiki/Bone_Marrow_Transplantation_(journal)
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A bone biopsy is a procedure in which a small bone sample is removed from the outer layers of bone for examination, unlike a bone marrow biopsy , which involves the innermost part of the bone. The bone biopsy sample retains the architecture of bone when seen using histopathological examination slide.
The technique of bone biopsy allows the histomorphometric analysis of the bone samples obtained from the iliac crest . Therefore, it can provide a direct assessment of regional bone metabolism. Hence, the reason why this method is considered the gold-standard technique for measuring bone remodelling. [ 1 ] Patients undergo double tetracycline labelling, and then samples of bone are collected using trephine under local anesthetic from the iliac crest as it is the only readily accessible site for bone biopsy. [ 2 ] This technique is subject to large measurement errors; it is complex and costly to perform and is invasive, meaning that it is painful to the patients. [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] For these reasons, a bone biopsy is not readily acceptable to patients. [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] Moreover, multiple biopsies using double tetracycline labelling are necessary for the same patient to assess treatment response or disease progression. Another drawback is that the iliac crest may not provide a true measurement of changes in bone metabolism at the lumbar spine or hip as considerable differences in regional bone metabolism estimates are observed at different skeletal sites. Revell et al. describes the measurement of various parameters such as trabecular bone volume, osteoid volume, osteoid surface, active osteoblastic surface, resorption surface, osteoclastic resorption surface, mineralization front, osteoid index, appositional rate, and osteoclastic index via histomorphometric analysis of bone samples. [ 8 ]
If a biopsy is to be obtained along with medical imaging examinations, as a rule, biopsy should be done after all necessary imaging has been performed. A bone biopsy can also be used to find out if cancer , [ 9 ] or infection , [ 10 ] or other abnormal cells are present in the bone tissue.
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https://en.wikipedia.org/wiki/Bone_biopsy
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Bone cements have been used very successfully to anchor artificial joints ( hip joints , knee joints , shoulder and elbow joints ) for more than half a century. Artificial joints (referred to as prostheses) are anchored with bone cement. The bone cement fills the free space between the prosthesis and the bone and plays the important role of an elastic zone. This is necessary because the human hip is acted on by approximately 10–12 times the body weight and therefore the bone cement must absorb the forces acting on the hips to ensure that the artificial implant remains in place over the long term.
Bone cement chemically is nothing more than Plexiglas (i.e. polymethyl methacrylate or PMMA). [ 1 ] PMMA was used clinically for the first time in the 1940s in plastic surgery to close gaps in the skull. Comprehensive clinical tests of the compatibility of bone cements with the body were conducted before their use in surgery . The excellent tissue compatibility of PMMA allowed bone cements to be used for anchorage of head prostheses in the 1950s.
Today several million procedures of this type are conducted every year all over the world and more than half of them routinely use bone cements – and the proportion is increasing. Bone cement is considered a reliable anchorage material with its ease of use in clinical practice and particularly because of its proven long survival rate with cemented-in prostheses. Hip and knee registers for artificial joint replacements such as those in Sweden and Norway [ 2 ] clearly demonstrate the advantages of cemented-in anchorage. A similar register for endoprosthesis was introduced in Germany in 2010. [ 3 ]
Synthetic, self-curing organic or inorganic material used to fill up a cavity or to create a mechanical fixation.
Note 1: In situ self-curing can be the source of released reagents that can cause local and/or systemic toxicity as in the case of the monomer released from methacrylics-based bone cement used in orthopedic surgery.
Note 2: In dentistry, polymer-based cements are also used as fillers of cavities. They are generally cured photochemically using UV radiation in contrast to bone cements. [ 4 ]
Bone cements are provided as two-component materials. Bone cements consist of a powder (i.e., pre-polymerized PMMA and or PMMA or MMA co-polymer beads and or amorphous powder, radio-opacifier, initiator) and a liquid (MMA monomer, stabilizer, inhibitor). The two components are mixed and a free radical polymerization occurs of the monomer when the initiator is mixed with the accelerator. The bone cement viscosity changes over time from a runny liquid into a dough like state that can be safely applied and then finally hardens into solid hardened material. [ 5 ] The set time can be tailored to help the physician safely apply the bone cement into the bone bed to either anchor metal or plastic prosthetic device to bone or used alone in the spine to treat osteoporotic compression fractures.
Bone cement heats up during the exothermic free-radical polymerization process, which reaches temperatures of around 82–86 °C in the body, a temperature higher than the critical level for protein denaturation in the body. This low polymerization temperature is determined by the relatively thin cement coating, which should not exceed 5 mm, and the temperature dissipation via the large prosthesis surface and the flow of blood. [ 6 ]
The individual components of the bone cement are also known in the area of dental filler materials. Acrylate -based plastics are also used in these applications. While the individual components are not always perfectly safe as pharmaceutical additives and active substances per se, as bone cement the individual substances are either converted or fully enclosed in the cement matrix during the polymerization phase from the increase in viscosity to curing. From current knowledge, cured bone cement can now be classified as safe, as originally demonstrated during the early studies on compatibility with the body conducted in the 1950s.
More recently bone cement has been used in the spine in either vertebroplasty or kyphoplasty procedures. The composition of these types of cement is mostly based on calcium phosphate and more recently magnesium phosphate. A novel biodegradable, non-exothermic, self-setting orthopedic cement composition based on amorphous magnesium phosphate (AMP) was developed. The occurrence of undesirable exothermic reactions was avoided through using AMP as the solid precursor. [ 7 ]
What is referred to as bone cement implantation syndrome (BCIS) is described in the literature. [ 8 ] For a long time it was believed that the incompletely converted monomer released from bone cement was the cause of circulation reactions and embolism . However, it is now known that this monomer (residual monomer) is metabolized by the respiratory chain and split into carbon dioxide and water and excreted. Embolisms can always occur during anchorage of artificial joints when material is inserted into the previously cleared femoral canal. The result is intramedullary pressure increase, potentially driving fat into the circulation.
If the patient is known to have any allergies to constituents of the bone cement, according to current knowledge bone cement should not be used to anchor the prosthesis. Anchorage without cement - cement-free implant placement - is the alternative.
New bone cement formulations require characterization according to ASTM F451. [ 9 ] This standard describes the test methods to assess cure rate, residual monomer, mechanical strength, benzoyl peroxide concentration, and heat evolution during cure.
Revision is the replacement of a prosthesis. This means that a prosthesis previously implanted in the body is removed and replaced by a new prosthesis. Compared to the initial operation revisions are often more complex and more difficult, because every revision involves the loss of healthy bone substance. Revision operations are also more expensive for a satisfactory result. The most important goal is therefore to avoid revisions by using a good surgical procedure and using products with good (long-term) results.
Unfortunately, it is not always possible to avoid revisions. [ 2 ] [ 5 ] There can also be different reasons for revisions and there is a distinction between septic or aseptic revision. [ 10 ] If it is necessary to replace an implant without confirmation of an infection—for example, aseptic—the cement is not necessarily removed completely. However, if the implant has loosened for septic reasons, the cement must be fully removed to clear an infection. In the current state of knowledge it is easier to remove cement than to release a well-anchored cement-free prosthesis from the bone site. Ultimately it is important for the stability of the revised prosthesis to detect possible loosening of the initial implant early to be able to retain as much healthy bone as possible.
A prosthesis fixed with bone cement offers very high primary stability combined with fast remobilization of patients. The cemented-in prosthesis can be fully loaded very soon after the operation because the PMMA gets most of its strength within 24 hours. [ 10 ] The necessary rehabilitation is comparatively simple for patients who have had a cemented-in prosthesis implanted. The joints can be loaded again very soon after the operation, but the use of crutches is still required for a reasonable period for safety reasons.
Bone cement has proven particularly useful because specific active substances, e.g. antibiotics , can be added to the powder component. The active substances are released locally after implant placement of the new joint, i.e. in the immediate vicinity of the new prosthesis and have been confirmed to reduce the danger of infection. The antibiotics act against bacteria precisely at the site where they are required in the open wound without subjecting the body in general to unnecessarily high antibiotic levels. This makes bone cement a modern drug delivery system that delivers the required drugs directly to the surgical site. The important factor is not how much active substance is in the cement matrix but how much of the active substance is actually released locally. Too much active substance in the bone cement would actually be detrimental, because the mechanical stability of the fixed prosthesis is weakened by a high proportion of active substance in the cement. The local active substance levels of industrially manufactured bone cements that are formed by the use of bone cements that contain active substances are approximate (assuming that there is no incompatibility) and are significantly below the clinical routine dosages for systemic single injections.
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https://en.wikipedia.org/wiki/Bone_cement
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Bone decalcification is the softening of bones due to the removal of calcium ions, and can be performed as a histological technique to study bones and extract DNA. [ 1 ] [ 2 ] This process also occurs naturally during bone development and growth, and when uninhibited, can cause diseases such as osteomalacia . [ 3 ]
Since calcium-rich bones are exceedingly difficult to study, scientists use bone decalcification to make specimens available for their research. [ 4 ] For example, bone decalcification has been used to examine cartilage and magnesium levels in order to understand bone decay. [ 1 ] There are two categories of decalcifying agents for removing calcium ions: chelating agents and acids. The acids are further divided into weak (picric, acetic and formic acid) and strong acids (nitric and hydrochloric acid ). The acids help produce a solution of calcium ions while the chelating agents take up the calcium ions. The most frequently used chelating agent is Ethylenediaminetetraacetic acid (EDTA). Decalcification is a lengthy procedure, as bone pieces have to be left in the decalcifying agent for days to weeks, depending on the size of the bone. There are numerous methods to test when bone decalcification is complete, such as X-ray examination, chemical analysis, and measurement of specimen flexibility. Decalcification is necessary to obtain soft sections of the bone using a microtome . Every thin section of the bone that is cut can be processed (see tissue processing ) like any other soft tissue of the body.
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https://en.wikipedia.org/wiki/Bone_decalcification
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In periodontal disease , not only does the bone that supports the teeth, known as alveolar bone , reduce in height in relation to the teeth , but the morphology of the remaining alveolar bone is altered. [ 1 ] The bone destruction patterns that occur as a result of periodontal disease generally take on characteristic forms.
There are four chief types of bone defects that present in the alveolar bone:
Generalized bone loss occurs most frequently as horizontal bone loss. [ 2 ] Horizontal bone loss manifests as a somewhat even degree of bone resorption so that the height of the bone in relation to the teeth has been uniformly decreased, as indicated in the radiograph to the rig defects occur adjacent to a tooth and usually in the form of a triangular area of missing bone, known as triangulation . [ 2 ]
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https://en.wikipedia.org/wiki/Bone_destruction_patterns_in_periodontal_disease
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Bone health refers to the overall condition and strength of the human skeletal system , which is crucial for maintaining mobility, preventing fractures, and supporting overall well-being throughout life. It is influenced by various factors, including genetics, nutrition, physical activity, and hormonal balance. [ 1 ] Optimal bone health is characterized by adequate bone mineral density (BMD) and proper bone microarchitecture, which together contribute to bone strength. [ 2 ] Osteoporosis, a skeletal disorder characterized by compromised bone strength and increased risk of fractures, is a major concern in bone health, particularly among older adults. [ 2 ] [ 3 ] Maintaining good bone health involves a combination of adequate calcium and vitamin D intake, regular weight-bearing exercise, and avoiding risk factors such as smoking and excessive alcohol consumption. [ 1 ] [ 4 ] Recent research has also highlighted the potential role of the gut microbiome in bone health, suggesting a complex interplay between various physiological systems in maintaining skeletal integrity. [ 2 ]
The human skeletal system is a complex organ in constant equilibrium with the rest of the body. In addition to supporting and giving structure to the body, a bone is the major reservoir for many minerals and compounds essential for maintaining a healthy pH balance. [ 5 ] The deterioration of the body with age renders the elderly particularly susceptible to and affected by poor bone health. Illnesses like osteoporosis , characterized by weakening of the bone's structural matrix, increases the risk of hip-fractures and other life-changing secondary symptoms. In 2010, over 258,000 people aged 65 and older were admitted to the hospital for hip fractures. [ 6 ] Incidence of hip fractures is expected to rise by 12% in America, with a projected 289,000 admissions in the year 2030. [ 7 ] Other sources estimate up to 1.5 million Americans will have an osteoporotic-related fracture each year. [ 8 ] The cost of treating these people is also enormous, in 1991 Medicare spent an estimated $2.9 billion for treatment and out-patient care of hip fractures, this number can only be expected to rise. [ 9 ]
When more sulfur containing amino acids , methionine and cystine , are consumed than the body can use for growth and repair, they are broken down yielding sulfate , or sulfuric acid among other products. Animal foods such as meat, dairy, and eggs are high in protein and "dietary animal protein intake is highly correlated with renal net acid excretion". [ 10 ] Research dating back to the early 1900s has shown correlations between high protein diets and increased acid excretion. [ 11 ] One measure of the acidic or basic effects foods have in the body is Potential Renal Acid Load (PRAL). Cheeses with protein content of 15 g protein/100g or higher have a high PRAL value of 23.6 mEq/100 g edible portion. Meats, fish, other cheeses and flour or noodles all have a PRAL around 8.0 mEq/100 g edible portion, where fruits and vegetables actually have a negative PRAL. [ 5 ] [ 12 ]
In healthy adults, bone undergoes constant repair and renewal. New bone is deposited by osteoblast cells and resorbed or destroyed by osteoclast cells. This addition and subtraction of bone usually yields no net change in the overall mass of the skeleton, but the turnover process can be significantly affected by pH. [ 5 ]
Bone mineral density (BMD) is a measure commonly used to quantify bone health. A lower BMD value indicates an increased risk of an osteoporosis or a fracture. [ 13 ] There is a large range of factors influencing BMD. Protein consumption has shown to be beneficial for bone density by providing amino acid substrates necessary for bone matrix formation. It is also thought that blood concentration of the bone formation stimulant, Insulin-like Growth Factor-I (IGF-I), is increased from high protein consumption and parathyroid hormone (PTH), a bone resorption stimulant, is decreased. [ 14 ] Although protein has shown to be beneficial for increasing bone mass, or bone mineral density, there is no significant association between protein intake and fracture incidence. [ 15 ] In other words, a low BMD can be predictive of osteoporosis and increased fracture risk, but a higher BMD does not necessarily mean better bone health. High BMD is also correlated with other health issues. [ 16 ] For example, a higher BMD has also been associated with increased risk of breast cancer. [ 17 ]
Osteoporosis is often asymptomatic until a fracture occurs. Common indicators include back pain, loss of height, a stooped posture, and fractures resulting from minor falls or movements. [ 18 ] [ 19 ]
A bone mineral density test, such as dual-energy X-ray absorptiometry , is commonly used to assess bone strength, particularly in the hip and spine. [ 20 ] Screening is generally recommended for women aged 65 and older, postmenopausal women with risk factors, [ 18 ] [ 21 ] and some men based on clinical evaluation. [ 18 ]
Most metabolic processes have a specific and narrow range of pH where operation is possible, multiple regulatory systems are in place to maintain homeostasis . Fluctuations away from optimal operating pH can slow or impair reactions and possibly cause damage to cellular structures or proteins. To maintain homeostasis the body may excrete excess acid or base through the urine , via gas exchange in the lungs, or buffer it in the blood. [ 22 ] The bicarbonate buffering system of blood plasma effectively holds a steady pH and helps to hold extracellular pH around 7.35. [ 23 ] The kidneys are responsible for the majority of acid-base regulation but can excrete urine no lower than a pH of 5. This means that a 330mL can of cola, for example, usually ranging in pH from 2.8 to 3.2, would need to be diluted 100 fold before being excreted. Instead of producing 33L of urine from one can of cola, the body relies on buffer to neutralize the acid. [ 5 ] Systemic acidosis can be the result of multiple factors, not just diet. Anaerobic exercise , diabetes , AIDS , aging, menopause , inflammation , infections , tumours , and other wounds and fractures all contribute to acidosis. Blood has an average pH of 7.40 but interstitial fluid can vary. Interstitial pH of the skin, for example, is ~7.1. There is no data available for bone. [ 24 ]
Homocysteine , a non-protein amino acid and analogue to the protein amino acid cystine , has been shown to have negative effects on bone health. Higher homocysteine concentrations are likely a result of folate , vitamin B 12 B 6 deficiencies. In addition, it was found that homocysteine concentration was significantly affected by physical activity. The stimulation of the skeleton through physical activity promotes positive bone remodelling and decreases levels of homocysteine, independently from nutritional intake. Four methods have been proposed regarding the interaction of homocysteine and bone; increase in osteoclast activity, decrease in osteoblast activity, decrease in bone blood flow, and direct action of homocysteine on bone matrix. Homocysteine inhibits lysyl oxidase which is responsible for post-translational modifications of collagen , a key component to bone structure [ 25 ]
Osteoclasts are located on the surface of bones and form resorption pits by excreting H+ to the bone surface removing hydroxyapatite , multiple bone minerals, and organic components: collagen and dentin . The purpose of bone resorption is to release calcium to the blood stream for various life processes. [ 25 ] These resorption pits are visible under electron microscopy and distinctive trails are formed from prolonged resorption. Osteoclasts have shown to be "absolutely dependent on extracellular acidification". [ 22 ] A drop in pH of <0.1 units can cause a 100% increase in osteoclast cell activity, this effect persists with prolonged acidosis with no desensitization, "amplifying the effects of modest pH differences". Osteoclast cells show little or no activity at pH 7.4 and are most active at pH 6.8 but can be further stimulated by other factors such as parathyroid hormone . [ 24 ]
Osteoblast are responsible for the mineralization and construction of bone matrix. They are responsible for the formation or production of bone tissue. [ 26 ] The origin of the osteoblasts and osteoclasts is from primitive precursor cells found in bone marrow. [ 26 ] Like osteoclast cells, osteoblast cell activity is directly related to extracellular pH mirroring of osteoclast activity. At pH 7.4, where osteoclasts are inactive, osteoblast are at peak activity. Likewise, at pH 6.9 osteoblast activity is non-existent. [ 24 ] The hormone estrogen is also important for osteoblast regulation. In postmenopausal women estrogen levels are decreased which has negative effects on bone remodeling. Homocysteine further exacerbates this problem by reducing estrogen receptor α mRNA transcription. Thus reducing any beneficial effect that estrogen plays on bone remodeling. [ 25 ]
Acidosis inhibits bone osteoblast matrix mineralization with reciprocal effect on osteoclast activation. The combined responses of these cells to acidosis maximizes the availability of hydroxyl ions in solution that can be used to buffer protons. [ 24 ] The utilization of bone to buffer even a small percentage of daily acid production can lead to significant loss of bone mass in the course of a decade. [ 10 ] Additionally, as the body ages there is a steady decline in renal function. Metabolic acidosis can become more severe as kidney function weakens, and the body will depend more heavily on bone and blood to maintain acid-base homeostasis. [ 14 ]
Bone Mineral Density (BMD) tends to peak at a young age. When children are younger, they start building up their BMD through their nutrition and through exercise. BMD peaks at around 12.5 years old for girls and around 14 years old for boys. [ 27 ] It could be caused by a deficiency in calcium or Vitamin D. Calcium is the main nutrient for bone health. It aids in the structure and density of the bone. Low BMD could be caused by the children not getting the proper exercise for adequate bone growth. Researchers suggest that children should get 20 minutes of vigorous activity 3 to 5 days a week to promote an increase in BMD. [ 28 ] Jumping for about 5 minutes a day also stimulates an increase in BMD. Researchers did a 10-year study on the effects of vigorous intensity activity and their bone health/strength. They studied 300 boys and girls. They found that in boys going through puberty (ages 11-13), they experienced a greater bone mass growth. [ 29 ] Their bone mass increased during this time because their bones are not ready for the mechanical stress from them growing. [ 29 ] However, that is how the bones grow stronger and why their BMD increases. Too much stress on the bones could cause BMD to decrease. Low BMD is dangerous because it can cause disorders inside the bone as the children grow and get older. These disorders can cause the bone to ossify, become brittle, fragile, more easily prone to fractures, and weak. Some of these disorders include osteopenia, osteoporosis, and scoliosis. [ 30 ] Scoliosis is very common in children. Low BMD plays a role in the child's scoliosis. When their bone density is low, there is a higher risk of microfractures in the vertebrae causing the spine to curve and bend. [ 31 ] These curves and bends cause pressure onto the vertebra which could cause progression of scoliosis. When the spine is in this shape, it makes it very difficult for the children to play and exercise. This will also improve the severity of the scoliosis. [ 31 ]
There is no one food or nutrient capable of providing adequate bone health on its own. Instead, a balanced diet sufficient in fruits and vegetables for their vitamins, minerals, and alkalinizing substrates is thought to be most beneficial. High protein diets supply larger amounts of amino acids that could be degraded to acidic compounds. Protein consumption above the Recommended Dietary Allowance is also known to be beneficial to calcium utilization. Overall it is understood that high-protein diets have a net benefit for bone health because changes in IGF-I and PTH concentrations outweigh the negative effects of metabolic acid production. [ 14 ] The source of protein, plant or animal, does not matter in terms of acid produced from amino acid metabolism. Any differences in methionine and cysteine content is not significant to affect the overall potential renal acid load (PRAL) of the food. In addition to their acid precursor protein content, plants also contain significant amounts of base precursors. Potassium bicarbonate , a basic salt, is produced via the metabolism of other organic potassium salts: citrate , malate , and gluconate , which are substantial in plants. The discrepancy observed in PRAL is accounted for by differences in base precursor content. [ 10 ] [ 12 ]
Obesity affects bone mineral density (BMD) and fracture risk. While increased weight may enhance BMD due to mechanical loading, it can also elevate fracture risk at specific skeletal sites. Studies suggest that obesity impacts bone quality, potentially increasing fragility. [ 32 ]
Magnesium is essential for bone health, contributing to bone formation and maintenance. [ 33 ] Lower magnesium intake has been linked to reduced BMD, while higher intake may help protect against fractures, particularly in postmenopausal women. [ 34 ]
While obesity may increase BMD, body fat distribution and metabolic factors can negatively affect bone quality, potentially raising fracture risk. [ 35 ]
Regular physical activity, particularly weight-bearing and resistance exercises, has been shown to improve bone density and reduce the likelihood of fractures. [ 36 ]
Adequate intake of calcium and vitamin D is essential for bone health. The National Osteoporosis Foundation recommends a daily calcium intake of 1,000 mg for men aged 50-70 and 1,200 mg for women aged 51 and older and men aged 71 and older. For vitamin D, a daily intake of 800-1,000 IU is recommended for adults aged 50 and older. [ 36 ]
Osteoporosis and compromised bone mineral density (BMD) are significant conditionss affecting the youth population. Weight-bearing physical activities are associated with bone development. Several studies have been made regarding different characteristics that affect bone development in youth such as gender, athletic status, type of exercise or sport, and intensity of exercise.
A common way children today receive their daily dose of exercise is within their chosen sport. Sports can vary in their benefit of bone mineral composition and can be sorted into two categories: Osteogenic and Non-Osteogenic. Osteogenic sports are impact sports such as football, baseball, track and field, etc; while non-osteogenic sports are non-impact sports such as swimming or cycling. A study was done examining the relationship between jumping exercise interventions and non-osteogenic sport bone mineral content. The study showed that a 9-month jumping exercise plan can increase the bone mineral content of a non-osteogenic sport participant by 5.6%-12.6%. [ 37 ] In conclusion, there is a strong correlation between physical activity and bone health in adolescents and physical activity should be a daily prescription in the lives of our youth today to maintain adequate bone health and development.
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Bone malrotation refers to the situation that results when a bone heals out of rotational alignment from another bone, or part of bone. It often occurs as the result of a surgical complication after a fracture where intramedullary nailing (IMN) occurs, [ 1 ] especially in the femur and tibial bones, but can also occur genetically at birth. The severity of this complication is often neglected due to its complexity to detect and treat, [ 1 ] yet if left untreated, bone malrotation can significantly impact regular bodily functioning, and even lead to severe arthritis . Detection throughout history has become more advanced and accurate, ranging from clinical assessment to ultrasounds to CT ( computed tomography ) scans. Treatment can include an osteotomy , a major surgical procedure where bones are cut and realigned correctly, or compensatory methods, where individuals learn to externally or internally rotate their limb to compensate for the rotation. Further research is currently being examined in this area to reduce occurrences of malrotation, including detailed computer navigation to improve visual accuracy during surgery. [ 2 ]
Bone malrotation predominantly occurs after an injury where a bone is fractured, however malrotation can genetically occur during foetal development . It usually occurs during a surgery which involves intramedullary nailing , which is the insertion of metal rods and nails to stabilise bones. Nailing is used as it requires minimal surgical dissection, less disruption of the fracture hematoma and allows faster functionality to a patient post-surgery. [ 1 ] [ 3 ] However, due to the semi-closed nature of IM, it is impossible to correct under direct vision, so there is less rotational control compared to traditional open methods such as plate fixation. [ 3 ] As a result, in many cases of intramedullary nailing, the bone is misaligned which causes malrotated regrowth. This torsional error is a major problem for femoral and tibial fractures, and occurs in 17 to 35% of patients who receive these surgeries, [ 4 ] and up to 40% of femur fracture patients. [ 1 ]
Femoral malrotation is the most significant bone malrotation issue, and these errors cause cosmetic problems but can also cause drastic physical problems. [ 4 ]
Historically, bone malrotation occurred due to a lack of adequate treatment measures, where fixation methods such as traction , casting and non-locked nails provided poor torsional stability. Currently, the utilisation of locked intramedullary nailing, has reduced the occurrence of rotational malalignment during fracture healing, yet femoral malrotation continues to remain very prevalent due to surgeon's inability to reliably restore the pre-injury alignment during operation. [ 1 ] A high attention to detail is necessary intra-operatively to avoid this complication when locking the intramedullary device. [ 5 ] The utilisation of both radiological and clinical assessment techniques to compare with an injured limb would also help prevent bone malrotation, however these can be difficult and inexact methods of assessment, which is why complications are so common. [ 1 ]
It is difficult to assess and diagnose the rotational malalignment of a bone after an operation, and many methodologies have been developed.
Clinical assessment and observation is one methodology, however it is unreliable, and can lead to complications. For femoral or tibial malrotation, many surgeons use the patient's ankle or patella to symmetrically align them with the injured side or to the floor but this method does not consider the position of the proximal fragment and could be moved during reduction attempts. [ 5 ] In order to measure femoral malalignment, many doctors will compare the internal and external rotation of both hips, while the patient is supine or prone, and a change in a patient's range of movement indicates malrotation. However, while clinical assessment can indicate the direction of malrotation, it often reports inaccurate measurements of the degree of malalignment, so it is unreliable in determining the potential impacts and necessary treatment methods. [ 3 ]
Another diagnosis methodology sometimes utilised are radiographs ; however, they are unreliable as they require difficult patient positioning to quantify the rotational deformity. [ 5 ] This difficulty is due to a patient's restriction in movement, as they may exhibit post-traumatic deformities and severe pain. To determine the level of femoral malrotation, with this method, two radiographs of the pelvis and upper legs must be made. Firstly, an anteroposterior (AP) perspective which shows the degree of difference between the femoral neck and femur, and another view where the hips and knees are both flexed to a right angle, which determines antetorsion. Both of these radiographs are utilised to calculate the angle of anteversion of the femoral neck. [ 3 ]
Ultrasounds can also be used to measure bone malrotation, and are considered highly reliable. The main issue with utilising ultrasound measurement is that it relies largely on the skills of an ultrasound technician, and consequently is not widely used. When measuring femoral malrotation with ultrasounds, a patient's thighs are fixed symmetrically while the degree of rotation of the femoral shaft is measured. This methodology requires exact positioning of a patient to correctly measure any deformity. [ 3 ]
MRI scans can be utilised and are proven to be reliable and effective at determining malrotation of bones. However, they are not as readily available as CT scanners, and are also time consuming and very expensive. [ 5 ]
The standard bone malrotation detection practice utilised are computed tomography scans , which are able to exactly quantify the amount of rotational malalignment. [ 5 ] It is also considered highly reliable and utilised because of its reproducibility. For femoral malrotation, the scan involves doctors measuring the angle between a line through the axis of the femoral neck and a line tangential to the femoral condyles. The angle difference between the uninjured and injured sides determines the degree of malrotation. An increase in the anteversion of the femoral neck of the injured side denotes internal rotation, and a decrease means external rotation has occurred. Another advantage of CT scans is that patient positioning does not impact the measurement accuracy of femoral torsion, which is unlike radiographs and ultrasounds. However, inaccurate measurements of malrotation can still occur in CT scans, but are mostly related difficulty in drawing clear and accurate lines along the femoral neck within the image. To avoid this inaccuracy, there needs to be improved accuracy of the line drawn, and this can be fixed by the utilisation of multi-image superimposed projection of the CT images so a more accurate measurement can be drawn. [ 3 ]
Whilst malrotation of a bone can be tolerated for most cases, it can still cause severe impacts on functional outcome for some patients. Whilst tibial fractures are the most common long bone fractures, it is malrotation of the femur which can cause the most significant impacts on regular functioning. [ 6 ]
If untreated, femoral malrotation can cause considerable gait disturbance and abnormal hip joint pressures. [ 2 ] Malrotation of the femur in the setting of a mid-shaft fracture has an impact on the axis of the entire leg, which shifts the centre of force in the knee away from its neutral position. Consequently, femoral malrotation has significant impacts on the mechanical axis and force vectors within the knee. This can cause pain in the hip and knee, and patients may be limited in their movement, which can impair their function, especially in physically demanding activities such as walking up stairs and running. [ 3 ] This can impact a person's satisfaction in life, as they may be physically unable to do things they want and need to, such as for laborious work, leisure activities, or raising a family, which can have significant impacts on their psychological health. Femoral malrotation can also cause an abnormally rotated foot, as the angle of a person's foot is directly related to the angle of the femur. [ 7 ]
Another significant long term consequence of femoral malrotation if untreated is degenerative arthritis of the hip and knee. [ 3 ] This joint arthrosis occurs as there is a proven correlation between rotational error, axis deviation and arthrosis of the knee and hip joints. However, the severity of the arthrosis is dependent on the percentage of malrotation. [ 4 ]
Whilst most malrotation problems occurred during surgery, patients with 10° or less difference of malrotation compared with the uninjured side rarely complained of any issues. [ 8 ] However, patients with differences greater than 15° found noticeable issues, and above 30° malrotation difference resulted in serious complaints. [ 5 ] External femoral malrotation is usually much better tolerated than internal malrotation. [ 1 ] However, older studies have found that external rotational deformities are more poorly tolerated, [ 9 ] which shows the need for more research in this area.
There are two main treatment methods; corrective surgery to fix the malrotation, or compensatory methods where patients learn to compensate for any malrotation when walking.
Many people with bone malrotation, such as femoral malrotation are able to functionally tolerate and learn compensatory methods , such as externally or internally adjusting their limb. Patients will compensate for even considerable rotational malalignment when they are active. However, femoral malrotation is more difficult to compensate for and maintain with non-operative treatment methods. [ 5 ] Patients with femoral malrotation of less than 15 degrees give less complaints than those with higher amounts of malalignment, yet many patients are able to tolerate the deformity well. [ 3 ]
In extreme cases, the malalignment can be treated by means of a derotational osteotomy which is a major surgical procedure. [ 3 ] It can be conducted around the existing intramedullary fixtures, but it usually requires a subtrochanteric osteotomy, which is an invasive surgical approach where bone is cut and realigned. As this is a major procedure, it is beneficial if discovered early, before callus has set, and consequently, patients should be assessed for malrotation in the early post-operative period and a CT scan should occur if abnormalities are found. [ 5 ] Correct measurement of bone malalignment with a CT scan is vital when considering an osteotomies in fixing rotational deformities, as torsional differences below 15 degrees are often easily compensated for with non surgical treatment. [ 3 ] Revision surgery should be avoided, if not necessary, as implementing femoral nails for a second time leads to higher rates of problems such as infection, nonunion, or nail destabilisation due to overlapping holes for the interlocking screws. [ 10 ]
There is currently limited clinical attention in the area of bone malrotation and research into more accurate methods, likely due to the complexity of the issue. [ 1 ] Whilst computed tomography scans are useful in determining the degree of bone malrotation after a surgery has occurred, research is being conducted into how to prevent this deformity occurring at all during surgery. CT scans are impractical intraoperatively due to high cost, lack of equipment portability and increased exposure to radiation. [ 10 ]
Consequently, one area being researched is that of computer navigation, which could be utilised during these surgeries to avoid malalignment issues. Computer assisted surgery (CAS) matches a patient's anatomy with pre or intraoperatively generated fluoroscopic image data, by using camera detected infrared signals. The computer then calculates the positioning of each component and creates a visual of their position on the monitor. As a result, the surgeon can monitor in real time the position of the surgical instruments in relation to the patient's anatomy and conducts the procedure accordingly. [ 11 ] The surgeon can plan the torsional adjustment and control the fracture reduction and nail insertion on a touchscreen of the navigation module.
Currently, this navigation may add extra time during surgery, so it is sometimes considered unnecessary in an urgent surgery. However, without computer navigation, the risk of bone malrotation is significantly increased. The benefit of computer navigation means that surgeons are able to view more clearly and restore axial alignment, but also ensure the injured limb and matches the alignment and length of the uninjured limb. [ 2 ] CAS provides increased surgical accuracy and safety for both patients and surgeons, radiation time is reduced, and it utilises minimally invasive techniques which means less tissue damage, improved wound healing, and reduced infections and scarring for patients. [ 11 ]
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Bone marrow examination refers to the pathologic analysis of samples of bone marrow obtained by bone marrow biopsy (often called trephine biopsy) and bone marrow aspiration . Bone marrow examination is used in the diagnosis of a number of conditions, including leukemia , multiple myeloma , lymphoma , anemia , and pancytopenia . The bone marrow produces the cellular elements of the blood , including platelets , red blood cells and white blood cells . While much information can be gleaned by testing the blood itself (drawn from a vein by phlebotomy ), it is sometimes necessary to examine the source of the blood cells in the bone marrow to obtain more information on hematopoiesis ; this is the role of bone marrow aspiration and biopsy.
Bone marrow samples can be obtained by aspiration and trephine biopsy. Sometimes, a bone marrow examination will include both an aspirate and a biopsy. The aspirate yields semi-liquid bone marrow, which can be examined by a pathologist under a light microscope and analyzed by flow cytometry , chromosome analysis , or polymerase chain reaction (PCR). Frequently, a trephine biopsy is also obtained, which yields a narrow, cylindrically shaped solid piece of bone marrow, 2 mm wide and 2 cm long (80 μL), which is examined microscopically (sometimes with the aid of immunohistochemistry ) for cellularity and infiltrative processes. An aspiration, using a 20 mL syringe, yields approximately 300 μL of bone marrow. [ 1 ] A volume greater than 300 μL is not recommended, since it may dilute the sample with peripheral blood. [ 1 ]
Aspiration does not always represent all cells since some such as lymphoma stick to the trabecula , and would thus be missed by a simple aspiration. [ citation needed ]
Bone marrow aspiration and trephine biopsy are usually performed on the back of the hipbone, or posterior iliac crest . An aspirate can also be obtained from the sternum (breastbone). For the sternal aspirate, the patient lies on their back, with a pillow under the shoulder to raise the chest. A trephine biopsy should never be performed on the sternum, due to the risk of injury to blood vessels , lungs or the heart . Bone marrow aspiration may also be performed on the tibial (shinbone) site in children up to 2 years of age while spinous process aspiration is frequently done in a lumbar puncture position and on the L3-L4 vertebrae. [ citation needed ]
Anesthesia is used to reduce surface pain at the spot where the needle is inserted. Pain may result from the procedure's insult to the marrow, which cannot be anesthetized, as well as short periods of pain from the anesthetic process itself. The experience is not uniform; different patients report different levels of pain, and some do not report any pain at certain expected points. [ 2 ]
A bone marrow biopsy may be done in a health care provider's office or in a hospital. Informed consent for the procedure is typically required. The patient is asked to lie on their abdomen ( prone position ) or on their side (lateral decubitus position). The skin is cleansed, and a local anesthetic such as lidocaine or procaine is injected to numb the area. Patients may also be pretreated with analgesics and/or anti-anxiety medications , although this is not a routine practice.
Typically, the aspirate is performed first. An aspirate needle is inserted through the skin using manual pressure and force until it hits the bone . Then, with a twisting motion of clinician's hand and wrist, the needle is advanced through the bony cortex (the hard outer layer of the bone) and into the marrow cavity. Once the needle is in the marrow cavity, a syringe is attached and used to aspirate ("suck out") liquid bone marrow. A twisting motion is performed during the aspiration to avoid excess content of blood in the sample, which might be the case if an excessively large sample from one single point is taken. Subsequently, the biopsy is performed if indicated. A different, larger trephine needle is inserted and anchored in the bony cortex. The needle is then advanced with a twisting motion and rotated to obtain a solid piece of bone marrow. This piece is then removed along with the needle. The entire procedure, once preparation is complete, typically takes 10–15 minutes.
If several samples are taken, the needle is removed between the samples to avoid blood coagulation.
After the procedure is complete, the patient is typically asked to lie flat for 5–10 minutes to provide pressure over the procedure site. After that, assuming no bleeding is observed, the patient can get up and go about their normal activities. Paracetamol (aka acetaminophen) or other simple analgesics can be used to ease soreness, which is common for 2–3 days after the procedure. Any worsening pain, redness, fever, bleeding or swelling may suggest a complication. Patients are also advised to avoid washing the procedure site for at least 24 hours after the procedure is completed.
There are few contraindications to bone marrow examination. It is important to note that thrombocytopenia or bleeding disorders are not contraindications as long as the procedure is performed by a skilled clinician. [ 3 ] Bone marrow aspiration and biopsy can be safely performed even in the setting of extreme thrombocytopenia (low platelet count). If there is a skin or soft tissue infection over the hip, a different site should be chosen for bone marrow examination. [ citation needed ]
While mild soreness lasting 12–24 hours is common after a bone marrow examination, serious complications are extremely rare. In a large review, an estimated 55,000 bone marrow examinations were performed, with 26 serious adverse events (0.05%), including one fatality. [ 4 ] The same author collected data on over 19,000 bone marrow examinations performed in the United Kingdom in 2003, and found 16 adverse events (0.08% of total procedures), the most common of which was bleeding. In this report, complications, while rare, were serious in individual cases. [ 5 ]
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Bone marrow suppression also known as myelotoxicity or myelosuppression , is the decrease in production of cells responsible for providing immunity ( leukocytes ), carrying oxygen ( erythrocytes ), and/or those responsible for normal blood clotting ( thrombocytes ). [ 1 ] Bone marrow suppression is a serious side effect of chemotherapy and certain drugs affecting the immune system such as azathioprine . [ 2 ] The risk is especially high in cytotoxic chemotherapy for leukemia . In the case of non-small-cell lung cancer , myelosuppression predisposition was shown to be modulated by enhancer mutations. [ 3 ]
Nonsteroidal anti-inflammatory drugs (NSAIDs), in some rare instances, may also cause bone marrow suppression. The decrease in blood cell counts does not occur right at the start of chemotherapy because the drugs do not destroy the cells already in the bloodstream (these are not dividing rapidly). Instead, the drugs affect new blood cells that are being made by the bone marrow. [ 4 ] When myelosuppression is severe, it is called myeloablation. [ 5 ]
Many other drugs including common antibiotics may cause bone marrow suppression. Unlike chemotherapy the effects may not be due to direct destruction of stem cells but the results may be equally serious. The treatment may mirror that of chemotherapy-induced myelosuppression or may be to change to an alternate drug or to temporarily suspend treatment.
Because the bone marrow is the manufacturing center of blood cells, the suppression of bone marrow activity causes a deficiency of blood cells. This condition can rapidly lead to life-threatening infection , as the body cannot produce leukocytes in response to invading bacteria and viruses , as well as leading to anaemia due to a lack of red blood cells and spontaneous severe bleeding due to deficiency of platelets .
Parvovirus B19 inhibits erythropoiesis by lytically infecting RBC precursors in the bone marrow and is associated with a number of different diseases ranging from benign to severe. In immunocompromised patients, B19 infection may persist for months, leading to chronic anemia with B19 viremia due to chronic marrow suppression. [ 6 ]
Bone marrow suppression due to azathioprine can be treated by changing to another medication such as mycophenolate mofetil (for organ transplants) or other disease-modifying drugs in rheumatoid arthritis or Crohn's disease .
Bone marrow suppression due to anti-cancer chemotherapy is much harder to treat and often involves hospital admission, strict infection control, and aggressive use of intravenous antibiotics at the first sign of infection. [ 7 ]
G-CSF is used clinically (see Neutropenia ) but tests in mice suggest it may lead to bone loss. [ 8 ] [ 9 ]
GM-CSF has been compared to G-CSF as a treatment of chemotherapy-induced myelosuppression/ Neutropenia . [ 10 ]
Trilaciclib (COSELA) , a CDK4/6 inhibitor , is administered before chemotherapy in small cell lung cancer to control chemotherapy-induced myelosuppression. [ 11 ]
In developing new chemotherapeutics, the efficacy of the drug against the disease is often balanced against the likely level of myelotoxicity the drug will cause. In-vitro colony forming cell (CFC) assays using normal human bone marrow grown in appropriate semi-solid media such as ColonyGEL have been shown to be useful in predicting the level of clinical myelotoxicity a certain compound might cause if administered to humans. [ 12 ] These predictive in-vitro assays reveal effects the administered compounds have on the bone marrow progenitor cells that produce the various mature cells in the blood and can be used to test the effects of single drugs or the effects of drugs administered in combination with others.
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1ES7 , 1REU , 1REW , 2GOO , 2H62 , 2H64 , 2QJ9 , 2QJA , 2QJB , 3BK3 , 3BMP , 4MID , 4N1D , 4UHY , 4UHZ , 4UI0 , 4UI1 , 4UI2
650
12156
ENSG00000125845
ENSMUSG00000027358
P12643
P21274
NM_001200
NM_007553
NP_001191
NP_031579
Bone morphogenetic protein 2 or BMP-2 belongs to the TGF-β superfamily of proteins . [ 5 ]
BMP-2 like other bone morphogenetic proteins , [ 6 ] plays an important role in the development of bone and cartilage. It is involved in the hedgehog pathway , TGF beta signaling pathway , and in cytokine -cytokine receptor interaction. It is also involved in cardiac cell differentiation and epithelial to mesenchymal transition .
Like many other proteins from the BMP family, BMP-2 has been demonstrated to potently induce osteoblast differentiation in a variety of cell types. [ 7 ]
BMP-2 may be involved in white adipogenesis [ 8 ] [ 9 ] and may have metabolic effects. [ 8 ] [ 9 ]
Bone morphogenetic protein 2 has been shown to interact with BMPR1A . [ 10 ] [ 11 ] [ 12 ] [ 13 ]
Bone morphogenetic protein 2 is shown to stimulate the production of bone. [ 14 ] [ 15 ] Recombinant human protein (rhBMP-2) is currently available for orthopaedic usage in the United States . [ 16 ] Implantation of BMP-2 is performed using a variety of biomaterial carriers ("metals, ceramics, polymers, and composites" [ 17 ] ) and delivery systems ("hydrogel, microsphere, nanoparticles, and fibers" [ 17 ] ). While used primarily in orthopedic procedures such as spinal fusion, [ 18 ] [ 19 ] BMP-2 has also found its way into the field of dentistry. [ 20 ] [ 21 ] [ 22 ]
The use of dual tapered threaded fusion cages and recombinant human bone morphogenetic protein-2 on an absorbable collagen sponge obtained and maintained intervertebral spinal fusion, improved clinical outcomes, and reduced pain after anterior lumbar interbody arthrodesis in patients with degenerative lumbar disc disease. [ 18 ] As an adjuvant to allograft bone or as a replacement for harvested autograft, bone morphogenetic proteins (BMPs) appear to improve fusion rates after spinal arthrodesis in both animal models and humans, while reducing the donor-site morbidity previously associated with such procedures. [ 19 ]
A study published in 2011 noted "reports of frequent and occasionally catastrophic complications associated with use of [BMP-2] in spinal fusion surgeries", with a level of risk far in excess of estimates reported in earlier studies. [ 23 ] [ 24 ] An additional review by Agrawal and Sinha of BMP-2 and its common delivery systems in early 2016 showed how "problems like ectopic growth, lesser protein delivery, [and] inactivation of the protein" reveal a further need "to modify the available carrier systems as well as explore other biomaterials with desired properties." [ 17 ]
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A bone sarcoma is a primary malignant bone tumour , a type of sarcoma that starts in the bones . [ 1 ] This is in contrast to most bone cancers that are secondary having developed as a metastasis from another cancer. Bone sarcomas are rare, and mostly affect the legs . The other type of sarcoma is a soft-tissue sarcoma .
There are three main types of bone sarcoma based on tissue type – an osteosarcoma , a Ewing's sarcoma , and a chondrosarcoma . [ 1 ]
The three main types of bone sarcoma are an osteosarcoma , most frequently found of the three; Ewing's sarcoma , and a chondrosarcoma . [ 2 ] There are many subtypes of these.
An osteosarcoma is predominantly found in childhood and adolescence. [ 1 ] They are primarily found in long bones , and may be secondary tumours. [ 3 ] Osteosarcomas are composed of mesenchymal cells that produce immature bone. [ 4 ] The tumour cells are unique in that they produce immature osteoid . [ 3 ]
Ewing's sarcoma is the next most commonly found sarcoma in adolescents and young adults. Ewing's is highly aggressive, typically developing from the medullary cavity of a bone with cells invading the Haversian system . [ 5 ] An immunohistochemistry test shows the tumour as having small rounded blue cells. [ 6 ] [ 7 ] The cells express high levels of CD99 . [ 5 ]
A chondrosarcoma is the type of bone cancer that starts in the cartilage cells. It is the most common type found in adults. Unlike the other types it is rarely found in those under the age of twenty. Most chondrosarcomas develop in the pelvis , legs or arms. Benign counterparts are known as enchondromas . Chondrosarcomas are classified by grade as a measurement of their growth rate – I, II, and III. The lower the grade the slower the rate of growth. Grade III are the most aggressive, and are liable to spread . [ 8 ]
Subtypes of chondrosarcomas have different features and different outlooks , they include: [ citation needed ]
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Bone segment navigation is a surgical method used to find the anatomical position of displaced bone fragments in fractures , or to position surgically created fragments in craniofacial surgery . Such fragments are later fixed in position by osteosynthesis . It has been developed for use in craniofacial and oral and maxillofacial surgery .
Bone segment navigation is a patented [ 1 ] [ 2 ] surgical procedure, using a frameless and markerless registration technique. It uses for the first time natural registration surfaces instead of single artificial x-ray visible markers, in order to achieve a higher precision (1 mm and better). [ 3 ] Previous methods of Cutting and Watzinger do not meet the criteria of bone segment navigation. [ 4 ]
After an accident or injury, a fracture can be produced and the resulting bony fragments can be displaced. In the oral and maxillofacial area, such a displacement could have a major effect both on facial aesthetics and organ function: a fracture occurring in a bone that delimits the orbit can lead to diplopia ; a mandibular fracture can induce significant modifications of the dental occlusion ; in the same manner, a skull ( neurocranium ) fracture can produce an increased intracranial pressure . [ citation needed ]
In severe congenital malformations of the facial skeleton surgical creation of usually multiple [ 5 ] [ 6 ] bone segments is required with precise movement of these segments to produce a more normal face.
An osteotomy is a surgical intervention that consists of cutting through bone and repositioning the resulting fragments in the correct anatomical place. To insure optimal repositioning of the bony structures by osteotomy , the intervention can be planned in advance and simulated. The surgical simulation is a key factor in reducing the actual operating time. Often, during this kind of operation, the surgical access to the bone segments is very limited by the presence of the soft tissues: muscles, fat tissue and skin - thus, the correct anatomical repositioning is very difficult to assess, or even impossible. Preoperative planning and simulation on models of the bare bony structures can be done. An alternate strategy is to plan the procedure entirely on a CT scan generated model and output the movement specifications purely numerically. [ 7 ]
The osteotomies performed in orthognathic surgery are classically planned on cast models of the tooth-bearing jaws, fixed in an articulator . For edentulous patients, the surgical planning may be made by using stereolithographic models . These tridimensional models are then cut along the planned osteotomy line, slid and fixed in the new position.
Since the 1990s, modern techniques of presurgical planning were developed – allowing the surgeon to plan and simulate the osteotomy in a virtual environment, based on a preoperative CT or MRI ; this procedure reduces the costs and the duration of creating, positioning, cutting, repositioning and refixing the cast models for each patient.
The usefulness of the preoperative planning, no matter how accurate, depends on the accuracy of the reproduction of the simulated osteotomy in the surgical field. The transfer of the planning was mainly based on the surgeon's visual skills. Different guiding headframes were further developed to mechanically guide bone fragment repositioning. [ citation needed ]
Such a headframe is attached to the patient's head, during CT or MRI, and surgery. There are certain difficulties in using this device. First, exact reproducibility of the headframe position on the patient's head is needed, both during CT or MRI registration, and during surgery. The headframe is relatively uncomfortable to wear, and very difficult or even impossible to use on small children, who can be uncooperative during medical procedures. For this reason headframes have been abandoned in favor of frameless stereotaxy of the mobilized segments with respect to the skull base. Intraoperative registration of the patient's anatomy with the computer model is done such that pre-CT placement of fiducial points is not necessary. [ citation needed ]
Initial bone fragment positioning efforts using an electro-magnetic system were abandoned due to the need for an environment without ferrous metals. [ 8 ] In 1991 Taylor at IBM working in collaboration with the craniofacial surgery team at New York University developed a bone fragment tracking system based on an infrared (IR) camera and IR transmitters attached to the skull. [ 9 ] [ 10 ] This system was patented by IBM in 1994. [ 11 ] At least three IR transmitters are attached in the neurocranium area to compensate the movements of the patient's head. There are three or more IR transmitters are attached to the bones where the osteotomy and bone repositioning is about to be performed onto. The 3D position of each transmitter is measured by the IR camera, using the same principle as in satellite navigation . A computer workstation is constantly visualizing the actual position of the bone fragments, compared with the predetermined position, and also makes real-time spatial determinations of the free-moving bony segments resulting from the osteotomy.
Thus, fragments can be very accurately positioned into the target position, predetermined by surgical simulation. More recently a similar system, the Surgical Segment Navigator (SSN), was developed in 1997 at the University of Regensburg, Germany , with the support of the Carl Zeiss Company . [ 12 ]
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Bone wax is a waxy substance used to help mechanically control bleeding from bone surfaces during surgical procedures.
It is generally made of beeswax [ 1 ] with a softening agent such as paraffin or petroleum jelly and is smeared across the bleeding edge of the bone, blocking the holes and causing immediate bone hemostasis through a tamponade effect. Bone wax is most commonly supplied in sterile sticks, and usually requires softening before it can be applied.
A note by Victor Horsley published in the British Medical Journal in 1892 described a formulation of "antiseptic wax" [ 1 ] having seven parts beeswax, one part almond oils, and 1% salicylic acid . The material was useful for controlling bleeding when pressed into the pores and channels of cut or damaged bone. The wax was sterilized by boiling and kept in stoppered bottles . This material soon became the standard of care for bleeding control in bone for general orthopedics, craniomaxillofacial surgery , and cardiothoracic surgery , where the sternum is often split longitudinally to provide access to the heart.
Ordinary bone wax is effective by virtue of its tamponade action, but is considered to have no active hemostatic properties (i.e. does not activate the blood clotting cascade ). In addition, bone wax is not soluble in the bodily fluids and thus remains at the site of implantation for long periods of time, if not indefinitely. The portion of traditional bone wax that departs the implant site is most likely carried away through the action of the foreign body response and is associated with a low-grade inflammatory response at and near the implant site. The residual product can also potentially serve as a nidus (breeding site) for post-operative infection .
Modern day bone wax is commercially available in substantially non-absorbable formulations similar to Horsley's original composition, as well as in absorbable/resorbable formats. Most are available as a firm wax in stick form that must be softened by kneading prior to use.
More recent advances have led to the introduction of a bone hemostat in putty format. Hemostatic putties act via tamponade in the same way as the stick waxes, but are ready to use and eliminate the requirement to soften the product prior to use.
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Bonnet–Dechaume–Blanc syndrome , also known as Wyburn-Mason syndrome , is a rare congenital disorder characterized by arteriovenous malformations of the brain , retina or facial nevi . [ 1 ] The syndrome has a number of possible symptoms and can, more rarely, affect the skin , bones , kidneys , muscles , and gastrointestinal tract . [ 2 ] When the syndrome affects the brain, people can experience severe headaches, seizures, acute stroke, meningism , and progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting. [ 2 ] [ 3 ]
In the retina, the syndrome causes retinocephalic vascular malformations that tend to be present with intracranial hemorrhage and lead to decreased visual acuity, proptosis , pupillary defects, optic atrophy, congestion of bulbar conjunctiva , and visual field defects. [ 4 ] [ 5 ] Retinal lesions can be unilateral and tortuous, and symptoms begin to appear in the second and third decades of life. [ 4 ]
The syndrome can present with cutaneous lesions, or skin with different texture, thickness, and color, usually on the face. [ 5 ] The facial features caused by the syndrome vary from slight discoloration to extensive nevi and angiomas of the skin. [ 3 ] In some cases, the frontal and maxillary sinus may also be affected. [ 5 ]
There have only been 52 reported cases of patients with Bonnet–Dechaume–Blanc syndrome as of 2012. [ 2 ] Symptoms are rarely noticed in children and the syndrome is often diagnosed in late childhood or early adulthood when visual impairment is noticed. [ 3 ] Fluorescein angiography is commonly used to diagnose the syndrome. [ 6 ]
There have been several methods in treating patients with Bonnet–Dechaume–Blanc syndrome. However, the optimal treatment is uncertain. Patients with intracranial lesions have been treated with surgical intervention and in some cases, this procedure has been successful. Other treatments include embolization , radiation therapy , and continued observation. [ 5 ]
With limited research on Bonnet–Dechaume–Blanc syndrome, researchers have focused on the clinical and radiological findings rather than how to manage this rare and non-heritable syndrome. [ 3 ]
Typically not diagnosed until late childhood or later, Bonnet–Dechaume–Blanc syndrome usually presents itself with a combination of central nervous system features ( midbrain ), ophthalmic features ( retina ), and facial features. [ 7 ] The degree of expression of the syndrome's components varies both clinically and structurally. Common symptoms that lead to diagnosis are headaches, retro-orbital pain, and hemianopia . [ 5 ]
The ophthalmic features of Bonnet–Dechaume–Blanc syndrome occur as retinal arteriovenous malformation (AVMs). There are three categories of AVMs based on their severity. The first category consists of the patient having small lesions that usually are asymptomatic . The second category, more severe than the first, is when the patient's malformation is missing a connecting capillary between an artery and a vein; without it, edema , hemorrhage, and visual impairment can result. Category three refers to malformations so severe that their dilated vessels no longer distinguish between artery and vein, and the patient has a significantly increased risk of vision loss. [ 3 ] Since the retinal lesions categorized vary from large vascular malformations that affect a majority of the retina to malformations that are barely visible, the lesions can cause a wide range of symptoms, including decrease in visual sharpness, proptosis , pupillary defects , optic nerve degeneration, and visual field defects. [ 5 ] The most common type of visual field impairment due to AVMs is homonymous hemianopia , [ 2 ] which is usually unilateral. [ 7 ]
Central nervous system (CNS) symptoms of Bonnet–Dechaume–Blanc syndrome are highly dependent on the locations and sizes of cerebral AVMs. [ 2 ] [ 5 ] [ 7 ] The most common CNS feature is an intracranial hemangioma in the midbrain . [ 3 ] Cerebral malformations can result in severe headaches, cerebral hemorrhages, vomiting, meningism , seizures, acute strokes, and progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting. [ 3 ]
The facial features of Bonnet–Dechaume–Blanc syndrome vary from case to case. A person showing signs of the syndrome may display faint skin discoloration, nevi , or angiomas of the skin. [ 3 ] Some patients with this disorder also present with high-flow AVMs in the maxillofacial or mandibular (jaw) regions. [ 8 ] Another facial indicator of this disease is malformations affecting the frontal or maxillary sinuses . [ 5 ]
Bonnet–Dechaume–Blanc syndrome results from arteriovenous malformations . The exact cause of this disorder is unknown, and no specific genetic abnormality has been identified. The syndrome is a congenital disorder that begins to develop around the seventh week of gestation when the maturation of retinal mesenchymal cells do not grow properly. [ 3 ] [ 7 ] [ 9 ] The abnormal development of vascular tissue leads to arteriovenous malformations, which affect both visual and cerebral structures. [ 9 ]
Diagnosis commonly occurs later in childhood and often occurs incidentally in asymptomatic patients or as a cause of visual impairment. [ 3 ]
A number of examinations can be used to determine the extent of the syndrome and its severity. Fluorescein angiography is quite useful in diagnosing retinal features of the disease, and the use of ultrasonography and optical coherence tomography (OCT) are helpful in confirming the disease. [ 6 ] Neuro-ophthalmic examinations reveal pupillary defects (e.g. Marcus Gunn Pupil ). Funduscopic examinations, examinations of the fundus of the eye , allow detection of arteriovenous malformations. [ 2 ] Neurological examination can determine neurological deficits such as hemiparesis and paresthesias . [ 2 ] MRI scans are used in imaging the brain and can allow visualization of the optic nerve and any possible atrophy . MRI, CT , and cerebral angiography may all be used to investigate the extent and location of any vascular lesions affecting the brain. [ 2 ] [ 5 ]
The treatment for Bonnet–Dechaume–Blanc syndrome is controversial due to a lack of consensus on the different therapeutic procedures for treating arteriovenous malformations. [ 9 ] The first successful treatment was performed by Morgan et al., [ 8 ] who combined intracranial resection, ligation of the ophthalmic artery , and selective arterial ligature of the external carotid artery . Notably, the patient did not have retinal vascular malformations. [ 7 ]
Lesions are watched closely for changes in size. Prognosis is best when lesions are less than 3 cm in length. Most complications occur when the lesions are greater than 6 cm in size. [ 2 ] Surgical intervention for intracranial lesions has been done successfully. Nonsurgical treatments include embolization , radiation therapy, and continued observation. [ 5 ]
When pursuing treatment, it is important to consider the size of the malformations, their locations, and neurological involvement. [ 7 ]
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Bonney's round ligament forceps , sometimes known as Berkely-Bonny's round ligament forceps , is a surgical instrument used in gynaecological surgery named after Victor Bonney . [ 1 ] [ 2 ]
This article related to medical equipment is a stub . You can help Wikipedia by expanding it .
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The Bonney myomectomy clamp is a surgical clamp developed in the interwar years by gynaecologist Victor Bonney to provide a blood free environment when performing a myomectomy to remove uterine fibroids . It allowed the conservation of the uterus and the resulting preservation of fertility in women of reproductive age who wished to have children. It is seldom used now. [ 1 ] [ 2 ] [ 3 ] [ 4 ]
This article related to medical equipment is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Bonney_myomectomy_clamp
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The Bonwill Triangle is a triangle formed by the contact point of the mandibular central incisors and the right and left mandibular condyles . [ 1 ] [ 2 ]
The distance between those points is equal in most humans and amounts on average to about 10 cm. [ 2 ] The triangle is therefore an equilateral triangle in those cases. William Gibson Arlington Bonwill (1833–1899) was the first to describe this. [ 2 ]
Two variants of the Bonwill Triangle have been described that differ in the exact location of the points on the condyles. In one the points are located on the articulating surfaces of the condyles whilst in the other they are located centrally within the heads of the mandible. [ 1 ]
In terms of practical application, the Bonwill Triangle is utilized in the construction and correct application of fixed articulators , which (in contrast to fully- and semi-adjustable articulators) are a type of articulator that does not allow for adjustments to imitate the specific movements of an individual's jaw. Instead, these articulators are designed to replicate the average movements of the jaw, and among others the Bonwill Triangle relationship is used to achieve this result. [ 3 ]
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https://en.wikipedia.org/wiki/Bonwill_Triangle
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The Borlaug Global Rust Initiative (BGRI - originally named the Global Rust Initiative) was founded in response to recommendations of a committee of international experts who met to consider a response to the threat the global food supply posed by the Ug99 strain of wheat rust . [ 1 ] [ 2 ] The BGRI was renamed the Borlaug Global Rust initiative in honor of Green Revolution pioneer and Nobel Peace Prize Laureate Dr. Norman Borlaug who worked to establish and lead the Global Rust Initiative. [ 3 ] [ 4 ]
The BGRI has the overarching objective of systematically reducing the world’s vulnerability to stem , yellow , and leaf rusts of wheat and advocating/facilitating the evolution of a sustainable international system to contain the threat of wheat rusts and continue the enhancements in productivity required to withstand future global threats to wheat. [ 5 ]
The organization focuses on addressing global challenges to wheat security through a collaborative network of researchers, policymakers, and agricultural practitioners. Its key objectives [ 6 ] include:
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Borna disease , also known as sad horse disease , [ 1 ] is an infectious neurological syndrome [ 2 ] of warm-blooded animals, caused by Borna disease viruses 1 and 2 (BoDV-1/2). BoDV-1/2 are neurotropic viruses of the species Orthobornavirus bornaense , and members of the Bornaviridae family within the Mononegavirales order. [ 3 ]
Borna disease is a severe neurological illness that predominantly affects horses and sheep , but it has been observed in a wide range of mammals. The disease is characterised by ataxia and abnormal depressive behaviour, frequently culminating in death. There have been rare cases of human fatalities associated with encephalitis caused by Borna disease virus infection. [ 4 ] Additionally, correlative evidence exists linking BoDV-1/2 infection with neuropsychiatric disorders such as bipolar disorder in humans. [ 5 ]
Borna disease was first described in 1885, when all horses belonging to a cavalry regiment stationed near the city of Borna in Saxony , Germany, died from a hitherto unknown disease, then termed hitzige Kopfkrankheit ("hot-tempered head illness"). In 1909, Ernst Joest and Kurt Degen discovered distinctive inclusions in the nerves of horses that had died of Borna disease, which were named Joest-Degen inclusion bodies. [ 6 ] This histopathological feature remains in use today to confirm the presence of Borna disease. In 1924, the Austrian virologist Wilhelm Zwick suggested a virus as the cause of the disease. [ citation needed ]
The mode of transmission of BoDV-1/2 is unclear but probably occurs through intranasal exposure to contaminated saliva or nasal secretions. Following infection, individuals may develop Borna disease, or may remain subclinical, possibly acting as a carrier of the virus. [ citation needed ] The only known animal reservoir of BoDV-1 is the bicolored shrew ( Crocidura leucodon ) , which is not susceptible to Borna disease. [ 7 ] It is unclear whether human or livestock infections are due to zoonotic transmission from the bicolored shrew.
Borna diseases viruses 1 and 2 appear to have wide host ranges, having been detected in horses , cattle , sheep , new world camelids , dogs , cats , and foxes . [ 8 ] [ 9 ] In 1995, BoDV-1 was isolated from cats with a "staggering disease" in Sweden . [ 10 ] BoDV-1 has been detected in animals in Europe, Asia , Africa and North America . [ citation needed ]
Symptoms of Borna disease in horses and sheep start after a four-week incubation period followed by the development of immune-mediated meningitis and encephalomyelitis . [ citation needed ] Clinical manifestations vary but may include excited or depressed behaviour, ataxia , teeth grinding, excessive salivating, ocular disorders and abnormal posture and movement. Later stages are characterised by bouts of fever and flailing of limbs while lying down. Death occurs a few days to weeks after symptom onset. Mortality rates are 80-100% in horses and greater than 50% in sheep. [ citation needed ]
Experimental infection of rats has been demonstrated to lead to learning impairments and altered social behaviour. The virus appears to be distributed primarily in the limbic system of the brain, including the hippocampus and entorhinal cortex . These areas of the brain are considered to be of importance in emotion . [ citation needed ]
Avian bornaviruses, a group of related viruses, have been reported, yet not proven, as the cause of proventricular dilatation disease (PDD), a disease of pet parrots. The use of a 'positive' brain cell culture containing ABV to inoculate another psittacine (parrot) bird resulted in the inoculated bird's death and subsequent histopathological diagnosis of PDD (mononuclear infiltrative ganglioneuritis). Earlier research with purified avian bornavirus inoculant (while did result in the death of parrots) did not reproduce histopathological changes associated with PDD. [ citation needed ]
Antibodies to BoDV-1 in humans were first discovered in the mid-1980s, suggesting that humans can be non-fatally infected. Antibodies to BoDV-1 and BoDV-1 antigen have also been detected in blood donors. [ citation needed ]
In 2018, three fatal cases of Borna disease in humans were confirmed in Germany. [ 11 ] [ 12 ] Three people were suspected to have been infected via organ transplants from the same donor, two of whom died. A third fatal case was unconnected to the organ donation. All three deaths were due to severe encephalitis . [ 11 ] [ 12 ]
In 2020, several additional cases of human infection were identified in the German federal state of Bavaria . [ 13 ] In total, there have been 24 cases of confirmed BoDV-1 infection of humans between 1996 and 2021 [ citation needed ] . The infection was almost always fatal. All cases occurred in known areas of spread of BoDV-1, including the federal states of Bavaria, Brandenburg , Thuringia , and Saxony-Anhalt . [ 4 ] [ 14 ] [ 15 ] [ 16 ] [ 17 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ] [ 22 ] [ 23 ] [ excessive citations ]
There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease. [ 5 ] [ 24 ]
In 1990, Janice E. Clements and colleagues reported in the journal Science that antibodies to a protein encoded by the BoDV-1 genome are found in the blood of patients with behavioral disorders. [ 25 ] In the early 1990s, researchers in Germany, America, and Japan conducted an investigation of 5000 patients with psychiatric disorders and 1000 controls, in which a significantly higher percentage of patients than controls were positive for BoDV-1 antibodies. [ 25 ] Subsequent studies have also presented evidence for an association between BoDV-1 and human psychiatric disorders. [ 26 ] [ 27 ] [ 28 ] However, not all researchers consider the link between BoDV-1 and human psychiatric disease to be conclusively proven. A study published in 2003 found no BoDV-1 antibodies in 62 patients with the deficit form of schizophrenia. [ 29 ]
Additional evidence for a role of BoDV-1 in psychiatric disorders comes from reports that the drug amantadine , which is used to treat influenza infections, has had some success in treating depression and clearing BoDV-1 infection. [ 30 ] [ 31 ]
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The Boston Diagnostic Aphasia Examination is a neuropsychological battery used to evaluate adults suspected of having aphasia , and is currently in its third edition. [ 1 ] It was created by Harold Goodglass and Edith Kaplan . The exam evaluates language skills based on perceptual modalities (auditory, visual, and gestural), processing functions (comprehension, analysis, problem-solving), and response modalities (writing, articulation, and manipulation). Administration time ranges from 20 to 45 minutes for the shortened version but it can last up to 120 minutes for the extended version of the assessment. There are five subtests which include: conversational & expository speech, auditory comprehension, oral expression, reading, and writing. In the extended version all questions are asked while in the shortened version only a few questions are asked within each subtest. [ 2 ] Many other tests are sometimes used by neurologists and speech language pathologists on a case-by-case basis, and other comprehensive tests exist like the Western Aphasia Battery .
The Boston Diagnostic Aphasia Examination provides a comprehensive exploration of a range of communicative abilities. Its results are used to classify patient's language profiles into one of the localization based classifications of aphasia: Broca's, Wernicke's, anomic, conduction, transcortical, transcortical motor, transcortical sensory, and global aphasia syndromes, although the test does not always provide a diagnosis or a therapeutic approach. The assessment provides a severity rating. [ 3 ] The Examination is designed to go beyond simple functional definitions of aphasia into the components of language dysfunctions (symptoms) that have been shown to underlie the various aphasic syndromes. Thus, this test evaluates various perceptual modalities (e.g., auditory, visual, and gestural), processing functions (e.g., comprehension, analysis, problem-solving), and response modalities (e.g., writing, articulation, and manipulation). This approach allows for the neuropsychological analysis and measurement of language-related skills and abilities from both ideographic and nomothetic bases, as well as a comprehensive approach to the symptom configurations that relate to neuropathologic conditions. The test is divided into five subtests and include assessment of conversation and expository speech (simple social responses, free conversation, and picture description), auditory comprehension (at the word-level, sentence level, and complex ideational material), oral expression (automatized sequences, repetition, and naming), reading (basic symbol recognition, number matching, word identification-picture-word matching, oral reading, and reading comprehension), and writing (mechanics, encoding skills, written picture naming, and narrative writing). [ 4 ]
The manual provides clear statements and rules for scoring protocols. Once the scores are collected, the examiner completes the Summary of Scores and inserts them into the Summary Profile of Standard Subtests in the Boston Diagnostic Aphasia Examination Record Booklet to get percentiles. The percentiles are listed as 0, 10, 20, 30, 40, 50, 60, 70, 80, 90, and 100 only. The scores that are collected are a tally of the number of correct responses, the number of cues given, number of phonemic cues, etc. [ 5 ]
Reliability of the subtests was studied by selecting protocols of 34 patients with a degree of severity of aphasia ranging from slight to severe. Kuder-Richardson reliability coefficients for subtests ranged from 0.68 to 0.98, with about two-thirds of the coefficients reported ranging from 0.90 upwards. Since test-retest reliability is difficult if not impossible to attain in patients with aphasic symptoms, the current reliability coefficients demonstrate good internal consistency in terms of what the items within the subtests are measuring. [ citation needed ]
Validity : A discriminant analysis comparing "unambiguous exemplars of a single syndrome" was carried out. Thus, unambiguous cases of Broca's aphasia, Wernicke's aphasia, conduction aphasia , and anomic aphasia were selected. Ten variables were selected on the assumption of providing the most useful data. From these, five variables were selected for the discriminant analysis (body part identification, repetition of high probability sentences, verbal paraphasias, articulatory agility rating, and automated sentence rating). This classification yielded no misclassifications.
Standardization of the revised Boston Diagnostic Aphasia Examination is based on a normative sample of 242 patients with aphasic symptoms tested at the Boston VA Medical Center between 1976 and 1982.
In Depth Review of the Boston Diagnostic Aphasia Examination (BDAE) - Stroke Engine. (2015). Retrieved November from [1] "BDAE 3 Boston Diagnostic Aphasia Examination Third Edition" . linguisystems . 2001. Archived from the original on 2016-03-04 . Retrieved 2015-11-14 .
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Bouffée délirante (BD) is an acute and transient psychotic disorder . [ 1 ] It is a uniquely French psychiatric diagnostic term with a long history in France [ 2 ] and various French speaking nations in the Caribbean (e.g., Haiti, Guadeloupe, Antilles) and Francophone Africa. [ 3 ] The term BD was originally coined and described by Valentin Magnan (1835–1916), fell into relative disuse, and was later revived by Henri Ey (1900–1977). [ 4 ]
The French word bouffée is often translated as a puff or waft (as of air), but can also mean a flash, rush, or surge. Chabrol translates the word délirante as "delusional". [ 5 ] Other common dictionary definitions include less useful meanings such as "crazy" or "incoherent". A reasonable English translation of the term bouffée délirante is "delusional flash".
Bouffée délirante is "an acute, brief nonorganic psychosis that typically presents with a sudden onset of fully formed, thematically variable delusions and hallucinations against a background of some degree of clouding of consciousness , unstable and fluctuating affect, and spontaneous recovery with some probability of relapse." [ 6 ] The following criteria have been suggested for a diagnosis of BD: a) abrupt onset, b) polymorphic delusions, emotional changes, mood swings, depersonalization, derealization, and/or hallucinations, c) complete remission within weeks or a few months, d) exclusion of organic causation, alcohol or drug use, e) no psychiatric antecedents with the exception of a previous episode of bouffée délirante. [ 7 ]
American academic investigators proposed the following definition in 2011: "The French concept of bouffée délirante refers to conditions with a sudden onset marked by prominent delusions with hallucinations, confusion, anxiety and affective symptoms. Symptoms vary rapidly, perhaps even by the hour, and there is a rapid return to the premorbid state of health." [ 8 ] A frequently quoted authority on BD, P. Pichot, of the Hôpital Sainte Anne, Paris, provides this description of BD:
Pichot's criteria can be refined further with these typical clinical characteristics:
In 1968 the French national organization INSERM (Institut National de la Santé et de la Recherche Médicale) classification of mental illness referenced two types of BD in their category 'acute delusional psychoses and confusional states' viz. reactive bouffée délirante and bouffée délirante (Magnan's type). [ 11 ] This classification scheme has been largely replaced by the two nosological systems discussed below.
The World Health Organization edition of the International Classification of Diseases 10th edition:version 2019 (ICD-10, CIM-10 en français), lists BD as the subentry "Bouffée délirante without symptoms of schizophrenia or unspecified" under diagnosis code F23: Acute and Transient Psychotic Disorders subsection, F23.0: Acute polymorphic psychotic disorder without symptoms of schizophrenia. [ 12 ] It is likely that the use of the term BD in French clinical psychiatry will decline further with the proposed 2022 implementation of ICD-11, which was released in May 2019. In contrast to the ICD-10, the term BD does not appear anywhere in ICD-11. The closest clinical match for BD in the ICD-11 is code 6A23, 'Acute and transient psychotic disorder' which is defined as
acute onset of psychotic symptoms that emerge without a prodrome and reach their maximal severity within two weeks. Symptoms may include delusions, hallucinations, disorganization of thought processes, perplexity or confusion, and disturbances of affect and mood. Catatonia-like psychomotor disturbances may be present. Symptoms typically change rapidly, both in nature and intensity, from day to day, or even within a single day. The duration of the episode does not exceed 3 months, and most commonly lasts from a few days to 1 month. The symptoms are not a manifestation of another health condition (e.g., a brain tumor) and are not due to the effect of a substance or medication on the central nervous system (e.g., corticosteroids), including withdrawal (e.g., alcohol withdrawal). [ 13 ]
The Diagnostic and Statistical Manual of Mental Disorders 5th edition ( DSM-5 ) diagnostic category brief psychotic disorder is probably the closest analog of BD. [ 14 ] The French term BD is nowhere mentioned in the DSM-5. [ 15 ] The diagnosis of bouffée délirante is still in use in the Classification Française des Troubles Mentaux (French Classification of Mental Disorder, CFTM) under the name bouffée délirante aiguë. [ 16 ]
The frequency of BD diagnoses in French hospitals has been declining due to the widespread acceptance of international classification systems such as the ICD-10 and DSM-5. However, the BD diagnosis has been used as recently as 2019 in Le Groupe Hospitalier Universitaire Paris psychiatrie & neurosciences (GHU Paris), Maison Blanche Bichat XVIII. [ 17 ] Older estimates of the incidence of BD in psychiatric hospitalizations range from 1–5%. [ 18 ] [ 19 ]
Psychiatric admission reviews show that 2–7% of first episode psychotic episodes are due to brief psychotic disorder; here serving as a surrogate diagnosis for BD. [ 20 ] Some authors state that the diagnostic category of BD can be eliminated because it can be fully integrated into the 'Polymorphic subgroup of Acute and Transient Psychotic Disorders' of the ICD-10. [ 21 ]
There are no current published guidelines in the English language psychiatric literature that discuss treatment for BD. A 2019 case of BD from GHU Paris treated the patient with largactil (chlorpromazine). [ 22 ] Assuming that BPD is an equivalent diagnosis, treatment depends on the severity of the episode. Mildly affected patients may receive supportive management and observation with additional outpatient therapy. More severe illness may require inpatient hospitalization and pharmacologic treatment with benzodiazepines and/or antipsychotic medication, for example: risperidone , though no clinical trials have examined the efficacy of therapy for BPD. [ 23 ]
It is difficult to firmly establish the prognosis of first episode BD patients with respect to progression to other psychiatric illness or relapse to another psychotic episode. This is due to the fact that high quality follow-up studies of large cohorts of BD patients are unavailable in part because of the uncommon nature of the illness and non-standardization of diagnostic methods. Investigators attempting to define the prognosis in BD have used data from similar conditions, i.e. acute transient psychotic disorder (ATPD) and brief psychotic disorder (BPD). [ 24 ]
A 2016 meta-analysis involving 11,000 patients estimated the rate of recurrent psychotic episodes in ATPD and BPD patients was 51% at 30 months compared to first episode schizophrenia patients who had an 84% recurrence rate at 36 months. As suggested by the various definitions of BD discussed above, rapid recovery and return to pre-morbid level of function is expected, though quantitative data is lacking. [ 25 ]
Psychiatric illnesses comparable to the unique French BD can be seen in the cycloid psychosis of German speaking countries and the psychogenic psychosis in Scandinavia. [ 26 ] It has been argued that acute and transient psychoses are more common in African and Afro-Caribbean populations and may be attributable to socio-cultural factors. This has led to the term " culture-bound syndrome ". It must be stressed that the term BD long predates any such socio-cultural, ethnic, or regional uses. The African and Caribbean nuances of the diagnosis and presentation of BD has been extensively reviewed by Henry Murphy. [ 27 ]
BD is a psychotic disorder of short duration generally considered to have a relatively good prognosis. The diagnosis has undergone numerous changes and re-evaluations since its description by Magnan in 1886. Though becoming replaced by more internationally recognized terminology, BD as a diagnostic category is still in use in France and other French speaking nations.
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Bovine Meat and Milk Factors ( BMMFs ) are circular, single-stranded DNA molecules (cssDNAs) originally found in beef and cow's milk which have been linked to the development of cancer—particularly colorectal and breast cancer . [ 1 ] They are formerly known as Slow Progressive Hidden INfections of variable X ( SPHINX ). Similar molecules have since been found in a much wider range of food. [ 2 ]
BMMF/SPHINX sequences are able to copy themselves in animal cells. They encode functional proteins that are expressed in some animal cells. Every BMMF/SPHINX contains at least a "Rep" open reading frame , which encodes a replication endonuclease that, in HEK 239TT cells , acts to replicate and retain the cssDNA. [ 3 ]
BMMF/SPHINX sequences are divided into four clades . Clades 1, 2, and 3 share sequence similarity with the plasmids of Acinetobacter baumannii . ( A. baumanii regularly produces outer membrane vesicles containing these plamids, and animal cells are known to take up these vesicles.) Clade 4 shares sequence similarity with Gemycircularvirus . [ 3 ]
The potential connection between BMMFs and cancer has been made based on assessments of epidemiological data [ 4 ] [ 5 ] [ 6 ] and the investigation of antibodies in human serum . [ 7 ] [ 8 ] Research has also suggested a potential link between BMMFs and neurodegenerative diseases such as multiple sclerosis . [ 7 ]
At the end of 2017, evidence was presented that BMMFs in human cells show long-term survival, through the identification of BMMFs' RNA and protein products. [ 7 ] [ 9 ] In February 2019, evidence was presented of a previously unknown infectious agent in the blood serum and milk of Eurasian cattle that could indirectly trigger the development of colorectal cancer. [ 5 ]
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The Bowen technique (or Bowen therapy) is an alternative type of physical manipulation named after Australian Thomas Ambrose Bowen (Tom Bowen) (1916–1982).
There is no clear evidence that the technique is a useful medical intervention. [ 1 ]
Bowen had no formal medical training [ 2 ] and described his approach as a "gift from God". [ 3 ] He referred to himself as an osteopath and tried to join the Australian register of osteopaths in 1981 but did not qualify for the title. [ 4 ] He died as an unlicensed practitioner of manual therapy. [ 5 ] In 1973 Bowen himself had referred to his ability to "average 65 patients per day", yet the technique as it is commonly practiced today is unlikely to achieve that volume. [ 5 ]
Bowen did not document his technique, so its practice after his death has followed one or other differing interpretation of his work. [ 5 ] It was not until some years after his death that the term "Bowen Technique" was coined. The technique goes by a wide variety of other names, including Smart Bowen, Fascial Kinetics, Integrated Bowen Therapy, Neurostructural Integration Technique (NST), Fascial Bowen, and Bowenwork. [ 5 ] The technique has been popularized by some of the six men who observed him at work, including Oswald Rentsch, an osteopath [ 6 ] whose interpretation has become the dominant, but not unchallenged, form. [ 5 ] Learning this technique requires 120 hours of instruction, [ 7 ] or as little as a weekend workshop. [ 8 ]
Recipients are generally fully clothed. Each session typically involves gentle rolling motions across the muscles , tendons , and fascia . [ 9 ] The therapy's distinctive features are the minimal nature of the physical intervention and pauses incorporated in the treatment. [ 10 ] Proponents claim these pauses allow the body to "reset" itself. [ 3 ]
In 2015, the Australian Government's Department of Health published the results of a review of alternative therapies that sought to determine if any were suitable for being covered by health insurance ; Bowen Technique was one of 17 therapies evaluated for which no clear evidence of effectiveness was found. [ 1 ] Quackwatch includes "Neuro-Structural Integration Technique (Bowen Therapy)" in its list of "questionable treatments." [ 11 ]
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https://en.wikipedia.org/wiki/Bowen_technique
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The Bower Manuscript is a collection of seven fragmentary Sanskrit treatises found buried in a Buddhist memorial stupa near Kucha , northwestern China . [ 1 ] [ 2 ] [ 3 ] Written in early Gupta script [ 4 ] (late Brahmi ) on birch bark , it is variously dated in 5th to early 6th century. [ 5 ] [ 6 ] The Bower manuscript includes the oldest dated fragments of an Indian medical text, the Navanitaka . [ 1 ] [ 7 ]
The seven treatises included in the collection three on Ayurvedic medicine , two on divination by dice, and two on incantations ( Dharani ) against snake bites. [ 8 ] The collection had at least four scribes, of which three were likely Buddhists because the second, the sixth and the seventh treatises open by invoking the Buddha and other Buddhist deities. [ 1 ] [ 9 ] Two invoke Shiva , Vishnu , Devi , and other Hindu deities. [ 9 ] The discovery of the manuscript in remote China near Central Asian region is considered evidence of the spread and sharing of ideas in ancient times between India, China and Central Asia. [ 10 ] It also contains excerpts of the Bhela Samhita , a medical text whose damaged manuscript is in Tanjavur , Tamil Nadu. [ 11 ] The medical fragments of the Bower manuscript have much in common with other ancient Sanskrit medical treatises such as those by Caraka , Ravigupta, Vagbhata and Kashyapa . [ 8 ]
The manuscript is named after Hamilton Bower – a British Lieutenant who bought the manuscript in March 1890 while on a mission to chase an assassin who was charged with hacking Andrew Dalgleish to death. The fragmentary manuscript was analyzed, edited, translated, and published by Calcutta -based Rudolf Hoernle . The Bower Manuscript is preserved in the collections of the Bodleian Library in Oxford. [ 12 ]
The Bower Manuscript is named after its accidental purchaser Hamilton Bower , a British Army Lieutenant. The story begins with the brutal murder of Andrew Dalgliesh, a Scotsman camping in the Karakoram mountains, north of Kashmir . He was hacked to death inside his tent by an Afghan named Dad Mahomed. The British government wanted to bring Mahomed to justice, and therefore sent Hamilton Bower with some troops to go after the killer, states Wujastyk. Mahomed learned about the effort and escaped. Bower, in the chase, followed Mahomed through the Himalayan valleys into the Takla Makan desert. Bower arrived near Kucha ( Xinjiang ) in early March 1890 and set his camp. On the night of 2 or 3 March, a man came to his tent and offered to sell him old manuscripts and artifacts that his treasure hunters had found. Bower bought them. [ 12 ]
Bower took the manuscripts with him when he returned to Simla and forwarded it to Colonel James Waterhouse , the then President of the Asiatic Society of Bengal . Waterhouse reported the manuscript at the monthly meeting of the Society on 5 November 1890, whose proceedings were widely distributed. [ 13 ] At the meeting, he stated that Bower visited the site where the manuscript was found, and referred to the stupa as something that looked like a huge " cottage loaf " near the "Ming–oi" Buddhist monastery ruins, 16 miles from Kucha near the banks of a river. [ 13 ] Waterhouse mentioned that the Bower manuscript had 56 leaves (the edition now preserved at Bodleian Library has 51 leaves). He reported that the Bower manuscript was bound with two wooden boards on either end and a string running through a hole. He had sought the help of Babu Sarat Chandra Das and Lama Phuntshog to decipher the manuscript. Neither was able to read the script and said it must be "very ancient", according to Waterhouse. [ 13 ] [ 7 ]
The Waterhouse report was reprinted in Bombay Gazette , where Hoernle learned about it and became very eager to study it. [ 14 ] After the meeting, in parallel, some attempts were made to decipher the manuscript, but they proved unsuccessful. German Indologist Georg Buhler succeeded in reading and translating two leaves of the manuscript, reproduced in the form of heliogravures in the Proceedings of the Asiatic Society of Bengal. [ citation needed ]
Immediately after his return to India in February 1891, Hoernle began to study the manuscript. He found that the manuscript leaves were jumbled out of sequence, but had the page numbers marked on the left. After re-arranging them, he concluded that it was an abridged collection of several different treatises. He presented the first decipherment two months later, at the meeting of the Society in April 1891, with evidence that it was "the oldest Indian written book that is known to exist". [ 14 ] Between 1893 and 1897 Hoernle published a complete edition of the text, featuring an annotated English translation and illustrated facsimile plates. A Sanskrit Index was published in 1908, and a revised translation of the medical portions (I, II, and III) in 1909; the Introduction appeared in 1912. [ 7 ]
The 'Bower Manuscript' is a collation of seven treatise manuscripts, compiled into a larger group and another a smaller one. The larger manuscript is a fragmentary convolute of six treatises (Part I, II, III, IV, V and VII), which are separately paginated, with each leaf approximately 29 square inches (11.5 inch x 2.5 inch). Part VI is written on smaller folio leaves, both in length and breadth, with each leaf approximately 18 square inches (9 inch x 2 inch). [ 7 ] The larger group and the smaller set likely came from different trees or region. The scribes wrote on both sides of the leaves but did not use both sides when the leaf was very thin. These seven constituent manuscripts are numbered as Parts I to VII in Hoernle's edition. [ 7 ]
The Bower manuscript, as discovered, had 56 birch bark leaves, cut into oblong palmyra shape (rectangular strips with rounded corners). This is the form commonly found in numerous ancient and medieval Indian manuscript books ( pothī ). The pages are bound in Indian style, with each leaf containing a hole about the middle of the left side, for the passage of the binding string. [ 7 ] The undamaged leaves of the Bower manuscript are numbered on the left edge of the reverse side, a tradition found in ancient pothi manuscripts in north India, in contrast to the historic south Indian tradition of numbering the obverse side in manuscripts. This suggests that the Bower manuscript scribes were trained in the north Indian tradition. [ 7 ]
The seven parts of the manuscript are written in an essentially identical script, the Gupta script (late Brahmi) found in north, northwest and western regions of ancient India. Early attempts to date the text placed it around 5th-century, largely on palaeographic grounds. [ 15 ] Hoernle determined that the manuscript belonged to the 4th or 5th–century because the script used matched with dated inscriptions and other texts of that period in the north and northwest India. [ 16 ] He also compared the style and script for numerals – particularly zero and position value – and the page numbering style in the manuscript with those found in Indian inscriptions and manuscripts. By combining such evidence with palaeographic evidence therein, he concluded that the Bower manuscript could not be dated in or after the second half of the 6th century. [ 16 ] Hoernle remarked that at least some treatises of the manuscript "must fall somewhere within that period [470 and 530 CE], that is, about 500 CE." [ 17 ]
Winand M. Callewaert dates it to c. 450 CE. [ 5 ] According to a 1986 analysis by Lore Sander, the Bower manuscript is best dated between 500 and 550 CE. [ 6 ]
The fragmentary treatises are copies of much older Indian texts authored by unknown scholars. These treatises were prepared by scribes, buried in a stupa built at some point to honor the memory of a Buddhist monk or some other regional influential person. Hoernle distinguished four scribes, based on their handwriting, subtle font and style differences. One scribe wrote Parts I, II and III; second wrote Part IV; third wrote Parts V and VII; while a fourth wrote Part VI. [ 7 ] He added that there may have been more than four scribes, because Part VI has some scribal differences, while V and VII too seems cursive and careless work of possibly more than one person. [ 18 ]
Based on the handwriting and fonts prevalent in the inscriptions discovered in India from that era, Hoernle suggested the first scribe who wrote Parts I through III likely grew up and came from Kashmir or Udyana (North India) to Kucha (China) because his writing shows early Sarada script influences. [ 18 ] Part VI, and possibly V and VII were written by scribe(s) who may have come to China from a region that is now the central India to Andhra Pradesh, for similar reasons. [ 18 ] The writer of part IV appears to have the style of someone used to "writing with a brush", and therefore may have been a local native or a Buddhist monk who came from interior China. [ 18 ]
The text consists of seven separate and different treatises, of which first three are on medicine, next two on divination, and last two on magical incantations. [ 19 ] The three medicinal treatises contain content that is also found in the ancient Indian text called the Caraka Samhita . [ 20 ] Treatises I to III are the medical treatises of the collection and contain 1,323 verses and some prose. The metrical writing suggests that the scribe of the three medical treatises was well versed in Sanskrit composition. The scribe of divination and incantation sections (Treatises IV-VII) was not conversant with classical Sanskrit, made grammatical errors and used a few Prakrit words. [ 16 ]
The manuscript is mostly in the Shloka verse style – a Vedic anuṣṭubh poetic meter (exceptions are found in Part I of the collection). [ 16 ] [ 7 ] The Bower Manuscript is written in the Gupta script – a type of late Brahmi script . [ 10 ]
Part I has 5 leaves, and the incomplete treatise ends abruptly. [ 7 ] It is a fragment of a treatise on garlic, it medicinal properties and recipes, its use for eye diseases. [ 1 ] It opens with a flowery description of the Himalayas, where a group of rishis reside, interested in the names and properties of medicinal plants. It mentions Hindu sages such as Ātreya , Hārīta , Parāśara , Bhela , Garga , Śāmbavya, Suśruta , Vasiṣṭha , Karāla, and Kāpya . Suśruta, whose curiosity is aroused by a particular plant, approaches muni Kāśirāja, enquiring about the nature of this plant. Kāśīrāja, granting his request, tells him about the origin of the plant, which proves to be garlic (Sanskrit laśuna ), its properties and uses. The section on garlic consists of 43 verses in poetic meter. This section also mentions the ancient Indian tradition of "garlic festival", as well as a mention of sage Sushruta in Benares ( Varanasi ). [ 20 ] This is the part where the initial 43 verses are in eighteen different, uncommon meters ( Sanskrit prosody ) such as the vasanta tilaka , trishtubh and arya , while the verses thereafter are in the shloka style. [ 19 ] The verses credit the knowledge to past sages. Verse 9, for example, attributes the knowledge to Susruta , who received it from the sage king of Kashi . [ 19 ]
Part II abruptly ends on the 33rd folio of the Bower manuscript. [ 7 ] It is voluminous, relative to the other six treatises, and contains medical prescriptions sections on powder, medicated ghee (clarified butter), oil, elixirs, aphrodisiacs, decoctions, dyes and ointments. [ 1 ] [ 19 ] It opens with a salutation addressed to the Tathāgatas , contains, as stated by the scribe, the Navanītaka text ( lit. "cream" text [ 19 ] ), a standard manual (siddhasaṃkarṣa). [ 21 ] Then it states its intention to provide 16 chapters of prescriptions (but the surviving fragment only provides 14, ending abruptly). [ 19 ] According to G.J. Meulenbeld, "an important peculiarity of the Bower MS consists of its varying attitude towards the number of the doṣas [humours]. In many instances, it accepts the traditional number of three, vāta, pitta, and kapha, but in a smaller number of passages it also appears to accept blood (rakta) as a doṣa." [ 22 ]
Part III consists of 4 leaves and also ends abruptly on the obverse side of the folio (Part IV starts on reverse). [ 7 ] It starts with the symbol Om as usual with the other treatises, and is a short treatise on 14 prescription formulary in a manner similar to Part II. It consists of 72 shlokas . [ 1 ] [ 7 ] It is a fragment whose contents correspond to chapters one to three of the Part II. [ 23 ]
Parts IV and V contain two short manuals of Pāśaka kevalī , or cubomancy, i.e., the art of foretelling a person's future by means of the cast of dice, a ritualistic practice found in Tibetan manuscripts. [ 24 ] Part IV is almost complete, while the manual constituting Part V is markedly more fragmentary and defective. The dice is stated to be a group of three dice, each with four faces ( tetrahedron ) numbered 1, 2, 3 and 4. When cast, it would yield one of 64 possible casts, of which 60 combinations are listed in Part IV (the missing 4 may be scribal error or lost; but those 4 are mentioned in later verses). [ 19 ] Hoernle mentioned that Part V is similar to other Sanskrit manuscripts discovered in Gujarat, and like it, these parts of the Bower manuscript may be one of the several recensions of a more ancient common source on divinatory work. [ 19 ] These are traditionally attributed to the ancient sage Garga , [ 25 ] but maybe an influence of the Greek oracle tradition during the post- Alexander the Great period. [ 19 ]
Parts VI and VII contain two different portions of the same text, the Mahāmāyurī , Vidyārājñī, a Buddhist dhāraṇī -genre incantations text. The Mayuri text, in later centuries, became a part of the Pancha-raksha magical incantations group – one of the highly popular dharani sets in Buddhist communities in and outside India. [ 19 ] Part VI of the Bower manuscript contains charms against cobra bite, [ 1 ] [ 26 ] while Part VII is for protecting against other evils befalling a person. [ 25 ] Both these parts are a small select portion of the actual Mayuri text, and tiny compared to the much larger dharani compilations. [ 19 ] Part VI is complete, written on better quality birch and is the most well preserved treatise in the Bower manuscript. [ 7 ] According to Watanabe, the verses of these treatises as found in folio 49 to 54 of the Bower manuscript completely correspond to those found in Mahamayurividya-rajni verses of the Chinese Tripitaka , in particular to the 705 CE translation by I-tsing, the 746–771 CE translation by Amoghavajra, and the 516 CE translation by Sanghapala. [ 27 ] Their shared source may be Pali verses in the Mora Jataka , with interpolations by Mahayana Buddhists of that era. These parts of the Bower manuscript also contain the name Yashomitra, likely the votary or the influential person for whom the manuscript was prepared. [ 27 ] According to Hoernle, Yashomitra may well have been a Buddhist monk of great repute, the one for whom the stupa was built, and in whose memory the manuscript was prepared and buried in the stupa mound. [ 7 ]
The discovery of the Bower Manuscript, its antiquity, and its decipherment by Hoernle triggered "enormous excitement" in the 1890s, states Wujastyk. [ 12 ] Famous explorers were commissioned by some of the world's major powers of the era – such as Britain, Germany, Japan, France, Russia – to go on a Central Asia and Xinjiang expedition. They were to seek manuscripts and other ancient treasures. These expeditions yielded major discoveries such as the Dunhuang manuscripts , [ 28 ] as well as famous forgeries such as those of Islam Akhun , in the decades that followed. [ 29 ] [ 30 ]
The European Union-funded International Dunhuang Project has continued the legacy of the Bower manuscript which in part inspired Rudolf Hornle to seek funds from the then Government of India to finance the first 1900–1901 expedition of Marc Aurel Stein . [ 31 ] [ 32 ]
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The Bowl of Hygeia , ⟨🕏⟩ , is one of the symbols of pharmacology , and along with the Rod of Asclepius , it is one of the most ancient and important symbols related to medicine in western countries. Hygeia was the Greek goddess of health, hygiene , cleanliness, and sanitation , and the daughter of Asclepius , whom she is often closely associated with e.g. in prayers and hymns. Asclepius' symbol is his rod , with a snake twined around it; correspondingly, Hygeia's symbol is a cup or chalice with a snake twined around its stem. Hygeia was also invoked, along with her father Asclepius, and Panacea in the original Hippocratic Oath .
The bowl of Hygeia has been used as a symbol of the pharmacy profession at least as far back as 1796, when it was used on a coin minted for the Parisian Society of Pharmacy. [ 1 ] It has since been adopted by many more pharmaceutical associations worldwide, such as the American Pharmacists Association , [ 2 ] the Canadian Pharmacists Association , [ 3 ] the Pharmaceutical Society of Australia , [ 4 ] and the Doctor of Pharmacy Association, [ 5 ] Conseil de l'Ordre des Pharmaciens in France [ 6 ] (where is written in law with another symbol, the green Greek cross). [ 7 ]
The bowl of Hygeia is a common symbol on signs outside of pharmacies in Europe. A mortar and pestle is a more common symbol in the United States.
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Brachial amyotrophic diplegia , also called Vulpian-Bernhardt Syndrome (VBS), flail arm syndrome, or man-in-barrel syndrome, is a rare motor neuron disease , often considered to be a phenotype or regional variant of amyotrophic lateral sclerosis . [ 1 ] In the first twelve to eighteen months, only a progressive weakness of one or both arms is observed. [ 2 ] Within the spectrum of ALS, this subtype has a relatively longer survival time. Because of its distinct symptoms, it was suggested that VBS is a separate entity, different from ALS.
The disease was described first in 1886 by the French neurologist Alfred Vulpian and the German neuropathologist Martin Bernhardt as a progressive weakness of the upper limbs but bulbar muscles unaffected. [ 3 ] It is a rare and atypical disease that can only be diagnosed after a significant time has elapsed. [ 4 ] A 2015 study found significant differences between ALS and VBS, most importantly the absence of signs of upper motor neuron compromise in patients with VBS. The study suggested that VBS is a different entity from ALS. [ 5 ]
While the cause is usually unknown, it can arise as a paraneoplastic syndrome . [ 6 ] There have been case reports linking the condition to SOD1 mutations. [ 7 ]
A study of 1,188 ALS cases in London between 1993 and 2007, and 432 in Melbourne, classified cases as flail arm syndrome when in the first 12 months only a weakness of upper limbs was reported. [ 8 ] Based on this criterium, 135 cases or 11% were classified as flail arm syndrome . At later stages, weakening of lower limbs and other ALS symptoms were observed. 16 per cent of these flail arm syndrome cases survived more than ten years, the highest of all variants of ALS in the study.
One of the few people with brachial amyotrophic diplegia who has spoken in public about the disease is Sonia Bustamante Dominguez, a Mexican woman who showed the first symptoms in 2012 and was diagnosed in 2016. In 2024 she described her body as a jail. [ 9 ]
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https://en.wikipedia.org/wiki/Brachial_amyotrophic_diplegia
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Brachial plexus block is a regional anesthesia technique that is sometimes employed as an alternative or as an adjunct to general anesthesia for surgery of the upper extremity . This technique involves the injection of local anesthetic agents in close proximity to the brachial plexus , temporarily blocking the sensation and ability to move the upper extremity. The subject can remain awake during the ensuing surgical procedure, or they can be sedated or even fully anesthetized if necessary.
There are several techniques for blocking the nerves of the brachial plexus. These techniques are classified by the level at which the needle or catheter is inserted for injecting the local anesthetic — interscalene block on the neck for example is considered the second most complete postoperative analgesia, [ 1 ] supraclavicular block immediately above the clavicle , infraclavicular block below the clavicle and axillary block in the axilla (armpit). [ 2 ]
General anesthesia may result in low blood pressure , undesirable decreases in cardiac output , central nervous system depression , respiratory depression , loss of protective airway reflexes (such as coughing), need for tracheal intubation and mechanical ventilation , and residual anesthetic effects. The most important advantage of brachial plexus block is that it allows for the avoidance of general anesthesia and therefore its attendant complications and side effects . Although brachial plexus block is not without risk, it usually affects fewer organ systems than general anesthesia. [ 3 ]
Brachial plexus blockade may be a reasonable option when all of the following criteria are met: [ citation needed ]
The brachial plexus is formed by the ventral rami of C5 - C6 - C7 - C8 - T1 , occasionally with small contributions by C4 and T2 . There are multiple approaches to blockade of the brachial plexus, beginning proximally with the interscalene block and continuing distally with the supraclavicular, infraclavicular, and axillary blocks. The concept behind all of these approaches to the brachial plexus is the existence of a sheath encompassing the neurovascular bundle extending from the deep cervical fascia to slightly beyond the borders of the axilla. [ 2 ]
Brachial plexus block is typically performed by an anesthesiologist . To achieve an optimal block, the tip of the needle should be close to the nerves of the plexus during the injection of local anesthetic solution. Commonly employed techniques for obtaining such a needle position include transarterial, elicitation of a paresthesia , and use of a peripheral nerve stimulator or a portable ultrasound scanning device. [ 4 ] If the needle is close to or contacts a nerve, the subject may experience a paresthesia (a sudden tingling sensation, often described as feeling like "pins and needles" or like an electric shock) in the arm, hand, or fingers. Injection close to the point of elicitation of such a paresthesia may result in a good block. [ 4 ] A peripheral nerve stimulator connected to an appropriate needle allows emission of electric current from the needle tip. When the needle tip is close to or contacts a motor nerve , characteristic contraction of the innervated muscle may be elicited. [ 4 ] Modern portable ultrasound devices allow the user to visualize internal anatomy , including the nerves to be blocked, neighboring anatomic structures and the needle as it approaches the nerves. Observation of local anesthetic surrounding the nerves during ultrasound-guided injection is predictive of a successful block. [ 5 ] Appropriate block per site-specific procedure are listed in the following table: [ 6 ]
1. Include musculocutaneous nerve 2. Include T1 - T2 if block is anesthetic
3. Include C3 - C4 if block is anesthetic
The interscalene block is performed by injecting local anesthetic to the nerves of the brachial plexus as it passes through the groove between the anterior and middle scalene muscles , at the level of the cricoid cartilage . This block is particularly useful in providing anesthesia and postoperative analgesia for surgery to the clavicle, shoulder, and arm. Advantages of this block include rapid blockade of the shoulder region, and relatively easily palpable anatomical landmarks. Disadvantages of this block include inadequate anesthesia in the distribution of the ulnar nerve , which makes this an unreliable block for operations involving the forearm and hand. [ 2 ]
Temporary paresis (impairment of the function) of the thoracic diaphragm occurs in virtually all people who have undergone interscalene or supraclavicular brachial plexus block. Significant respiratory impairment can be demonstrated in these people by pulmonary function testing . [ 7 ] In certain people — such as those with severe chronic obstructive pulmonary disease — this can result in respiratory failure requiring tracheal intubation and mechanical ventilation until the block dissipates. [ 8 ] Horner's syndrome may be observed if the local anesthetic solution tracks cephalad and blocks the stellate ganglion . This may be accompanied by difficulty swallowing and vocal cord paresis . These signs and symptoms are transient however, and do not commonly result in any long-term problems, although they may be significantly distressing to patients until the effects subside. [ citation needed ]
Contraindications include severe chronic obstructive pulmonary disease, [ 8 ] and paresis of the phrenic nerve on the opposite side as the block. [ 9 ]
Providing a rapid onset of dense anesthesia of the arm with a single injection, the supraclavicular block is ideal for operations involving the arm and forearm, from the lower humerus down to the hand. The brachial plexus is most compact at the level of the trunks formed by the C5–T1 nerve roots , so nerve block at this level has the greatest likelihood of blocking all of the branches of the brachial plexus. This results in rapid onset times and, ultimately, high success rates for surgery and analgesia of the upper extremity, excluding the shoulder. [ 10 ]
Surface landmarks can be used to identify the appropriate location for injection of local anesthetic, which is typically lateral to (outside) the lateral border of the sternocleidomastoid muscle and above the clavicle, with the first rib generally considered to represent the limit below which the needle must not be directed (the pleural cavity and uppermost part of the lung are located at this level). Palpation or ultrasound visualization of the subclavian artery just above the clavicle provides a useful anatomic landmark for locating the brachial plexus, which is lateral to the artery at this level. [ 10 ] Proximity to the brachial plexus can be determined using by elicitation of a paresthesia, use of a peripheral nerve stimulator, or ultrasound guidance. [ 11 ]
Compared to the interscalene block, the supraclavicular block — despite eliciting a more complete block of the median , radial ulnar and musculocutaneous nerves — does not improve postoperative analgesia. However, the supraclavicular block is often quicker to perform and may result in fewer side effects than the interscalene block. Compared to the infraclavicular block and axillary blocks, the successful achievement of adequate anesthesia for surgery of the upper extremity is about the same with supraclavicular block. [ 11 ]
Unlike the interscalene block — which results in diaphragmatic hemiparesis in all subjects — only half of those who undergo supraclavicular block experience this side effect. Disadvantages of the supraclavicular block include the risk of pneumothorax , which is estimated to be between 1%–4% when using paresthesia or peripheral nerve stimulator guided techniques. Ultrasound guidance allows the operator to visualize the first rib and the pleura, thereby helping to ensure that the needle does not puncture the pleura; this presumably reduces the risk of pneumothorax. [ 11 ]
For infraclavicular block, current evidence suggests that — when using a peripheral nerve stimulator for nerve localization — a double-stimulation technique is better than a single-stimulation technique. When compared to a multiple-stimulation axillary block, infraclavicular block provides similar efficacy. However it may be associated with a shorter performance time and less procedure-related pain for the patient. [ 11 ]
The axillary block is particularly useful in providing anesthesia and postoperative analgesia for surgery to the elbow, forearm, wrist, and hand. The axillary block is also the safest of the four main approaches to the brachial plexus, as it does not risk paresis of the phrenic nerve, nor does it have the potential to cause pneumothorax . [ 12 ] In the axilla, the nerves of the brachial plexus and the axillary artery are enclosed together in a fibrous sheath which is a continuation of the deep cervical fascia . The easily palpated axillary artery thus serves as a reliable anatomical landmark for this block, and the injection of local anesthetic close to this artery frequently leads to a good block of the brachial plexus. The axillary block is commonly performed due to its ease of performance and relatively high success rate. [ 4 ]
Disadvantages of the axillary block include inadequate anesthesia in the distribution of the musculocutaneous nerve. This nerve supplies motor function to the biceps , brachialis , and coracobrachialis muscles and one of its branches supplies sensation to the skin of the forearm. If the musculocutaneous nerve is missed, it may be necessary to block this nerve separately. This can be accomplished by using a peripheral nerve stimulator to identify the location of the nerve as it passes through the coracobrachialis muscle. The intercostobrachial nerves (which are branches of the second and third intercostal nerves ) are also frequently missed with the axillary block. Because these nerves supply sensation to the skin of the medial and posterior aspects of the arm and axilla, a tourniquet on the arm may be poorly tolerated in such cases. Subcutaneous injection of local anesthetic over the medial aspect of the arm in the axilla helps patients tolerate an arm tourniquet by blocking these nerves. [ 13 ]
Single-injection techniques provide unreliable blockade in the areas supplied by the musculocutaneous and radial nerves. Current evidence suggests that a triple-stimulation technique — with injections on the musculocutaneous, median and radial nerves — is the best technique for the axillary block. [ 11 ]
Despite the fact that people have been performing brachial plexus blocks for over a hundred years, [ 14 ] there is as yet no clear evidence to support the assertion that one method of nerve localization is better than another. There are however numerous case reports documenting cases in which use of a portable ultrasound scanning device has detected abnormal anatomy that would otherwise not have been evident using a "blind" approach. On the other hand, use of ultrasound may create a false sense of security in the operator, which may lead to errors, especially if the needle tip is not adequately visualized at all times. [ 10 ]
For interscalene block, it is not clear whether nerve stimulation provides a better interscalene block than elicitation of paresthesiae. [ 11 ] However, a recent study using ultrasound to follow the spread of local anesthetic demonstrated an improved success rate of the block (relative to blocks done with nerve stimulator alone) even at the inferior roots of the plexus. [ 2 ]
For supraclavicular block, nerve stimulation with a minimal threshold of 0.9 mA can offer a dependable block. [ 11 ] Although ultrasound-guided supraclavicular block has been shown to be a safe alternative to the peripheral nerve stimulator guided technique, there is little evidence to support that ultrasound guidance provides a better block, or is associated with fewer complications. [ 10 ] There is some evidence to suggest that the use of ultrasound guidance in combination with nerve stimulation can shorten the performance time of supraclavicular block. [ 11 ]
For axillary block, success rates are greatly improved with multiple injection techniques whether using nerve stimulation or ultrasound guidance. [ 12 ]
The duration of a "single-shot" brachial plexus block is highly variable, commonly lasting anywhere from 45 minutes to 24 hours. The block can be extended by placing an indwelling catheter , which may be connected to a mechanical or electronic infusion pump for continuous administration of local anesthetic solution. A catheter may be inserted at the interscalene, supraclavicular, infraclavicular or axillary location, depending on the desired location of nerve block. Specific branches of the brachial plexus can also be blocked individually, for example the suprascapular nerve. [ 15 ] The infusion of local anesthetic can be programmed to be a continuous flow or patient-controlled analgesia . In some cases, people can maintain the catheters and infusions at home after release from the facility where the surgery was performed. [ 2 ]
As with any procedure involving disruption of the integrity of the skin, brachial plexus block can be associated with infection or bleeding . In people who are using anticoagulant agents, there is a greater risk of complications related to bleeding. [ 2 ]
Complications associated with brachial plexus block include intra-arterial or intravenous injection, which can lead to local anesthetic toxicity . This may be characterized by serious central nervous system problems such as epileptic seizure , central nervous system depression , and coma . [ 16 ] Cardiovascular effects of local anesthetic toxicity include slowing of the heart rate and impairment of its ability to pump blood through the circulatory system, which may lead to circulatory collapse . In severe cases, cardiac dysrhythmia , cardiac arrest and death may occur. [ 17 ] Other rare but serious complications from brachial plexus block include pneumothorax and persistent paresis of the phrenic nerve . [ 18 ]
Complications associated with interscalene and supraclavicular blocks include inadvertent subarachnoid or epidural injection of local anesthetic, which can result in respiratory failure. [ 18 ]
Because of the close proximity of the lung to the brachial plexus at the level of the clavicle, the complication most often associated with this block is pneumothorax — with a risk as high as 6.1%. [ 10 ] Further complications of supraclavicular block include subclavian artery puncture, and spread of local anesthetic to cause paresis of the stellate ganglion, the phrenic nerve and recurrent laryngeal nerve. [ 10 ]
Depending on the circumstances, alternatives to brachial plexus block may include general anesthesia , monitored anesthesia care , Bier block , or local anesthesia . [ citation needed ]
In 1855, Friedrich Gaedcke (1828–1890) became the first to chemically isolate cocaine , the most potent alkaloid of the coca plant. Gaedcke named the compound "erythroxyline". [ 19 ] [ 20 ] In 1884, Austrian ophthalmologist Karl Koller (1857–1944) instilled a 2% solution of cocaine into his own eye and tested its effectiveness as a local anesthetic by pricking the eye with needles. [ 21 ] His findings were presented a few weeks later at annual conference of the Heidelberg Ophthalmological Society. [ 22 ] The following year, William Halsted (1852–1922) performed the first brachial plexus block. [ 23 ] [ 24 ] Using a surgical approach in the neck, Halsted applied cocaine to the brachial plexus. [ 25 ] In January 1900, Harvey Cushing (1869–1939) — who was at that time one of Halsted's surgical residents — applied cocaine to the brachial plexus prior to dividing it, during a forequarter amputation for sarcoma . [ 26 ]
The first percutaneous supraclavicular block was performed in 1911 by German surgeon Diedrich Kulenkampff (1880–1967). [ 14 ] Just as his older colleague August Bier (1861–1949) had done with spinal anesthesia in 1898, [ 27 ] Kulenkampff subjected himself to the supraclavicular block. [ 14 ] Later that year, Georg Hirschel (1875–1963) described a percutaneous approach to the brachial plexus from the axilla. [ 28 ] In 1928, Kulenkampff and Persky published their experiences with a thousand blocks without apparent major complications. They described their technique with the patient in the sitting position or in the supine position with a pillow between the shoulders. The needle was inserted above the midpoint of the clavicle where the pulse of the subclavian artery could be felt and it was directed medially toward the second or third thoracic spinous process . [ 29 ]
By the late 1940s, clinical experience with brachial plexus block in both peacetime and wartime surgery was extensive, [ 30 ] and new approaches to this technique began to be described. For example, In 1946, F. Paul Ansbro was the first to describe a continuous brachial plexus block technique. He secured a needle in the supraclavicular fossa and attached tubing connected to a syringe through which he could inject incremental doses of local anesthetic. [ 31 ] The subclavian perivascular block was first described by Winnie and Collins in 1964. [ 32 ] This approach became popular due to its lower risk of pneumothorax compared to the traditional Kulenkampff approach. The infraclavicular approach was first developed by Raj. [ citation needed ] In 1977, Selander described a technique for continuous brachial plexus block using an intravenous catheter secured in the axilla. [ 33 ] In 1977, James K. Sims described the use of the coracoid process of the scapula as a landmark for the performance of brachial plexus block. The Sims approach, now referred to as Infracoracoid Block has certain advantages: a) The needle tip is directed away from the apex of the lung, not toward it, b) the skin at the point of initial needle penetration is easier to clean than the axilla, c) the Musculocutaneous nerve is still within the sheath at this point making this terchnique more consistently useful for upper forearm surgery, and d) a percutaneous indwelling catheter may be placed for postoperative pain control. [ 34 ]
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Bracht–Wachter bodies are a finding in infective endocarditis [ 1 ] consisting of yellow-white miliary spots in the myocardium .
Histologically , these are collections of chronic inflammatory cells, mainly lymphocytes [ 2 ] and histiocytes .
They were described by two Germans, Erich Franz Eugen Bracht , a pathologist and obstetrician-gynecologist, and Hermann Julius Gustav Wächter , a physician. [ 3 ]
Other findings in infective endocarditis are:
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Brachyturricephaly is a form of complex craniosynostosis (a combination of brachycephaly and turricephaly ) in which the head has both an abnormally high vertical height and a shortened length from anterior to posterior. Malformations of the occipital region are also often present. [ 1 ] [ 2 ] [ 3 ]
Brachyturricephaly is seen in the following conditions: [ 1 ]
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Bradyphrenia is the slowness of thought common to many disorders of the brain. [ 1 ] Disorders characterized by bradyphrenia include Parkinson's disease and forms of schizophrenia consequently causing a delayed response and fatigue . [ 2 ] Patients with bradyphrenia may describe or may manifest slowed thought processes, evidenced by increased latency of response and also involve severe memory impairment and poor motor control. [ 3 ] The word 'bradyphrenia' originates from the ancient Greek meaning 'slow mind.' [ 4 ]
In his research, Steck found that almost half the patients with Parkinson's disease in the psychiatric ward during the post-encephalitic period had bradyphrenia. [ 2 ] Neurologists often saw the condition as an additional trait of Parkinson's disease as they found that patients with Parkinson's disease had often impaired traits that would be defined by bradyphrenia. [ 2 ] In the study conducted in 1966, Wilson et al. had found that bradyphrenia found in the patients with Parkinson's disease had increased their reaction time of retaining information. [ 5 ] [ 6 ] [ 7 ] Other studies exploring this theory confirmed that bradyphrenia was commonly seen in their studies of patients with Parkinson's disease [ 8 ] In addition, some researchers found that the condition does not impact all patients with Parkinson's disease.
Some neurologists had also suggested that bradyphrenia could exist without the presence of parkinsonism. [ 8 ] In some cases, it has been found that bradyphrenia has been mistaken for an inability to strategically complete tasks and therefore may often be categorised as the condition incorrectly. [ 6 ] Collectively, it was concluded that bradyphrenia does not commonly appear in parkinsonism but rather as a single entity that occurs in other conditions and not only in the single presence of Parkinson's disease. [ 6 ]
Despite the collective agreement of bradyphrenia being classified as a nosological entity, the neurological condition is still more often described in case studies where the subjects are analysed for having Parkinson's disease. [ citation needed ]
There are several symptoms in Parkinson's disease which are influenced by the presence of bradyphrenia. Researcher Norberg discovered that a gradual cognitive slowing impacted the eating behaviour of these patients. [ 9 ] It was found that patients with Parkinson's disease would often experience extended periods of time attempting to process the food that they are eating, causing an increase in the time it took for them to consume their food. [ 9 ]
In another study examining the presence of bradyphrenia in Parkinson's disease, researchers had discovered that bradyphrenia was one of the reasons for slow auditory feedback as measured by the DAF (Delayed Auditory Feedback). [ 8 ] Dobbs et al., completed an experiment whereby the experimenter would communicate to the patient via a microphone and would ask the participant to complete a series of tasks. The participant, with or without Parkinson's disease, would receive this information through their headphones and respond via a microphone. The experimenters had asked the participants to complete the following tasks; counting to 20, repeat several simple sentences and read a series of words from a card. [ 8 ] The researchers concluded that bradyphrenia was present in Parkinson's disease however also in older patients as they also had delayed feedback when completing the task. [ 8 ]
Researchers Rogers et al. found bradyphrenia in light of Parkinson's disease was considerably similar to what is referred to as ' Psychomotor retardation . [ 10 ] Psychomotor retardation was proposed by the researchers as a condition particularly seen in major depressive disorders. Researchers had conducted a study to examine in ways in which the two conditions share similarities in analysing diagnosed Parkinson Disease patients and patients who had been diagnosed with depression. The participants were given two tasks to complete, one of the tasks is known as the digit symbol substitution test which consisted of the participants filling in a row of numbers which had a specific connection to a symbol. Another task which been referred to as the 'simpler task' which was to match the number on the screen that they had seen by pressing the same number on the keyboard. [ 10 ] Both of these measurements required a fast reaction time as their response was based on how quickly (in seconds) they would respond to each of the tasks. Researchers found that there had been no significant decrease in the response time for this test in participants with Parkinson's disease as their reaction time had been longer. [ 10 ] However, for participants having major depressive disorder, there had been an overall improvement in reaction time. Rogers, Lees and Smith had then eventually concluded that bradyphrenia explored in the presence of Parkinson's disease was very similar to psychomotor retardation in a major depressive disorder with a few differences. They had found that there had been notable impairments in their dopaminergic areas seen in both groups of disorders that could call for some similarities between the two conditions. [ 10 ]
Alzheimer's disease , another neurological condition involving cognition impairment. [ 11 ] Researchers found that there was a presence of cognitive slowing in patients with Alzheimer's. [ 11 ] Pate and Margolin, found that this was caused by damage to the cortical central. [ 12 ] The cortical central is the outer region of the cerebellum , a major component of the brain that controls motor functions. [ 13 ] Particularly in the older population, evidence of bradyphrenia had been seen in patients with Alzheimer's.
Evidence of bradyphrenia in patients with depression had been present if they had previous neurological damage. [ 13 ] In a study of elderly patients, it was found that patients with depression had not shown a significant delay in thought processing as did patients with depression and additional neurological damage to a part of their brain. [ 14 ]
Yet, Rogers et al., examined bradyphrenia and whether or not it was indicated by 'mental rotation' in melancholic and non-melancholic depressed patients. Researchers would ask the participants to participate in numerous tasks whereby their performance would be measured by their reaction time and accuracy of response. [ 15 ] The tasks that participants were asked to perform included being able to determine which direction a stimulus on the screen was pointing towards and were also told to determine if a stimulus shown was the normal positioning or whether it had been reversed. [ 15 ] From this study, researchers had concluded that in melancholic participants with major depression their slowing in reaction time was higher, in contrast to the control group, which indicated the presence of bradyphrenia. Researchers had drawn the conclusion that the lesser slowness of the non-melancholic depressed groups in these tasks had not been intense enough to draw it to bradyphrenia. [ 15 ]
Bradyphrenia had also been observed in Huntington's disease and schizophrenia . [ 16 ] To examine the role of bradyphrenia within these conditions the researchers used the Tower of London Test which is a task that requires cognitive processing. [ 16 ] This study had shown that there had been a significant increase in time that it took for patients with Huntington's to solve the problem. [ 16 ] Participants with schizophrenia, however, performed the tasks in a smaller amount of time, faster than those in the control group within the experiment. [ 16 ] Hanes had suggested that bradyphrenia in schizophrenia was not as common as it was seen in Huntington's disease. [ 16 ]
Experts including Martin et al. discovered that bradyphrenia is seen as one of the first stages of the ramifications of overdosing on an opioid like heroin . Bradyphrenia, however, had been considered the presence of bradyphrenia to be the most 'minor' of the ramifications. [ 17 ] Martin et al. found that stage three of symptoms of overdose entailed the high risk around 20% of those that reach what has been described as 'stage three' will die. [ 17 ] A case report had been done on a 63-year-old man who had been hospitalised for ten days and has been released with no notable impairments. The patient was hospitalised again several days later after showing abnormal behaviours in which specialists could only describe it as being bradyphrenia. [ 18 ] The patient's abnormal behaviour included having a diminished attention span as well as being unable to remember minor details. Researchers had justified this worsening of behaviour by abnormal neurological activity within the pre-frontal cortex . [ 18 ] The patient's cognitive abilities had improved with the use of an antioxidant therapy yet with some acts of abnormal behaviours still showing. [ 18 ] [ 19 ]
Currently, there are no pharmaceutical medications that will directly increase the rate of thoughts in patients with bradyphrenia experience. [ 20 ] The treatments for Parkinson's disease have been imposed as a model for treatment of bradyphrenia as in some cases the researchers have been able to treat the condition in patients with Parkinson's. [ 2 ]
During the time of the encephalitis lethargica period, the rise of bradyphrenia was seen in many of the cases. In one case in Russia it was believed that this condition could be treated with steroid therapy after the patient's condition had improved after three months using steroid. [ 21 ] In another more recent case, an 80-year-old woman had been diagnosed with Cerebral Amyloid Angiopathy (CAA) and was described to have symptoms of bradyphrenia after showing abnormalities within the pre-frontal cortex of the brain through a magnetic resonance imaging system (MRI) that had shown a significant increase in lesions. [ 22 ] The patient had been put on steroid therapy which researchers McHugh et al. had found a significant improvement of cognitive abilities over time. [ 22 ] The effectiveness of steroid therapy had been observed within an MRI improvement as the number of lesions had decreased as well as the shift in behaviours of participants. [ 22 ] [ 23 ]
In one trial it was found that bradyphrenia as well as bradykinesia , could be treated using the combination of a L-DOPA and carbidopa regimen. This combination was believed to alter these effects of Parkinson's disease. [ 24 ] In the short term, this combination had brought positive results as behaviours of these patients had improved. [ 24 ] Yet these researchers found that in the long-term this combination provided a reverse effect, accelerating the cognitive slowing of the brain (bradyphrenia) and motor movement ( bradykinesia ). [ 24 ]
H2 antagonists is a class of drugs that was found to provide positive outcomes throughout the treatment of Parkinson's disease. [ 25 ] [ 26 ] Some studies have shown that through oral admission, the H-2 antagonist will target specific receptors in the brain by crossing the blood–brain barrier and will alter the rate of cognitive thought processing. [ 25 ] Psychiatrist Kaminski found an improvement of this condition in Parkinson's disease with a positive correlation between the decrease of time in cognitive thought processing and the decrease in reaction time for tasks to be completed. [ 25 ]
The first sightings of bradyphrenia were documented by French neurologist Naville in the early 20th century, during the time of the epidemic of encephalitis lethargica , as it appears, he was investigating this disorder. [ 2 ] This epidemic involved inflammation of the brain ( encephalitis ), and affected people tended to experience mental delays and remain motionless for extended periods of time due to an unknown cause. [ 27 ] Naville was dealing with patients experiencing several symptoms which he could only describe as a gradual brain impairment. Several symptoms listed included decreased attention span, memory and lack of motivation to perform any tasks. [ 2 ] Naville had also observed the facial expressions of his patients with these symptoms' had become stagnant and disinterested over time. [ 2 ] Since Naville's publications in 1922, researchers often referred to this condition as 'psychic torpor' being translated as 'mental inactivity.' [ 28 ]
Swiss neurologist Steck completed a study investigating the case of bradyphrenia post- an epidemic, in 27 mental institutions. Within his research, he found that more than half of the patients hospitalised had the condition [ 2 ] Following Steck's discovery, for some period there had been no active research into the causes of bradyphrenia. [ 2 ] Steck's work stimulated the interest of other neurologists including Aubrun, who investigated bradyphrenia creating a new direction by linking it to Parkinson's disease. [ 2 ] Gradually, more neurologists began exploring bradyphrenia in the presence of other disorders including Alzheimer's disease , loss of motor control and psychiatric disorders . [ citation needed ]
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Brain Research UK , formerly known as the Brain Research Trust , is a United Kingdom medical research charity dedicated to the research of neurological diseases and conditions.
Registered charity no. 1137560
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Brain injury ( BI ) is the destruction or degeneration of brain cells . Brain injuries occur due to a wide range of internal and external factors. In general, brain damage refers to significant, undiscriminating trauma-induced damage.
A common category with the greatest number of injuries is traumatic brain injury (TBI) following physical trauma or head injury from an outside source, and the term acquired brain injury (ABI) is used in appropriate circles to differentiate brain injuries occurring after birth from injury, from a genetic disorder (GBI), or from a congenital disorder (CBI). [ 1 ] Primary and secondary brain injuries identify the processes involved, while focal and diffuse brain injury describe the severity and localization. [ citation needed ]
Impaired function of affected areas can be compensated through neuroplasticity by forming new neural connections.
Symptoms of brain injuries vary based on the severity of the injury or how much of the brain is affected. The four categories used for classifying the severity of brain injuries are mild, moderate, or severe. [ 2 ]
Symptoms of a mild brain injury include headaches , confusions , tinnitus , fatigue , changes in sleep patterns , mood or behavior . Other symptoms include trouble with memory , concentration , attention or thinking . [ 3 ] Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident.
Cognitive symptoms include confusion, aggressiveness, abnormal behavior, slurred speech , and coma or other disorders of consciousness . Physical symptoms include headaches that worsen or do not go away, vomiting or nausea, convulsions , brain pulsation, abnormal dilation of the eyes , inability to awaken from sleep, weakness in extremities, and loss of coordination . [ 3 ]
Symptoms observed in children include changes in eating habits, persistent irritability or sadness, changes in attention, or disrupted sleeping habits. [ 3 ]
Symptoms of brain injuries can also be influenced by the location of the injury and as a result impairments are specific to the part of the brain affected. Lesion size is correlated with severity, recovery, and comprehension. [ 4 ] Brain injuries often create impairment or disability that can vary greatly in severity.
In cases of severe brain injuries, the likelihood of areas with permanent disability is great, including neurocognitive deficits , delusions (often, to be specific, monothematic delusions ), speech or movement problems, and intellectual disability . There may also be personality changes. The most severe cases result in coma or even persistent vegetative state . Even a mild incident can have long-term effects or cause symptoms to appear years later. [ 5 ]
Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomia , unknowingly making up words ( neologisms ), and problems with comprehension. The symptoms of Wernicke's aphasia are caused by damage to the posterior section of the superior temporal gyrus . [ 6 ] [ 7 ]
Damage to the Broca's area typically produces symptoms like omitting functional words ( agrammatism ), sound production changes, dyslexia , dysgraphia , and problems with comprehension and production. Broca's aphasia is indicative of damage to the posterior inferior frontal gyrus of the brain. [ 8 ]
An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired, however. For example, in pure alexia , the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca's area and Wernicke's area). However, this does not mean one with pure alexia is incapable of comprehending speech—merely that there is no connection between their working visual cortex and language areas—as is demonstrated by the fact that people with pure alexia can still write, speak, and even transcribe letters without understanding their meaning. [ 9 ]
Lesions to the fusiform gyrus often result in prosopagnosia , the inability to distinguish faces and other complex objects from each other. [ 10 ] Lesions in the amygdala would eliminate the enhanced activation seen in occipital and fusiform visual areas in response to fear with the area intact. Amygdala lesions change the functional pattern of activation to emotional stimuli in regions that are distant from the amygdala. [ 11 ]
Other lesions to the visual cortex have different effects depending on the location of the damage. Lesions to V1 , for example, can cause blindsight in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure . [ 12 ] Lesions to V4 can cause color-blindness , [ 13 ] and bilateral lesions to MT/V5 can cause the loss of the ability to perceive motion. Lesions to the parietal lobes may result in agnosia , an inability to recognize complex objects, smells, or shapes, or amorphosynthesis , a loss of perception on the opposite side of the body. [ 14 ]
Brain injuries have far-reaching and varied consequences due to the nature of the brain as the main source of bodily control. Brain-injured people commonly experience issues with memory. [ 15 ] This can be issues with either long or short-term memories depending on the location and severity of the injury. Sometimes memory can be improved through rehabilitation, although it can be permanent. Behavioral and personality changes are also commonly observed due to changes of the brain structure in areas controlling hormones or major emotions.
Headaches and pain can occur as a result of a brain injury, either directly from the damage or due to neurological conditions stemming from the injury. Due to the changes in the brain as well as the issues associated with the change in physical and mental capacity, depression and low self-esteem are common side effects that can be treated with psychological help. Antidepressants must be used with caution in brain injury people due to the potential for undesired effects because of the already altered brain chemistry.
There are multiple responses of the body to brain injury, occurring at different times after the initial occurrence of damage, as the functions of the neurons , nerve tracts, or sections of the brain can be affected by damage. The immediate response can take many forms. Initially, there may be symptoms such as swelling, pain, bruising, or loss of consciousness. [ 16 ] Post-traumatic amnesia is also common with brain damage, as is temporary aphasia , or impairment of language. [ 17 ]
As time progresses, and the severity of injury becomes clear, there are further responses that may become apparent. Due to loss of blood flow or damaged tissue, sustained during the injury, amnesia and aphasia may become permanent, and apraxia has been documented in patients. Amnesia is a condition in which a person is unable to remember things. [ 18 ] Aphasia is the loss or impairment of word comprehension or use. Apraxia is a motor disorder caused by damage to the brain, and may be more common in those who have been left brain damaged, with loss of mechanical knowledge critical. [ 19 ] Headaches, occasional dizziness, and fatigue—all temporary symptoms of brain trauma—may become permanent, or may not disappear for a long time.
There are documented cases of lasting psychological effects as well, such as emotional changes often caused by damage to the various parts of the brain that control human emotions and behavior. [ 20 ] Individuals who have experienced emotional changes related to brain damage may have emotions that come very quickly and are very intense, but have very little lasting effect. [ 20 ] Emotional changes may not be triggered by a specific event, and can be a cause of stress to the injured party and their family and friends. [ 21 ] Often, counseling is suggested for those who experience this effect after their injury, and may be available as an individual or group session.
The long term psychological and physiological effects will vary by person and injury. For example, perinatal brain damage has been implicated in cases of neurodevelopmental impairments and psychiatric illnesses. [ citation needed ]
Brain injuries can result from a number of conditions, including: [ 22 ]
Chemotherapy can cause brain damage to the neural stem cells and oligodendrocyte cells that produce myelin . Radiation and chemotherapy can lead to brain tissue damage by disrupting or stopping blood flow to the affected areas of the brain. This damage can cause long term effects such as but not limited to; memory loss, confusion, and loss of cognitive function . The brain damage caused by radiation depends on where the brain tumor is located, the amount of radiation used, and the duration of the treatment. Radiosurgery can also lead to tissue damage that results in about 1 in 20 patients requiring a second operation to remove the damaged tissue. [ 28 ] [ 29 ]
Wernicke–Korsakoff syndrome can cause brain damage and results from a Vitamin B deficiency (specifically vitamin B1, thiamine ). [ 30 ] [ 31 ] This syndrome presents with two conditions, Wernicke's encephalopathy and Korsakoff psychosis . Typically Wernicke's encephalopathy precedes symptoms of Korsakoff psychosis. Wernicke's encephalopathy results from focal accumulation of lactic acid , causing problems with vision, coordination, and balance. [ 30 ]
Korsakoff psychosis typically follows after the symptoms of Wernicke's decrease. [ 30 ] [ 31 ] Wernicke-Korsakoff syndrome is typically caused by conditions causing thiamine deficiency, such as chronic heavy alcohol use or by conditions that affect nutritional absorption, including colon cancer, eating disorders and gastric bypass. [ 30 ]
Brain lesions are sometimes intentionally inflicted during neurosurgery , such as the carefully placed brain lesion used to treat epilepsy and other brain disorders. These lesions are induced by excision or by electric shocks (electrolytic lesions) to the exposed brain or commonly by infusion of excitotoxins to specific areas. [ medical citation needed ]
Diffuse axonal injury is caused by shearing forces on the brain leading to lesions in the white matter tracts of the brain. [ 32 ] These shearing forces are seen in cases where the brain had a sharp rotational acceleration, and is caused by the difference in density between white matter and grey matter. [ 33 ]
Unlike some of the more obvious responses to brain damage, the body also has invisible physical responses which can be difficult to notice. These will generally be identified by a healthcare provider, especially as they are normal physical responses to brain damage. Cytokines are known to be induced in response to brain injury. [ 34 ] These have diverse actions that can cause, exacerbate, mediate and/or inhibit cellular injury and repair. TGFβ seems to exert primarily neuroprotective actions, whereas TNFα might contribute to neuronal injury and exert protective effects. IL-1 mediates ischaemic, excitotoxic, and traumatic brain injury , probably through multiple actions on glia, neurons, and the vasculature. Cytokines may be useful in order to discover novel therapeutic strategies. At the current time, they are already in clinical trials. [ 35 ]
Glasgow Coma Scale (GCS) is the most widely used scoring system used to assess the level of severity of a brain injury. This method is based on the objective observations of specific traits to determine the severity of a brain injury. It is based on three traits: eye opening, verbal response, and motor response, gauged as described below. [ 36 ] Based on the Glasgow Coma Scale severity is classified as follows, severe brain injuries score 3–8, moderate brain injuries score 9–12 and mild score 13–15. [ 36 ]
There are several imaging techniques that can aid in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) magnetic resonance spectroscopy (MRS), positron emission tomography (PET), and single-photon emission tomography (SPECT) . CT scans and MRI are the two techniques widely used and are most effective. CT scans can show brain bleeds, fractures of the skull, fluid build up in the brain that will lead to increased cranial pressure. [ 37 ]
MRI is able to better to detect smaller injuries, detect damage within the brain, diffuse axonal injury, injuries to the brainstem, posterior fossa, and subtemporal and subfrontal regions. However, patients with pacemakers, metallic implants, or other metal within their bodies are unable to have an MRI done. Typically the other imaging techniques are not used in a clinical setting because of the cost, lack of availability. [ 38 ]
The treatment for emergency traumatic brain injuries focuses on assuring the person has enough oxygen from the brain's blood supply, and on maintaining normal blood pressure to avoid further injuries of the head or neck. The person may need surgery to remove clotted blood or repair skull fractures, for which cutting a hole in the skull may be necessary. Medicines used for traumatic injuries are diuretics , anti-seizure or coma -inducing drugs. Diuretics reduce the fluid in tissues lowering the pressure on the brain. In the first week after a traumatic brain injury, a person may have a risk of seizures, which anti-seizure drugs help prevent. Coma-inducing drugs may be used during surgery to reduce impairments and restore blood flow. Mouse NGF has been licensed in China since 2003 and is used to promote neurological recovery in a range of brain injuries, including intracerebral hemorrhage. [ 39 ]
In the case of brain damage from traumatic brain injury , dexamethasone and/or Mannitol may be used. [ 40 ]
Various professions may be involved in the medical care and rehabilitation of someone with an impairment after a brain injury. Neurologists , neurosurgeons , and physiatrists are physicians specialising in treating brain injury. Neuropsychologists (especially clinical neuropsychologists ) are psychologists specialising in understanding the effects of brain injury and may be involved in assessing the severity or creating rehabilitation strategies. Occupational therapists may be involved in running rehabilitation programs to help restore lost function or help re-learn essential skills. Registered nurses , such as those working in hospital intensive care units , are able to maintain the health of the severely brain-injured with constant administration of medication and neurological monitoring, including the use of the Glasgow Coma Scale used by other health professionals to quantify extent of orientation. [ 41 ]
Physiotherapists also play a significant role in rehabilitation after a brain injury. In the case of a traumatic brain injury (TBI), physiotherapy treatment during the post-acute phase may include sensory stimulation, serial casting and splinting, fitness and aerobic training, and functional training. [ 42 ] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention. [ 43 ] Serial casting and splinting are often used to reduce soft tissue contractures and muscle tone. Evidence based research reveals that serial casting can be used to increase passive range of motion (PROM) and decrease spasticity . [ 43 ]
Functional training may also be used to treat patients with TBIs. To date, no studies supports the efficacy of sit to stand training, arm ability training and body weight support systems (BWS). [ 44 ] [ 45 ] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills. [ 46 ] More research is required to better understand the efficacy of the treatments mentioned above. [ 47 ]
Other treatments for brain injury can include medication , psychotherapy , neuropsychological rehabilitation , neurotherapy and/or surgery . [ 48 ]
Prognosis, or the likely progress of a disorder, depends on the nature, location, and cause of the brain damage (see Traumatic brain injury , Focal and diffuse brain injury , Primary and secondary brain injury ).
In general, neuroregeneration can occur in the peripheral nervous system but is much rarer and more difficult to assist in the central nervous system (brain or spinal cord). However, in neural development in humans , areas of the brain can learn to compensate for other damaged areas, and may increase in size and complexity and even change function, just as someone who loses a sense may gain increased acuity in another sense—a process termed neuroplasticity . [ 49 ]
There are many misconceptions that revolve around brain injuries and brain damage. One misconception is that if someone has brain damage then they cannot fully recover. Recovery depends a variety of factors; such as severity and location. Testing is done to note severity and location. Not everyone fully heals from brain damage, but it is possible to have a full recovery. Brain injuries are very hard to predict in outcome. Many tests and specialists are needed to determine the likelihood of the prognosis. People with minor brain damage can have debilitating side effects; not just severe brain damage has debilitating effects. [ 50 ]
The side-effects of a brain injury depend on location and the body's response to injury. [ 50 ] Even a mild concussion can have long term effects that may not resolve. [ 51 ] Another misconception is that children heal better from brain damage. Children are at greater risk for injury due to lack of maturity. It makes future development hard to predict. [ 51 ] [ dead link ] This is because different cortical areas mature at different stages, with some major cell populations and their corresponding cognitive faculties remaining unrefined until early adulthood. In the case of a child with frontal brain injury, for example, the impact of the damage may be undetectable until that child fails to develop normal executive functions in his or her late teens and early twenties. [ 52 ]
The foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case studies by Paul Broca. The first case study on Phineas Gage's head injury is one of the most astonishing brain injuries in history. In 1848, Phineas Gage was paving way for a new railroad line when he encountered an accidental explosion of a tamping iron straight through his frontal lobe. Gage observed to be intellectually unaffected but was claimed by some to have exemplified post-injury behavioral deficits. [ 53 ] [ failed verification ]
Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca's first patient lacked productive speech. He saw this as an opportunity to address language localization. It was not until Leborgne, informally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left cerebral hemisphere. The affected area is known today as Broca's area and the condition as Broca's aphasia . [ 54 ]
A few years later, a German neuroscientist, Carl Wernicke , consulted on a stroke patient. The patient experienced neither speech nor hearing impairments, but had a few brain deficits. These deficits included lacking the ability to comprehend what was spoken to him and the words written down. After his death, Wernicke examined his autopsy that found a lesion located in the left temporal region. This area became known as Wernicke's area . Wernicke later hypothesized the relationship between Wernicke's area and Broca's area, which was proven fact. [ 55 ]
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Brain death is the permanent, irreversible, and complete loss of brain function , which may include cessation of involuntary activity (e.g., breathing ) necessary to sustain life. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] It differs from persistent vegetative state , in which the person is alive and some autonomic functions remain. [ 6 ] It is also distinct from comas as long as some brain and bodily activity and function remain, and it is also not the same as the condition locked-in syndrome . A differential diagnosis can medically distinguish these differing conditions.
Brain death is used as an indicator of legal death in many jurisdictions, [ 7 ] but it is defined inconsistently and often confused by the public. [ 8 ] Various parts of the brain may keep functioning when others do not anymore, bringing questions about whether they should truly be considered dead. The term "brain death" has been used to refer to various combinations. For example, although one major medical dictionary considers "brain death" to be synonymous with "cerebral death" (death of the cerebrum ), [ 9 ] the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem . The distinctions are medically significant because, for example, in someone with a dead cerebrum but a living brainstem, spontaneous breathing may continue unaided, whereas in whole-brain death (which includes brainstem death ), only life support equipment would maintain ventilation . In certain countries, patients classified as brain-dead may legally have their organs surgically removed for organ donation . [ citation needed ]
Brain death is a medicolegal death of a person due to the complete and irreversible loss of all brain functions, including the brain stem. The definition of brain death is accepted in numerous regions, it is one of the most complicated topics in medical ethics today. In operational definitions of death have obvious medicolegal implications (in medical jurisprudence and medical law ). Traditionally, both the legal and medical communities determined death through the permanent end of certain bodily functions in clinical death , especially respiration and heartbeat . With the increasing ability of the medical community to resuscitate people with no respiration, heartbeat, or other external signs of life, the need for another definition of death occurred, raising questions of legal death . This gained greater urgency with the widespread use of life support equipment and the rising capabilities and demand for organ transplantation .
Since the 1960s, laws governing the determination of death have been implemented in all countries that have active organ transplantation programs. The first European country to adopt brain death as a legal definition (or indicator) of death was Finland in 1971, while in the United States , the state of Kansas had enacted a similar law earlier. [ 10 ]
An ad hoc committee at Harvard Medical School published a pivotal 1968 report to define irreversible coma . [ 11 ] [ 12 ] The Harvard criteria gradually gained consensus toward what is now known as brain death. In the wake of the 1976 Karen Ann Quinlan case , state legislatures in the United States moved to accept brain death as an acceptable indication of death. In 1981, a presidential commission issued a landmark report entitled Defining Death: Medical, Legal, and Ethical Issues in the Determination of Death , [ 13 ] which rejected the "higher-brain" approach to death in favor of a "whole-brain" definition. This report formed the basis for the Uniform Determination of Death Act , since enacted in 39 states. [ 14 ] Today, both the legal and medical communities in the US use "brain death" as a legal definition of death, allowing a person to be declared legally dead even if life support equipment maintains the body's metabolic processes . [ 15 ]
In the UK, the Royal College of Physicians reported in 1995, abandoning the 1979 claim that the tests published in 1976 sufficed for the diagnosis of brain death, and suggesting a new definition of death based on the irreversible loss of brain-stem function alone. [ 16 ] This new definition, the irreversible loss of the capacity for consciousness and for spontaneous breathing, and the essentially unchanged 1976 tests held to establish that state, have been adopted as a basis of death certification for organ transplant purposes in subsequent Codes of Practice. [ 17 ] [ 18 ] The Australia and New Zealand Intensive Care Society (ANZICS) states that the "determination of brain death requires that there is unresponsive coma, the absence of brain-stem reflexes and the absence of respiratory centre function, in the clinical setting in which these findings are irreversible. In particular, there must be definite clinical or neuro-imaging evidence of acute brain pathology (e.g. traumatic brain injury, intracranial haemorrhage, hypoxic encephalopathy) consistent with the irreversible loss of neurological function." [ 19 ] In Brazil, the Federal Council of Medicine revised its regulations in 2017, including "a requirement for the patient to meet specific physiological prerequisites and for the physician to provide optimized care to the patient before starting the procedures for diagnosing brain death and to perform complementary tests, as well as the need for specific training for physicians who make this diagnosis." [ 20 ]
In 2020, an international panel of experts, the World Brain Death Project, published a guideline that: [ 21 ]
provides recommendations for the minimum clinical standards for determination of brain death/death by neurologic criteria (BD/DNC) in adults and children with clear guidance for various clinical circumstances. The recommendations have widespread international society endorsement and can serve to guide professional societies and countries in the revision or development of protocols and procedures for determination of brain death/death by neurologic criteria, leading to greater consistency within and between countries.
The World Brain Death Project, published in 2020 by Greer et al., provides some of the most comprehensive and globally recognized recommendations for determining brain death. Their *JAMA* The agreement statement offers detailed evidence in protocols for diagnosing brain death in adults and children. It focuses on a standard clinical process, additional testing when necessary, and special considerations in difficult cases. One of the project's main goals is to reduce variability in brain death diagnosis by creating a consistent, internationally framework (Greer et al., 2020).
Natural movements also known as the Lazarus sign or Lazarus reflex can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem; these cells come from the spinal cord . Sometimes these body movements can cause false hope for family members.
A brain-dead individual has no clinical evidence of brain function upon physical examination . This includes no response to pain and no cranial nerve reflexes . Reflexes include pupillary response (fixed pupils), oculocephalic reflex , corneal reflex , no response to the caloric reflex test , and no spontaneous respirations .
Brain death can sometimes be difficult to differentiate from other medical states such as barbiturate overdose , acute alcohol poisoning , sedative overdose, hypothermia , hypoglycemia , coma , and chronic vegetative states . Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly .
Brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest . [ 22 ] Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria. [ 23 ]
The diagnosis of brain death is often required to be highly rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), [ 24 ] and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria.
Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time. [ 25 ]
CT angiography is neither required nor sufficient test to make the diagnosis. [ 26 ]
Confirmatory testing is only needed under the age of 1. [ 2 ] For children and adults, testing is optional. Other situations possibly requiring confirmatory testing include severe facial trauma where determination of brainstem reflexes will be difficult, pre-existing pupillary abnormalities, and patients with severe sleep apnea and/or pulmonary disease. [ 2 ] Confirmatory tests include: cerebral angiography, electroencephalography, transcranial Doppler ultrasonography, and cerebral scintigraphy (technetium Tc 99m exametazime). Cerebral angiography is considered the most sensitive confirmatory test in the determination of brain death. [ 2 ]
While the diagnosis of brain death has become accepted as a basis for the certification of death for legal purposes, it is a very different state from biological death – the state universally recognized and understood as death. [ 27 ] The continuing function of vital organs in the bodies of those diagnosed brain-dead, if mechanical ventilation and other life-support measures are continued, provides optimal opportunities for their transplantation.
When mechanical ventilation is used to support the body of a brain-dead organ donor pending a transplant into an organ recipient, the donor's date of death is listed as the date that brain death was diagnosed. [ 28 ]
In some countries (for instance, Spain , [ 29 ] Finland , the United Kingdom , [ 30 ] Portugal , France , and by 2026 Switzerland ), everyone is automatically an organ donor after diagnosis of death on legally accepted criteria, although some jurisdictions (such as Singapore , Spain, the United Kingdom, France, Czech Republic , Poland and Portugal) allow opting out of the system. Elsewhere, consent from family members or next-of-kin may be required for organ donation. In New Zealand , Australia and most states in the United States , drivers are asked upon application if they wish to be registered as an organ donor. [ 31 ]
In the United States, if the patient is at or near death, the hospital must notify a designated Organ Procurement Organization (OPO) of the details, and maintain the patient while the patient is being evaluated for suitability as a donor. [ 32 ] The OPO searches to see if the deceased is registered as a donor, which serves as legal consent; if the deceased has not registered or otherwise noted consent (e.g., on a driver's license), the OPO will ask the next of kin for authorization. [ 33 ] The patient is kept on ventilator support until the organs have been surgically removed. If the patient has indicated in an advance health care directive that they do not wish to receive mechanical ventilation or has specified a do-not-resuscitate (DNR) order and the patient has also indicated that they wish to donate their organs, some vital organs such as the heart and lungs may not be able to be recovered. [ 34 ]
Brain death is responsible for 2% of all adult and 5% of pediatric in-hospital deaths in the United States. [ 35 ] In a nationwide survey of pediatric intensive care units (PICU) in the United States in 2019; there were more than 3,000 pediatric brain deaths out of a total of more than 15,344 children who died in PICUs. According to a national study, "brain death evaluations are performed infrequently, even in large PICUs." [ 36 ]
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Brain healing is the process that occurs after the brain has been damaged. If an individual survives brain damage, the brain has a remarkable ability to adapt. When cells in the brain are damaged and die, for instance by stroke , there will be no repair or scar formation for those cells. The brain tissue will undergo liquefactive necrosis , and a rim of gliosis will form around the damaged area.
Apart from a small amount in the blood vessels , there are no fibroblasts in the brain. A scar is formed by fibroblasts producing collagen to repair an area, which will later contract. If scars did form in the brain, the contraction would cause even more damage.
Around the edge of necrosis, astrocytes proliferate. These cells extend processes, and form a delicate rim of gliosis around the margin of damage. The empty space left by brain tissue fills up with cerebrospinal fluid .
Brain injury will commonly be accompanied by acute swelling, which impairs function in brain tissue that remains alive. Resolution of swelling is an important factor for the individual's function to improve. The greatest factor in functional recovery after brain injury comes from the brain's ability to learn, called neuroplasticity . After injury, neuroplasticity allows intact areas of the brain to adapt and attempt to compensate for damaged parts of the brain. Although axons and the peripheral nervous system in the developing brain can regenerate, they cannot in the adult brain. This is partly because of factors produced by cells in the brain that inhibit this regeneration. Dendrites , however, will develop from intact axons, as part of the neuroplasticity process. After severe brain injury, improvement in function related to neuroplasticity is unlikely to occur without help from health professionals skilled in rehabilitation . Recent studies have found collagen is extensively distributed throughout the brain and may be essential in protecting the brain against degeneration such as that in Alzheimers. [ 1 ] [ 2 ]
A study done in Tel Aviv University showed severe brain damage can be reversed through oxygen rich air. Patients were treated with hyperbaric oxygen therapy (HBOT) in high pressure chambers containing oxygen rich air which increased oxygen levels in body tenfold.
After two months of treatment, patients who were previously unable to perform simple daily activities such as bathing, cooking, climbing stairs or reading a book regained these abilities following treatment. [ 3 ]
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Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage . People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders . Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system (CNS) functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity .
Air pollution may increase the risk of developmental disorders (e.g., autism ), [ 3 ] [ 4 ] [ 5 ] [ 6 ] neurodegenerative disorders, [ 7 ] [ 8 ] mental disorders, [ 9 ] [ 10 ] [ 11 ] and suicide . [ 9 ] [ 11 ] [ 12 ] It is associated with neurological conditions including stroke , multiple sclerosis , dementia , Parkinson disease , [ 13 ] Alzheimer's disease , [ 1 ] schizophrenia [ 14 ] and headaches . [ 13 ]
A 2008 study compared children and dogs raised in Mexico City (a location known for high pollution levels) with children and dogs raised in Polotitlán , Mexico (a city whose pollution levels meet the current US National Ambient Air Quality Standards ). [ 15 ] Children raised in areas of higher pollution were found to score lower in intelligence (i.e., on IQ tests), and showed signs of lesions in MRI scanning of the brain. In contrast, children from the low pollution area scored as expected on IQ tests and showed no significant sign of the risk of brain lesions. Concerning traffic-related air pollution, children of mothers exposed to higher levels during the first trimester of pregnancy were at increased risk of allergic sensitization at one year age. [ 16 ]
Effects of physical activity and air pollution on neuroplasticity may counteract. Physical activity is known for its benefits to the cardiovascular system, brain plasticity processes, cognition and mental health. The neurotrophine, brain-derived neurotrophic factor (BDNF) is thought to play a key role in exercise-induced cognitive improvements. Brief bouts of physical activity may increase serum levels of BDNF, but this increase may be offset by increased exposure to traffic-related air pollution. [ 17 ] Over longer periods of physical exercise, the cognitive improvements which were demonstrated in rural joggers were found to be absent in urban joggers who were partaking in the same 12-week start-2-run training programme. [ 18 ] During exercise, traffic-related air pollution may reduce the beneficial effects of that exercise. [ 19 ]
Analyzing 2017 and 2018 data from Lost in Migration , a phone game that test players' ability to keep their focus, researchers found effects of wildfire smoke and pollution particulates on brain performance. [ 20 ]
"We found evidence suggesting that fine particulate matter (PM2.5) can reduce attention in adults within just hours of exposure. This is a very quick turnaround between exposure and decreased cognitive performance and may have implications when thinking about time-sensitive public health communication during extreme air pollution events like wildfires ," Cleland, a predoctoral ORISE fellow at EPA , explained. [ 20 ] It was also found that prolonged exposure to particulate pollution shortens attention spans in younger populations specifically. In both the long-term and short-term analyses, exposure to harmful particulates caused lower game scores. [ 20 ]
Airborne particulate matter is a Group 1 carcinogen . [ 21 ] Particulates are the most harmful form (other than ultra-fines ) of air pollution [ 22 ] as they can penetrate deep into the lungs and brain from blood streams, causing health problems such as heart disease , lung disease , and premature death . [ 23 ] There is no safe level of particulates. [ 24 ] Ultrafine particles are both manufactured and naturally occurring. Hot volcanic lava , ocean spray , and smoke are common natural UFPs sources. UFPs can be intentionally fabricated as fine particles to serve a vast range of applications in both medicine and technology. Other UFPs are byproducts, like emissions, from specific processes, combustion reactions, or equipment such as printer toner and automobile exhaust . [ 25 ] [ 26 ] Anthropogenic sources of UFPs include combustion of gas, coal or hydrocarbons, biomass burning (i.e. agricultural burning, forest fires and waste disposal), vehicular traffic and industrial emissions, tire wear and tear from car brakes, air traffic , seaport, maritime transportation, construction , demolition , restoration and concrete processing , domestic wood stoves, outdoor burning , kitchen, and cigarette smoke. [ 27 ]
While hand-held power tools are very helpful (e.g., in renovation and construction), they also produce large amounts of vibrations [ 28 ] and particulates (particulate matter), including ultrafine particles , [ 29 ] from both fuel combustion and the mechanical tasks. Not only power tools, hand tools also generate UFPs. [ 30 ]
Many construction tasks create dust. High dust levels are caused by one of more the following:
Examples of high dust level tasks include:
Currently there seems to be no or little regulations on the size and amount of dust emitted by power tools. Some industry standards do exist, [ 32 ] [ 33 ] though it appears that they are not widely known or used globally. Knowing that dust is generated throughout the construction process and can cause serious health hazards, [ 34 ] manufacturers are now marketing power tools that are equipped with dust collection system (e.g. HEPA vacuum cleaner) or integrated water delivery system which extract the dust after emission. [ 35 ] [ 36 ] However, the use of such products is still not common in most places. As Q1 2024 petrol powered tools are banned in California. [ 37 ]
Organohalogen compounds, such as dioxins , are commonly found in pesticides or created as by-products of pesticide manufacture or degradation . These compounds can have a significant impact on the neurobiology of exposed organisms. Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion (Ca 2+ ), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance. [ 38 ] A study of 350 chemical plant employees exposed to a dioxin precursor for herbicide synthesis between 1965 and 1968 showed that 80 of the employees displayed signs of dioxin poisoning. [ 39 ] The study suggested that the effects of dioxins were not limited to initial toxicity . Dioxins, through neuroplastic effects, may cause long-term damage that may not manifest itself for years or even decades. [ 39 ]
Heavy metal exposure can result in an increased risk of various neurological diseases. The two most neurotoxic heavy metals are mercury and lead . The impact of the two heavy metals is highly dependent upon the individual due to genetic variations . Mercury and lead are particularly neurotoxic for many reasons: they easily cross cell membranes , have oxidative effects on cells, react with sulfur in the body (leading to disturbances in the many functions that rely upon sulfhydryl groups), and reduce glutathione levels inside cells. Methylmercury , in particular, has an extremely high affinity for sulfhydryl groups. [ 40 ] Organomercury is a particularly damaging form of mercury because of its high absorbability [ 41 ] Lead also mimics calcium , a very important mineral in the CNS, and this mimicry leads to many adverse effects. [ 42 ] Mercury's neuroplastic mechanisms work by affecting protein production. Elevated mercury levels increase glutathione levels by affecting gene expression , and this in turn affects two proteins (MT1 and MT2) that are contained in astrocytes and neurons. [ 43 ]
Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione. [ 44 ] Blood lead concentrations ≥ 5·0 μg/dL could result in children scoring 3–5 points lower in intelligence tests than those with the concentrations < 5·0 μg/dL . Higher blood lead concentrations are also associated with serious cognitive function losses. "Lead-related IQ losses are associated with increased rates of school failure, behavioural disorders, diminished economic productivity, and global economic losses of almost $1 trillion annually." [ 45 ]
Heavy metal exposure , when combined with certain genetic predispositions , can place individuals at increased risk for developing autism . Many examples of CNS pathophysiology , such as oxidative stress , neuroinflammation , and mitochondrial dysfunction, could be by-products of environmental stressors such as pollution , as found in a 2010 study. [ 46 ] There have been reports of autism outbreaks occurring in specific locations. [ 47 ]
Early-life exposure to air pollution may be a risk factor for autism. Children of mothers living near a freeway , and traffic-related pollution, during the third trimester of pregnancy were twice as likely to develop ASD. [ 48 ] A distance of 1,014 feet, or a little less than 3.5 football fields, was considered near a freeway. Children with a mutation in a gene called MET , combined with high levels of exposure to air pollution, may have increased risk. [ 48 ]
Prenatal and early childhood exposure to heavy metals , like mercury , lead , or arsenic ; altered levels of essential metals like zinc or manganese ; pesticides ; and other contaminants cause concern. [ 48 ] A study of twins used baby teeth to determine and compare levels of lead, manganese, and zinc in children with autism to their twin without the condition. [ 48 ] Autistic children were low on manganese and zinc, metals essential to life, but had higher levels of lead, a harmful metal during specific developmental time periods studied. Altered zinc-copper cycles , which regulate metal metabolism in the body, are disrupted in ASD cases. [ 48 ]
Maternal exposure to insecticides during early pregnancy was associated with higher risk of autism in their children. Contaminants such as Bisphenol A , phthalates , flame retardants , and polychlorinated biphenyls are also being studied. [ 48 ]
Neuroinflammation is associated with increased rates of neurodegeneration . [ 49 ] Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the CNS to age more quickly. Many late-onset diseases are caused by neurodegeneration. Multiple sclerosis , Parkinson's disease , amyotrophic lateral sclerosis (ALS), and Alzheimer's disease are all believed to be exacerbated by inflammatory processes, resulting in individuals displaying signs of these diseases at an earlier age than is typically expected. [ 49 ]
Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes , which in turn leads to the destruction of the myelin sheath . Then axons begin exhibiting signs of damage, which in turn leads to neuron death. Multiple sclerosis has been correlated to living in areas with high particulate matter levels in the air. [ 50 ]
According to Lancet (2021), exposure to "environmental pollution with toxins, such as pesticides (eg, paraquat) or chemicals (eg, trichloroethylene), known to be harmful to Parkinson's disease-related neurons and brain circuits," is associated with Parkinson's disease. [ 51 ] Multi-decade studies have identified an increased likelihood of Parkinson's in association with agricultural work, pesticide exposure, and rural habitation. Chlorinated solvents, used in commercial and industrial application like dry cleaning and degreasing, are associated with increased PD risk, particularly trichloroethylene . [ 52 ] [ 53 ] Other chemical risk factors include manganese , suspended particles from traffic fumes, and exposure to other heavy metals such as mercury and lead . [ 53 ] [ 54 ]
In the case of Alzheimer's disease, inflammatory processes lead to neuron death by inhibiting growth at axons and activating astrocytes that produce proteoglycans . This product can only be deposited in the hippocampus and cortex , indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's disease. [ 55 ] Tiny particles (e.g., engineered nanoparticles and combustion nanoparticle emissions, also called nanomaterials , including those containing manganese ) can bypass the blood-brain barrier (the body's filtering system) and enter the brain as they are breathed in. [ 56 ] [ 57 ] [ 58 ]
A study on the young adult citizens in Metropolitan Mexico City (MMC) found association between air pollution exposure and olfactory dysfunction and pathology in the olfactory bulb . [ 1 ] The young adults demonstrated olfactory bulb endothelial hyperplasia , neuronal accumulation of particles , and immunoreactivity to Aβ and/or α-synuclein in neurons, glial cells and/or blood vessels. There were ultrafine particles deposited in their endothelial cytoplasm and basement membranes of the olfactory bulb. [ 1 ]
Studies consistently suggested a strong link between chronic exposure to PM, especially PM2.5 and UFPM, with the onset of dementia and AD, as well as neurodegenerative-like pathology and cognitive deficits . [ 1 ] The central role of oxidative stress was highlighted in the neuronal injury caused by PM. Neuroinflammation could further damage the neurons and other cells such as the endothelial cells in the neurovascular unit (NVU). [ 1 ] The neurovascular unit consists of neurons, astrocytes , vasculature ( endothelial and vascular mural cells ), the vasomotor apparatus ( smooth muscle cells and pericytes ), and microglia . [ 59 ] Targeting the HMGB1 / TLR4 / NF-κB pathways or oxidative stress by pharmacological inhibitors or genetic knockdown has demonstrated potential as an therapeutic intervention. [ 1 ]
Effects of PM on metabolism should be further studied according to the results in the neurometabolomics analysis as studies not only showed the implication of disturbed glutathione metabolism in the pathogenesis of PM-induced neuronal injury but also demonstrated that PM may affect the fatty acid and energy metabolism in the neurons. [ 1 ] Injury in the NVU after exposure to PM would also impair energy metabolism in the affected brain regions. [ 1 ] Therefore, the disturbed metabolic homeostasis may also play a crucial pathogenic role in the development of PM-induced neuropathology . [ 1 ] Restoring these metabolic disturbances may enhance the resistance of neurons against the stress caused by exposure to PM. [ 1 ]
Exposure to air pollution was positively associated with an increased risk of stroke hospital admission (PM2.5, PM10, SO2, NO2, CO, and O3), incidence (PM2.5, SO2, and NO2), and mortality (PM2.5, PM10, SO2, and NO2). [ 60 ] There is a "well-recognized link between PM2.5 and vascular injury and the role of vascular injury in dementia". [ 61 ] Air pollution in the cerebrovascular system may result in “stroke, vascular dementia, or other types of dementia". [ 62 ] The risk of dementia, including Alzheimer's disease and vascular dementia , may be increased by long-term exposure to PM2.5. [ 63 ]
Interest in the possible effects of air pollutants on the brain began in about 2002 when Calderon-Garciduenas and colleagues reported that dogs exposed to air pollution in Mexico City showed neuropathological changes of the type associated with Alzheimer's disease. This work was an extension of studies undertaken in the 1990s on the effects of Mexico City air pollution on the olfactory epithelium of humans and dogs. Later, interest in possible effects on the brain has been strengthened by epidemiological studies, which suggest that exposure to air pollutants is associated with a decline of cognitive function and the development of dementia. [ 64 ]
Magnetite nanoparticles have been found in the brain with a morphology that suggests an exogenous origin. Similar ferrous nanoparticles were found in air collected at traffic roadsides in the UK. These nanoparticles may be able to reach the brain via the olfactory nerves and olfactory bulb, or via the circumventricular organs where the blood-brain barrier is more permeable. In addition, the blood-brain barrier could be made less impermeable by systemic inflammation for which exposure to air pollutants is a known risk factor. The blood-brain barrier is also more permeable in the very young and old, making these two life stages opportunities for the entry of nanoparticles into the brain, and potential elicitation of neurological damage. [ 64 ]
In addition to the possible direct effects from nanoparticles reaching the brain, there are indirect mechanisms by which pollutants could potentially lead to brain injury. These include damage to the vasculature , leading to cerebral ischaemia or extravasation of neurotoxic proteins such as fibrinogen. Brain injury could also be secondary to systemic inflammatory responses to air pollution. [ 64 ]
Calderon-Garciduenas et al. reviewed their work in children and youngsters in Mexico City and reported neuropathological changes in children and young adults similar to those in Alzheimer's disease. There was increased neuro-inflammation and vascular damage: upregulated mRNA cyclooxygenase-2, interleukin-1β and CD14, and clusters of mononuclear cells around blood vessels and activated microglia in the frontal and temporal cortex, subiculum and brain stem. They also found deposits of amyloid-β42, α-synuclein , hyperphosphorylated tau , and evidence of oxidative stress, neuronal damage and death. Children in Mexico City (with high levels of air pollution) also had low serum BDNF concentrations. [ 64 ]
Studies of white matter volume found associations between exposure to air pollution and reduced white matter volume. [ 64 ] Evidence suggests that long-term exposure to air pollutants is associated with cognitive decline and with the risk of development of dementia. [ 64 ] There is epidemiological evidence suggestive of a causal association between exposure to a range of air pollutants and a number of effects on the nervous system including the acceleration of cognitive decline and the induction of dementia. [ 64 ]
Dementia is an umbrella term for a range of conditions that affect how the brain works, reducing the ability to remember, think and reason. It mainly affects older people and gets worse over time. Health and lifestyle factors such as high blood pressure and smoking are known to increase the risk of developing dementia. [ 65 ]
The Committee on the Medical Effects of Air Pollutants (COMEAP) in UK have reviewed nearly 70 studies in human populations (epidemiological studies) and think it is likely that air pollution can contribute to a decline in mental ability and dementia in older people. It is known that air pollution, particularly small particle pollution, can affect the heart and the circulatory system, including circulation to the brain. These effects are linked to vascular dementia (a form of dementia), which is caused by damage to the blood vessels in the brain. [ 65 ] Therefore, it is likely that air pollution contributes to mental decline and dementia caused by effects on the blood vessels.
Air pollution might also stimulate the immune cells in the brain, which can then damage nerve cells. [ 65 ]
In 2022, COMEAP has concluded that the evidence is suggestive of an association between ambient air pollutants and an acceleration of the decline in cognitive function often associated with ageing, and with the risk of developing dementia. [ 65 ] There are a number of plausible biological mechanisms by which air pollutants could cause effects on the brain leading to accelerated cognitive decline and dementia. Some of these have been demonstrated in experimental studies. There is a strong case for the effects of air pollutants on the cardiovascular system having a secondary effect on the brain. COMEAP has already concluded that long-term exposure to air pollutants damages the cardiovascular system (COMEAP 2006, 2018). It is likely that such effects have an effect on the blood supply to the brain . That such an effect might well lead to damage to the brain seems likely. Therefore it is regarded that the association between exposure to air pollutants and effects on cognitive decline and dementia as likely to be causal with respect to this mechanism. [ 65 ]
A number of mechanisms have been suggested by which air pollutants could have direct effects on the brain. These include the translocation of small particles from the lung to the blood stream and thence to the brain. The evidence suggests that a small proportion of very small particles that are inhaled can enter the brain, both from the blood and via the olfactory nerves leading from the nasal passages to the olfactory bulbs . [ 65 ] What is much less clear is whether exposure to ambient concentrations of particulate material results in sufficient translocation to produce damage to the brain. Study of the literature has suggested that particles which enter the brain are cleared from the brain only slowly, if at all. This is clearly a point in favour of the suggestion that particulate material which does enter the brain might produce detrimental effects. [ 65 ] Animal and in vitro studies of ultrafine particulate material, diesel engine exhaust or ozone have all shown effects on the brain or brain cells. The mechanisms involved include the generation and release of free radicals within the brain and the induction of an inflammatory response ; these 2 mechanisms seem likely to be linked. A number of common pollutants may affect brain function. [ 65 ]
COMEAP concluded that:
Exposure to air pollution may be associated with elevated risk of schizophrenia . [ 14 ]
Multiple air pollutants are probably associated with the risk of epilepsy , [ 66 ] e.g., carbon monoxide , ozone , sulfur dioxide , nitrogen dioxide , large particulate matter, and fine particulate matter . It was hypothesized that air pollutants increase epilepsy risk by increasing inflammatory mediators, and by providing a source of oxidative stress , eventually altering the blood–brain barrier 's function and cause brain inflammation . Brain inflammation is known to be a risk factor for epilepsy; thus, the sequence of events provides a plausible mechanism by which pollution may increase epilepsy risk in individuals who are genetically vulnerable to the disease. [ 66 ] [ medical citation needed ]
Dementia is a pressing public health challenge. Its prevalence is strongly age-related: doubling every 5–6 years over the age of 65 years. The number of people living with dementia worldwide is estimated at 50 million and expected to reach 152 million by 2050. Its current economic cost worldwide is US$818 billion/year (as of 2015) and it will rise in proportion to the numbers affected (WHO, 2019). [ 64 ]
For point-source pollution:
Do not produce the pollutants.
If produced, remove at source as soon as possible.
If not removed at source, use barriers.
If barriers do not work well or not installed properly (i.e., pollutants escaped), neighbours need filtration, sealing, and/or proper ventilation / pollutant dilution, etc. for their premises. Large scale air cleaning system may also help as a passive measure. Clean-up programmes may be needed to prevent further secondary contamination or pollution.
At individual level, exposure reduction of air pollutants maybe achieved by better choice of places that one stays, prevention of cross-contamination or secondary contamination (between persons and/or their personal belongings/environment), better personal hygiene, use of face masks and air purifiers, etc.
Priority areas in “Education and Awareness included: (8) making this unrecognised public health issue known; (9) developing educational products; (10) attaching air pollution and brain health to existing strategies and campaigns; and (11) providing publicly available monitoring, assessment and screening tools...” [ 67 ]
NIEHS -funded studies have found taking prenatal vitamins may help lower autism risk. Taking vitamins and supplements might provide protective effects for those exposed to certain environmental contaminants during pregnancy. [ 48 ] Women were less likely to have a child with autism if they took a daily prenatal vitamin during the three months before and first month of pregnancy, compared to women not taking vitamins. This finding was more evident in women and children with genetic variants that made them more susceptible to developing autism. [ 48 ]
Folic acid is a source of the protective effects of prenatal vitamins. Women who took the daily recommended dosage during the first month of pregnancy had a reduced risk of having a child with autism. [ 48 ] Folic acid intake during early pregnancy may reduce the risk of having a child with autism for those women with high exposure to air pollution, and pesticides. [ 48 ]
Pregnant mothers who used multivitamins , with or without additional iron or folic acid, were less likely to have a child with autism and intellectual disability . [ 48 ] Maternal prenatal vitamin intake during the first month of pregnancy may also reduce ASD recurrence in siblings of children with ASD in high-risk families. [ 48 ]
Pollutants
Sources
Others
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Brain implants , often referred to as neural implants , are technological devices that connect directly to a biological subject's brain – usually placed on the surface of the brain, or attached to the brain 's cortex . A common purpose of modern brain implants and the focus of much current research is establishing a biomedical prosthesis circumventing areas in the brain that have become dysfunctional after a stroke or other head injuries . [ 1 ] This includes sensory substitution , e.g., in vision . Other brain implants are used in animal experiments simply to record brain activity for scientific reasons. Some brain implants involve creating interfaces between neural systems and computer chips . This work is part of a wider research field called brain–computer interfaces . (Brain–computer interface research also includes technology such as EEG arrays that allow interface between mind and machine but do not require direct implantation of a device.)
Neural implants such as deep brain stimulation and vagus nerve stimulation are increasingly becoming routine for patients with Parkinson's disease and clinical depression , respectively.
Brain implants electrically stimulate, block [ 2 ] or record [ 3 ] (or both record and stimulate simultaneously [ 4 ] ) signals from single neurons or groups of neurons ( biological neural networks ) in the brain. This can only be done where the functional associations of these neurons are approximately known. Because of the complexity of neural processing and the lack of access to action potential related signals using neuroimaging techniques, the application of brain implants has been seriously limited until recent advances in neurophysiology and computer processing power. Much research is also being done on the surface chemistry of neural implants in effort to design products which minimize all negative effects that an active implant can have on the brain, and that the body can have on the function of the implant. Researchers are also exploring a range of delivery systems, such as using veins, to deliver these implants without brain surgery; by leaving the skull sealed shut, patients could receive their neural implants without running as great a risk of seizures, strokes, or permanent neural impairments, all of which can be caused by open-brain surgery. [ 5 ]
Research in sensory substitution has made significant progress since 1970. Especially in vision, due to the knowledge of the working of the visual system , eye implants (often involving some brain implants or monitoring) have been applied with demonstrated success. For hearing , cochlear implants are used to stimulate the auditory nerve directly. The vestibulocochlear nerve is part of the peripheral nervous system , but the interface is similar to that of true brain implants.
Multiple projects have demonstrated success at recording from the brains of animals for long periods of time. As early as 1976, researchers at the NIH led by Edward Schmidt made action potential recordings of signals from rhesus monkey motor cortexes using immovable "hatpin" electrodes, [ 6 ] including recording from single neurons for over 30 days, and consistent recordings for greater than three years from the best electrodes.
The "hatpin" electrodes were made of pure iridium and insulated with parylene , materials that are currently used in the cyberkinetics implementation of the Utah array. [ 7 ] These same electrodes, or derivations thereof using the same biocompatible electrode materials, are currently used in visual prosthetics laboratories, [ 8 ] laboratories studying the neural basis of learning, [ 9 ] and motor prosthetics approaches other than the cyberkinetics probes. [ 10 ]
Other laboratory groups produce their own implants to provide unique capabilities not available from the commercial products. [ 11 ] [ 12 ] [ 13 ] [ 14 ]
Breakthroughs include: studies of the process of functional brain re-wiring throughout the learning of a sensory discrimination, [ 15 ] control of physical devices by rat brains, [ 16 ] monkeys over robotic arms, [ 17 ] remote control of mechanical devices by monkeys and humans, [ 18 ] remote control over the movements of roaches , [ 19 ] the first reported use of the Utah Array in a human for bidirectional signaling. [ 20 ] Currently a number of groups are conducting preliminary motor prosthetic implants in humans. These studies are presently limited to several months by the longevity of the implants. The array now forms the sensor component of the Braingate .
Much research is also being done on the surface chemistry of neural implants in effort to design products which minimize all negative effects that an active implant can have on the brain, and that the body can have on the function of the implant.
Another type of neural implant that is being experimented on is prosthetic neuronal memory silicon chips , which imitate the signal processing done by functioning neurons that allows peoples' brains to create long-term memories.
For implants, potentially including brain implants, all-organic devices could be advantageous because they could be biocompatible . [ 21 ] If organic neuromorphic devices reach that point, "implants could allow humans to control powered exoskeletons" for example. [ 21 ] Genetically modified neurons may enable connecting external components – such as prosthetic limbs – to nerves. [ 22 ] There also is research of potentially implantable [ 23 ] physical artificial neurons .
There is research of potential implants for drug delivery to the brain . [ 24 ] [ 25 ]
In 2016, scientists at the University of Illinois at Urbana–Champaign announced development of tiny brain sensors for use postoperative monitoring, which melt away when they are no longer needed. [ 26 ]
In 2020, scientists out of the University of Melbourne , who formed the company Synchron in 2016, published clinical data related to a discovery for Stentrode , a device implanted via the jugular vein , without the need for open brain surgery. The technology was shown to enable two patients to control a computer using thought alone. It may ultimately help diagnose and treat a range of brain pathologies, such as epilepsy and Parkinson's disease . [ 27 ] In 2023, researchers reported no serious adverse events during the first year in all four patients who used the device to operate a computer. [ 28 ] [ 29 ]
DARPA has announced its interest in developing "cyborg insects" to transmit data from sensors implanted into the insect during the pupal stage. The insect's motion would be controlled from a Micro-Electro-Mechanical System (MEMS) and could conceivably survey an environment or detect explosives and gas. [ 30 ] Similarly, DARPA is developing a neural implant to remotely control the movement of sharks . The shark's unique senses would then be exploited to provide data feedback in relation to enemy ship movement or underwater explosives. [ 31 ]
In 2006, researchers at Cornell University invented [ 32 ] a new surgical procedure to implant artificial structures into insects during their metamorphic development. [ 33 ] [ 34 ] The first insect cyborgs, moths with integrated electronics in their thorax , were demonstrated by the same researchers. [ 35 ] [ 36 ] The initial success of the techniques has resulted in increased research and the creation of a program called Hybrid-Insect-MEMS, HI-MEMS. Its goal, according to DARPA 's Microsystems Technology Office , is to develop "tightly coupled machine-insect interfaces by placing micro-mechanical systems inside the insects during the early stages of metamorphosis". [ 37 ]
The use of neural implants has recently been attempted, with success, on cockroaches. Surgically applied electrodes were put on the insect, which were remotely controlled by a human. The results, although sometimes different, basically showed that the cockroach could be controlled by the impulses it received through the electrodes. DARPA is now funding this research because of its obvious beneficial applications to the military and other areas [ 38 ]
In 2009 at the Institute of Electrical and Electronics Engineers (IEEE) Micro-electronic mechanical systems (MEMS) conference in Italy , researchers demonstrated the first "wireless" flying-beetle cyborg. [ 39 ] Engineers at the University of California at Berkeley pioneered the design of a " remote controlled beetle ", funded by the DARPA HI-MEMS Program. [ 40 ] This was followed later that year by the demonstration of wireless control of a "lift-assisted" moth-cyborg. [ 41 ]
Eventually researchers plan to develop HI-MEMS for dragonflies, bees, rats and pigeons. [ 42 ] [ 43 ] For the HI-MEMS cybernetic bug to be considered a success, it must fly 100 metres (330 ft) from a starting point, guided via computer into a controlled landing within 5 metres (16 ft) of a specific end point. Once landed, the cybernetic bug must remain in place. [ 42 ]
In 2012, DARPA provided seed funding [ 44 ] to Dr. Thomas Oxley , a neurointerventionist at Mount Sinai Hospital in New York City, for a technology that became known as Stentrode. Oxley's group in Australia was the only non-US-based funded by DARPA as part of the Reliable Neural Interface Technology (RE-NET) program. [ 45 ] This technology is the first to attempt to provide neural implants through a minimally invasive surgical procedure that does not require cutting into the skull. That is, an electrode array built onto a self-expanding stent, implanted into the brain via cerebral angiography. This pathway can provide safe, easy access and capture a strong signal for a number of indications beyond addressing paralysis, and is currently in clinical trials [ 46 ] in patients with severe paralysis seeking to regain the ability to communicate.
In 2015 it was reported that scientists from the Perception and Recognition Neuro-technologies Laboratory at the Southern Federal University in Rostov-on-Don suggested using rats with microchips planted in their brains to detect explosive devices. [ 47 ] [ 48 ] [ 49 ]
In 2016 it was reported that American engineers are developing a system that would transform locusts into "remote controlled explosive detectors" with electrodes in their brains beaming information about dangerous substances back to their operators. [ 50 ]
Neurostimulators have been in use since 1997 to ease the symptoms of such diseases as epilepsy , Parkinson's disease , dystonia and recently depression . Rapid advancements in neurostimulation technologies are providing relief to an unprecedented number of patients affected by debilitating neurologic and psychiatric disorders. Neurostimulation therapies include invasive and noninvasive approaches that involve the application of electrical stimulation to drive neural function within a circuit.
Brain implants are also being explored by DARPA as part of the Reliable Neural-Interface Technology (RE-NET) program launched in 2010 to directly address the need for high-performance neural interfaces to control the dexterous functions made possible by DARPA's advanced prosthetic limbs. The goal is to provide high-bandwidth, intuitive control interface for these limbs.
Individuals and companies exploring brain–computer interface include: Elon Musk , Bill Gates , Mark Zuckerberg , Jeff Bezos , Neuralink, CTRL Labs, and Synchron.
Current brain implants are made from a variety of materials such as tungsten , silicon , platinum - iridium , or even stainless steel . Future brain implants may make use of more exotic materials such as nanoscale carbon fibers ( nanotubes ), and polycarbonate urethane . Nearly all implants require open brain surgery, but, in 2019, a company called Synchron was able to successfully implant a brain–computer interface via the blood vessels.
There have been a number of advances in technological spinal cord injury treatment, including the use of implants that provided a “digital bridge” between the brain and the spinal cord. In a study published in May 2023 in the journal Nature , researchers in Switzerland described such implants which allowed a 40-year-old man, paralyzed from the hips down for 12 years, to stand, walk and ascend a steep ramp with only the assistance of a walker. More than a year after the implant was inserted, he has retained these abilities and could walk with crutches even when the implant was switched off. [ 51 ] It turns out that walking with the implant has encouraged the recovery of neurological function beyond what prior traditional rehabilitation had done. [ 52 ]
In 1870, Eduard Hitzig and Gustav Fritsch demonstrated that electrical stimulation of the brains of dogs could produce movements. Robert Bartholow showed the same to be true for humans in 1874. By the start of the 20th century, Fedor Krause began to systematically map human brain areas, using patients that had undergone brain surgery .
Prominent research was conducted in the 1950s. Robert G. Heath experimented with mental patients, aiming to influence his subjects' moods through electrical stimulation. [ 53 ]
Yale University physiologist Jose Delgado demonstrated limited control of animal and human subjects' behaviours using electronic stimulation. He invented the stimoceiver or transdermal stimulator , a device implanted in the brain to transmit electrical impulses that modify basic behaviours such as aggression or sensations of pleasure.
Delgado was later to write a popular book on mind control, called Physical Control of the Mind , where he stated: "the feasibility of remote control of activities in several species of animals has been demonstrated [...] The ultimate objective of this research is to provide an understanding of the mechanisms involved in the directional control of animals and to provide practical systems suitable for human application."
In the 1950s, the CIA also funded research into mind control techniques, through programs such as MKULTRA . Perhaps because he received funding for some research through the US Office of Naval Research , it has been suggested (but not proven) that Delgado also received backing through the CIA. He denied this claim in a 2005 article in Scientific American describing it only as a speculation by conspiracy-theorists. He stated that his research was only progressively scientifically motivated to understand how the brain works.
Current research is focused on enabling paralyzed patients to move external devices through thought as well as facilitating thought-to-text capability in this population.
In 2012, a landmark study in Nature, led by pioneer Leigh Hochberg , MD, PhD, demonstrated that two people with tetraplegia were able to control robotic arms through thought when connected to the BrainGate neural interface system. [ 54 ] The two participants were able to reach for and grasp objects in three-dimensional space, and one participant used the system to serve herself coffee for the first time since becoming paralyzed nearly 15 years prior.
In October 2020, two patients were able to wirelessly control a Surface Book 2 running Windows 10 to text, email, shop and bank using direct thought through the Stentrode brain computer interface. [ 55 ] This was the first time a brain–computer interface was implanted via the patient's blood vessels, eliminating the need for open-brain surgery.
Ethical questions raised include who are good candidates to receive neural implants and what are good and bad uses of neural implants.
Whilst deep brain stimulation is increasingly becoming routine for patients with Parkinson's disease, there may be some behavioural side effects. Reports in the literature describe the possibility of apathy, hallucinations, compulsive gambling, hypersexuality, cognitive dysfunction, and depression. However, these may be temporary and related to correct placement and calibration of the stimulator and so are potentially reversible. [ 56 ]
Some transhumanists , such as Ray Kurzweil and Kevin Warwick , see brain implants as part of the next step for humans in progress and evolution , whereas others, especially bioconservatives , view them as unnatural , with humankind losing essential human qualities. It raises controversy similar to other forms of human enhancement . For instance, it is argued that implants would technically change people into cybernetic organisms ( cyborgs ). It is also expected that all research will comply with the Declaration of Helsinki . Yet further, the usual legal duties apply such as information to the person wearing implants and that the implants are voluntary, with (very) few exceptions.
Other concerns involve vulnerabilities of neural implants to cybercrime or intrusive surveillance as neural implants could be hacked, misused, or misdesigned. [ 57 ]
Sadja states that "one's private thoughts are important to protect" and does not consider it a good idea to just charge the government or any company with protecting them. Walter Glannon, a neuroethicist of the University of Calgary notes that "there is a risk of the microchips being hacked by third parties" and that "this could interfere with the user's intention to perform actions, violate privacy by extracting information from the chip". [ 58 ]
Brain implants are now part of modern culture but there were early philosophical references of relevance as far back as René Descartes .
In his 1641 Meditations , Descartes argued that it would be impossible to tell if all one's apparently real experiences were in fact being produced by an evil demon intent on deception. A modern twist on Descartes' argument is provided by the " brain in a vat " thought experiment, which imagines a brain, sustained apart from its body in a vat of nutrients, and hooked up to a computer which is capable of stimulating it in such a way as to produce the illusion that everything is normal. [ 59 ]
Popular science fiction discussing brain implants and mind control became widespread in the 20th century, often with a dystopian outlook. Literature in the 1970s delved into the topic, including The Terminal Man by Michael Crichton , where a man with brain damage receives an experimental surgical brain implant designed to prevent seizures, which he abuses by triggering for pleasure. Another example is Larry Niven 's science fiction writing of wire-heads in his " Known Space " stories.
A somewhat more positive view of brain implants used to communicate with a computer as a form of augmented intelligence is seen in Algis Budrys 1976 novel Michaelmas .
Fear that the technology will be misused by the government and military is an early theme. In the 1981 BBC serial The Nightmare Man the pilot of a high-tech mini submarine is linked to his craft via a brain implant but becomes a savage killer after ripping out the implant.
Perhaps the most influential novel exploring the world of brain implants was William Gibson 's 1984 novel Neuromancer . This was the first novel in a genre that came to be known as " cyberpunk ". It follows a computer hacker through a world where mercenaries are augmented with brain implants to enhance strength, vision, memory, etc. Gibson coins the term "matrix" and introduces the concept of "jacking in" with head electrodes or direct implants. He also explores possible entertainment applications of brain implants such as the "simstim" (simulated stimulation) which is a device used to record and playback experiences.
Gibson's work led to an explosion in popular culture references to brain implants. Its influences are felt, for example, in the 1989 roleplaying game Shadowrun , which borrowed his term "datajack" to describe a brain–computer interface. The implants in Gibson's novels and short stories formed the template for the 1995 film Johnny Mnemonic and later, The Matrix Trilogy .
Pulp fiction with implants or brain implants include the novel series Typers , film Spider-Man 2 , the TV series Earth: Final Conflict , and numerous computer/video games.
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Brain injury ( BI ) is the destruction or degeneration of brain cells . Brain injuries occur due to a wide range of internal and external factors. In general, brain damage refers to significant, undiscriminating trauma-induced damage.
A common category with the greatest number of injuries is traumatic brain injury (TBI) following physical trauma or head injury from an outside source, and the term acquired brain injury (ABI) is used in appropriate circles to differentiate brain injuries occurring after birth from injury, from a genetic disorder (GBI), or from a congenital disorder (CBI). [ 1 ] Primary and secondary brain injuries identify the processes involved, while focal and diffuse brain injury describe the severity and localization. [ citation needed ]
Impaired function of affected areas can be compensated through neuroplasticity by forming new neural connections.
Symptoms of brain injuries vary based on the severity of the injury or how much of the brain is affected. The four categories used for classifying the severity of brain injuries are mild, moderate, or severe. [ 2 ]
Symptoms of a mild brain injury include headaches , confusions , tinnitus , fatigue , changes in sleep patterns , mood or behavior . Other symptoms include trouble with memory , concentration , attention or thinking . [ 3 ] Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident.
Cognitive symptoms include confusion, aggressiveness, abnormal behavior, slurred speech , and coma or other disorders of consciousness . Physical symptoms include headaches that worsen or do not go away, vomiting or nausea, convulsions , brain pulsation, abnormal dilation of the eyes , inability to awaken from sleep, weakness in extremities, and loss of coordination . [ 3 ]
Symptoms observed in children include changes in eating habits, persistent irritability or sadness, changes in attention, or disrupted sleeping habits. [ 3 ]
Symptoms of brain injuries can also be influenced by the location of the injury and as a result impairments are specific to the part of the brain affected. Lesion size is correlated with severity, recovery, and comprehension. [ 4 ] Brain injuries often create impairment or disability that can vary greatly in severity.
In cases of severe brain injuries, the likelihood of areas with permanent disability is great, including neurocognitive deficits , delusions (often, to be specific, monothematic delusions ), speech or movement problems, and intellectual disability . There may also be personality changes. The most severe cases result in coma or even persistent vegetative state . Even a mild incident can have long-term effects or cause symptoms to appear years later. [ 5 ]
Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomia , unknowingly making up words ( neologisms ), and problems with comprehension. The symptoms of Wernicke's aphasia are caused by damage to the posterior section of the superior temporal gyrus . [ 6 ] [ 7 ]
Damage to the Broca's area typically produces symptoms like omitting functional words ( agrammatism ), sound production changes, dyslexia , dysgraphia , and problems with comprehension and production. Broca's aphasia is indicative of damage to the posterior inferior frontal gyrus of the brain. [ 8 ]
An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired, however. For example, in pure alexia , the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca's area and Wernicke's area). However, this does not mean one with pure alexia is incapable of comprehending speech—merely that there is no connection between their working visual cortex and language areas—as is demonstrated by the fact that people with pure alexia can still write, speak, and even transcribe letters without understanding their meaning. [ 9 ]
Lesions to the fusiform gyrus often result in prosopagnosia , the inability to distinguish faces and other complex objects from each other. [ 10 ] Lesions in the amygdala would eliminate the enhanced activation seen in occipital and fusiform visual areas in response to fear with the area intact. Amygdala lesions change the functional pattern of activation to emotional stimuli in regions that are distant from the amygdala. [ 11 ]
Other lesions to the visual cortex have different effects depending on the location of the damage. Lesions to V1 , for example, can cause blindsight in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure . [ 12 ] Lesions to V4 can cause color-blindness , [ 13 ] and bilateral lesions to MT/V5 can cause the loss of the ability to perceive motion. Lesions to the parietal lobes may result in agnosia , an inability to recognize complex objects, smells, or shapes, or amorphosynthesis , a loss of perception on the opposite side of the body. [ 14 ]
Brain injuries have far-reaching and varied consequences due to the nature of the brain as the main source of bodily control. Brain-injured people commonly experience issues with memory. [ 15 ] This can be issues with either long or short-term memories depending on the location and severity of the injury. Sometimes memory can be improved through rehabilitation, although it can be permanent. Behavioral and personality changes are also commonly observed due to changes of the brain structure in areas controlling hormones or major emotions.
Headaches and pain can occur as a result of a brain injury, either directly from the damage or due to neurological conditions stemming from the injury. Due to the changes in the brain as well as the issues associated with the change in physical and mental capacity, depression and low self-esteem are common side effects that can be treated with psychological help. Antidepressants must be used with caution in brain injury people due to the potential for undesired effects because of the already altered brain chemistry.
There are multiple responses of the body to brain injury, occurring at different times after the initial occurrence of damage, as the functions of the neurons , nerve tracts, or sections of the brain can be affected by damage. The immediate response can take many forms. Initially, there may be symptoms such as swelling, pain, bruising, or loss of consciousness. [ 16 ] Post-traumatic amnesia is also common with brain damage, as is temporary aphasia , or impairment of language. [ 17 ]
As time progresses, and the severity of injury becomes clear, there are further responses that may become apparent. Due to loss of blood flow or damaged tissue, sustained during the injury, amnesia and aphasia may become permanent, and apraxia has been documented in patients. Amnesia is a condition in which a person is unable to remember things. [ 18 ] Aphasia is the loss or impairment of word comprehension or use. Apraxia is a motor disorder caused by damage to the brain, and may be more common in those who have been left brain damaged, with loss of mechanical knowledge critical. [ 19 ] Headaches, occasional dizziness, and fatigue—all temporary symptoms of brain trauma—may become permanent, or may not disappear for a long time.
There are documented cases of lasting psychological effects as well, such as emotional changes often caused by damage to the various parts of the brain that control human emotions and behavior. [ 20 ] Individuals who have experienced emotional changes related to brain damage may have emotions that come very quickly and are very intense, but have very little lasting effect. [ 20 ] Emotional changes may not be triggered by a specific event, and can be a cause of stress to the injured party and their family and friends. [ 21 ] Often, counseling is suggested for those who experience this effect after their injury, and may be available as an individual or group session.
The long term psychological and physiological effects will vary by person and injury. For example, perinatal brain damage has been implicated in cases of neurodevelopmental impairments and psychiatric illnesses. [ citation needed ]
Brain injuries can result from a number of conditions, including: [ 22 ]
Chemotherapy can cause brain damage to the neural stem cells and oligodendrocyte cells that produce myelin . Radiation and chemotherapy can lead to brain tissue damage by disrupting or stopping blood flow to the affected areas of the brain. This damage can cause long term effects such as but not limited to; memory loss, confusion, and loss of cognitive function . The brain damage caused by radiation depends on where the brain tumor is located, the amount of radiation used, and the duration of the treatment. Radiosurgery can also lead to tissue damage that results in about 1 in 20 patients requiring a second operation to remove the damaged tissue. [ 28 ] [ 29 ]
Wernicke–Korsakoff syndrome can cause brain damage and results from a Vitamin B deficiency (specifically vitamin B1, thiamine ). [ 30 ] [ 31 ] This syndrome presents with two conditions, Wernicke's encephalopathy and Korsakoff psychosis . Typically Wernicke's encephalopathy precedes symptoms of Korsakoff psychosis. Wernicke's encephalopathy results from focal accumulation of lactic acid , causing problems with vision, coordination, and balance. [ 30 ]
Korsakoff psychosis typically follows after the symptoms of Wernicke's decrease. [ 30 ] [ 31 ] Wernicke-Korsakoff syndrome is typically caused by conditions causing thiamine deficiency, such as chronic heavy alcohol use or by conditions that affect nutritional absorption, including colon cancer, eating disorders and gastric bypass. [ 30 ]
Brain lesions are sometimes intentionally inflicted during neurosurgery , such as the carefully placed brain lesion used to treat epilepsy and other brain disorders. These lesions are induced by excision or by electric shocks (electrolytic lesions) to the exposed brain or commonly by infusion of excitotoxins to specific areas. [ medical citation needed ]
Diffuse axonal injury is caused by shearing forces on the brain leading to lesions in the white matter tracts of the brain. [ 32 ] These shearing forces are seen in cases where the brain had a sharp rotational acceleration, and is caused by the difference in density between white matter and grey matter. [ 33 ]
Unlike some of the more obvious responses to brain damage, the body also has invisible physical responses which can be difficult to notice. These will generally be identified by a healthcare provider, especially as they are normal physical responses to brain damage. Cytokines are known to be induced in response to brain injury. [ 34 ] These have diverse actions that can cause, exacerbate, mediate and/or inhibit cellular injury and repair. TGFβ seems to exert primarily neuroprotective actions, whereas TNFα might contribute to neuronal injury and exert protective effects. IL-1 mediates ischaemic, excitotoxic, and traumatic brain injury , probably through multiple actions on glia, neurons, and the vasculature. Cytokines may be useful in order to discover novel therapeutic strategies. At the current time, they are already in clinical trials. [ 35 ]
Glasgow Coma Scale (GCS) is the most widely used scoring system used to assess the level of severity of a brain injury. This method is based on the objective observations of specific traits to determine the severity of a brain injury. It is based on three traits: eye opening, verbal response, and motor response, gauged as described below. [ 36 ] Based on the Glasgow Coma Scale severity is classified as follows, severe brain injuries score 3–8, moderate brain injuries score 9–12 and mild score 13–15. [ 36 ]
There are several imaging techniques that can aid in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) magnetic resonance spectroscopy (MRS), positron emission tomography (PET), and single-photon emission tomography (SPECT) . CT scans and MRI are the two techniques widely used and are most effective. CT scans can show brain bleeds, fractures of the skull, fluid build up in the brain that will lead to increased cranial pressure. [ 37 ]
MRI is able to better to detect smaller injuries, detect damage within the brain, diffuse axonal injury, injuries to the brainstem, posterior fossa, and subtemporal and subfrontal regions. However, patients with pacemakers, metallic implants, or other metal within their bodies are unable to have an MRI done. Typically the other imaging techniques are not used in a clinical setting because of the cost, lack of availability. [ 38 ]
The treatment for emergency traumatic brain injuries focuses on assuring the person has enough oxygen from the brain's blood supply, and on maintaining normal blood pressure to avoid further injuries of the head or neck. The person may need surgery to remove clotted blood or repair skull fractures, for which cutting a hole in the skull may be necessary. Medicines used for traumatic injuries are diuretics , anti-seizure or coma -inducing drugs. Diuretics reduce the fluid in tissues lowering the pressure on the brain. In the first week after a traumatic brain injury, a person may have a risk of seizures, which anti-seizure drugs help prevent. Coma-inducing drugs may be used during surgery to reduce impairments and restore blood flow. Mouse NGF has been licensed in China since 2003 and is used to promote neurological recovery in a range of brain injuries, including intracerebral hemorrhage. [ 39 ]
In the case of brain damage from traumatic brain injury , dexamethasone and/or Mannitol may be used. [ 40 ]
Various professions may be involved in the medical care and rehabilitation of someone with an impairment after a brain injury. Neurologists , neurosurgeons , and physiatrists are physicians specialising in treating brain injury. Neuropsychologists (especially clinical neuropsychologists ) are psychologists specialising in understanding the effects of brain injury and may be involved in assessing the severity or creating rehabilitation strategies. Occupational therapists may be involved in running rehabilitation programs to help restore lost function or help re-learn essential skills. Registered nurses , such as those working in hospital intensive care units , are able to maintain the health of the severely brain-injured with constant administration of medication and neurological monitoring, including the use of the Glasgow Coma Scale used by other health professionals to quantify extent of orientation. [ 41 ]
Physiotherapists also play a significant role in rehabilitation after a brain injury. In the case of a traumatic brain injury (TBI), physiotherapy treatment during the post-acute phase may include sensory stimulation, serial casting and splinting, fitness and aerobic training, and functional training. [ 42 ] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention. [ 43 ] Serial casting and splinting are often used to reduce soft tissue contractures and muscle tone. Evidence based research reveals that serial casting can be used to increase passive range of motion (PROM) and decrease spasticity . [ 43 ]
Functional training may also be used to treat patients with TBIs. To date, no studies supports the efficacy of sit to stand training, arm ability training and body weight support systems (BWS). [ 44 ] [ 45 ] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills. [ 46 ] More research is required to better understand the efficacy of the treatments mentioned above. [ 47 ]
Other treatments for brain injury can include medication , psychotherapy , neuropsychological rehabilitation , neurotherapy and/or surgery . [ 48 ]
Prognosis, or the likely progress of a disorder, depends on the nature, location, and cause of the brain damage (see Traumatic brain injury , Focal and diffuse brain injury , Primary and secondary brain injury ).
In general, neuroregeneration can occur in the peripheral nervous system but is much rarer and more difficult to assist in the central nervous system (brain or spinal cord). However, in neural development in humans , areas of the brain can learn to compensate for other damaged areas, and may increase in size and complexity and even change function, just as someone who loses a sense may gain increased acuity in another sense—a process termed neuroplasticity . [ 49 ]
There are many misconceptions that revolve around brain injuries and brain damage. One misconception is that if someone has brain damage then they cannot fully recover. Recovery depends a variety of factors; such as severity and location. Testing is done to note severity and location. Not everyone fully heals from brain damage, but it is possible to have a full recovery. Brain injuries are very hard to predict in outcome. Many tests and specialists are needed to determine the likelihood of the prognosis. People with minor brain damage can have debilitating side effects; not just severe brain damage has debilitating effects. [ 50 ]
The side-effects of a brain injury depend on location and the body's response to injury. [ 50 ] Even a mild concussion can have long term effects that may not resolve. [ 51 ] Another misconception is that children heal better from brain damage. Children are at greater risk for injury due to lack of maturity. It makes future development hard to predict. [ 51 ] [ dead link ] This is because different cortical areas mature at different stages, with some major cell populations and their corresponding cognitive faculties remaining unrefined until early adulthood. In the case of a child with frontal brain injury, for example, the impact of the damage may be undetectable until that child fails to develop normal executive functions in his or her late teens and early twenties. [ 52 ]
The foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case studies by Paul Broca. The first case study on Phineas Gage's head injury is one of the most astonishing brain injuries in history. In 1848, Phineas Gage was paving way for a new railroad line when he encountered an accidental explosion of a tamping iron straight through his frontal lobe. Gage observed to be intellectually unaffected but was claimed by some to have exemplified post-injury behavioral deficits. [ 53 ] [ failed verification ]
Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca's first patient lacked productive speech. He saw this as an opportunity to address language localization. It was not until Leborgne, informally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left cerebral hemisphere. The affected area is known today as Broca's area and the condition as Broca's aphasia . [ 54 ]
A few years later, a German neuroscientist, Carl Wernicke , consulted on a stroke patient. The patient experienced neither speech nor hearing impairments, but had a few brain deficits. These deficits included lacking the ability to comprehend what was spoken to him and the words written down. After his death, Wernicke examined his autopsy that found a lesion located in the left temporal region. This area became known as Wernicke's area . Wernicke later hypothesized the relationship between Wernicke's area and Broca's area, which was proven fact. [ 55 ]
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3N56 , 1YK1
4879
18158
ENSG00000120937
ENSMUSG00000029019
P16860
P40753
NM_002521
NM_001287348 NM_008726
NP_002512 NP_002512
NP_001274277 NP_032752
Brain natriuretic peptide ( BNP ), also known as B-type natriuretic peptide , is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. [ 5 ] BNP is one of the three natriuretic peptides, in addition to atrial natriuretic peptide ( ANP ) and C-type natriuretic peptide ( CNP ). [ 6 ] BNP was first discovered in porcine brain tissue in 1988, which led to its initial naming as "brain natriuretic peptide", although subsequent research revealed that BNP is primarily produced and secreted by the ventricular myocardium (heart muscle) in response to increased ventricular blood volume and stretching. To reflect its true source, BNP is now often referred to as "B-type natriuretic peptide" while retaining the same acronym. [ 7 ]
The 32-amino acid polypeptide BNP-32 is secreted attached to a 76–amino acid N-terminal fragment in the prohormone called NT-proBNP (BNPT), which is biologically inactive. Once released, BNP binds to and activates the atrial natriuretic factor receptor NPRA , and to a lesser extent NPRB , in a fashion similar to atrial natriuretic peptide (ANP) but with 10-fold lower affinity. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better targets than ANP for diagnostic blood testing.
The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis . The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. [ 8 ]
BNP is synthesized as a 134-amino acid preprohormone (preproBNP), encoded by the human gene NPPB. Removal of the 26-residue N-terminal signal peptide generates the prohormone, proBNP, which is stored intracellularly as an O-linked glycoprotein ; proBNP is subsequently cleaved between arginine-102 and serine-103 by a specific convertase (probably furin or corin ) into NT-proBNP and the biologically active 32-amino acid polypeptide BNP-32, which are secreted into the blood in equimolar amounts. [ 9 ] [ 10 ] Cleavage at other sites produces shorter BNP peptides with unknown biological activity. [ 11 ] Processing of proBNP may be regulated by O-glycosylation of residues near the cleavage sites. [ 12 ] The synthesis of BNP in cardiomyocytes is stimulated by pro-inflammatory cell factors, such as interleukin-1β, interleukin-6 and tumor necrosis factor-α. [ 13 ]
BNP decreases sodium reabsorption in the distal convoluted tubule (interaction with NCC ) [ 14 ] and cortical collecting duct of the nephron via guanosine 3',5'-cyclic monophosphate ( cGMP ) dependent phosphorylation of ENaC .
BNP and NT-proBNP are measured by immunoassay . [ 15 ]
A preoperative BNP can be predictive of a risk of an acute cardiac event during vascular surgery. A cutoff of 100 pg/ml has a sensitivity of approximately 100%, a negative predictive value of approximately 100%, a specificity of 90%, and a positive predictive value of 78% according to data from the United Kingdom . [ 20 ]
BNP is cleared by binding to natriuretic peptide receptors (NPRs) and neutral endopeptidase (NEP). Less than 5% of BNP is cleared renally. NT-proBNP is the inactive molecule resulting from cleavage of the prohormone Pro-BNP and is reliant solely on the kidney for excretion. The achilles heel of the NT-proBNP molecule is the overlap in kidney disease in the heart failure patient population. [ 21 ] [ 22 ]
Some laboratories report in units ng per Litre (ng/L), which is equivalent to pg/mL
There is a diagnostic 'gray area', often defined as between 100 and 500 pg/mL, for which the test is considered inconclusive, but, in general, levels above 500 pg/ml are considered to be an indicator of heart failure. This so-called gray zone has been addressed in several studies, and using clinical history or other available simple tools can help make the diagnosis. [ 23 ] [ 24 ]
BNP has been suggested as a predictor for a variety of medical states , including cardiovascular mortality in diabetics [ 25 ] and cardiac impairment in cancer patients. [ 26 ] [ 27 ]
BNP was found to have an important role in prognostication of heart surgery patients [ 28 ] and in the emergency department. [ 29 ] It has been shown that combining BNP with other tools like impedance cardiography (ICG) can improve early diagnosis of heart failure and advance prevention strategies. [ 30 ] [ 31 ] Utility of BNP has also been explored in various settings like preeclampsia , intensive care , shock and end-stage renal disease (ESRD). [ 32 ] [ 33 ] [ 34 ]
The effect or race and gender on value of BNP and its utility in that context has been studied extensively. [ 35 ] [ 36 ]
The BNP test is used as an aid in the diagnosis and assessment of severity of heart failure. A recent meta-analysis concerning effects of BNP testing on clinical outcomes of patients presenting to the emergency department with acute dyspnea revealed that BNP testing led to a decrease in admission rates and decrease in mean length of stay, although neither was statistically significant. Effects on all cause hospital mortality was inconclusive. [ 38 ] The BNP test is also used for the risk stratification of patients with acute coronary syndromes. [ 39 ] [ 40 ]
When interpreting an elevated BNP level, values may be elevated due to factors other than heart failure. Lower levels are often seen in obese patients. [ 41 ] Higher levels are seen in those with renal disease, in the absence of heart failure.
Recombinant BNP, nesiritide , has been suggested as a treatment for decompensated heart failure. However, a clinical trial failed to show a benefit of nesiritide in patients with acute decompensated heart failure . [ 42 ] Blockade of neprilysin , a protease known to degrade members of the natriuretic peptide family, has also been suggested as a possible treatment for heart failure. Dual administration of neprilysin inhibitors and angiotensin receptor blockers has been shown to be advantageous to ACE inhibitors , the current first-line therapy, in multiple settings. [ 43 ] [ 44 ]
attribution : copied from Brain natriuretic peptide version as of 13:57, 4 December 2019
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The anatomical study of Vladimir Lenin 's brain by the German neurologist and psychiatrist Oskar Vogt in 1924 was a significant event in the history of neuroscience . The study aimed to understand the neural basis of Lenin's political and intellectual abilities. The research was conducted at the request of the Soviet government, which wanted to prove that Lenin's supposed genius was the result of his brain's superior structure. [ 1 ] Under Vogt's leadership, the Kaiser Wilhelm Institute for Brain Research in Berlin was established, and the study of Lenin's brain was one of the institute's first major projects. [ 2 ] The histological analysis methods used to examine tissue samples and helped establish the procedure as a viable way of studying the brain. Though certain structural aspects in Lenin's brain had been said to contribute to heightened cognitive ability , Vogt was nonetheless unable to identify any particular region within Lenin's brain which provided structural proof to Lenin's genius abilities. [ 3 ] While the study has limitations and controversies, it is significant in the context of the field of neuropsychology. [ 4 ]
The study and dissection of Lenin's brain is directly attributed to the field of phrenology, the neuroscientific field developed by Franz Joseph Gall that examines the relationship between mental ability and brain structure. [ 5 ] [ 6 ] The reasons behind dissecting Lenin's brain was by no means a pursuit of Soviet deification of Lenin, nor was it a unique event; rather, it was due to the fact that Lenin was considered to be a genius and that his geniusness was identifiable within his brain structure. [ 7 ]
The historical search for biological roots of extraordinary brain capacity was of particular interest throughout the 19th and 20th centuries. It built off of Franz Joseph Gall's late 18th century idea that it would be scientifically beneficial to examine the brains of geniuses as mental qualities and faculties are derived from the brain. [ 6 ] [ 8 ] In conjunction with the lifelong consideration of Lenin as one of the greatest geniuses of the time, the immediate action to examine his brain upon his death sought to provide insight on the relationship between intellectual capabilities and brain structure. [ 5 ] The expectation of the results of dissecting Lenin's brain was that due to Lenin being a mentally extraordinary and gifted individual, his brain must be unique and identifiable as such within his brain structure. [ 5 ]
Vladimir Ilyich Ulyanov's death occurred on January 21, 1924, in Gorki , near Moscow. On January 24, an autopsy was performed by Professor Aleksey Abrikosov , with 27 Russian pathologists and Professor Otfried Foerster in attendance, and his brain was examined. [ 9 ] Lenin's brain weighed 1340 grams and showed signs of degeneration, particularly in the left hemisphere. [ 10 ] Additionally, two areas of softening were observed in the right occipitotemporal border. The blood vessels above the corpora quadrigemina were congested with blood, and there were signs of hemorrhage. Abrikosov diagnosed the deceased with diffuse atherosclerosis primarily in the brain arteries. However, researchers have since argued that Lenin should have been diagnosed with neurosyphilis or, according to recent studies, with a mutation of the NT5E gene. Given the Soviet Union’s attempts to conceal Lenin's venereal disease as well as to hide his illness entirely, the diagnosis remains up for debate.
Neuroanatomical research in pursuit of identifying intellectual genius had been a recurrent in Russian universities. Medical faculties collected the brains of medical professors and other notable individuals who had donated their organs for scientific research. Lenin "was considered to be the greatest of geniuses, and his brain was expected to be unique". [ 5 ] Therefore, following his death, Oskar Vogt - a neuroanatomist from the University of Berlin - was requested to conduct histological examinations at the Moscow Brain Research Institute [ ru ] . [ 11 ] The institute was especially established for Vogt to conduct analyses on Lenin's brain. [ 2 ] Between 1925 and 1927, Vogt conducted a comprehensive analysis of Lenin's brain, involving 153 pages, fifteen albums, and 30,953 brain slices. [ 12 ] [ 13 ] [ 14 ] Some of the methodologies adopted by Vogt included the "cutting, mounting, and staining in serial sections the entire brain" to obtain a "a minute parcellation of the cerebral cortex". [ 15 ] The most significant finding was an unusually high number and size of pyramidal cells in the third layer of the cerebral cortex. [ 16 ] Vogt called these "association neurons" and were seen as confirmation of Lenin's supposed genius. [ 11 ]
On November 10, 1929, Vogt presented his findings to high-ranking officials in the Pantheon Hall of the Moscow Brain Research Institute. [ 17 ] The abundance of pyramidal neurons was attributed to Lenin's exceptional intellectual and organizational skills as well as to his rigorous mental training and political activities. [ 11 ] Wilder Penfield wrote a letter to his mother in 1929, confirming the validity of Vogt's study on Lenin's brain. According to Penfield, during his visit to the Brain Research Institute in Berlin, he and other visitors were shown many large nerve cells in the third layer of the gray matter of Lenin's brain. The lack of reliable morphometric and statistical controls limited the significance of the cytoarchitectonic observations, but the finding of association neurons was sufficient to please the Politburo without compromising Vogt's integrity or Germany's relationship with Russia. [ 17 ] At the presentation, Vogt emphasized the need for further comparative quantitative research including the brains of "elite" individuals, as well as those from diverse ethnic groups. Due to Hitler's rise to power, the changing political climate between Germany and Russia was now bringing an end to their cooperation on neuroscientific research. Vogt’s activities at the Moscow Brain Research Institute ceased and he did not proceed with the comparative experimentation. In 1937, Vogt was fired from the directorship of the Kaiser Wilhelm Institute for Brain Research. [ 18 ]
Contrary to Lenin’s autopsy which found many irregularities related to his deteriorated condition upon the last years of his life, the dissection of his brain for the purpose of physically identifying extraordinary mental prowess was generally unreliable. [ 3 ] [ 19 ] Today it is of general agreement among neuroscientists that broad concepts of genius or extraordinary mental prowess cannot be pinned down to physical locations in the brain. [ 3 ] Furthermore, upon the conclusion of the dissection of Lenin's brain, there existed many indications expressing perplexity on the matter amongst the neuroscience community as well as regret within Vogt about potentially overexposing himself in his project. [ 3 ] This in turn brings the question of validity and acceptance to the project's conclusions. Despite this, Vogt concluded his dissection of Lenin's brain by exclaiming Lenin to have been "a brain athlete and association giant" with a heightened ability in his brain, a conclusion on Lenin still prevalent to this day. [ 3 ] [ 20 ]
The overseers of the dissection of the brain were a married couple; neurologists Oskar and Cecile Vogt . Born in Husum , Germany, the neuroatonomist graduated from Jena University 's medical school in 1893, marrying Cécile six years later. [ 21 ] Before they met, Vogt worked in the Burghölzli psychiatric hospital for Auguste Forel where Vogt thoroughly studied hypnosis and the effect it bore on patients and its relations with brain components. [ 22 ] [ 23 ] As a hypnotist, he advocated for the use of hypermnesia to return suppressed, traumatic memories of patients. Vogt moved to Paris for more extensive training in 1896. [ 24 ] By 1914, Vogt was made director of the Kaiser Wilhelm Institute located in Berlin. Together, the Vogts had a significant influence on their field. Amongst their findings, their discovery of the cytoarchitectural organization of the cerebral cortex and thalamus had international influence. [ 25 ] The German Empire-era institute was responsible for dissecting the brains of murdered patients, with both Cecile and Oskar studying the brains of the "elite". [ 26 ]
Despite the Vogts' work in the KWI, they were opponents of the National Social Party dominating Germany in the following decades. The couple had analysed the supposedly "elite" brains of high-profile figures, but they nevertheless resisted hiring staff based on race, culminating in raids on the KWI building by the Nazi Party . Vogt allegedly threw Nazi Propaganda Minister Joseph Goebbels down the stairs at one point. [ 26 ] The regime eventually removed Vogt as the head of the KWI in 1937, replacing him with Hugo Spatz . Vogt’s friend and a Foreign Service official in Germany, Gustav Krupp , eventually helped the former create the German Brain Research Society .
Vogt was not a communist, but a socialist, although he sympathised with the communist beliefs echoed by the Soviet Union, which he found progressive. [ 11 ] As a result, upon Russian invitation, Vogt went to Moscow to form the Brain Research Institute in 1924 to study the brain of Vladimir Lenin. By this time, the neurologist had become renowned for his work as a brain researcher and garnered the attention of the Soviet Union. As mentioned previously, Vogt sought to study the brains of those whom he viewed as intellectuals and elite minds with the backing of Germany's Weimar Republic , which wanted to improve relations with Russia. [ 27 ]
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A brain stem tumor is a tumor in the part of the brain that connects to the spinal cord (the brain stem ).
The symptoms of brain stem tumors vary greatly and can include ataxia , cranial nerve palsy, headaches , problems with speech and swallowing, hearing loss, weakness, hemiparesis , vision abnormalities, ptosis , and behavioral changes. Another possible symptom is vomiting. Headaches related to brainstem tumors may be worse shortly after waking up in the morning. [ 1 ]
An MRI is better than a CT scan when a brainstem tumor is in the differential diagnosis. [ citation needed ]
The most common form of brainstem tumor is the brainstem glioma .
Treatment typically consists of radiotherapy and steroids for palliation of symptoms. [ citation needed ] Radiotherapy may result in minimally extended survival time. [ citation needed ]
Prognosis is very poor, with only 37% of treated patients surviving one year or more. [ citation needed ] Topotecan has been studied in the treatment of brainstem glioma, [ citation needed ] otherwise, chemotherapy is probably ineffective, though further study is needed. [ 2 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
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A brain transplant or whole-body transplant is a procedure in which the brain of one organism is transplanted into the body of another organism. It is a procedure distinct from head transplantation , which involves transferring the entire head to a new body, as opposed to the brain only. Theoretically, a person with complete organ failure could be given a new and functional body while keeping their own personality , memories , and consciousness through such a procedure. Neurosurgeon Robert J. White has grafted the head of a monkey onto the headless body of another monkey. Electroencephalography (EEG) readings showed the brain was later functioning normally. Initially, it was thought to prove that the brain was an immunologically privileged organ, as the host's immune system did not attack it at first, [ 1 ] but immune rejection caused the monkey to die after nine days. [ 2 ]
One of the most significant barriers to the procedure is the inability of nerve tissue to heal properly; scarred nerve tissue does not transmit signals well, which is why spinal cord injuries devastate muscle function and sensation .
Alternatively, a brain–computer interface can be used connecting the subject to their own body. A study [ 3 ] using a monkey as a subject shows that it is possible to directly use commands from the brain, bypass the spinal cord and enable hand function. An advantage is that this interface can be adjusted after the surgical interventions are done where nerves can not be reconnected without surgery.
Also, for the procedure to be practical, the age of the donated body must be close to that of the recipient brain: an adult brain cannot fit into a skull that has not reached its full growth, which occurs at age 9–12 years.
When organs are transplanted, aggressive transplant rejection by the host's immune system can occur. Because immune cells of the central nervous system (CNS) contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood, the brain has been hypothesized to be an immunologically privileged (unrejectable) organ. [ 4 ] [ 5 ] [ 6 ] However, immunorejection of a functional transplanted brain has been reported in monkeys. [ 7 ]
In 1982, Dr. Dorothy T. Krieger, chief of endocrinology at Mount Sinai Medical Center in New York City, achieved success with a partial brain transplant in mice . [ 8 ]
In 1998, a team of surgeons from the University of Pittsburgh Medical Center attempted to transplant a group of brain cells to Alma Cerasini, who had suffered a severe stroke that caused the loss of mobility in her right limbs as well as had limited speech . The team hoped that the cells would correct the listed damage. She died later on. [ 9 ]
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In human neuroanatomy , brainstem auditory evoked potentials ( BAEPs ), also called brainstem auditory evoked responses ( BAERs ), are very small auditory evoked potentials in response to an auditory stimulus, which are recorded by electrodes placed on the scalp. They reflect neuronal activity in the auditory nerve , cochlear nucleus , superior olive , and inferior colliculus of the brainstem . They typically have a response latency of no more than six milliseconds with an amplitude of approximately one microvolt.
Due to their small amplitude, 500 or more repetitions of the auditory stimulus are required in order to average out the random background electrical activity. Although it is possible to obtain a BAEP to a pure tone stimulus in the hearing range , a more effective auditory stimulus contains a range of frequencies in the form of a short sharp click.
Long and Allen [ 1 ] were the first to report the abnormal BAEPs in an alcoholic woman who recovered from acquired central hypoventilation syndrome . These investigators hypothesized that their patient's brainstem was poisoned, but not destroyed, by her chronic alcoholism.
BAER testing is also recommended for dogs [ 2 ] and white cats . [ 3 ]
This neuroscience article is a stub . You can help Wikipedia by expanding it .
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Brainstem death is a clinical syndrome defined by the absence of reflexes with pathways through the brainstem – the "stalk" of the brain, which connects the spinal cord to the mid-brain , cerebellum and cerebral hemispheres – in a deeply comatose , ventilator -dependent patient.
Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days, although it may continue for weeks if intensive support is maintained. [ 1 ]
In the United Kingdom , death can be certified on the basis of a formal diagnosis of brainstem death, so long as this is done in accordance with a procedure established in "A Code of Practice for the Diagnosis and Confirmation of Death", published in 2008 by the Academy of Medical Royal Colleges . [ 1 ] The premise of this is that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brainstem alone is sufficient to produce this state. [ 2 ]
This concept of brainstem death is also accepted as grounds for pronouncing death for legal purposes in India [ 3 ] and Trinidad & Tobago . [ 4 ] Elsewhere in the world, the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain – whole brain death – with which the British concept should not be confused. The United States ' President's Council on Bioethics made it clear, for example, in its White Paper of December 2008, that the British concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States. [ 5 ]
The United Kingdom (UK) criteria were first published by the Conference of Medical Royal Colleges (with advice from the Transplant Advisory Panel) in 1976, as prognostic guidelines. [ 6 ] They were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought "to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery". The published criteria – negative responses to bedside tests of some reflexes with pathways through the brainstem and a specified challenge to the brainstem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects – were held to be "sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists". Recognition of that state required the withdrawal of further artificial support so that death is allowed to occur, thus "sparing relatives from the further emotional trauma of sterile hope". [ 6 ]
In 1979, the Conference of Medical Royal Colleges promulgated its conclusion that identification of the state defined by those same criteria – then thought sufficient for a diagnosis of brain death – "means that the patient is dead". [ 7 ] Death certification on those criteria has continued in the United Kingdom (where there is no statutory legal definition of death) since that time, particularly for organ transplantation purposes, although the conceptual basis for that use has changed.
In 1995, after a review by a Working Group of the Royal College of Physicians of London , the Conference of Medical Royal Colleges [ 2 ] formally adopted the "more correct" term for the syndrome, "brainstem death" – championed by Pallis in a set of 1982 articles in the British Medical Journal [ 8 ] – and advanced a new definition of human death as the basis for equating this syndrome with the death of the person. The suggested new definition of death was the "irreversible loss of the capacity for consciousness, combined with irreversible loss of the capacity to breathe". It was stated that the irreversible cessation of brainstem function will produce this state and "therefore brainstem death is equivalent to the death of the individual". [ 2 ]
In the UK, the formal rules for the diagnosis of brainstem death have undergone only minor modifications since they were first published [ 6 ] in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death [ 1 ] reaffirms the preconditions for its consideration. These are:
With these pre-conditions satisfied, the definitive criteria are:
Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after "a short period of time ... to allow return of the patient's arterial blood gases and baseline parameters to the pre-test state". These criteria for the diagnosis of death are not applicable to infants below the age of two months.
With due regard for the cause of the coma, and the rapidity of its onset, testing for the purpose of diagnosing death on brainstem death grounds may be delayed beyond the stage where brainstem reflexes may be absent only temporarily – because the cerebral blood flow is inadequate to support synaptic function, although there is still sufficient blood flow to keep brain cells alive [ 9 ] and capable of recovery. There has recently [ when? ] been renewed interest in the possibility of neuronal protection during this phase by use of moderate hypothermia and by correction of the neuroendocrine abnormalities commonly seen in this early stage. [ 13 ]
Published studies of patients meeting the criteria for brainstem death or whole brain death – the American standard which includes brainstem death diagnosed by similar means – record that even if ventilation is continued after diagnosis, the heart stops beating within only a few hours or days. [ 14 ] However, there have been some very long-term survivals [ 15 ] and it is noteworthy that expert management can maintain the bodily functions of pregnant brain dead women for long enough to bring them to term. [ 16 ]
The diagnostic criteria were originally published for the purpose of identifying a clinical state associated with a fatal prognosis (see above). The change of use, in the UK, to criteria for the diagnosis of death itself was protested immediately. [ 17 ] [ 18 ] The initial basis for the change of use was the claim that satisfaction of the criteria sufficed for the diagnosis of the death of the brain as a whole, despite the persistence of demonstrable activity in parts of the brain. [ 19 ] In 1995, that claim was abandoned [ 7 ] and the diagnosis of death (acceptable for legal purposes in the UK in the context of organ procurement for transplantation) by the specified testing of brainstem functions was based on a new definition of death – the permanent loss of the capacity for consciousness and spontaneous breathing. There are doubts that this concept is generally understood and accepted and that the specified testing is stringent enough to determine that state. It is, however, associated with substantial risk of exacerbating the brain damage and even causing the death of the apparently dying patient so tested (see "the apnoea test" above). This raises ethical problems which seem not to have been addressed.
It has been argued [ by whom? ] that sound scientific support is lacking for the claim that the specified purely bedside tests have the power to diagnose true and total death of the brainstem, the necessary condition for the assumption of permanent loss of the intrinsically untestable consciousness-arousal function of those elements of the reticular formation which lie within the brainstem (there are elements also within the wider brain). [ 19 ] Knowledge of this arousal system is based upon the findings from animal experiments [ 20 ] [ 21 ] [ 22 ] as illuminated by pathological studies in humans. [ 23 ] The current neurological consensus is that the arousal of consciousness depends upon reticular components which reside in the midbrain, diencephalon and pons . [ 24 ] [ 25 ] It is said that the midbrain reticular formation may be viewed as a driving centre for the higher structures, loss of which produces a state in which the cortex appears, on the basis of electroencephalographic (EEG) studies, to be awaiting the command or ability to function. The role of diencephalic (higher brain) involvement is stated to be uncertain and we are reminded that the arousal system is best regarded as a physiological rather than a precise anatomical entity. There should, perhaps, also be a caveat about possible arousal mechanisms involving the first and second cranial nerves (serving sight and smell) which are not tested when diagnosing brainstem death but which were described in cats in 1935 and 1938. [ 20 ] In humans, light flashes have been observed to disturb the sleep-like EEG activity persisting after the loss of all brainstem reflexes and of spontaneous respiration. [ 26 ]
There is also concern about the permanence of consciousness loss, based on studies in cats, dogs and monkeys which recovered consciousness days or weeks after being rendered comatose by brainstem ablation and on human studies of brainstem stroke syndrome raising thoughts about the "plasticity" of the nervous system. [ 23 ] Other theories of consciousness place more stress on the thalamocortical system. [ 27 ] Perhaps the most objective statement to be made is that consciousness is not currently understood. That being so, proper caution must be exercised in accepting a diagnosis of its permanent loss before all cerebral blood flow has permanently ceased.
The ability to breathe spontaneously depends upon functioning elements in the medulla – the 'respiratory centre'. In the UK, establishing a neurological diagnosis of death involves challenging this centre with the strong stimulus offered by an unusually high concentration of carbon dioxide in the arterial blood, but it is not challenged by the more powerful drive stimulus provided by anoxia – although the effect of that ultimate stimulus is sometimes seen after final disconnection of the ventilator in the form of agonal gasps .
No testing of testable brain stem functions such as oesophageal and cardiovascular regulation is specified in the UK Code of Practice for the diagnosis of death on neurological grounds. There is published evidence [ 28 ] [ 29 ] [ 30 ] strongly suggestive of the persistence of brainstem blood pressure control in organ donors .
A small minority of medical practitioners working in the UK have argued that neither requirement of the UK Health Department's Code of Practice basis for the equation of brainstem death with death is satisfied by its current diagnostic protocol [ 1 ] and that in terms of its ability to diagnose de facto brainstem death it falls far short.
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https://en.wikipedia.org/wiki/Brainstem_death
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A brain–computer interface ( BCI ), sometimes called a brain–machine interface ( BMI ), is a direct communication link between the brain 's electrical activity and an external device, most commonly a computer or robotic limb. BCIs are often directed at researching, mapping , assisting, augmenting , or repairing human cognitive or sensory-motor functions . [ 1 ] They are often conceptualized as a human–machine interface that skips the intermediary of moving body parts (e.g. hands or feet). BCI implementations range from non-invasive ( EEG , MEG , MRI ) and partially invasive ( ECoG and endovascular) to invasive ( microelectrode array ), based on how physically close electrodes are to brain tissue. [ 2 ]
Research on BCIs began in the 1970s by Jacques Vidal at the University of California, Los Angeles (UCLA) under a grant from the National Science Foundation , followed by a contract from the Defense Advanced Research Projects Agency ( DARPA ). [ 3 ] [ 4 ] Vidal's 1973 paper introduced the expression brain–computer interface into scientific literature.
Due to the cortical plasticity of the brain, signals from implanted prostheses can, after adaptation, be handled by the brain like natural sensor or effector channels. [ 5 ] Following years of animal experimentation, the first neuroprosthetic devices were implanted in humans in the mid-1990s.
The history of brain-computer interfaces (BCIs) starts with Hans Berger 's discovery of the brain's electrical activity and the development of electroencephalography (EEG). In 1924 Berger was the first to record human brain activity utilizing EEG. Berger was able to identify oscillatory activity , such as the alpha wave (8–13 Hz), by analyzing EEG traces.
Berger's first recording device was rudimentary. He inserted silver wires under the scalps of his patients. These were later replaced by silver foils attached to the patient's head by rubber bandages. Berger connected these sensors to a Lippmann capillary electrometer , with disappointing results. However, more sophisticated measuring devices, such as the Siemens double-coil recording galvanometer , which displayed voltages as small as 10 −4 volt, led to success.
Berger analyzed the interrelation of alternations in his EEG wave diagrams with brain diseases . EEGs permitted completely new possibilities for brain research.
Although the term had not yet been coined, one of the earliest examples of a working brain-machine interface was the piece Music for Solo Performer (1965) by American composer Alvin Lucier . The piece makes use of EEG and analog signal processing hardware (filters, amplifiers, and a mixing board) to stimulate acoustic percussion instruments. Performing the piece requires producing alpha waves and thereby "playing" the various instruments via loudspeakers that are placed near or directly on the instruments. [ 6 ]
Jacques Vidal coined the term "BCI" and produced the first peer-reviewed publications on this topic. [ 3 ] [ 4 ] He is widely recognized as the inventor of BCIs. [ 7 ] [ 8 ] [ 9 ] A review pointed out that Vidal's 1973 paper stated the "BCI challenge" [ 10 ] of controlling external objects using EEG signals, and especially use of Contingent Negative Variation (CNV) potential as a challenge for BCI control. Vidal's 1977 experiment was the first application of BCI after his 1973 BCI challenge. It was a noninvasive EEG (actually Visual Evoked Potentials (VEP)) control of a cursor-like graphical object on a computer screen. The demonstration was movement in a maze. [ 11 ]
1988 was the first demonstration of noninvasive EEG control of a physical object, a robot. The experiment demonstrated EEG control of multiple start-stop-restart cycles of movement, along an arbitrary trajectory defined by a line drawn on a floor. The line-following behavior was the default robot behavior, utilizing autonomous intelligence and an autonomous energy source. [ 12 ] [ 13 ] [ 14 ] [ 15 ]
In 1990, a report was given on a closed loop, bidirectional, adaptive BCI controlling a computer buzzer by an anticipatory brain potential, the Contingent Negative Variation (CNV) potential. [ 16 ] [ 17 ] The experiment described how an expectation state of the brain, manifested by CNV, used a feedback loop to control the S2 buzzer in the S1-S2-CNV paradigm. The resulting cognitive wave representing the expectation learning in the brain was termed Electroexpectogram (EXG). The CNV brain potential was part of Vidal's 1973 challenge.
Studies in the 2010s suggested neural stimulation's potential to restore functional connectivity and associated behaviors through modulation of molecular mechanisms. [ 18 ] [ 19 ] This opened the door for the concept that BCI technologies may be able to restore function.
Beginning in 2013, DARPA funded BCI technology through the BRAIN initiative, which supported work out of teams including University of Pittsburgh Medical Center , [ 20 ] Paradromics, [ 21 ] Brown, [ 22 ] and Synchron. [ 23 ]
Neuroprosthetics is an area of neuroscience concerned with neural prostheses, that is, using artificial devices to replace the function of impaired nervous systems and brain-related problems, or of sensory or other organs (bladder, diaphragm, etc.). As of December 2010, cochlear implants had been implanted as neuroprosthetic devices in some 736,900 people worldwide. [ 24 ] Other neuroprosthetic devices aim to restore vision, including retinal implants . The first neuroprosthetic device, however, was the pacemaker .
The terms are sometimes used interchangeably. Neuroprosthetics and BCIs seek to achieve the same aims, such as restoring sight, hearing, movement, ability to communicate, and even cognitive function . [ 1 ] Both use similar experimental methods and surgical techniques.
Several laboratories have managed to read signals from monkey and rat cerebral cortices to operate BCIs to produce movement. Monkeys have moved computer cursors and commanded robotic arms to perform simple tasks simply by thinking about the task and seeing the results, without motor output. [ 25 ] In May 2008 photographs that showed a monkey at the University of Pittsburgh Medical Center operating a robotic arm by thinking were published in multiple studies. [ 26 ] Sheep have also been used to evaluate BCI technology including Synchron's Stentrode.
In 2020, Elon Musk 's Neuralink was successfully implanted in a pig. [ 27 ] In 2021, Musk announced that the company had successfully enabled a monkey to play video games using Neuralink's device. [ 28 ]
In 1969 operant conditioning studies by Fetz et al. at the Regional Primate Research Center and Department of Physiology and Biophysics, University of Washington School of Medicine showed that monkeys could learn to control the deflection of a biofeedback arm with neural activity. [ 29 ] Similar work in the 1970s established that monkeys could learn to control the firing rates of individual and multiple neurons in the primary motor cortex if they were rewarded accordingly. [ 30 ]
Algorithms to reconstruct movements from motor cortex neurons , which control movement, date back to the 1970s. In the 1980s, Georgopoulos at Johns Hopkins University found a mathematical relationship between the electrical responses of single motor cortex neurons in rhesus macaque monkeys and the direction in which they moved their arms. He also found that dispersed groups of neurons, in different areas of the monkey's brains, collectively controlled motor commands. He was able to record the firings of neurons in only one area at a time, due to equipment limitations. [ 31 ]
Several groups have been able to capture complex brain motor cortex signals by recording from neural ensembles (groups of neurons) and using these to control external devices. [ citation needed ]
Phillip Kennedy (Neural Signals founder (1987) and colleagues built the first intracortical brain–computer interface by implanting neurotrophic-cone electrodes into monkeys. [ citation needed ]
In 1999, Yang Dan et al. at University of California, Berkeley decoded neuronal firings to reproduce images from cats. The team used an array of electrodes embedded in the thalamus (which integrates the brain's sensory input). Researchers targeted 177 brain cells in the thalamus lateral geniculate nucleus area, which decodes signals from the retina . Neuron firings were recorded from watching eight short movies. Using mathematical filters, the researchers decoded the signals to reconstruct recognizable scenes and moving objects. [ 32 ]
Duke University professor Miguel Nicolelis advocates using multiple electrodes spread over a greater area of the brain to obtain neuronal signals.
After initial studies in rats during the 1990s, Nicolelis and colleagues developed BCIs that decoded brain activity in owl monkeys and used the devices to reproduce monkey movements in robotic arms. Monkeys' advanced reaching and grasping abilities and hand manipulation skills, made them good test subjects.
By 2000, the group succeeded in building a BCI that reproduced owl monkey movements while the monkey operated a joystick or reached for food. [ 33 ] The BCI operated in real time and could remotely control a separate robot. But the monkeys received no feedback ( open-loop BCI).
Later experiments on rhesus monkeys included feedback and reproduced monkey reaching and grasping movements in a robot arm. Their deeply cleft and furrowed brains made them better models for human neurophysiology than owl monkeys. The monkeys were trained to reach and grasp objects on a computer screen by manipulating a joystick while corresponding movements by a robot arm were hidden. [ 34 ] [ 35 ] The monkeys were later shown the robot and learned to control it by viewing its movements. The BCI used velocity predictions to control reaching movements and simultaneously predicted gripping force .
In 2011 O'Doherty and colleagues showed a BCI with sensory feedback with rhesus monkeys. The monkey controlled the position of an avatar arm while receiving sensory feedback through direct intracortical stimulation (ICMS) in the arm representation area of the sensory cortex . [ 36 ]
Other laboratories that have developed BCIs and algorithms that decode neuron signals include John Donoghue at the Carney Institute for Brain Science at Brown University , Andrew Schwartz at the University of Pittsburgh , and Richard Andersen at Caltech . These researchers produced working BCIs using recorded signals from far fewer neurons than Nicolelis (15–30 neurons versus 50–200 neurons).
The Carney Institute reported training rhesus monkeys to use a BCI to track visual targets on a computer screen (closed-loop BCI) with or without a joystick. [ 37 ] The group created a BCI for three-dimensional tracking in virtual reality and reproduced BCI control in a robotic arm. [ 38 ] The same group demonstrated that a monkey could feed itself pieces of fruit and marshmallows using a robotic arm controlled by the animal's brain signals. [ 39 ] [ 40 ] [ 41 ]
Andersen's group used recordings of premovement activity from the posterior parietal cortex , including signals created when experimental animals anticipated receiving a reward. [ 42 ]
In addition to predicting kinematic and kinetic parameters of limb movements, BCIs that predict electromyographic or electrical activity of the muscles of primates are in process. [ 43 ] Such BCIs could restore mobility in paralyzed limbs by electrically stimulating muscles.
Nicolelis and colleagues demonstrated that large neural ensembles can predict arm position. This work allowed BCIs to read arm movement intentions and translate them into actuator movements. Carmena and colleagues [ 34 ] programmed a BCI that allowed a monkey to control reaching and grasping movements by a robotic arm. Lebedev and colleagues argued that brain networks reorganize to create a new representation of the robotic appendage in addition to the representation of the animal's own limbs. [ 35 ]
In 2019, a study reported a BCI that had the potential to help patients with speech impairment caused by neurological disorders. Their BCI used high-density electrocorticography to tap neural activity from a patient's brain and used deep learning to synthesize speech. [ 44 ] [ 45 ] In 2021, those researchers reported the potential of a BCI to decode words and sentences in an anarthric patient who had been unable to speak for over 15 years. [ 46 ] [ 47 ]
The biggest impediment to BCI technology is the lack of a sensor modality that provides safe, accurate and robust access to brain signals. The use of a better sensor expands the range of communication functions that can be provided using a BCI.
Development and implementation of a BCI system is complex and time-consuming. In response to this problem, Gerwin Schalk has been developing BCI2000 , a general-purpose system for BCI research, since 2000. [ 48 ]
A new 'wireless' approach uses light-gated ion channels such as channelrhodopsin to control the activity of genetically defined subsets of neurons in vivo . In the context of a simple learning task, illumination of transfected cells in the somatosensory cortex influenced decision-making in mice. [ 49 ]
BCIs led to a deeper understanding of neural networks and the central nervous system . Research has reported that despite neuroscientists' inclination to believe that neurons have the most effect when working together, single neurons can be conditioned through the use of BCIs to fire in a pattern that allows primates to control motor outputs. BCIs led to development of the single neuron insufficiency principle that states that even with a well-tuned firing rate, single neurons can only carry limited information and therefore the highest level of accuracy is achieved by recording ensemble firings. Other principles discovered with BCIs include the neuronal multitasking principle, the neuronal mass principle, the neural degeneracy principle, and the plasticity principle. [ 50 ]
BCIs are proposed to be applied by users without disabilities. Passive BCIs allow for assessing and interpreting changes in the user state during Human–computer interaction (HCI). In a secondary, implicit control loop, the system adapts to its user, improving its usability . [ 51 ]
BCI systems can potentially be used to encode signals from the periphery. These sensory BCI devices enable real-time, behaviorally-relevant decisions based upon closed-loop neural stimulation. [ 52 ]
The BCI Research Award is awarded annually in recognition of innovative research. Each year, a renowned research laboratory is asked to judge projects. The jury consists of BCI experts recruited by that laboratory. The jury selects twelve nominees, then chooses a first, second, and third-place winner, who receive awards of $3,000, $2,000, and $1,000, respectively. [ citation needed ]
Invasive BCI requires surgery to implant electrodes under the scalp for accessing brain signals. The main advantage is to increase accuracy. Downsides include side effects from the surgery, including scar tissue that can obstruct brain signals, or the body potentially rejecting the implanted electrodes. [ 53 ]
Invasive BCI research has targeted repairing damaged sight and providing new functionality for people with paralysis. Invasive BCIs are implanted directly into the grey matter of the brain during neurosurgery. Because they lie in the grey matter, invasive devices produce the highest quality signals of BCI devices but are prone to scar-tissue build-up, causing the signal to weaken, or disappear, as the body reacts to the foreign object. [ 54 ]
In vision science , direct brain implants have been used to treat non- congenital (acquired) blindness. One of the first scientists to produce a working brain interface to restore sight was private researcher William Dobelle . Dobelle's first prototype was implanted into "Jerry", a man blinded in adulthood, in 1978. A single-array BCI containing 68 electrodes was implanted onto Jerry's visual cortex and succeeded in producing phosphenes , the sensation of seeing light. The system included cameras mounted on glasses to send signals to the implant. Initially, the implant allowed Jerry to see shades of grey in a limited field of vision at a low frame-rate. This also required him to be hooked up to a mainframe computer , but shrinking electronics and faster computers made his artificial eye more portable and now enable him to perform simple tasks unassisted. [ 55 ]
In 2002, Jens Naumann, also blinded in adulthood, became the first in a series of 16 paying patients to receive Dobelle's second generation implant, one of the earliest commercial uses of BCIs. The second generation device used a more sophisticated implant enabling better mapping of phosphenes into coherent vision. Phosphenes are spread out across the visual field in what researchers call "the starry-night effect". Immediately after his implant, Jens was able to use his imperfectly restored vision to drive an automobile slowly around the parking area of the research institute. [ 56 ] Dobelle died in 2004 before his processes and developments were documented, leaving no one to continue his work. [ 57 ] Subsequently, Naumann and the other patients in the program began having problems with their vision, and eventually lost their "sight" again. [ 58 ] [ 59 ]
BCIs focusing on motor neuroprosthetics aim to restore movement in individuals with paralysis or provide devices to assist them, such as interfaces with computers or robot arms.
Kennedy and Bakay were first to install a human brain implant that produced signals of high enough quality to simulate movement. Their patient, Johnny Ray (1944–2002), developed ' locked-in syndrome ' after a brain-stem stroke in 1997. Ray's implant was installed in 1998 and he lived long enough to start working with the implant, eventually learning to control a computer cursor; he died in 2002 of a brain aneurysm . [ 60 ]
Tetraplegic Matt Nagle became the first person to control an artificial hand using a BCI in 2005 as part of the first nine-month human trial of Cyberkinetics 's BrainGate chip-implant. Implanted in Nagle's right precentral gyrus (area of the motor cortex for arm movement), the 96-electrode implant allowed Nagle to control a robotic arm by thinking about moving his hand as well as a computer cursor, lights and TV. [ 61 ] One year later, Jonathan Wolpaw received the Altran Foundation for Innovation prize for developing a Brain Computer Interface with electrodes located on the surface of the skull, instead of directly in the brain. [ 62 ]
Research teams led by the BrainGate group and another at University of Pittsburgh Medical Center , both in collaborations with the United States Department of Veterans Affairs (VA), demonstrated control of prosthetic limbs with many degrees of freedom using direct connections to arrays of neurons in the motor cortex of tetraplegia patients. [ 63 ] [ 64 ]
In May 2021, a Stanford University team reported a successful proof-of-concept test that enabled a quadraplegic participant to produce English sentences at about 86 characters per minute and 18 words per minute. The participant imagined moving his hand to write letters, and the system performed handwriting recognition on electrical signals detected in the motor cortex, utilizing Hidden Markov models and recurrent neural networks . [ 65 ] [ 66 ]
A 2021 study reported that a paralyzed patient was able to communicate 15 words per minute using a brain implant that analyzed vocal tract motor neurons. [ 67 ] [ 46 ]
In a review article, authors wondered whether human information transfer rates can surpass that of language with BCIs. Language research has reported that information transfer rates are relatively constant across many languages. This may reflect the brain's information processing limit. Alternatively, this limit may be intrinsic to language itself, as a modality for information transfer. [ 68 ]
In 2023 two studies used BCIs with recurrent neural network to decode speech at a record rate of 62 words per minute and 78 words per minute. [ 69 ] [ 70 ] [ 71 ]
There exist a number of technical challenges to recording brain activity with invasive BCIs. Advances in CMOS technology are pushing and enabling integrated, invasive BCI designs with smaller size, lower power requirements, and higher signal acquisition capabilities. [ 72 ] Invasive BCIs involve electrodes that penetrate brain tissue in an attempt to record action potential signals (also known as spikes) from individual, or small groups of, neurons near the electrode. The interface between a recording electrode and the electrolytic solution surrounding neurons has been modelled using the Hodgkin-Huxley model . [ 73 ] [ 74 ]
Electronic limitations to invasive BCIs have been an active area of research in recent decades. While intracellular recordings of neurons reveal action potential voltages on the scale of hundreds of millivolts, chronic invasive BCIs rely on recording extracellular voltages which typically are three orders of magnitude smaller, existing at hundreds of microvolts. [ 75 ] Further adding to the challenge of detecting signals on the scale of microvolts is the fact that the electrode-tissue interface has a high capacitance at small voltages. Due to the nature of these small signals, for BCI systems that incorporate functionality onto an integrated circuit, each electrode requires its own amplifier and ADC , which convert analog extracellular voltages into digital signals. [ 75 ] Because a typical neuron action potential lasts for one millisecond, BCIs measuring spikes must have sampling rates ranging from 300 Hz to 5 kHz. Yet another concern is that invasive BCIs must be low-power, so as to dissipate less heat to surrounding tissue; at the most basic level more power is traditionally needed to optimize signal-to-noise ratio . [ 74 ] Optimal battery design is an active area of research in BCIs. [ 76 ]
Challenges existing in the area of material science are central to the design of invasive BCIs. Variations in signal quality over time have been commonly observed with implantable microelectrodes. [ 77 ] Optimal material and mechanical characteristics for long term signal stability in invasive BCIs has been an active area of research. [ 78 ] It has been proposed that the formation of glial scarring , secondary to damage at the electrode-tissue interface, is likely responsible for electrode failure and reduced recording performance. [ 79 ] Research has suggested that blood-brain barrier leakage, either at the time of insertion or over time, may be responsible for the inflammatory and glial reaction to chronic microelectrodes implanted in the brain. [ 79 ] [ 80 ] As a result, flexible [ 81 ] [ 82 ] [ 83 ] and tissue-like designs [ 84 ] [ 85 ] have been researched and developed to minimize foreign-body reaction by means of matching the Young's modulus of the electrode closer to that of brain tissue. [ 84 ]
Partially invasive BCI devices are implanted inside the skull but rest outside the brain rather than within the grey matter. They produce higher resolution signals than non-invasive BCIs where the bone tissue of the cranium deflects and deforms signals and have a lower risk of forming scar-tissue in the brain than fully invasive BCIs. Preclinical demonstration of intracortical BCIs from the stroke perilesional cortex has been conducted. [ 86 ]
A systematic review published in 2020 detailed multiple clinical and non-clinical studies investigating the feasibility of endovascular BCIs. [ 87 ]
In 2010, researchers affiliated with University of Melbourne began developing a BCI that could be inserted via the vascular system. Australian neurologist Thomas Oxley conceived the idea for this BCI, called Stentrode, earning funding from DARPA . Preclinical studies evaluated the technology in sheep. [ 2 ]
Stentrode is a monolithic stent electrode array designed to be delivered via an intravenous catheter under image-guidance to the superior sagittal sinus , in the region which lies adjacent to the motor cortex . [ 88 ] This proximity enables Stentrode to measure neural activity. The procedure is most similar to how venous sinus stents are placed for the treatment of idiopathic intracranial hypertension . [ 89 ] Stentrode communicates neural activity to a battery-less telemetry unit implanted in the chest, which communicates wirelessly with an external telemetry unit capable of power and data transfer. While an endovascular BCI benefits from avoiding a craniotomy for insertion, risks such as clotting and venous thrombosis exist.
Human trials with Stentrode were underway as of 2021. [ 88 ] In November 2020, two participants with amyotrophic lateral sclerosis were able to wirelessly control an operating system to text, email, shop, and bank using direct thought using Stentrode, [ 90 ] marking the first time a brain-computer interface was implanted via the patient's blood vessels, eliminating the need for brain surgery. In January 2023, researchers reported no serious adverse events during the first year for all four patients, who could use it to operate computers. [ 91 ] [ 92 ]
Electrocorticography (ECoG) measures brain electrical activity from beneath the skull in a way similar to non-invasive electroencephalography, using electrodes embedded in a thin plastic pad placed above the cortex, beneath the dura mater . [ 93 ] ECoG technologies were first trialled in humans in 2004 by Eric Leuthardt and Daniel Moran from Washington University in St. Louis . In a later trial, the researchers enabled a teenage boy to play Space Invaders . [ 94 ] This research indicates that control is rapid, requires minimal training, balancing signal fidelity and level of invasiveness. [ note 1 ]
Signals can be either subdural or epidural, but are not taken from within the brain parenchyma . Patients are required to have invasive monitoring for localization and resection of an epileptogenic focus. [ citation needed ]
ECoG offers higher spatial resolution, better signal-to-noise ratio, wider frequency range, and less training requirements than scalp-recorded EEG, and at the same time has lower technical difficulty, lower clinical risk, and may have superior long-term stability than intracortical single-neuron recording. [ 96 ] This feature profile and evidence of the high level of control with minimal training requirements shows potential for real world application for people with motor disabilities. [ 97 ] [ 98 ]
Edward Chang and Joseph Makin from UCSF reported that ECoG signals could be used to decode speech from epilepsy patients implanted with high-density ECoG arrays over the peri-Sylvian cortices. [ 99 ] [ 100 ] They reported word error rates of 3% (a marked improvement from prior efforts) utilizing an encoder-decoder neural network , which translated ECoG data into one of fifty sentences composed of 250 unique words. [ citation needed ]
In 2014, a BCI using functional near-infrared spectroscopy for "locked-in" patients with amyotrophic lateral sclerosis (ALS) was able to restore basic ability to communicate. [ 101 ]
After Vidal stated the BCI challenge, the initial reports on non-invasive approaches included control of a cursor in 2D using VEP, [ 102 ] control of a buzzer using CNV, [ 103 ] control of a physical object, a robot, using a brain rhythm (alpha), [ 104 ] control of a text written on a screen using P300. [ 105 ] [ 10 ]
In the early days of BCI research, another substantial barrier to using EEG was that extensive training was required. For example, in experiments beginning in the mid-1990s, Niels Birbaumer at the University of Tübingen in Germany trained paralysed people to self-regulate the slow cortical potentials in their EEG to such an extent that these signals could be used as a binary signal to control a computer cursor. (Birbaumer had earlier trained epileptics to prevent impending fits by controlling this low voltage wave.) The experiment trained ten patients to move a computer cursor. The process was slow, requiring more than an hour for patients to write 100 characters with the cursor, while training often took months. The slow cortical potential approach has fallen away in favor of approaches that require little or no training, are faster and more accurate, and work for a greater proportion of users. [ 106 ]
Another research parameter is the type of oscillatory activity that is measured. Gert Pfurtscheller founded the BCI Lab 1991 and conducted the first online BCI based on oscillatory features and classifiers. Together with Birbaumer and Jonathan Wolpaw at New York State University they focused on developing technology that would allow users to choose the brain signals they found easiest to operate a BCI, including mu and beta rhythms. [ citation needed ]
A further parameter is the method of feedback used as shown in studies of P300 signals. Patterns of P300 waves are generated involuntarily ( stimulus-feedback ) when people see something they recognize and may allow BCIs to decode categories of thoughts without training. [ citation needed ]
A 2005 study reported EEG emulation of digital control circuits, using a CNV flip-flop. [ 107 ] A 2009 study reported noninvasive EEG control of a robotic arm using a CNV flip-flop. [ 108 ] A 2011 study reported control of two robotic arms solving Tower of Hanoi task with three disks using a CNV flip-flop. [ 109 ] A 2015 study described EEG-emulation of a Schmitt trigger , flip-flop, demultiplexer , and modem . [ 110 ]
Advances by Bin He and his team at University of Minnesota suggest the potential of EEG-based brain-computer interfaces to accomplish tasks close to invasive brain-computer interfaces. Using advanced functional neuroimaging including BOLD functional MRI and EEG source imaging, They identified the co-variation and co-localization of electrophysiological and hemodynamic signals. [ 111 ] Refined by a neuroimaging approach and a training protocol, They fashioned a non-invasive EEG based brain-computer interface to control the flight of a virtual helicopter in 3-dimensional space, based upon motor imagination. [ 112 ] In June 2013 they announced a technique to guide a remote-control helicopter through an obstacle course. [ 113 ] They also solved the EEG inverse problem and then used the resulting virtual EEG for BCI tasks. Well-controlled studies suggested the merits of such a source analysis-based BCI. [ 114 ]
A 2014 study reported that severely motor-impaired patients could communicate faster and more reliably with non-invasive EEG BCI than with muscle-based communication channels. [ 115 ]
A 2019 study reported that the application of evolutionary algorithms could improve EEG mental state classification with a non-invasive Muse device, enabling classification of data acquired by a consumer-grade sensing device. [ 116 ]
In a 2021 systematic review of randomized controlled trials using BCI for post-stroke upper-limb rehabilitation, EEG-based BCI was reported to have efficacy in improving upper-limb motor function compared to control therapies. More specifically, BCI studies that utilized band power features, motor imagery , and functional electrical stimulation were reported to be more effective than alternatives. [ 117 ] Another 2021 systematic review focused on post-stroke robot-assisted EEG-based BCI for hand rehabilitation. Improvement in motor assessment scores was observed in three of eleven studies. [ 118 ]
In the early 1990s Babak Taheri, at University of California, Davis demonstrated the first single and multichannel dry active electrode arrays. [ 119 ] The arrayed electrode was demonstrated to perform well compared to silver / silver chloride electrodes. The device consisted of four sensor sites with integrated electronics to reduce noise by impedance matching . The advantages of such electrodes are:
The active electrode array is an integrated system containing an array of capacitive sensors with local integrated circuitry packaged with batteries to power the circuitry. This level of integration was required to achieve the result.
The electrode was tested on a test bench and on human subjects in four modalities, namely:
Performance compared favorably with that of standard wet electrodes in terms of skin preparation, no gel requirements (dry), and higher signal-to-noise ratio. [ 120 ]
In 1999 Hunter Peckham and others at Case Western Reserve University used a 64-electrode EEG skullcap to return limited hand movements to a quadriplegic . As he concentrated on simple but opposite concepts like up and down. A basic pattern was identified in his beta-rhythm EEG output and used to control a switch: Above average activity was interpreted as on, below average off. The signals were also used to drive nerve controllers embedded in his hands, restoring some movement. [ 121 ]
In 2009, the NCTU Brain-Computer-Interface-headband was announced. Those researchers also engineered silicon-based microelectro-mechanical system (MEMS) dry electrodes designed for application to non-hairy body sites. These electrodes were secured to the headband's DAQ board with snap-on electrode holders. The signal processing module measured alpha activity and transferred it over Bluetooth to a phone that assessed the patients' alertness and cognitive capacity. When the subject became drowsy, the phone sent arousing feedback to the operator to rouse them. [ 122 ]
In 2011, researchers reported a cellular based BCI that could cause a phone to ring. The wearable system was composed of a four channel bio-signal acquisition/amplification module , a communication module, and a Bluetooth phone. The electrodes were placed to pick up steady state visual evoked potentials ( SSVEPs ). [ 123 ] SSVEPs are electrical responses to flickering visual stimuli with repetition rates over 6 Hz [ 123 ] that are best found in the parietal and occipital scalp regions of the visual cortex. [ 124 ] [ 125 ] [ 126 ] It was reported that all study participants were able to initiate the phone call with minimal practice in natural environments. [ 127 ]
The scientists reported that a single channel fast Fourier transform (FFT) and multiple channel system canonical correlation analysis ( CCA ) algorithm can support mobile BCIs. [ 123 ] [ 128 ] The CCA algorithm has been applied in experiments investigating BCIs with claimed high accuracy and speed. [ 129 ] Cellular BCI technology can reportedly be translated for other applications, such as picking up sensorimotor mu / beta rhythms to function as a motor-imagery based BCI. [ 123 ]
In 2013, comparative tests performed on Android cell phone, tablet, and computer based BCIs, analyzed the power spectrum density of resultant EEG SSVEPs. The stated goals of this study were to "increase the practicability, portability, and ubiquity of an SSVEP-based BCI, for daily use". It was reported that the stimulation frequency on all mediums was accurate, although the phone's signal was not stable. The amplitudes of the SSVEPs for the laptop and tablet were reported to be larger than those of the cell phone. These two qualitative characterizations were suggested as indicators of the feasibility of using a mobile stimulus BCI. [ 128 ]
One of the difficulties with EEG readings is susceptibility to motion artifacts. [ 130 ] In most research projects, the participants were asked to sit still in a laboratory setting, reducing head and eye movements as much as possible. However, since these initiatives were intended to create a mobile device for daily use, [ 128 ] the technology had to be tested in motion. In 2013, researchers tested mobile EEG-based BCI technology, measuring SSVEPs from participants as they walked on a treadmill. Reported results were that as speed increased, SSVEP detectability using CCA decreased. Independent component analysis (ICA) had been shown to be efficient in separating EEG signals from noise. [ 131 ] The researchers stated that CCA data with and without ICA processing were similar. They concluded that CCA demonstrated robustness to motion artifacts. [ 125 ] EEG-based BCI applications offer low spatial resolution. Possible solutions include: EEG source connectivity based on graph theory , EEG pattern recognition based on Topomap and EEG- fMRI fusion.
Non-invasive BCIs have been applied to prosthetic upper and lower extremity devices in people with paralysis. For example, Gert Pfurtscheller of Graz University of Technology and colleagues demonstrated a BCI-controlled functional electrical stimulation system to restore upper extremity movements in a person with tetraplegia due to spinal cord injury . [ 132 ] Between 2012 and 2013, researchers at University of California, Irvine demonstrated for the first time that BCI technology can restore brain-controlled walking after spinal cord injury . In their study , a person with paraplegia operated a BCI-robotic gait orthosis to regain basic ambulation. [ 133 ] [ 134 ] In 2009 independent researcher Alex Blainey used the Emotiv EPOC to control a 5 axis robot arm. [ 135 ] He made several demonstrations of mind controlled wheelchairs and home automation .
Magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI) have both been used as non-invasive BCIs. [ 136 ] In a widely reported experiment, fMRI allowed two users to play Pong in real-time by altering their haemodynamic response or brain blood flow through biofeedback . [ 137 ]
fMRI measurements of haemodynamic responses in real time have also been used to control robot arms with a seven-second delay between thought and movement. [ 138 ]
In 2008 research developed in the Advanced Telecommunications Research (ATR) Computational Neuroscience Laboratories in Kyoto , Japan, allowed researchers to reconstruct images from brain signals at a resolution of 10x10 pixels . [ 139 ]
A 2011 study reported second-by-second reconstruction of videos watched by the study's subjects, from fMRI data. [ 140 ] This was achieved by creating a statistical model relating videos to brain activity. This model was then used to look up 100 one-second video segments, in a database of 18 million seconds of random YouTube videos, matching visual patterns to brain activity recorded when subjects watched a video. These 100 one-second video extracts were then combined into a mash-up image that resembled the video. [ 141 ] [ 142 ] [ 143 ]
Motor imagery involves imagining the movement of body parts, activating the sensorimotor cortex , which modulates sensorimotor oscillations in the EEG. This can be detected by the BCI and used to infer user intent. Motor imagery typically requires training to acquire acceptable control. Training sessions typically consume hours over several days. Regardless of the duration of the training session, users are unable to master the control scheme. This results in very slow pace of the gameplay. [ 144 ] Machine learning methods were used to compute a subject-specific model for detecting motor imagery performance. The top performing algorithm from BCI Competition IV in 2022 [ 145 ] dataset 2 for motor imagery was the Filter Bank Common Spatial Pattern, developed by Ang et al. from A*STAR , Singapore . [ 146 ]
Biofeedback can be used to monitor a subject's mental relaxation. In some cases, biofeedback does not match EEG, while parameters such as electromyography (EMG), galvanic skin resistance (GSR), and heart rate variability (HRV) can do so. Many biofeedback systems treat disorders such as attention deficit hyperactivity disorder (ADHD) , sleep problems in children, teeth grinding, and chronic pain. EEG biofeedback systems typically monitor four brainwave bands (theta: 4–7 Hz, alpha:8–12 Hz, SMR: 12–15 Hz, beta: 15–18 Hz) and challenge the subject to control them. Passive BCI uses BCI to enrich human–machine interaction with information on the user's mental state, for example, simulations that detect when users intend to push brakes during emergency vehicle braking. [ 51 ] Game developers using passive BCIs understand that through repetition of game levels the user's cognitive state adapts. During the first play of a given level, the player reacts differently than during subsequent plays: for example, the user is less surprised by an event that they expect. [ 144 ]
A VEP is an electrical potential recorded after a subject is presented with a visual stimuli. The types of VEPs include SSVEPs and P300 potential.
Steady-state visually evoked potentials (SSVEPs) use potentials generated by exciting the retina , using visual stimuli modulated at certain frequencies. SSVEP stimuli are often formed from alternating checkerboard patterns and at times use flashing images. The frequency of the phase reversal of the stimulus used can be distinguished by EEG; this makes detection of SSVEP stimuli relatively easy. SSVEP is used within many BCI systems. This is due to several factors. The signal elicited is measurable in as large a population as the transient VEP and blink movement. Electrocardiographic artefacts do not affect the frequencies monitored. The SSVEP signal is robust; the topographic organization of the primary visual cortex is such that a broader area obtains afferents from the visual field's central or fovial region. SSVEP comes with problems. As SSVEPs use flashing stimuli to infer user intent, the user must gaze at one of the flashing or iterating symbols in order to interact with the system. It is, therefore, likely that the symbols become irritating and uncomfortable during longer play sessions.
Another type of VEP is the P300 potential . This potential is a positive peak in the EEG that occurs roughly 300 ms after the appearance of a target stimulus (a stimulus for which the user is waiting or seeking) or oddball stimuli . P300 amplitude decreases as the target stimuli and the ignored stimuli grow more similar. P300 is thought to be related to a higher level attention process or an orienting response. Using P300 requires fewer training sessions. The first application to use it was the P300 matrix. Within this system, a subject chooses a letter from a 6 by 6 grid of letters and numbers. The rows and columns of the grid flashed sequentially and every time the selected "choice letter" was illuminated the user's P300 was (potentially) elicited. However, the communication process, at approximately 17 characters per minute, was slow. P300 offers a discrete selection rather than continuous control. The advantage of P300 within games is that the player does not have to learn how to use a new control system, requiring only short training instances to learn gameplay mechanics and the basic BCI paradigm. [ 144 ]
Human-computer interaction can exploit other recording modalities, such as electrooculography and eye-tracking. These modalities do not record brain activity and therefore do not qualify as BCIs. [ 147 ]
In 1989, a study reported control of a mobile robot by eye movement using electrooculography signals. A mobile robot was driven to a goal point using five EOG commands, interpreted as forward, backward, left, right, and stop. [ 148 ]
A 2016 article described a new non-EEG-based HCI that required no visual fixation , or ability to move the eyes. [ 149 ] The interface is based on covert interest ; directing attention to a chosen letter on a virtual keyboard, without the need to look directly at the letter. Each letter has its own (background) circle which micro-oscillates in brightness differently from the others. Letter selection is based on best fit between unintentional pupil-size oscillation and the background circle's brightness oscillation pattern. Accuracy is additionally improved by the user's mental rehearsal of the words 'bright' and 'dark' in synchrony with the brightness transitions of the letter's circle.
In the 1960s a researcher after training used EEG to create Morse code using alpha waves. [ 150 ] On 27 February 2013 Miguel Nicolelis 's group at Duke University and IINN-ELS connected the brains of two rats, allowing them to share information, in the first-ever direct brain-to-brain interface . [ 151 ] [ 152 ] [ 153 ]
Gerwin Schalk reported that ECoG signals can discriminate vowels and consonants embedded in spoken and imagined words, shedding light on the mechanisms associated with their production and could provide a basis for brain-based communication using imagined speech. [ 98 ] [ 154 ]
In 2002 Kevin Warwick had an array of 100 electrodes fired into his nervous system in order to link his nervous system to the Internet. Warwick carried out a series of experiments. Electrodes were implanted into his wife's nervous system, allowing them to conduct the first direct electronic communication experiment between the nervous systems of two humans. [ 155 ] [ 156 ] [ 157 ] [ 158 ]
Other researchers achieved brain-to-brain communication between participants at a distance using non-invasive technology attached to the participants' scalps. The words were encoded in binary streams by the cognitive motor input of the person sending the information. Pseudo-random bits of the information carried encoded words "hola" ("hi" in Spanish) and "ciao" ("goodbye" in Italian) and were transmitted mind-to-mind. [ 159 ]
Researchers have built devices to interface with neural cells and entire neural networks in vitro . Experiments on cultured neural tissue focused on building problem-solving networks, constructing basic computers and manipulating robotic devices. Research into techniques for stimulating and recording individual neurons grown on semiconductor chips is neuroelectronics or neurochips . [ 160 ]
Development of the first neurochip was claimed by a Caltech team led by Jerome Pine and Michael Maher in 1997. [ 161 ] The Caltech chip had room for 16 neurons.
In 2003 a team led by Theodore Berger, at the University of Southern California , worked on a neurochip designed to function as an artificial or prosthetic hippocampus . The neurochip was designed for rat brains. The hippocampus was chosen because it is thought to be the most structured and most studied part of the brain. Its function is to encode experiences for storage as long-term memories elsewhere in the brain. [ 162 ]
In 2004 Thomas DeMarse at the University of Florida used a culture of 25,000 neurons taken from a rat's brain to fly a F-22 fighter jet aircraft simulator . After collection, the cortical neurons were cultured in a petri dish and reconnected themselves to form a living neural network. The cells were arranged over a grid of 60 electrodes and used to control the pitch and yaw functions of the simulator. The study's focus was on understanding how the human brain performs and learns computational tasks at a cellular level. [ 163 ]
The idea of combining/integrating brain signals from multiple individuals was introduced at Humanity+ @Caltech, in December 2010, by Adrian Stoica, who referred to the concept as multi-brain aggregation. [ 164 ] [ 165 ] [ 166 ] A patent was applied for in 2012. [ 167 ] [ 168 ] [ 169 ] Stoica's first paper on the topic appeared in 2012, after the publication of his patent application. [ 170 ]
Concerns center on the safety and long-term effects on users. These include obtaining informed consent from individuals with communication difficulties, the impact on patients' and families' quality of life, health-related side effects, misuse of therapeutic applications, safety risks, and the non-reversible nature of some BCI-induced changes. Additionally, questions arise about access to maintenance, repair, and spare parts, particularly in the event of a company's bankruptcy. [ 171 ]
The legal and social aspects of BCIs complicate mainstream adoption. Concerns include issues of accountability and responsibility, such as claims that BCI influence overrides free will and control over actions, inaccurate translation of cognitive intentions, personality changes resulting from deep-brain stimulation, and the blurring of the line between human and machine. [ 172 ] Other concerns involve the use of BCIs in advanced interrogation techniques, unauthorized access ("brain hacking"), [ 173 ] social stratification through selective enhancement, privacy issues related to mind-reading, tracking and "tagging" systems, and the potential for mind, movement, and emotion control. [ 174 ]
In their current form, most BCIs are more akin to corrective therapies that engage few of such ethical issues. Bioethics is well-equipped to address the challenges posed by BCI technologies, with Clausen suggesting in 2009 that "BCIs pose ethical challenges, but these are conceptually similar to those that bioethicists have addressed for other realms of therapy." [ 175 ] Haselager and colleagues highlighted the importance of managing expectations and value. [ 176 ]
The evolution of BCIs mirrors that of pharmaceutical science, which began as a means to address impairments and now enhances focus and reduces the need for sleep. As BCIs progress from therapies to enhancements, the BCI community is working to create consensus on ethical guidelines for research, development, and dissemination. [ 177 ] [ 178 ]
Various companies are developing inexpensive BCIs for research and entertainment. Toys such as the NeuroSky and Mattel MindFlex have seen some commercial success.
A consortium of 12 European partners completed a roadmap to support the European Commission in their funding decisions for the Horizon 2020 framework program. The project was funded by the European Commission. It started in November 2013 and published a roadmap in April 2015. [ 195 ] A 2015 publication describes this project, as well as the Brain-Computer Interface Society. [ 196 ] It reviewed work within this project that further defined BCIs and applications, explored recent trends, discussed ethical issues, and evaluated directions for new BCIs.
Other recent publications too have explored future BCI directions for new groups of disabled users. [ 7 ] [ 197 ]
Some people have a disorder of consciousness (DOC). This state is defined to include people in a coma and those in a vegetative state (VS) or minimally conscious state (MCS). BCI research seeks to address DOC. A key initial goal is to identify patients who can perform basic cognitive tasks, which would change their diagnosis, and allow them to make important decisions (such as whether to seek therapy, where to live, and their views on end-of-life decisions regarding them). Patients incorrectly diagnosed may die as a result of end-of-life decisions made by others. The prospect of using BCI to communicate with such patients is a tantalizing prospect. [ 198 ] [ 199 ]
Many such patients cannot use BCIs based on vision. Hence, tools must rely on auditory and/or vibrotactile stimuli. Patients may wear headphones and/or vibrotactile stimulators placed on responsive body parts. Another challenge is that patients may be able to communicate only at unpredictable intervals. Home devices can allow communications when the patient is ready.
Automated tools can ask questions that patients can easily answer, such as "Is your father named George?" or "Were you born in the USA?" Automated instructions inform patients how to convey yes or no, for example by focusing their attention on stimuli on the right vs. left wrist. This focused attention produces reliable changes in EEG patterns that can help determine whether the patient is able to communicate. [ 200 ] [ 201 ] [ 202 ]
People may lose some of their ability to move due to many causes, such as stroke or injury. Research in recent years has demonstrated the utility of EEG-based BCI systems in aiding motor recovery and neurorehabilitation in patients who have had a stroke. [ 203 ] [ 204 ] [ 205 ] [ 206 ] Several groups have explored systems and methods for motor recovery that include BCIs. [ 207 ] [ 208 ] [ 209 ] [ 210 ] In this approach, a BCI measures motor activity while the patient imagines or attempts movements as directed by a therapist. The BCI may provide two benefits: (1) if the BCI indicates that a patient is not imagining a movement correctly (non-compliance), then the BCI could inform the patient and therapist; and (2) rewarding feedback such as functional stimulation or the movement of a virtual avatar also depends on the patient's correct movement imagery.
So far, BCIs for motor recovery have relied on the EEG to measure the patient's motor imagery. However, studies have also used fMRI to study different changes in the brain as persons undergo BCI-based stroke rehab training. [ 211 ] [ 212 ] [ 213 ] Imaging studies combined with EEG-based BCI systems hold promise for investigating neuroplasticity during motor recovery post-stroke. [ 213 ] Future systems might include the fMRI and other measures for real-time control, such as functional near-infrared, probably in tandem with EEGs. Non-invasive brain stimulation has also been explored in combination with BCIs for motor recovery. [ 214 ] In 2016, scientists out of the University of Melbourne published preclinical proof-of-concept data related to a potential brain-computer interface technology platform being developed for patients with paralysis to facilitate control of external devices such as robotic limbs, computers and exoskeletons by translating brain activity. [ 215 ] [ 216 ] [ 217 ]
In 2014, some 400,000 people underwent brain mapping during neurosurgery. This procedure is often required for people who do not respond to medication . [ 218 ] During this procedure, electrodes are placed on the brain to precisely identify the locations of structures and functional areas. Patients may be awake during neurosurgery and asked to perform tasks, such as moving fingers or repeating words. This is necessary so that surgeons can remove the desired tissue while sparing other regions. Removing too much brain tissue can cause permanent damage, while removing too little can mandate additional neurosurgery. [ citation needed ]
Researchers explored ways to improve neurosurgical mapping. This work focuses largely on high gamma activity, which is difficult to detect non-invasively. Results improved methods for identifying key functional areas. [ 219 ]
Flexible electronics are polymers or other flexible materials (e.g. silk , [ 220 ] pentacene , PDMS , Parylene , polyimide [ 221 ] ) printed with circuitry ; the flexibility allows the electronics to bend. The fabrication techniques used to create these devices resembles those used to create integrated circuits and microelectromechanical systems (MEMS). [ citation needed ]
Flexible neural interfaces may minimize brain tissue trauma related to mechanical mismatch between electrode and tissue. [ 222 ]
Neural dust is millimeter-sized devices operated as wirelessly powered nerve sensors that were proposed in a 2011 paper from the University of California, Berkeley Wireless Research Center. [ 223 ] [ 224 ] In one model, local field potentials could be distinguished from action potential "spikes", which would offer greatly diversified data vs conventional techniques. [ 223 ]
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https://en.wikipedia.org/wiki/Brain–computer_interface
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Branchial hearts are accessory pumps that supplement the action of the systemic heart in a cephalopod 's body. They are myogenic in nature. [ 1 ] Branchial hearts are always in pairs located at the base of the gills . Each branchial heart consists of a single chamber. [ 1 ] [ 2 ] They pump blood through the gills via the afferent branchial veins. Since they only circulate venous blood , branchial hearts function under predominantly anaerobic conditions. [ 1 ] Branchial hearts also appear to be involved in hemocyanin synthesis. [ 3 ] [ 2 ]
Each branchial heart is directly connected to a branchial heart appendage or pericardial gland. [ 4 ] The action of the branchial hearts is necessary for the production of primary urine in these appendages via pressure filtration. [ 5 ] Branchial hearts may have evolved from the pericardial glands of nautiloids , such as those still found in modern nautiluses . [ 6 ]
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The Breakthrough Prize in Life Sciences is a scientific award, funded by internet entrepreneurs Mark Zuckerberg and Priscilla Chan of Facebook; Sergey Brin of Google; entrepreneur and venture capitalist Yuri Milner ; and Anne Wojcicki , one of the founders of the genetics company 23andMe . [ 1 ]
The award of $3 million, the largest award in the sciences, [ 2 ] is given to researchers who have made discoveries that extend human life. The Prize is awarded annually, beginning in 2013, with six awards given in each subsequent year. Winners are expected to give public lectures and form the committee to decide future winners. [ 1 ] The ceremony takes place in the San Francisco Bay Area, with the symposiums alternating between University of California, Berkeley , University of California, San Francisco , and Stanford University .
[ 11 ]
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https://en.wikipedia.org/wiki/Breakthrough_Prize_in_Life_Sciences
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Breast Cancer Research is a bimonthly peer-reviewed medical journal covering research into breast cancer . The journal was established in 1999 and is published by BioMed Central . The editor-in-chief is Lewis Chodosh ( University of Pennsylvania ).
The journal is abstracted and indexed in: [ 1 ]
According to the Journal Citation Reports , the journal has a 2021 impact factor of 8.4. [ 2 ]
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Breast Cancer Research and Treatment is a scientific journal focused on the treatment of and investigations in breast cancer . It is targeted towards a wide audience of clinical researchers , epidemiologists , immunologists , or cell biologists interested in breast cancer.
The types of articles in this journal include original research, invited reviews, discussions on controversial issues, book reviews, meeting reports, letters to the editors, and editorials. Manuscripts are peer-reviewed by an international and multidisciplinary panel of advisory editors. According to the Journal Citation Reports , the journal has a 2020 impact factor of 4.872. [ 1 ]
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Breast atrophy is the normal or spontaneous atrophy or shrinkage of the breasts . [ 1 ]
Breast atrophy commonly occurs in women during menopause when estrogen levels decrease. [ 2 ] [ 3 ] [ 4 ] It can also be caused by hypoestrogenism and/or hyperandrogenism in women in general, [ 1 ] such as in antiestrogen treatment for breast cancer , in polycystic ovary syndrome (PCOS), [ 5 ] [ 6 ] and in malnutrition such as that associated with eating disorders like anorexia nervosa or with chronic disease . [ 1 ] [ 7 ] [ 8 ] It can also be an effect of weight loss . [ 8 ] [ 9 ]
In the treatment of gynecomastia in males and macromastia in women, and in hormone replacement therapy (HRT) for trans men , [ 10 ] breast atrophy may be a desired effect.
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A breast biopsy is a medical procedure used to remove a small sample of breast tissue to examine it more closely under a microscope. It is usually done after a suspicious lesion is discovered on either mammography or ultrasound to get tissue for pathological diagnosis. [ 1 ] Several methods for a breast biopsy now exist. [ 2 ] The most appropriate method of biopsy for a patient depends upon a variety of factors, including the size, location, appearance and characteristics of the abnormality. [ 3 ] The different types of breast biopsies include fine-needle aspiration (FNA), vacuum-assisted biopsy , core needle biopsy , and surgical excision biopsy. [ 3 ] [ 4 ] [ 5 ] Breast biopsies can be done utilizing ultrasound, MRI or a stereotactic biopsy imaging guidance. [ 2 ] [ 5 ] [ 4 ] [ 6 ] Vacuum assisted biopsies are typically done using stereotactic techniques when the suspicious lesion can only be seen on mammography. [ 5 ] On average, 5–10 biopsies of a suspicious breast lesion will lead to the diagnosis of one case of breast cancer . [ 7 ] Needle biopsies have largely replaced open surgical biopsies in the initial assessment of imaging as well as palpable abnormalities in the breast. [ 8 ]
There are many reasons why a doctor may order a breast biopsy. [ 7 ] Typical indications include:
Fine-needle aspiration (FNA) is a percutaneous ("through the skin") procedure that uses a fine needle and a syringe to sample fluid from a breast cyst or remove clusters of cells from a solid mass. [ 6 ] It is mainly used to differentiate between a cyst and a mass. [ 6 ] If the aspirated contents are not cyst-like, then a tissue sample must be taken to better evaluate the mass. [ 6 ] Fine-needle aspiration is one of the most commonly used initial diagnostic tools for suspicious lesions. [ 12 ] The doctor will typically use a 22 or 27 gauge needle to aspirate out free fluid and cells. [ 12 ] It can be done in an outpatient setting and is associated with minimal pain. [ 12 ] However, in up to 30% of cases, pathological slides from fine-needle aspiration of breast lesions may be inconclusive, necessitating the need for further testing. [ 12 ] FNA can be done to aspirate the contents of a cyst, which may relieve any pain that the cyst caused, or can be used to aspirate a suspicious lesion in conjunction with cytology (cellular analysis). [ 13 ] If aspirating the contents of a cyst, the aspirate is usually not sent for cytology unless it is bloody. [ 13 ] If the cyst is not detectable by touch, it may be located using ultrasound, MRI, or stereotactic mammography. [ 13 ] Recovery time from an outpatient FNA is minimal. [ 13 ]
Core needle biopsy (CNB) is another percutaneous ("through the skin") method of breast biopsy that became more popular than FNA in the 1990s due to the larger sample of tissue CNB provides. [ 14 ] This method is usually done under ultrasound guidance and involves using two needles, one inner "puncture" needle that is inserted into the mass, and a wider gauge needle with an open "gap" or "trough" on one side that allows for tissue to enter. [ 11 ] A spring-loaded sheath then is triggered by the technician that covers the trough in the needle to allow sample tissue to be separated and removed for analysis. [ 11 ] Typically four tissue samples are removed to minimize sample error. To prevent the need to pierce the breast repeatedly, a coaxial needle is left in place on top of the mass as a guide. [ 11 ] CNB has a higher sensitivity for cancer than FNA, has lower false negatives, and has proven more successful in finding rare breast diseases like lobular carcinoma . However, this method still has relatively high rates of false negatives compared to surgical or vacuum-assisted methods due to the overall low volume of tissue removed. [ 14 ] [ 11 ] Also, because breast tissue can be difficult to target on ultrasound, as many as 5–10% of suspicious lesions are missed by the needle and may result in a high rate of false negatives, or the need for additional biopsies. [ 14 ]
Stereotactic biopsy is done with the help of a specialized device, which provides mammographic guidance. For a stereotactic biopsy, morbid obesity is a relative contraindication due to weight limitations of the devices. Pregnancy and breast compression size may also be contraindications depending on the modality being used. [ 15 ]
Vacuum-assisted breast biopsy (VABB) is a more recent version of core needle biopsy using a vacuum technique to assist the collection of the tissue sample. Similarly to core needle biopsy, the needle has a lateral ("from the side") opening and can be rotated, allowing multiple samples to be collected through a single skin incision. This method has become more popular than FNA, CNB, and surgical biopsies due to the benefits of low invasiveness while still obtaining a larger tissue sample. [ 14 ] Taking more tissue helps reduce sampling error since breast lesions are often heterogeneous (cancer cells are spread unevenly) and therefore cancer can be missed if not enough tissue is taken. VABB can be guided by stereotactic (most popular), ultrasound, and MRI, and can yield as much as 2g of tissue sample. [ 14 ] The vacuum-assisted biopsy category also includes automated rotational core devices. [ 16 ]
The direct and frontal biopsy systems can even be considered relatively painless. The quality of the sample is sufficient for research on molecular biology. [ 17 ] [ 18 ] [ 19 ]
Excisional biopsy involves surgically removing the suspicious area of the breast to examine it under the microscope for diagnosis. One method is wire-guided (or wire-localized) excisional biopsy, where a wire is inserted into the breast and repeatedly imaged using breast ultrasound or mammography until the technician sees that the tip is located in the suspicious area. The suspicious area is then removed entirely in one block by the surgeon with the help of the wire. [ 10 ] [ 20 ] When the tissue is removed, it is processed by a pathologist, who describes the tissue as it appears by eye and inks the sides to help orient the tissue under the microscope after it is sliced. [ 10 ] Each color corresponds to a direction, such as superior, inferior, medial, lateral, anterior, and posterior (these correspond to top, bottom, outside, inside, front, and back). [ 10 ] When the tissue is then looked at under the microscope, the margins can then be evaluated to see if they are free of cancer cells, or if the surgeon needs to go back and remove more tissue from that area. [ 10 ] Titanium surgical clips are often left behind by surgeons to help future physicians locate the site and monitor for future disease or target the area with radiation if needed. [ 10 ] Percutaneous ("through the skin") biopsy methods have become more favored over surgical biopsies due to the high rate of benign findings (80%) and the reduction of adverse effects such as scarring. [ 11 ]
Adverse effects of breast biopsies tend to vary depending on what type of biopsy is performed. The more invasive, such as surgery, tend to have more severe types of adverse incidents, whereas less invasive such as FNA or CNB tend to have less severe. For vacuum-assisted biopsies, some complications of the procedure can include bleeding, post-operative pain, and hematoma formation. [ 14 ] However, most can be avoided with proper application of pressure and rest. [ 14 ] Some examples of adverse effects of core needle biopsies can include rare biopsy risks like infection, abscess formation, fistula formation, migration of any markers placed in the breast, and potential seeding of the tumor (causing displacement of cancer cells due to the procedure that can start new tumors elsewhere). [ 1 ] [ 21 ] Another potential adverse effect occurs when taking a biopsy of an area of microcalcification. If the entire area of microcalcification is removed, it is then very difficult to find the suspicious area in the future for treatment. A marker is placed in the suspicious area to help localize the proper area for possible removal at a later date; if this is removed during biopsy, it can be difficult to make sure that the correct area was excised in surgery. [ 21 ] Bleeding into the site of the suspicious lesion caused by the biopsy procedure can appear to look like a complex cyst on ultrasound, which could lead to additional unnecessary management. [ 13 ] The false negative rate of the results of a breast biopsy is approximately 1%. [ 13 ]
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Breast development , also known as mammogenesis , is a complex biological process in primates that takes place throughout a female 's life.
It occurs across several phases, including prenatal development , puberty , and pregnancy . At menopause , breast development ceases and the breasts atrophy . Breast development results in prominent and developed structures on the chest known as breasts in primates, which serve primarily as mammary glands . The process is mediated by an assortment of hormones (and growth factors ), the most important of which include estrogen , progesterone , prolactin , and growth hormone .
The master regulators of breast development are the steroid hormones , estrogen , and progesterone , growth hormone (GH), mostly via its secretory product, insulin-like growth factor 1 (IGF-1), and prolactin . [ 1 ] These regulators induce the expression of growth factors , such as amphiregulin , epidermal growth factor (EGF), IGF-1, and fibroblast growth factor (FGF), which in turn have specific roles in breast growth and maturation. [ 1 ]
At puberty , gonadotropin-releasing hormone (GnRH) is secreted in a pulsatile manner from the hypothalamus . [ 2 ] [ 3 ] GnRH induces the secretion of the gonadotropins , follicle-stimulating hormone (FSH) and luteinizing hormone (LH), from the pituitary gland . [ 2 ] [ 3 ] The secreted gonadotropins travel through the bloodstream to the ovaries and trigger the secretion of estrogen and progesterone in fluctuating amounts during each menstrual cycle . [ 2 ] [ 3 ] Growth hormone (GH), which is secreted from the pituitary gland, and insulin-like growth factor 1 (IGF-1), which is produced in the body in response to GH, are growth-mediating hormones. [ 4 ] During prenatal development , infancy, and childhood, GH and IGF-1 levels are low, but progressively increase and reach a peak at puberty, [ 5 ] with a 1.5- to 3-fold increase in pulsatile GH secretion and a 3-fold or greater increase in serum IGF-1 levels being capable of occurring at this time. [ 6 ] In late adolescence and early adulthood, GH and IGF-1 levels significantly decrease, [ 7 ] and continue to decrease throughout the rest of life. [ 5 ] It has been found that both estrogen and GH are essential for breast development at puberty – in the absence of either, no development will take place. [ 8 ] [ 9 ] Moreover, most of the role of GH in breast development has been found to be mediated by its induction of IGF-1 production and secretion, as IGF-1 administration rescues breast development in the absence of GH. [ 9 ] GH induction of IGF-1 production and secretion occurs in almost all types of tissue in the body, but especially in the liver , which is the source of approximately 80% of circulating IGF-1, [ 10 ] as well as locally in the breasts. [ 5 ] [ 11 ] Although IGF-1 is responsible for most of the role of GH in mediating breast development, GH itself has been found to play a direct, augmenting role as well, as it increases estrogen receptor (ER) expression in breast stromal (connective) tissue , while IGF-1, in contrast, has been found to not do this. [ 12 ] [ 13 ] In addition to estrogen and GH/IGF-1 both being essential for pubertal breast development, they are synergistic in bringing it about. [ 8 ] [ 9 ] [ 14 ]
Despite the apparent necessity of GH/IGF-1 signaling in pubertal breast development however, women with Laron syndrome , in whom the growth hormone receptor (GHR) is defective and insensitive to GH and serum IGF-1 levels are very low, puberty, including breast development, is delayed, although full sexual maturity is always eventually reached. [ 15 ] Moreover, breast development and size are normal (albeit delayed) in spite of GH/IGF-1 axis insufficiency, and in some the breasts may actually be large in relation to body size. [ 15 ] [ 16 ] The relatively large breasts in women with Laron syndrome have been suggested to be due to increased secretion of prolactin (which is known to produce breast enlargement) caused by a drift phenomenon from somatomammotrophic cells in the pituitary gland with a high GH secretion. [ 15 ] [ 16 ] An animal model of Laron syndrome, the GHR knockout mouse , shows severely impaired ductal outgrowth at 11 weeks of age. [ 17 ] [ 18 ] [ 19 ] However, by 15 weeks, ductal development has caught up with that of normal mice and the ducts have fully distributed throughout the mammary fat pad, although the ducts remain narrower than those of wild-type mice. [ 17 ] [ 18 ] [ 19 ] In any case, female GHR knockout mice can lactate normally. [ 17 ] [ 19 ] As such, it has been said that the phenotypes of women with Laron syndrome and GHR knockout mice are identical, with diminished body size and delayed sexual maturation accompanied by normal lactation. [ 17 ] These data indicate that very low circulating levels of IGF-1 can nonetheless allow for full pubertal breast development. [ 15 ] [ 17 ]
Development of the breasts during the prenatal stage of life is independent of biological sex and sex hormones . [ 20 ] During embryonic development , the breast buds, in which networks of tubules are formed, are generated from the ectoderm . [ 21 ] These rudimentary tubules will eventually become the matured lactiferous (milk) ducts , which connect the lobules (milk "containers") of the breast, grape-like clusters of alveoli , to the nipples. [ 22 ] Until puberty, the tubule networks of the breast buds remain rudimentary and quiescent, [ 1 ] and the male and female breast do not show any differences. [ 20 ] During puberty in females, estrogen, in conjunction with GH/IGF-1, through activation of ERα specifically (and notably not ERβ or GPER ), [ 23 ] [ 24 ] causes growth of and transformation of the tubules into the matured ductal system of the breasts. [ 20 ] [ 21 ] [ 25 ] Under the influence of estrogen, the ducts sprout and elongate, and terminal end buds (TEBs), bulbous structures at the tips of the ducts, penetrate into the fat pad and branch as the ducts elongate. [ 20 ] [ 21 ] [ 25 ] This continues until a tree-like network of branched ducts that is embedded into and fills the entire fat pad of the breast is formed. [ 1 ] [ 20 ] [ 21 ] [ 25 ] In addition to its role in mediating ductal development, estrogen causes stromal tissue to grow and adipose (fat) tissue to accumulate, [ 20 ] [ 21 ] as well as the nipple-areolar complex to increase in size. [ 26 ]
Progesterone, in conjunction with GH/IGF-1 similarly to estrogen, affects the development of the breasts during puberty and thereafter as well. [ 20 ] [ 21 ] [ 25 ] To a lesser extent than estrogen, progesterone contributes to ductal development at this time, as evidenced by the findings that progesterone receptor (PR) knockout mice or mice treated with the PR antagonist mifepristone show delayed (albeit eventually normal, due to estrogen acting on its own) ductal growth during puberty and by the fact that progesterone has been found to induce ductal growth on its own in the mouse mammary gland mainly via the induction of the expression of amphiregulin, the same growth factor that estrogen primarily induces to mediate its actions on ductal development. [ 27 ] In addition, progesterone produces modest lobuloalveolar development (alveolar bud formation or ductal sidebranching) starting at puberty, [ 20 ] [ 25 ] specifically through activation of PRB (and notably not PRA ), [ 28 ] with growth and regression of the alveoli occurring to some degree with each menstrual cycle. [ 20 ] [ 21 ] However, only rudimentary alveoli develop in response to pre-pregnancy levels of progesterone and estrogen, and lobuloalveolar development will remain at this stage until pregnancy occurs, if it does. [ 21 ] In addition to GH/IGF-1, estrogen is required for progesterone to affect the breasts, [ 20 ] [ 25 ] as estrogen primes the breasts by inducing the expression of the progesterone receptor (PR) in breast epithelial tissue . [ 28 ] In contrast to the case of the PR, ER expression in the breast is stable and differs relatively little in the contexts of reproductive status, stage of the menstrual cycle, or exogenous hormonal therapy . [ 28 ]
During pregnancy , pronounced breast growth and maturation occurs in preparation of lactation and breastfeeding . [ 20 ] [ 29 ] [ 30 ] Estrogen and progesterone levels increase dramatically, [ 20 ] reaching levels by late pregnancy that are several hundred-fold higher than usual menstrual cycle levels. [ 31 ] Estrogen and progesterone cause the secretion of high levels of prolactin from the anterior pituitary , [ 32 ] [ 33 ] which reach levels as high as 20 times greater than normal menstrual cycle levels. [ 31 ] IGF-1 and IGF-2 levels also increase dramatically during pregnancy, due to secretion of placental growth hormone (PGH). [ 34 ] Further ductal development, by estrogen, again in conjunction with GH/IGF-1, occurs during pregnancy. [ 21 ] [ 22 ] In addition, the concert of estrogen, progesterone (again specifically through PRB), [ 28 ] prolactin, and other lactogens such as human placental lactogen (hPL) and PGH, in conjunction with GH/IGF-1, as well as insulin-like growth factor 2 (IGF-2), [ 35 ] [ 36 ] acting together, mediate the completion of lobuloalveolar development of the breasts during pregnancy. [ 21 ] [ 22 ] [ 37 ] [ 38 ] Both PR and prolactin receptor (PRLR) knockout mice fail to show lobuloalveolar development, and progesterone and prolactin have been found to be synergistic in mediating growth of alveoli, demonstrating the essential role of both of these hormones in this aspect of breast development. [ 39 ] [ 40 ] Growth hormone receptor (GHR) knockout mice also show greatly impaired lobuloalveolar development. [ 41 ] In addition to their role in lobuloalveolar growth, prolactin and hPL act to increase the size of the nipple-areolar complex during pregnancy. [ 42 ] By the end of the fourth month of pregnancy, at which time lobuloalveolar maturation is complete, the breasts are fully prepared for lactation and breastfeeding. [ 30 ]
Insulin , glucocorticoids such as cortisol (and by extension adrenocorticotropic hormone (ACTH)), and thyroid hormones such as thyroxine (and by extension thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH)) also play permissive but less well-understood/poorly-characterized roles in breast development during both puberty and pregnancy, and are required for full functional development. [ 43 ] [ 44 ] [ 45 ] [ 46 ] Leptin has also been found to be an important factor in mammary gland development, and has been found to promote mammary epithelial cell proliferation. [ 2 ] [ 47 ]
In contrast to the female-associated sex hormones, estrogen and progesterone, the male-associated sex hormones, the androgens , such as testosterone and dihydrotestosterone (DHT), powerfully suppress the action of estrogen in the breasts. [ 37 ] [ 46 ] [ 48 ] [ 49 ] At least one way that they do this is by reducing the expression of the estrogen receptor in breast tissue. [ 48 ] [ 49 ] [ 50 ] In the absence of androgenic activity, such as in women with complete androgen insensitivity syndrome (CAIS), modest levels of estrogen (50 pg/mL) are capable of mediating significant breast development, with CAIS women showing breast volumes that are even above-average. [ 37 ] The combination of much higher levels of androgens (about 10-fold higher) and much lower levels of estrogen (about 10-fold less), [ 51 ] due to the ovaries in females producing high amounts of estrogens but low amounts of androgens and the testes in males producing high amounts of androgens but low amounts of estrogens, [ 52 ] are why males generally do not grow prominent or well-developed breasts relative to females. [ 46 ] [ 53 ]
Calcitriol , the hormonally active form of vitamin D , acting through the vitamin D receptor (VDR), has, like the androgens, been reported to be a negative regulator of mammary gland development in mice, for instance, during puberty. [ 41 ] VDR knockout mice show more extensive ductal development relative to wild-type mice, [ 54 ] as well as precocious mammary gland development. [ 55 ] In addition, VDR knockout has also been shown to result in increased responsiveness of mouse mammary gland tissue to estrogen and progesterone, which was represented by increased cell growth in response to these hormones. [ 54 ] Conversely however, it has been found that VDR knockout mice show reduced ductal differentiation, represented by an increased number of undifferentiated TEBs, [ 56 ] and this finding has been interpreted as indicating that vitamin D may be essential for lobuloalveolar development. [ 40 ] As such, calcitriol, via the VDR, may be a negative regulator of ductal development but a positive regulator of lobuloalveolar development in the mammary gland. [ 57 ]
A possible mechanism of the negative regulatory effects of the VDR on breast development may be indicated by a study of vitamin D 3 supplementation in women which found that vitamin D 3 suppresses cyclooxygenase-2 (COX-2) expression in the breast, and by doing so, reduces and increases, respectively, the levels of prostaglandin E 2 (PGE 2 ) and transforming growth factor β2 (TGF-β2), a known inhibitory factor in breast development. [ 58 ] Moreover, suppression of PGE 2 in breast tissue is relevant because, via activation of prostaglandin EP receptors , PGE 2 potently induces amphiregulin expression in breast tissue, and activation of the EGFR by amphiregulin increases COX-2 expression in breast tissue, in turn resulting in more PGE 2 , and thus, a self-perpetuating, synergistic cycle of growth amplification due to COX-2 appears to potentially be present in normal breast tissue. [ 59 ] [ 60 ] Accordingly, overexpression of COX-2 in mammary gland tissue produces mammary gland hyperplasia as well as precocious mammary gland development in female mice, mirroring the phenotype of VDR knockout mice, and demonstrating a strong stimulatory effect of COX-2, which is downregulated by VDR activation, on the growth of the mammary glands. [ 59 ] [ 60 ] Also in accordance, COX-2 activity in the breasts has been found to be positively associated with breast volume in women. [ 61 ]
Estrogen, progesterone, and prolactin, as well as GH/IGF-1, produce their effects on breast development by modulating the local expression in breast tissue of an assortment of autocrine and paracrine growth factors, [ 25 ] [ 44 ] [ 62 ] [ 63 ] [ 64 ] including IGF-1, IGF-2, amphiregulin, [ 65 ] EGF, FGF, hepatocyte growth factor (HGF), [ 66 ] tumor necrosis factor α (TNF-α), tumor necrosis factor β (TNF-β), transforming growth factor α (TGF-α), [ 67 ] transforming growth factor β (TGF-β), [ 68 ] heregulin , [ 69 ] Wnt , [ 40 ] RANKL , [ 40 ] and leukemia inhibitory factor (LIF). [ 40 ] These factors regulate cellular growth , proliferation , and differentiation via activation of intracellular signaling cascades that control cell function , such as Erk , Akt , JNK , and Jak/Stat . [ 10 ] [ 70 ] [ 71 ] [ 72 ]
Based on research with epidermal growth factor receptor (EGFR) knockout mice , the EGFR, which is the molecular target of EGF, TGF-α, amphiregulin, and heregulin, has, similarly to the insulin-like growth factor-1 receptor (IGF-1R), [ 1 ] been found to be essential for mammary gland development. [ 73 ] Estrogen and progesterone mediate ductal development mainly through induction of amphiregulin expression, and thus downstream EGFR activation. [ 27 ] [ 65 ] [ 70 ] [ 74 ] [ 75 ] Accordingly, ERα, amphiregulin , and EGFR knockout mice copy each other phenotypically in regards to their effects on ductal development. [ 74 ] Also in accordance, treatment of mice with amphiregulin or other EGFR ligands like TGF-α or heregulin induces ductal and lobuloalveolar development in the mouse mammary gland, actions that occur even in the absence of estrogen and progesterone. [ 69 ] [ 76 ] As both the IGF-1R and the EGFR are independently essential for mammary gland development, and as combined application of IGF-1 and EGF, through their respective receptors, has been found to synergistically stimulate the growth of human breast epithelial cells, these growth factor systems appear to work together in mediating breast development. [ 77 ] [ 78 ] [ 79 ]
Elevated levels of HGF and, to a lesser extent, IGF-1 (by 5.4-fold and 1.8-fold, respectively), in breast stromal tissue, have been found in macromastia , a very rare condition of extremely and excessively large breast size. [ 80 ] Exposure of macromastic breast stromal tissue to non-macromastic breast epithelial tissue was found to cause increased alveolar morphogenesis and epithelial proliferation in the latter. [ 80 ] A neutralizing antibody for HGF, but not for IGF-1 or EGF, was found to attenuate the proliferation of breast epithelial tissue caused by exposure to macromastic breast stromal cells, potentially directly implicating HGF in the breast growth and enlargement seen in macromastia . [ 80 ] Also, a genome-wide association study has highly implicated HGF and its receptor, c-Met , in breast cancer aggressiveness. [ 81 ]
Upon parturition (childbirth), estrogen and progesterone rapidly drop to very low levels, with progesterone levels being undetectable. [ 20 ] Conversely, prolactin levels remain elevated. [ 20 ] [ 29 ] As estrogen and progesterone block prolactin-induced lactogenesis by suppressing prolactin receptor (PRLR) expression in breast tissue, their sudden absence results in the commencement of milk production and lactation by prolactin. [ 20 ] [ 29 ] Expression of the PRLR in breast tissue may increase by as much as 20-fold when estrogen and progesterone levels drop upon childbirth. [ 20 ] With suckling from the infant, prolactin and oxytocin are secreted and mediate milk production and letdown , respectively. [ 20 ] [ 21 ] [ 29 ] Prolactin suppresses the secretion of LH and FSH, which in turn results in continued low levels of estrogen and progesterone, and temporary amenorrhea (absence of menstrual cycles) occurs. [ 29 ] In the absence of regular, episodic suckling, which keeps prolactin concentrations high, levels of prolactin will quickly drop, the menstrual cycle will resume and hence normal estrogen and progesterone levels will return, and lactation will cease (that is, until next parturition, or until induced lactation (i.e., with a galactogogue ), occurs). [ 29 ]
Some factors of breast morphology, including their density, are clearly implicated in breast cancer . While breast size is moderately heritable, the relationship between breast size and cancer is uncertain. The genetic variants influencing breast size have not been identified. [ 82 ]
Through genome-wide association studies , a variety of genetic polymorphisms have been linked to breast size. [ 82 ] Some of these include rs7816345 near ZNF703 (zinc finger protein 703); rs4849887 and rs17625845 flanking INHBB (inhibin βB); rs12173570 near ESR1 (ERα); rs7089814 in ZNF365 (zinc finger protein 365); rs12371778 near PTHLH (parathyroid hormone-like hormone); rs62314947 near AREG (amphiregulin); [ 82 ] as well as rs10086016 at 8p11.23 (which is in complete linkage disequilibrium with rs7816345) and rs5995871 at 22q13 (contains the MKL1 gene, which has been found to modulate the transcriptional activity of ERα). [ 83 ] Many of these polymorphisms are also associated with the risk of developing breast cancer, revealing a potential positive association between breast size and breast cancer risk. [ 82 ] [ 83 ] However, conversely, some polymorphisms show a negative association between breast size and breast cancer risk. [ 83 ] In any case, a meta-analysis concluded that breast size and risk of breast cancer are indeed importantly related. [ 84 ]
Circulating IGF-1 levels are positively associated with breast volume in women. [ 85 ] In addition, the absence of the common 19-repeat allele in the IGF1 gene is also positively associated with breast volume in women, as well as with high IGF-1 levels during oral contraceptive use and with lessening of the normal age-associated decline in circulating IGF-1 concentrations in women. [ 85 ] There is great variation in the prevalence of the IGF1 19-repeat allele between ethnic groups, and its absence has been reported to be highest among African-American women. [ 85 ]
Genetic variations in the androgen receptor (AR) have been linked to both breast volume (as well as body mass index ) and breast cancer aggressiveness. [ 86 ]
COX-2 expression has been positively associated with breast volume and inflammation in breast tissue, as well as with breast cancer risk and prognosis. [ 61 ]
Women with CAIS, who are completely insensitive to the AR-mediated actions of androgens, have, as a group, above-average sized breasts. This is true despite the fact that they simultaneously have relatively low levels of estrogen, which demonstrates the powerful suppressant effect of androgens on estrogen-mediated breast development. [ 37 ]
Aromatase excess syndrome , an extremely rare condition characterized by marked hyperestrogenism , is associated with precocious breast development and macromastia in females and similarly precocious gynecomastia (women's breasts) in males. [ 87 ] [ 88 ] [ 89 ] In complete androgen insensitivity syndrome, a condition in which the AR is defective and insensitive to androgens, there is full breast development with breast volumes that are in fact above average in spite of relatively low levels of estrogen (50 pg/mL estradiol). [ 37 ] In aromatase deficiency , a form of hypoestrogenism in which aromatase is defective and cannot synthesize estrogen, and in complete estrogen insensitivity syndrome , a condition in which ERα is defective and insensitive to estrogen, breast development is completely absent. [ 90 ] [ 91 ] [ 92 ]
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Breast duct endoscopy is a method used to examine the lining of the lactiferous ducts to look for abnormal tissue . A very thin, flexible , lighted tube attached to a camera is inserted through the nipple , and threaded into the breast ducts deep in the breast. Tissue and fluid samples may be removed during the procedure.
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A breast implant is a prosthesis used to change the size, shape, and contour of a person's breast . In reconstructive plastic surgery , breast implants can be placed to restore a natural looking breast following a mastectomy , to correct congenital defects and deformities of the chest wall or, cosmetically, to enlarge the appearance of the breast through breast augmentation surgery .
Complications of implants may include breast pain , rashes, skin changes, infection, rupture, cosmetic changes to the breasts such as asymmetry and hardness, and a fluid collection around the breast. [ 1 ]
A rare complication associated with textured surfaced implants and polyurethane foam-covered implants is a type of lymphoma (cancer of the immune system) known as breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL). [ 2 ]
There are four general types of breast implants, defined by their filler material: saline solution, silicone gel, structured and composite filler. The saline implant has an elastomer silicone shell filled with sterile saline solution during surgery; the silicone implant has an elastomer silicone shell pre-filled with viscous silicone gel; structured implants use nested elastomer silicone shells and two saline-filled lumen; and the alternative composition implants featured miscellaneous fillers, such as hydrogel, soy oil or polypropylene string . [ citation needed ]
In surgical practice, for the reconstruction of a breast, the tissue expander device is a temporary breast prosthesis used to form and establish an implant pocket for the future permanent breast implant. For the correction of male breast defects and deformities, the pectoral implant is the breast prosthesis used for the reconstruction and the aesthetic repair of a man's chest wall (see: gynecomastia and mastopexy ). [ citation needed ]
A mammoplasty procedure for the placement of breast implant devices has three purposes:
The operating room time of post– mastectomy breast reconstruction , and of breast augmentation surgery is determined by the procedure employed, the type of incisions, the breast implant (type and materials), and the pectoral locale of the implant pocket.
Recent research has indicated that mammograms should not be done with any greater frequency than that used in normal procedure in patients undergoing breast surgery, including breast implant, augmentation, mastopexy, and breast reduction. [ 3 ]
The breast augmentation patient usually is a young woman whose personality profile indicates psychological distress about her personal appearance and her bodily self image , and a history of having endured criticism (teasing) about the aesthetics of her person. [ 4 ] The studies Body Image Concerns of Breast Augmentation Patients (2003) [ full citation needed ] and Body Dysmorphic Disorder and Cosmetic Surgery (2006) [ full citation needed ] reported that the woman who underwent breast augmentation surgery also had undergone psychotherapy , suffered low self-esteem , presented frequent occurrences of psychological depression , had attempted suicide , and had body dysmorphia , a type of mental illness.
Post-operative patient surveys about mental health and quality-of-life, reported improved physical health, physical appearance, social life, self-confidence, self-esteem, and satisfactory sexual functioning . Furthermore, the women reported long-term satisfaction with their breast implant outcomes; some despite having medical complications that required surgical revision, either corrective or aesthetic. Likewise, in Denmark, 8% of breast augmentation patients had a pre-operative history of psychiatric hospitalization. [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ] [ 14 ]
In 2008, the longitudinal study Excess Mortality from Suicide and other External Causes of Death Among Women with Cosmetic Breast Implants (2007), reported that women who sought breast implants are almost 3 times as likely to commit suicide as are women who have not sought breast implants. Compared to the standard suicide-rate for women of the general populace, the suicide-rate for women with augmented breasts remained constant until 10-years post-implantation, yet, it increased to 4.5 times greater at the 11-year mark, and so remained until the 19-year mark, when it increased to 6 times greater at 20-years post-implantation. Moreover, additional to the suicide-risk, women with breast implants also faced a trebled death-risk from alcoholism and the abuse of prescription and recreational drugs. [ 15 ] [ 16 ] Although seven studies have statistically connected a woman's breast augmentation to a greater suicide-rate, the research indicates that breast augmentation surgery does not increase the death rate; and that, in the first instance, it is the psychopathologically -inclined woman who is more likely to undergo a breast augmentation procedure. [ 17 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ] [ 22 ]
The study Effect of Breast Augmentation Mammoplasty on Self-Esteem and Sexuality: A Quantitative Analysis (2007), reported that the women attributed their improved self image , self-esteem , and increased, satisfactory sexual functioning to having undergone breast augmentation; the cohort, aged 21–57 years, averaged post-operative self-esteem increases that ranged from 20.7 to 24.9 points on the 30-point Rosenberg self-esteem scale , which data supported the 78.6 per cent increase in the woman's libido , relative to her pre-operative level of libido. [ 23 ] Therefore, before agreeing to any surgery, the plastic surgeon evaluates and considers the woman's mental health to determine if breast implants can positively affect her self-esteem and sexual functioning .
The plastic surgical emplacement of breast implant devices, either for breast reconstruction or for aesthetic purpose , presents the same health risks common to surgery , such as adverse reaction to anesthesia , hematoma (post-operative bleeding), late hematoma (post-operative bleeding after 6 months or more), [ 24 ] seroma (fluid accumulation), incision-site breakdown (wound infection). Complications specific to breast augmentation include breast pain, altered sensation, impeded breast-feeding function, visible wrinkling, asymmetry, thinning of the breast tissue, and symmastia , the "bread loafing" of the bust that interrupts the natural plane between the breasts. Specific treatments for the complications of indwelling breast implants— capsular contracture and capsular rupture—are periodic MRI monitoring and physical examinations. Furthermore, complications and re-operations related to the implantation surgery, and to tissue expanders (implant place-holders during surgery) can cause unfavorable scarring in approximately 6–7 percent of the patients. [ 25 ] [ 26 ] [ 27 ] Statistically , 20 percent of women who underwent cosmetic implantation, and 50 percent of women who underwent breast reconstruction implantation, required their explantation (surgical removal) at the 10-year mark. [ 28 ]
In the 1990s, several reports reviewed the few studies evaluating any increased risk of systemic and auto-immune diseases among women with breast implants. The conclusion at that time was that there was no evidence establishing a causal connection between the implantation of silicone breast implants and either type of disease. [ 29 ] [ 30 ] However, the Institute of Medicine report pointed out that these earlier studies included too few women to conclusively evaluate the impact on these rare diseases. [ 29 ] In addition, many of the studies included women who had breast implants for just a few months, which would be too early to develop a diagnosed autoimmune disease. In recent years, large epidemiological studies have reported clinically and statistically significant increases in some of these diseases. A study by Watad and colleagues that was published in 2018 compared and examined the medical records of more than 24,000 women with breast implants to more than 98,000 "matched controls" who did not have breast implants but shared very similar demographic traits. [ 31 ] The study found a statistically significant 22% overall increase in diagnosed autoimmune or rheumatic disorders. The greatest increases in diagnoses for women with breast implants was for Sjögren's syndrome , Multiple Sclerosis (MS), and sarcoidosis, each of which were 58%-98% higher in women with breast implants. That analysis was based on Israeli women with breast implants as confirmed by medical records, and the analyses of diseases were based on diagnoses made after the women got breast implants that were included in medical records during up to 20 years of follow-up. [ 31 ]
A published study of U.S. women with similar results was published in 2019 by Coroneos and his colleagues at MD Anderson Medical Center. [ 32 ] The data were based on two studies with a combined total of almost 100,000 women with breast implants, but many dropped out of the study within a few years of their breast implant surgery. However, of the women in the study for at least two years, the researchers reported an 800% increase in Sjögren syndrome, 700% increase in scleroderma, and almost 600% increase in rheumatoid arthritis among women with breast implants compared to the general population of women of the same age and demographics.
Recent research on women who reported autoimmune and other system symptoms but were not diagnosed with an autoimmune disease evaluated whether the women's symptoms changed after their implants were removed. A 2020 study on the effectiveness of explant surgery on women with breast implant illness found that nearly all of 750 women who underwent explant surgery reported a significant improvement in their health within a month after their surgery. Researchers focused on the following symptoms: hair loss, memory loss, dry eyes and/or blurred vision, numbness or tingling in the extremities, chronic fatigue, joint pain, rashes, breast pain, food intolerance, flu-like symptoms, and difficulty breathing. The same authors also published a study on the impact of breast implant removal on breathing difficulties and found a statistically significant improvement in well-established objective measures of pulmonary function following explant surgery. [ 33 ]
English translation: "We did not observe connective tissue diseases to be directly or indirectly associated by the presence of a breast implant, in particular one of silicone gel...."
Because a breast implant is a Class III medical device of limited product-life, the principal rupture-rate factors are its age and design; nonetheless, a breast implant device can retain its mechanical integrity for decades in a woman's body. [ 44 ] When a saline breast implant ruptures, leaks, and empties, it quickly deflates, and thus can be readily explanted (surgically removed). In some cases, saline implant rupture can result in an infection due to bacteria or mold that had been within the implant, though this is uncommon. [ 45 ] The follow-up report, Natrelle Saline-filled Breast Implants: a Prospective 10-year Study (2009) indicated rupture-deflation rates of 3–5 per cent at 3-years post-implantation, and 7–10 per cent rupture-deflation rates at 10-years post-implantation. [ 46 ] In a study of his 4761 augmentation mammaplasty patients, Eisenberg reported that overfilling saline breast implants 10-13% significantly reduced the rupture-deflation rate to 1.83% at 8-years post-implantation. [ 47 ]
When a silicone breast implant ruptures it usually does not deflate, yet the filler gel does leak from it, which can migrate to the implant pocket; therefore, an intracapsular rupture (in-capsule leak) can become an extracapsular rupture (out-of-capsule leak), and each occurrence is resolved by explantation. Although the leaked silicone filler-gel can migrate from the chest tissues to elsewhere in the woman's body, most clinical complications are limited to the breast and armpit areas, usually manifested as granulomas (inflammatory nodules) and axillary lymphadenopathy (enlarged lymph glands in the armpit area). [ 48 ] [ 49 ] [ 50 ]
The suspected mechanisms of breast implant rupture are:
Silicone implant rupture can be evaluated using magnetic resonance imaging; from the long-term MRI data for single-lumen breast implants, the European literature about second generation silicone-gel breast implants (1970s design), reported silent device-rupture rates of 8–15 per cent at 10-years post-implantation (15–30% of the patients). [ 52 ] [ 53 ] [ 54 ] [ 55 ] Additionally, high-resolution ultrasound is another effective method of evaluating silicone implant integrity. [ 56 ]
The study Safety and Effectiveness of Mentor's MemoryGel Implants at 6 Years (2009), which was a branch study of the U.S. FDA's core clinical trials for primary breast augmentation surgery patients, reported low device-rupture rates of 1.1 per cent at 6-years post-implantation. [ 57 ] The first series of MRI evaluations of the silicone breast implants with thick filler-gel reported a device-rupture rate of 1 percent, or less, at the median 6-year device-age. [ 58 ] Statistically, the manual examination (palpation) of the woman is inadequate for accurately evaluating if a breast implant has ruptured. The study, The Diagnosis of Silicone Breast implant Rupture: Clinical Findings Compared with Findings at Magnetic Resonance Imaging (2005), reported that, in asymptomatic patients, only 30 per cent of the ruptured breast implants are accurately palpated and detected by an experienced plastic surgeon, whereas MRI examinations accurately detected 86 per cent of breast implant ruptures. [ 59 ] Therefore, the U.S. FDA recommended scheduled MRI examinations, as silent-rupture screenings, beginning at the 3-year-mark post-implantation, and then every two years, thereafter. [ 25 ] Nonetheless, beyond the U.S., the medical establishments of other nations have not endorsed routine MRI screening, and, in its stead, proposed that such a radiologic examination be reserved for two purposes: (i) for the woman with a suspected breast implant rupture; and (ii) for the confirmation of mammographic and ultrasonic studies that indicate the presence of a ruptured breast implant. [ 60 ]
Furthermore, The Effect of Study design Biases on the Diagnostic Accuracy of Magnetic Resonance Imaging for Detecting Silicone Breast Implant Ruptures: a Meta-analysis (2011) reported that the breast-screening MRIs of asymptomatic women might overestimate the incidence of breast implant rupture. [ 61 ] In the event, the U.S. Food and Drug Administration emphasised that "breast implants are not lifetime devices. The longer a woman has silicone gel-filled breast implants, the more likely she is to experience complications." [ 62 ]
The human body's immune response to a surgically installed foreign object—breast implant, cardiac pacemaker , orthopedic prosthesis —is to encapsulate it with scar tissue capsules of tightly woven collagen fibers, in order to maintain the integrity of the body by isolating the foreign object, and so tolerate its presence. Capsular contracture —which should be distinguished from normal capsular tissue—occurs when the collagen-fiber capsule thickens and compresses the breast implant; it is a painful complication that might distort either the breast implant, or the breast, or both. Capsular contracture is diagnosed through a visual and physical examiniation according to level of increasing severity based on the Baker Grade scale: Baker Grade I, Baker Grade II, Baker Grade III, and Baker Grade IV.
The cause of capsular contracture is unknown, but the common incidence factors include bacterial contamination, device-shell rupture, filler leakage, and hematoma . The surgical implantation procedures that have reduced the incidence of capsular contracture include submuscular emplacement, the use of breast implants with a textured surface (polyurethane-coated); [ 63 ] [ 64 ] [ 65 ] limited pre-operative handling of the implants, limited contact with the chest skin of the implant pocket before the emplacement of the breast implant, and irrigation of the recipient site with triple-antibiotic solutions. [ 66 ] [ 67 ]
The correction of capsular contracture might require an open capsulotomy (surgical release) of the collagen-fiber capsule, or the removal, and possible replacement, of the breast implant. Furthermore, in treating capsular contracture, the closed capsulotomy (disruption via external manipulation) once was a common maneuver for treating hard capsules, but now is a discouraged technique, because it can rupture the breast implant. Non-surgical treatments for collagen-fiber capsules include massage, external ultrasonic therapy, leukotriene pathway inhibitors such as zafirlukast (Accolate) or montelukast (Singulair), and pulsed electromagnetic field therapy (PEMFT). [ 68 ] [ 69 ] [ 70 ] [ 71 ]
When the patient is unsatisfied with the outcome of the augmentation mammoplasty; or when technical or medical complications occur; or because of the breast implants' limited product life, it is likely she might require replacing the breast implants. Common revision surgery indications include major and minor medical complications, capsular contracture , shell rupture, and device deflation. [ 51 ] Revision incidence rates were greater for breast reconstruction patients, because of the post-mastectomy changes to the soft-tissues and to the skin envelope of the breast, and to the anatomical borders of the breast, especially in women who received adjuvant external radiation therapy . [ 51 ] Moreover, besides breast reconstruction, breast cancer patients usually undergo revision surgery of the nipple-areola complex (NAC), and symmetry procedures upon the opposite breast, to create a bust of natural appearance, size, form, and feel. Carefully matching the type and size of the breast implants to the patient's pectoral soft-tissue characteristics reduces the incidence of revision surgery. Appropriate tissue matching, implant selection, and proper implantation technique, the re-operation rate was 3 percent at the 7-year-mark, compared with the re-operation rate of 20 per cent at the 3-year-mark, as reported by the U.S. Food and Drug Administration. [ 72 ] [ 73 ]
In the 1990s, the national health ministries of the listed countries reviewed the pertinent studies for causal links among silicone-gel breast implants and systemic and diagnosed autoimmune diseases and breast cancer. [ 74 ] [ 38 ] [ 75 ] A study by researchers at the U.S. National Institute of Health reported an increase in four types of cancer among women with breast implants compared to other plastic surgery patients of the same age and similar demographic traits and health habits. [ 17 ] This increase in cancer was attenuated but did not disappear when the researchers followed the women for 5 more years, with a 43% increase in brain cancer and a 63% increase in respiratory cancer compared to other plastic surgery patients. [ 76 ] A study by Watad et al. evaluated the medical records of more than 24,000 women with breast implants compared to more than 98,000 women with the same demographic traits who did not have breast implants. The researchers found a statistically significant 22 percent increase in several diagnosed diseases, increasing to more than 60% for Sjogren's syndrome , multiple sclerosis , and sarcoidosis [ 31 ] After investigating this issue, in 2021 the U.S. FDA revised its "black box warnings" on breast implants to acknowledge the association between breast implants and systemic autoimmune, rheumatologic, and neurological symptoms to state: "Patients receiving breast implants have reported a variety of systemic symptoms, such as joint pain, muscle aches, confusion, chronic fatigue, autoimmune diseases, and others. Individual patient risk for developing these symptoms has not been well established. Some patients report complete resolution of symptoms when the implants are removed without replacement". [ 77 ]
A 2021 study by Cleveland Clinic physicians investigated the outcome of breast implant removal on women with breast implants who had reported difficulty breathing or tightness in their chest; this is one of the symptoms associated with breast implant illness . [ 33 ] The study examined breast implant patients who reported problems breathing, comparing their scores on 6 pulmonary function tests before and after their implants and scar capsules were removed. The researchers reported that 74% of the patients reported significant improvements on at least 3 of the pulmonary function tests. In self-reports, all study participants reported that their breathing improved after their implant surgery.
Platinum is a catalyst used in the making of silicone implant polymer shells and other silicone devices used in medicine. The literature indicates that small amounts of platinum leaches (leaks) from these implants and is present in the surrounding tissue. The FDA reviewed the available studies from the medical literature on platinum and breast implants in 2002 and concluded there was little evidence suggesting toxicity from platinum in implant patients. [ 78 ] The FDA revisited this study and additional literature several years later, reaffirming prior conclusions that platinum catalysts used in implants is likely not ionized and therefore would not represent a risk to women. [ 79 ]
The FDA has identified that breast implants may be associated with a rare form of cancer called anaplastic large-cell lymphoma (ALCL), which some experts believe is believed to be associated with chronic bacterial inflammation. [ 80 ] Similar ALCL phenomena have been seen with other types of medical implants including vascular access ports, orthopedic hip implants, and jaw (TMJ) implants. The causal association between breast implants and ALCL was conclusively established in December 2013, when researchers at MD Anderson Cancer Center published a study of 60 women with breast implants who were diagnosed with ALCL in the breast. In 2015, plastic surgeons published an article reviewing 37 articles in the literature on 79 patients and collected another 94 unreported cases, resulting in 173 women with breast implants who had developed ALCL of the breast. They concluded that "Breast implant-associated ALCL is a novel manifestation of site- and material-specific lymphoma originating in a specific scar location, presenting a wide array of diverse characteristics and suggesting a multifactorial cause." They stated that "There was no preference for saline or silicone fill or for cosmetic or reconstructive indications." Where implant history was known, the patient had received at least one textured-surface device. In 2016, the World Health Organization (WHO) officially recognized BIA-ALCL. [ 81 ]
As of April 2022, the FDA has received 1,130 global medical device reports (MDRs) of BIA-ALCL, including 59 deaths. [ 82 ] Since ALCL was thought to be diagnosed in only 1 woman in half a million, 60 women was a much higher number than would be expected. The researchers pointed out that BIA-ALCL could be fatal. [ 83 ] If women with implants present with delayed swelling or fluid collection, cytologic studies and a test for the marker CD30 are suggested. The American Society of Plastic Surgery (ASPS) states, "CD30 is the main diagnostic test that must be performed on the seroma fluid as routine pathology or H&E staining can frequently miss the diagnosis." [ 84 ] Diagnosis and treatment of breast implant-associated ALCL now follows standardized guidelines established by the National Comprehensive Cancer Network. [ 85 ]
The current lifetime risk of BIA-ALCL in the U.S. is unknown, but estimates have ranged between one in 70,000 and one in 500,000 women with breast implants, according to the MD Anderson Cancer Center . [ 86 ] Countries with breast implant registries have the best data on the risks of BIA-ALCL. For example, as of October 2020, the Therapeutic Goods Administration of Australia and New Zealand reported a "1:3,345 risk with Allergan Biocell and a 1:86,029 risk with Mentor Siltex." [ 84 ] AIn the U.S, estimates of the risk of BIA-ALCL in textured implants ranges from 1.79 per 1,000 (1 woman with BIA-ALCL per 559 implants) to 2.82 per 1,000 (1 woman per 355 implants)[2]. As of April 2022, the FDA reported 1,130 medical device reports (MDRs) of BIA-ALCL. Of those MDRs, 59 of the women died. FDA states that 798 of the 1,130 MDRs for BIA-ALCL involved textured breast implants, 37 MDRs involved smooth-surfaced implants, and 295 MDRs did not specify whether the implants were textured or smooth. [ 82 ] In some cases, the women who developed BIA-ALCL after smooth breast implants had textured expanders prior to their implants. Most patients had BIA-ALCL affect only one breast with only 8 patients diagnosed with bilateral BIA-ALCL. The most common reported symptom of BIA-ALCL according to the FDA was seroma, followed by breast swelling and pain, capsular contracture, and peri-implant mass or lump. Furthermore, 84 percent of the reported implants were made by Allergan, the largest breast implant manufacturer at the time. [ 82 ]
A study conducted at Memorial Sloan Kettering cancer center of women undergoing prophylactic mastectomies indicated that 1 in 355 women were subsequently diagnosed with BIA-ALCL. [ 87 ] Almost all those women had Allergan biocell implants and expanders. These reports strongly suggest that BIA-ALCL develops primarily in patients with textured implants or expanders. In all cases, however, many researchers suspect that BIA-ALCL is an under-recognized, misdiagnosed, and under-reported complication of breast implants.
The ASPS and the Plastic Surgery Foundation (PSF) have partnered with the FDA to study this condition and in doing so created the Patient Registry and Outcomes for Breast Implants and Anaplastic Large Cell Lymphoma Etiology and Epidemiology (PROFILE). The United States FDA strongly encourages all physicians to report cases to PROFILE in an effort to better understand the role of breast implants in ALCL and the management of this disease. [ 88 ]
In September 2022, the FDA announced new information regarding other types of cancers related to breast implants, based on medical device reports (MDRs) of cases of patients with squamous-cell carcinoma or various lymphomas found in the scar tissue around breast implants. The agency reported 10 MDRs about squamous-sell carcinoma found in the capsule scar tissue and 12 MDRs about various lymphomas also in the scar tissue around the breast implants. These new cases do not overlap with cases of BIA-ALCL. SCC and other lymphomas have been found in smooth-surface and textured implants as well as silicone-gel-filled and saline-filled implants. Patients who reported symptoms specified swelling, pain, lumps, and changes to their skin. As of 2022, neither the incidence rate nor prevalence is known. [ 89 ]
Breast implant emplacement is performed with five types of surgical incisions:
The five surgical approaches to emplacing a breast implant to the implant pocket are often described in anatomical relation to the pectoralis major muscle .
The surgical scars of a breast augmentation mammoplasty develop approximately at 6-weeks post-operative, and fade within months. Depending upon the daily-life physical activities required of the woman, the breast augmentation patient usually resumes her normal life at 1-week post-operative. Moreover, women whose breast implants were emplaced beneath the chest muscles (submuscular placement) usually have a longer, slightly more painful convalescence, because of the healing of the incisions to the chest muscles. Usually, she does not exercise or engage in strenuous physical activities for approximately 6 weeks. During the initial post-operative recovery, the woman is encouraged to regularly exercise (flex and move) her arm to alleviate pain and discomfort; if required, analgesic indwelling medication catheters can alleviate pain [ 95 ] [ 96 ] Moreover, significantly improved patient recovery has resulted from refined breast-device implantation techniques (submuscular, subglandular) that allow 95 per cent of women to resume their normal lives at 24-hours post-procedure, without bandages, fluid drains, pain pumps, catheters, medical support brassières, or narcotic pain medication. [ 97 ] [ 98 ] [ 99 ] [ 100 ]
Today, there are three types of breast implants commonly used for mammaplasty , breast reconstruction , and breast augmentation procedures: [ 101 ]
A fourth type of implant, composite (or alternative-composite) implants, have largely been discontinued. These types featured fillers such as soy oil and polypropylene string. Other discontinued materials include ox cartilage, Terylene wool, ground rubber, silastic rubber, and teflon-silicone prostheses. [ 102 ]
The saline breast implant—filled with saline solution (biological-concentration salt water 0.90% w/v of NaCl , ca. 300 mOsm /L.)—was first manufactured by the Laboratoires Arion company, in France, and was introduced for use as a prosthetic medical device in 1964. The contemporary models of saline breast implant are manufactured with thicker, room-temperature vulcanized (RTV) shells made of a silicone elastomer . The study In vitro Deflation of Pre-filled Saline Breast Implants (2006) reported that the rates of deflation (filler leakage) of the pre-filled saline breast implant made it a second-choice prosthesis for corrective breast surgery. [ 103 ] Nonetheless, in the 1990s, the saline breast implant was the prosthesis most common device used for breast augmentation surgery in the United States, because of the U.S. FDA's restriction against the implantation of silicone-filled breast implants outside of clinical studies. Saline breast implants have enjoyed little popularity in the rest of the world, possessing negligible market share.
The technical goal of saline-implant technology was a physically less invasive surgical technique for emplacing an empty breast implant device through a smaller surgical incision. [ 104 ] In surgical praxis, after having emplaced the empty breast implants to the implant pockets, the plastic surgeon then filled each device with saline solution , and, because the required insertion-incisions are short and small, the resultant incision-scars will be smaller and shorter than the surgical scars usual to the long incisions required for inserting pre-filled, silicone-gel implants.
When compared to the results achieved with a silicone-gel breast implant, the saline implant can yield acceptable results, of increased breast-size, smoother hemisphere-contour, and realistic texture; yet, it is likelier to cause cosmetic problems, such as the rippling and the wrinkling of the breast-envelope skin, accelerated lower breast pole stretch, and technical problems, such as the presence of the implant being noticeable to the eye and to the touch. The occurrence of such cosmetic problems is likelier in the case of the woman with very little breast tissue, and in the case of the woman who requires post-mastectomy breast reconstruction; thus, the silicone-gel implant is the technically superior prosthetic device for breast augmentation, and for breast reconstruction. In the case of the woman with much breast tissue, for whom sub-muscular emplacement is the recommended surgical approach, saline breast implants can produce an aesthetic result much like that afforded by silicone breast implants. [ 105 ] [ 106 ] Ultrasound examination and outcome studies have revealed that saline and silicone breast implants look and feel similar. [ 107 ]
As a medical device technology , there are five generations of silicone breast implant, each defined by common model-manufacturing techniques. [ citation needed ]
The modern prosthetic breast was invented in 1961 by the American plastic surgeons Thomas Cronin and Frank Gerow, and manufactured by the Dow Corning Corporation ; in due course, the first augmentation mammoplasty was performed in 1962.
The Cronin–Gerow Implant, prosthesis model 1963, was a silicone rubber envelope-sac, shaped like a teardrop, which was filled with viscous silicone-gel. To reduce the rotation of the emplaced breast implant upon the chest wall, the model 1963 prosthesis was affixed to the implant pocket with a fastener-patch, made of Dacron material ( Polyethylene terephthalate ), which was attached to the rear of the breast implant shell. [ 108 ]
In the 1970s, manufacturers presented the second generation of breast implant prostheses that featured functional developments and aesthetic improvements to the technology:
In the 1980s, the models of the third and of the fourth generations of breast implant devices were sequential advances in manufacturing technology, such as elastomer -coated shells that decreased gel-bleed (filler leakage), and a thicker (increased-cohesion) filler gel. Sociologically , the manufacturers of prosthetic breasts then designed and made anatomic models (natural breast) and shaped models (round, tapered) that realistically corresponded with the breast- and body- types of women. The tapered models of breast implant have a uniformly textured surface, which reduces the rotation of the prosthesis within the implant pocket; the round models of breast implant are available in smooth-surface- and textured-surface- types.
Since the mid-1990s, the fifth generation of silicone-gel breast implant is made of a high-strength, highly cohesive silicone gel that mostly eliminates the occurrences of filler leakage ("silicone gel bleed") and of the migration of the silicone filler from the implant pocket to elsewhere in the woman's body. These implants are commonly referred to as "gummy bear breast implants" for their firm, pliant consistency, which is similar to gummy candies. The studies Experience with Anatomical Soft Cohesive Silicone gel Prosthesis in Cosmetic and Reconstructive Breast Implant Surgery (2004) and Cohesive Silicone gel Breast Implants in Aesthetic and Reconstructive Breast Surgery (2005) reported low incidence-rates of capsular contracture and of device-shell rupture; and greater rates of improved medical-safety and technical-efficacy than that of early generation breast implant devices. [ 111 ] [ 112 ] [ 113 ]
The presence of breast implants currently presents no contraindication to breast feeding, and no evidence to support that the practice may present health issues to a breastfeeding infant is recognized by the USFDA.
Women with breast implants may have functional breast-feeding difficulties; mammoplasty procedures that feature periareolar incisions are especially likely to cause breastfeeding difficulties. Surgery may also damage the lactiferous ducts and the nerves in the nipple-areola area. [ 114 ] [ 115 ] [ 116 ]
Functional breastfeeding difficulties arise if the surgeon cut the milk ducts or the major nerves innervating the breast, or if the milk glands were otherwise damaged. Milk duct and nerve damage are more common if the incisions cut tissue near the nipple. The milk glands are most likely to be affected by subglandular implants (under the gland), and by large-sized breast implants, which pinch the lactiferous ducts and impede milk flow. Small-sized breast implants, and submuscular implantation, cause fewer breast-function problems; however, it is impossible to predict whether a woman who undergoes breast augmentation will be able to successfully breast feed since some women are able to breast-feed after periareolar incisions and subglandular placement and some are not able to after augmentation using submuscular and other types of surgical incisions. [ 116 ]
The presence of radiologically opaque breast implants (either saline or silicone) might interfere with the radiographic sensitivity of the mammograph , that is, the image might not show any tumor(s) present. In this case, an Eklund view mammogram is required to ascertain either the presence or the absence of a cancerous tumor, wherein the breast implant is manually displaced against the chest wall and the breast is pulled forward, so that the mammograph can visualize a greater volume of the internal tissues; nonetheless, approximately one-third of the breast tissue remains inadequately visualized, resulting in an increased incidence of mammograms with false-negative results. [ 117 ] [ 118 ]
The breast cancer studies Cancer in the Augmented Breast: Diagnosis and Prognosis (1993) and Breast Cancer after Augmentation Mammoplasty (2001) of women with breast implant prostheses reported no significant differences in disease-stage at the time of the diagnosis of cancer; prognoses are similar in both groups of women, with augmented patients at a lower risk for subsequent cancer recurrence or death. [ 119 ] [ 120 ] Conversely, the use of implants for breast reconstruction after breast cancer mastectomy appears to have no negative effect upon the incidence of cancer-related death. [ 121 ] That patients with breast implants are more often diagnosed with palpable—but not larger—tumors indicates that equal-sized tumors might be more readily palpated in augmented patients, which might compensate for the impaired mammogram images. [ 122 ] The ready palpability of the breast-cancer tumor(s) is consequent to breast tissue thinning by compression, innately in smaller breasts a priori (because they have lesser tissue volumes), and that the implant serves as a radio-opaque base against which a cancerous tumor can be differentiated. [ 123 ]
The breast implant has no clinical bearing upon lumpectomy breast-conservation surgery for women who developed breast cancer after the implantation procedure, nor does the breast implant interfere with external beam radiation treatments (XRT); moreover, the post-treatment incidence of breast-tissue fibrosis is common, and thus a consequent increased rate of capsular contracture . [ 124 ] There is tentative evidence that women who have had breast augmentation, have worse breast cancer prognosis. [ 125 ] The use of implants for breast reconstruction after breast cancer mastectomy appears to have no negative effect upon cancer-related death. [ 121 ] [ 126 ]
There have been multiple reported cases of other adverse effects of mammography of women with breast implants; ruptures resulting from pressure exerted on the breast implant make up a majority of these cases. [ 127 ] Compression may also lead to pain or exacerbate already existing pain in the breasts. [ 127 ]
Since the late nineteenth century, breast implants have been used to surgically augment the size (volume), modify the shape (contour), and enhance the feel (tact) of a woman's breasts. In 1895, surgeon Vincenz Czerny effected the earliest breast implant emplacement when he used the patient's autologous adipose tissue , harvested from a benign lumbar lipoma , to repair the asymmetry of the breast from which he had removed a tumor. [ 128 ] In 1889, surgeon Robert Gersuny experimented with paraffin injections, with disastrous results arising from the breakup of the paraffin into smaller bodies following the procedure. [ 129 ]
From the first half of the twentieth century, physicians used other substances as breast implant fillers— ivory , glass balls, ground rubber, ox cartilage , Terylene wool , gutta-percha , Dicora, polyethylene chips, Ivalon ( polyvinyl alcohol —formaldehyde polymer sponge), a polyethylene sac with Ivalon, polyether foam sponge (Etheron), polyethylene tape (Polystan) strips wound into a ball, polyester (polyurethane foam sponge) Silastic rubber, and teflon-silicone prostheses. [ 130 ]
In the mid-twentieth century, Morton I. Berson, in 1945, and Jacques Maliniac, in 1950, each performed flap-based breast augmentations by rotating the patient's chest wall tissue into the breast to increase its volume. Furthermore, throughout the 1950s and the 1960s, plastic surgeons used synthetic fillers—including silicone injections received by some 50,000 women, from which developed silicone granulomas and breast hardening that required treatment by mastectomy . [ 131 ] In 1961, the American plastic surgeons Thomas Cronin and Frank Gerow, and the Dow Corning Corporation , developed the first silicone breast prosthesis, filled with silicone gel; in due course, the first augmentation mammoplasty was performed in 1962 using the Cronin–Gerow Implant, prosthesis model 1963. In 1964, the French company Laboratoires Arion developed and manufactured the saline breast implant, filled with saline solution , and then introduced for use as a medical device in 1964. [ 103 ]
In 1988, twenty-six years after the 1962 introduction of breast implants filled with silicone gel, the U.S. Food and Drug Administration (FDA) investigated breast implant failures and the subsequent complications, and re-classified breast implant devices as Class III medical devices, and required from manufacturers the documentary data substantiating the safety and efficacy of their breast implant devices. [ 132 ] In 1992, the FDA placed silicone-gel breast implants in moratorium in the U.S., because there was "inadequate information to demonstrate that breast implants were safe and effective". Nonetheless, medical access to silicone-gel breast implant devices continued for clinical studies of post-mastectomy breast reconstruction , the correction of congenital deformities, and the replacement of ruptured silicone-gel implants. The FDA required from the manufacturers the clinical trial data, and permitted their providing breast implants to the breast augmentation patients for the statistical studies required by the U.S. Food and Drug Administration. [ 132 ] In mid-1992, the FDA approved an adjunct study protocol for silicone-gel filled implants for breast reconstruction patients, and for revision-surgery patients. Also in 1992, the Dow Corning Corporation , a silicone products and breast implant manufacturer, announced the discontinuation of five implant-grade silicones , but would continue producing 45 other, medical-grade, silicone materials—three years later, in 1995, the Dow Corning Corporation went bankrupt when it faced large class action lawsuits claiming a variety of illnesses. [ 132 ]
The U.S. Food and Drug Administration established the age ranges for women seeking breast implants; for breast reconstruction, silicone-gel filled implants and saline-filled implants were approved for women of all ages; for breast augmentation, saline implants were approved for women 18 years of age and older; silicone implants were approved for women 22 years of age and older. [ 141 ] Because each breast implant device entails different medical risks, the minimum age of the patient for saline breast implants is different from the minimum age of the patient for silicone breast implants—because of the filler leakage and silent shell-rupture risks; thus, periodic MRI screening examinations are the recommended post-operative, follow-up therapy for the patient. [ 141 ] In other countries, in Europe and Oceania, the national health ministries' breast implant policies do not endorse periodic MRI screening of asymptomatic patients, but suggest palpation proper—with or without an ultrasonic screening—to be sufficient post-operative therapy for most patients.
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https://en.wikipedia.org/wiki/Breast_implant
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Breast implant illness ( BII ), also known as autoimmune/autoinflammatory syndrome induced by adjuvants ( ASIA ), along with other terms, is a purported condition that is said to affect certain women with breast implants . Its acceptance as a legitimate disease is controversial, [ 2 ] [ 3 ] but some evidence exists supporting the idea that silicone -based breast implants can trigger autoimmune responses in patients with underlying allergies or autoimmune diseases . [ 1 ] Nonetheless, it remains poorly defined, and its existence has still not been conclusively proven. [ 3 ] [ 4 ] The idea of BII has existed since the 1960s, [ 2 ] but it has more recently been popularized on social media — particularly among non-experts — a process that may increase fear and anxiety regarding the condition and encourage self-diagnosis . [ 4 ] There are currently no diagnostic criteria nor specific diagnostic tests, thus BII is considered to be a diagnosis of exclusion . [ 5 ] [ 6 ]
• En Bloc: Involves removing both the implant and the capsule tissue surrounding it in one piece. The idea is to eliminate any potential toxins or inflammatory cells that might be contributing to symptoms.
• Non-En Bloc: Involves removing the implant but leaving the surrounding capsule tissue, which may still harbor inflammation or bacteria, but not necessarily in a manner that causes ongoing symptoms.
Studies have found that women who undergo en bloc explantation vs. non-en bloc explantation both report significant improvements in symptoms, including fatigue, brain fog, joint pain, and other BII-related issues. [ 7 ]
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https://en.wikipedia.org/wiki/Breast_implant_illness
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Breathwork is a term [ 1 ] [ 2 ] for various breathing practices in which the conscious control of breathing is said to influence a person's mental, emotional, or physical state, with a therapeutic effect. [ 3 ]
Edzard Ernst writes that breathwork (or 'rebirthing') is a form of alternative medicine first devised by Leonard Orr in the 1970s. [ 4 ] [ inconsistent ]
Breathwork is the use of breathing techniques to achieve altered states of consciousness and to have a variety of effects on physical and mental well-being. [ 3 ] Breathwork has been seen as derived from multiple spiritual and pre-scientific traditions from around the world. [ 3 ] According to Jack Raso, breathwork is described by proponents as a multiform "healing modality" characterized by stylized breathing. Its purported design is to effect physical, emotional, and spiritual change. Such a process can allegedly "dissolve limiting programs" that are "stored" in the mind and body, and increases one's ability to handle more "energy". [ 5 ] Breathwork practitioners believe that an individual's particular pattern of passive breathing can lead to insights about their unconscious mind. [ 3 ]
During a breathwork session, individuals will typically lie down and be instructed to breathe using particular methods, depending on the sub-type of breathwork. [ 6 ] Most breathwork sessions last around an hour. [ 6 ] Alternatively, breathwork is advocated to be done by individuals alone, for shorter periods. [ 7 ]
A practice that uses rapid breathing and other elements such as music to put individuals in altered states of consciousness. It was developed by Stanislav Grof as a successor to his LSD -based psychedelic therapy , following the suppression of legal LSD use in the late 1960s. [ 8 ] Side effects of the hyperventilation aspect of holotropic breathwork can include cramping in the hands and around the mouth. [ 3 ] As the expressed goal of holotropic breathwork is to attain an altered state, it should not be attempted alone. [ 3 ] Following a 1993 report commissioned by the Scottish Charities Office , concerns about the risk that the hyperventilation technique could cause seizure or lead to psychosis in vulnerable people caused the Findhorn Foundation to suspend its breathwork programme. [ 9 ]
A process described as releasing suppressed traumatic childhood memories, especially those related to one's own birth. [ 10 ] Orr proposed that correct breathing can cure disease and relieve pain. [ 11 ] Orr devised rebirthing therapy in the 1970s after he supposedly re-lived his own birth while in the bath. [ 10 ] He believed that breathing techniques could be used to purge traumatic childhood memories that had been repressed. [ 10 ] [ 12 ] There is no evidence that individuals can remember their births. [ 13 ] Memories of one's birth that appear to resurface during a rebirthing-breathwork practice are believed to be the result of false memories . [ 14 ] Rebirthing-breathwork is one of the practices critiqued by anti-cult experts Margaret Singer and Janja Lalich in the book Crazy Therapies: What Are They? Do They Work? [ 11 ] Singer and Lalich write that proponents of such "bizarre" practices are proud of their non-scientific approach, and that this finds favor with an irrational clientele. [ 11 ] In 2006, a panel that consisted of over one hundred experts participated in a survey of psychological treatments; they considered rebirthing therapy to be discredited. [ 15 ]
In addition to a practitioner, breathwork sessions will often have "sitters" present. Sitters are individuals who provide emotional or physical support to those practicing breathwork. [ 3 ]
Some common side effects include "sleepiness; tingling in the hands, feet, or face; and a sense of altered consciousness that can be distressing to some." [ 6 ] Breathwork is generally considered safe when done with a skilled practitioner, but there are contraindications such as cardiovascular disease , glaucoma , high blood pressure , mental illness , severe asthma , or seizure disorders , among others. [ 3 ] [ 6 ]
A 2018 review found that research to date had been limited, and that studies showed "limited evidence of a relationship between physiological parameters and psychological/behavioral outcomes in healthy subjects undergoing slow breathing techniques." [ 16 ] A 2023 review said that results showed that breathwork may be effective for improving stress and mental health, but urged caution until more research has been done. [ 17 ]
Breathwork may be helpful for relaxation and stress in a similar way to meditation . [ 6 ] [ 18 ] Anxiety may be helped by breathwork. [ 19 ]
Media related to New Age practices at Wikimedia Commons
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Brenda Banwell is Chief of the Division of Neurology and Co-Director of the Neuroscience Center, and Professor of Neurology at Children's Hospital of Philadelphia and holder of the Grace R. Loeb Endowed Chair in Neurosciences. She also holds the title of Professor of Pediatrics and Neurology at the Perelman School of Medicine at the University of Pennsylvania .
Banwell is the co-director of the Pediatric Multiple Sclerosis and Neuroinflammatory Disorders Clinic at the Children's Hospital of Philadelphia . She has published extensively on pediatric demyelinating diseases including multiple sclerosis , neuromyelitis optica and MOG antibody disease . Banwell is the co-director of the Canadian Pediatric Demyelinating Disease Network, [ 1 ] the chair of the International Pediatric Multiple Sclerosis Study Group , [ 2 ] and the chair of the International Medical and Scientific Board of the MS International Federation . [ 3 ] Banwell also sits on the International Advisory Committee on Clinical Trials of New Drugs in Multiple Sclerosis. [ 4 ]
Banwell is a fellow of the American Academy of Neurology , [ 5 ] and serves as vice chair of the Academic Neurology Committee. [ 6 ] She has been active in the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), delivering the 2022 ECTRIMS lecture. [ 7 ]
Banwell was born in Winnipeg, Canada. [ 8 ] She did her undergraduate training at the University of Western Ontario , where she remained for her MD and her residency in pediatrics. She completed her pediatric neurology residency at the University of Toronto Hospital for Sick Children , where she was chief resident. She then went to Mayo Clinic for a two year fellowship in neuromuscular disease . [ 9 ]
Banwell returned to the University of Toronto Hospital for Sick Children as an assistant professor in 1999. She became a full professor at the University of Toronto in 2012. In July 2012, she took a position as full professor in neurology and pediatrics at and chief of neurology at the Children's Hospital of Philadelphia . [ 10 ]
Banwell initially took her position at the University of Toronto intending to focus on neuromuscular disease in children. When she inherited five patients with multiple sclerosis from a retiring physician, she reports that her focus shifted to pediatric demyelinating disease. [ 11 ]
To better study a rare disease, Banwell created the Canadian Pediatric Demyelinating Disease Network in 2004, a multi-site network including all pediatric health-care facilities in Canada. [ 12 ] This has allowed Banwell and co-investigators to better understand diagnosis, treatment, and comorbidities of pediatric demyelinating disease.
Diagnosis: Banwell has been instrumented in evaluating the use of the McDonald criteria - standardized criteria to diagnose multiple sclerosis through determination of dissemination of central nervous system demyelination in space and time - in pediatric multiple sclerosis . [ 13 ] She has been the primary pediatric neurologist involved in international work to develop updates of the McDonald criteria for adults and children in 2010 [ 14 ] and in 2017. [ 15 ]
Treatment: While many medications have become available for the treatment of multiple sclerosis over the last three decades, testing in children has been challenging due to the rarity of pediatric multiple sclerosis and ethical considerations with the use of placebo. [ 16 ] To facilitate and improve clinical trial design, Banwell created and currently chairs the International Pediatric Multiple Sclerosis Study Group. This allowed for the success of the PARADIGMS clinical trial, studying the safety and efficacy of fingolimod in a comparison with interferon beta-1a , [ 17 ] and led to approval of fingolimod by the Food and Drug Administration for pediatric multiple sclerosis, the first approval of a medication for this indication. [ 18 ]
Comorbidities: Banwell's work has shown that while children may recover physically from flares of multiple sclerosis, neuropsychological deficits may be apparent on testing, particularly in those who present at a younger age. [ 19 ] [ 20 ] This knowledge has changed how families are counseled and supported through the diagnosis of multiple sclerosis. [ 21 ]
Because demyelinating diseases in the pediatric population can be difficult to distinguish from each other, Banwell has worked to define and provide clinical guidelines for physicians working to delineate the diseases. [ 22 ]
In 2015, Banwell was on the International Panel for NMO Diagnosis (IPND) to develop international consensus diagnostic criteria for what became termed neuromyelitis optica spectrum disorder (NMO-SD). [ 23 ] She has also worked to determine the best treatment options for pediatric NMO-SD .
MOG antibody disease (MOGAD) was first described in the early 2000s as a subset of cases of neuromyelitis optica with antibodies to myelin oligocyte glycoprotein (MOG). [ 24 ] Banwell and colleagues worked to characterize pediatric MOGAD to determine methods of diagnosis, [ 25 ] treatment options, [ 26 ] and prognosis. [ 27 ]
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https://en.wikipedia.org/wiki/Brenda_Banwell
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The Brighton trunk murders were two murders linked to Brighton , England, in 1934. In each, the body of a murdered woman was placed in a trunk . The murders are not believed to have any connection with each other aside from how they were carried out, and the first of the two victims remains unidentified; a suspect was arrested and tried for the second murder but was found not guilty.
The murders led to Brighton being dubbed "The Queen of Slaughtering Places" (a play on "The Queen of Watering Places"). [ 1 ]
The first murder was discovered on 17 June 1934, when an unclaimed plywood trunk was noticed by William Joseph Vinnicombe at the left luggage office of Brighton railway station as he investigated a smell. He alerted the police and Chief Inspector Robert (Bob) Donaldson opened the trunk to find the dismembered torso of a woman. When other stations were alerted a suitcase at King's Cross railway station was found to contain the legs. The head and arms were never found. The press named the victim 'The Girl with the Pretty Feet' or simply 'Pretty Feet' because the corpse had 'Dancer's Feet', thought beautiful. [ 2 ]
The post-mortem , conducted by Sir Bernard Spilsbury , revealed that the woman was about 25 and five months pregnant. [ 3 ] Neither the victim nor her murderer was ever identified.
Chief Inspector Donaldson suspected a local abortionist named Massiah based on what was known about him and on Spilsbury's notes:
Internal examination of the torso had not revealed the cause of death; the legs and feet found at King's Cross belonged to the torso; the victim had been well nourished; she had been not younger than twenty-one and not older than twenty-eight, had stood about five feet two inches, and had weighed roughly eight and a half stones; she was five months pregnant at the time of death.
[ citation needed ]
Donaldson asked officers to watch Massiah covertly. One, drafted from Hove, confronted Massiah, expecting him to come quietly. Instead, the doctor wrote a list of names of such prominent and powerful persons that "...it seemed to the policeman that the sun had gone in: all of a sudden the consulting room was a place of sombre shadows....". [ 4 ] [ citation needed ]
The policeman did not tell Donaldson about the confrontation; he heard only when he was warned by a senior officer to back off Massiah. Massiah moved to London where a woman died while he was performing an abortion, yet he evaded prosecution. He remained on the General Medical Register and was removed only after he failed to re-register in 1952, following his retirement to Port of Spain , Trinidad . [ citation needed ] Spilsbury, always on the lookout for evidence of illegal abortions, described no evidence of interference with the pregnancy, and noted that the dismemberment showed no particular anatomical skill. [ 5 ]
In 2020, the BBC One documentary Dark Land: Hunting the Killers suggested that George Shotton could be the murderer of the unidentified woman. George Shotton was posthumously named as the murderer of his wife Mamie Stuart at the inquest into her death in 1961. [ 6 ]
Although the first murder was unrelated to the second, it did lead to the discovery of the second trunk murder.
The victim was Violette Kaye (née Watts, also known as Saunders), aged 42. She had been a dancer and sex worker in London, where she had met Toni Mancini, aged 26, who had a criminal record, including theft and loitering, but who worked as a waiter and bouncer. [ 7 ] He was also known as Cecil Louis England (his real name), Jack Notyre, Tony English and Hyman Gold. [ 8 ] They moved to Brighton together in September 1933 and lived at various addresses.
Kaye and Mancini's relationship was tempestuous. One argument occurred on 10 May 1934 at the Skylark café on the seafront, where Mancini worked, when a drunk Kaye accused him of being romantically involved with a teenage waitress called Elizabeth Attrell. [ 9 ] Kaye was never seen again and the following day Mancini told friends she had gone to Paris and gave some of her clothes and belongings to Attrell. Her sister-in-law also received a telegram that read "Going abroad. Good job. Sail Sunday. Will write. --Vi"; it was later established that this had been sent from Brighton that morning, by which time Kaye was already dead. [ 10 ]
Mancini then took new lodgings in 52 Kemp Street, close to the station, and transported a trunk to his new flat by handcart . He put the trunk, with Kaye's non-dismembered body inside it, at the foot of his bed, covered it with a cloth and used it as a coffee table – in spite of the smell and leaking fluids, of which visitors complained. [ 10 ]
Kaye's absence had been noted by police and Mancini was questioned. Apparently panicked, he went on the run. During the investigation related to the unsolved trunk murder, police searched premises close to the station and stumbled upon Kaye's remains in Mancini's lodgings. Mancini was arrested in South East London. The post mortem was also carried out by Sir Bernard Spilsbury . [ 8 ]
Mancini's trial opened in December 1934 in Lewes Assizes and lasted five days. The prosecution was led by J.C. Cassells and on his team was Quintin Hogg (later Lord Hailsham). Norman Birkett was the defence counsel. [ 8 ]
The prosecution focused on Kaye's death by a blow to the head. A graphologist confirmed the handwriting on the form for the telegram sent to Kaye's sister matched that on menus Mancini had written at the Skylark café. One witness, Doris Saville, said Mancini had asked her to provide a false alibi. Other witnesses, friends of Mancini, claimed he boasted in the days after the murder of giving his "missus" the biggest hiding of her life. [ citation needed ]
Birkett's defence focused on Kaye's work as a prostitute and her character. Mancini claimed he had discovered Kaye's body at the flat at 44 Park Crescent, Brighton . Thinking the police would not believe his story because he had a criminal record, he kept the matter a secret and put her body in a trunk. Birkett speculated she could have been murdered by a client or fallen down steps into the flat. [ 8 ]
The quality and nature of the forensic evidence were also drawn into doubt by the defence who queried the amount of morphine in Kaye's blood and proved that items of clothing stained with blood had been purchased after Kaye's death. The testimony of Sir Bernard Spilsbury, whose illustrious career as Principal Home Office Pathologist was already in decline, was effectively demolished by the well-planned cross-examination and closing speech of Norman Birkett. [ 11 ] A number of witnesses also confirmed that Mancini and Kaye had seemed a contented couple. [ citation needed ]
After two and a quarter hours the jury returned a verdict of not guilty. [ 8 ]
In 1976 Mancini confessed to a News of the World journalist. He explained that during a blazing row with Kaye, she had attacked him with the hammer he had used to break coal for their fire. He had wrestled the hammer from her, but when she had demanded it back, he had thrown it at her, hitting her on the left temple. A prosecution of Mancini for perjury was considered but rejected due to lack of corroboration. [ 12 ]
The case was dramatised in a 1951 episode of Orson Welles ' radio drama The Black Museum titled "The Hammerhead" (with the story being changed to reveal the victim's sister as the killer). [ citation needed ]
The press attention to the 1934 trunk murders revived interest in a previous Brighton trunk murder. In the 19th century, John Holloway murdered his wife Celia Holloway, a painter on the Chain Pier , then transported her body in a trunk on a wheelbarrow to Lover's Walk in Preston Park, Brighton and buried the remains. Holloway was arrested, tried in Lewes and hanged at Horsham gaol on 16 December 1831. [ 13 ]
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https://en.wikipedia.org/wiki/Brighton_trunk_murders
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Between 1977 and 2006, the Bristol-Myers Squibb Foundation presented annual award s of US$50,000 to scientists for distinguished achievements in fields such as cancer , infectious disease , neuroscience , nutrition , and cardiovascular disease . [ 1 ] The recipients of these awards were selected by pre-eminent members of each field and past award recipients. Bristol-Myers Squibb had no role in determining the recipients of the awards. [ 2 ]
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https://en.wikipedia.org/wiki/Bristol-Myers_Squibb_Awards
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