In addition to mutations in the SEPN1 gene, other genetic and environmental factors may also play a role in the development of rigid spine syndrome. However, further research is needed to fully understand these factors and their contribution to the condition. [ 10 ]


Diagnosing rigid spine syndrome can be challenging due to its rarity and the variability of symptoms among affected individuals. However, the following approaches are commonly used to diagnose the condition:


A thorough physical examination is often the first step in diagnosing rigid spine syndrome. The healthcare provider will assess the patient's muscle tone, range of motion, and any signs of spinal deformities or joint contractures. [ 11 ] [ 2 ]


X-rays ,  CT scans , or  MRI scans  may be used to evaluate the spine for any abnormalities, such as kyphosis, scoliosis, or other spinal deformities. These imaging studies can also help assess the severity of the condition and guide treatment planning. [ 4 ]


Genetic testing is essential for confirming a diagnosis of rigid spine syndrome. Testing typically involves analyzing the SEPN1 gene for mutations. Identifying mutations in this gene can help confirm the diagnosis and provide valuable information about the genetic basis of the condition. [ 4 ]


In some cases, a  muscle biopsy  may be recommended to evaluate the structure and function of the muscles. This can help differentiate rigid spine syndrome from other muscle disorders and provide additional information about the underlying cause of the condition. [ 4 ]


EMG  may be used to assess the electrical activity of the muscles and  nerves . This test can help identify abnormalities in muscle function and may be used to support a diagnosis of rigid spine syndrome. [ 4 ]


A detailed family history can also be helpful in diagnosing rigid spine syndrome, as it is an autosomal recessive condition and often runs in families. [ 4 ]


The  prognosis  of rigid spine syndrome is variable and can be influenced by several factors, including the severity of symptoms, the age of onset, and the effectiveness of treatment. In general, the condition is progressive, meaning that symptoms tend to worsen over time. However, the rate of progression can vary widely among affected individuals.


The severity of symptoms at the time of diagnosis can have a significant impact on prognosis. Individuals with milder symptoms may experience slower progression of the condition and better overall outcomes compared to those with more severe symptoms. [ 6 ]


The age at which symptoms of rigid spine syndrome first appear can also influence prognosis. Early onset of symptoms, particularly in  infancy  or early childhood, is often associated with a more severe form of the condition and a poorer prognosis. [ 5 ] [ 6 ]


The effectiveness of treatment in managing symptoms and complications of rigid spine syndrome can greatly impact prognosis. Early and aggressive management, including physical therapy, orthopedic interventions, and respiratory support, can help improve quality of life and slow disease progression. [ 10 ] [ 12 ]


The development of complications, such as respiratory problems or severe joint contractures, can also affect prognosis. Complications may require additional interventions and can further impact mobility and overall health. [ 10 ]


Each individual responds differently to treatment, and the effectiveness of various interventions can vary. Regular monitoring and adjustments to the treatment plan are essential to managing the condition and optimizing outcomes.


Despite the progressive nature of rigid spine syndrome, many individuals are able to maintain a good quality of life with appropriate care and support. Access to multidisciplinary care and assistive devices can greatly improve mobility and independence.


Rigid spine syndrome is a rare neuromuscular disorder, and accurate epidemiological data is limited. However, the condition appears to be extremely rare, with only a few dozen cases reported in medical literature.


The exact prevalence of rigid spine syndrome is unknown, but it is believed to be very low. The condition has been reported in various populations worldwide, suggesting that it is not limited to any specific ethnic or geographic group. [ 13 ]


Similarly, the incidence of rigid spine syndrome is not well-established due to its rarity. The condition is typically diagnosed in infancy or early childhood, but cases of adult onset have also been reported, albeit rarely. [ citation needed ]


Rigid spine syndrome can affect individuals of any age or gender, but it is most commonly diagnosed in childhood. The condition does not appear to have a significant gender bias, affecting males and females equally. [ 13 ]


Rigid spine syndrome has been reported in various countries around the world, indicating that it is not limited to any specific geographic region. However, due to its rarity, there may be underreporting in some areas. [ 13 ]


The autosomal recessive inheritance pattern of rigid spine syndrome suggests that individuals with a family history of the condition are at increased risk. Genetic counseling and testing can help identify carriers and inform family planning decisions. [ 11 ]


Research on rigid spine syndrome is ongoing, with a focus on understanding the underlying genetic and molecular mechanisms of the condition, developing new treatment approaches, and improving the quality of life for affected individuals. Some key areas of research include:


Researchers are conducting genetic studies to identify additional genes that may be involved in the development of rigid spine syndrome. This research may lead to a better understanding of the condition's genetic basis and the development of targeted therapies. [ 5 ]


Studies are underway to investigate the molecular mechanisms underlying muscle stiffness and rigidity in rigid spine syndrome. This research may uncover new targets for therapeutic interventions aimed at improving muscle function. [ 4 ]


Clinical trials are being conducted to evaluate the safety and efficacy of potential treatments for rigid spine syndrome. These trials may involve medications, physical therapies, or surgical interventions aimed at improving mobility and quality of life for affected individuals. [ 10 ]


Some researchers are exploring the use of regenerative medicine approaches, such as stem cell therapy, to repair damaged muscles and improve muscle function in individuals with rigid spine syndrome. This area of research holds promise for future treatment options. [ 10 ]


Patient registries are being established to collect data on individuals with rigid spine syndrome, including information on symptoms, disease progression, and treatment outcomes. These registries are valuable resources for researchers studying the condition.


Collaborative research efforts among healthcare providers, researchers, and patient advocacy groups are essential for advancing our understanding of rigid spine syndrome. These collaborations can help facilitate the sharing of data and resources, leading to more rapid progress in the field.


Future research in rigid spine syndrome is likely to focus on personalized medicine approaches, aimed at tailoring treatments to the specific genetic and molecular characteristics of individual patients. Additionally, research may continue to explore the role of environmental factors in the development and progression of the condition. [ 12 ]


The  sarcoglycanopathies  are a collection of diseases resulting from  mutations  in any of the five  sarcoglycan  genes: α, β, γ, δ or ε.
The five sarcoglycanopathies are: α-sarcoglycanopathy,  LGMD2D ; β-sarcoglycanopathy, LGMD2E; γ-sarcoglycanopathy, LGMD2C; δ-sarcoglycanopathy, LGMD2F and ε-sarcoglycanopathy, myoclonic dystonia. The four different sarcoglycan genes encode proteins that form a  tetrameric  complex at the muscle  cell plasma membrane . This complex stabilizes the association of  dystrophin  with the  dystroglycans  and contributes to the stability of the plasma membrane  cytoskeleton . The four sarcoglycan genes are related to each other structurally and functionally, but each has a distinct  chromosome  location.


In outbred populations, the relative frequency of mutations in the four genes is alpha >> beta >> gamma >> delta in an 8:4:2:1 ratio. No common mutations have been identified in outbred populations except the R77C mutation, which accounts for up to one-third of the mutated  SGCA   alleles . Founder mutations have been observed in certain populations. [ 1 ]  A 1997 Italian clinical study demonstrated variations in  muscular dystrophy  progression dependent on the sarcoglycan gene affected. [ 2 ]


Sphincter paralysis  is  paralysis  of one of the body's many  sphincters , preventing it from constricting normally.


Case studies have shown patients may remain  continent  for many years despite being affected by anal sphincter paralysis. [ 1 ]


This article about a  disease , disorder, or medical condition is a  stub . You can help Wikipedia by  expanding it .


A  strain  is an acute or  chronic   soft tissue injury  that occurs to a  muscle ,  tendon , or both. The equivalent injury to a  ligament  is a  sprain . [ 1 ]  Generally, the muscle or tendon overstretches and partially tears, under more physical stress than it can withstand, often from a sudden increase in duration, intensity, or frequency of an activity. Strains most commonly occur in the foot, leg, or back. Immediate treatment typically used to include four steps abbreviated as  R.I.C.E.  (rest, ice, compression, elevation) before the role of inflammation was found to be helpful.


Typical  signs  and  symptoms  of a strain include  pain , functional loss of the involved structure,  muscle weakness ,  contusion , and localized  inflammation . [ 2 ]  A strain can range from mild overstretching to severe  tears, depending on the extent of injury. [ 1 ]


A strain can occur as a result of improper body mechanics with any activity (e.g.,  contact sports , lifting heavy objects) that can induce mechanical trauma or injury. Generally, the muscle or tendon overstretches and is placed under more physical stress than it can withstand. [ 1 ]  Strains commonly result in a partial or complete tear of a tendon or muscle, or they can be severe in the form of a complete tendon rupture. Strains most commonly occur in the  foot ,  leg , or  back. [ 3 ]  Acute strains are more closely associated with recent mechanical trauma or injury. Chronic strains typically result from repetitive movement of the muscles and tendons over a long period of time. [ 1 ]


Degrees of Injury (as classified by the  American College of Sports Medicine ): [ 4 ]


To establish a uniform definition amongst healthcare providers, in 2012 a Consensus Statement on suggested new terminology and classification of muscle injuries was published. [ 5 ]


The classifications suggested were:


Indirect Muscle Injury
FUNCTIONAL (Negative MSK US & MRI) [ 6 ]


• Type 2: Neuromuscular muscle disorder


STRUCTURAL MUSCLE INJURY (Positive MSK US & MRI) [ 6 ]
• Type 3: Partial Muscle Tear
• Type 4: (Sub) total tear


DIRECT MUSCLE INJURY
•  Bump or Cut: Contact-related


Although strains are not restricted to athletes and can happen while doing everyday tasks, people who play sports are more at risk for developing a strain. It is common for an  injury  to develop when there is a sudden increase in duration, intensity, or frequency of an activity. [ 3 ]


The first-line treatment for a muscular strain in the  acute phase  include five steps commonly known as  P.R.I.C.E. [ 7 ] [ 8 ]


Immediate treatment is usually an adjunctive therapy of  NSAIDs  and  Cold compression therapy . Cold compression therapy acts to reduce swelling and pain by reducing  leukocyte extravasation  into the injured area. [ 9 ] [ 10 ]  NSAIDs such as  Ibuprofen/paracetamol  work to reduce the immediate inflammation by inhibiting  Cox-1  and  Cox-2  enzymes, which are the enzymes responsible for converting  arachidonic acid  into  prostaglandin . However, NSAIDs, including  aspirin  and ibuprofen, affect platelet function (this is why they are known as "blood thinners") and should not be taken during the period when tissue is bleeding because they will tend to increase blood flow, inhibit clotting, and thereby increase bleeding and swelling. After the bleeding has stopped, NSAIDs can be used with some effectiveness to reduce inflammation and pain. [ 11 ]


A new treatment for acute strains is the use of  platelet rich plasma  (PRP) injections which have been shown to accelerate recovery from non-surgical muscular injuries. [ 12 ]


It is recommended that the person injured should consult a medical provider if the injury is accompanied by severe pain, if the limb cannot be used, or if there is noticeable tenderness over an isolated spot. These can be signs of a broken or  fractured bone , a  sprain , or a complete muscle tear. [ 13 ]


Thyrotoxic periodic paralysis  ( TPP ) is a rare condition featuring attacks of  muscle weakness  in the presence of  hyperthyroidism  (overactivity of the  thyroid  gland).  Hypokalemia  (a decreased  potassium  level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the  breathing muscles  leads to  respiratory failure , or if the low potassium levels lead to  abnormal heart rhythms . [ 1 ] [ 2 ]  If untreated, it is typically recurrent in nature. [ 1 ]


The condition has been linked with  genetic mutations  in genes that code for certain  ion channels  that transport  electrolytes  ( sodium  and  potassium ) across  cell membranes . The main ones are the  L-type calcium channel α1-subunit [ 1 ]  and  potassium inward rectifier 2.6 ; [ 3 ]  it is therefore classified as a  channelopathy . [ 3 ]  The abnormality in the channel is thought to lead to shifts of potassium into  cells , under conditions of high  thyroxine  (thyroid hormone) levels, usually with an additional precipitant.


Treatment of the low levels of potassium in the blood, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks. It occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent. [ 1 ]  TPP is one of several conditions that can cause  periodic paralysis . [ 4 ]


An attack often begins with muscle pain, cramping, and stiffness. [ 5 ]  This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical; [ 5 ]  the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the  mouth and throat ,  eyes , and  breathing  are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening  respiratory failure . Attacks typically resolve within several hours to several days, even in the absence of treatment. [ 1 ] [ 2 ] [ 5 ]  On  neurological examination  during an attack,  flaccid weakness  of the limbs is noted;  reflexes  are usually diminished, but the  sensory system  is unaffected. [ 1 ] [ 5 ]  Mental status is not affected. [ 5 ]


Attacks may be brought on by  physical exertion , drinking  alcohol , or eating food high in  carbohydrates  or  salt . This may explain why attacks are more common in summer when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may, therefore, be recommended to abort an attack. [ 1 ]


There may be symptoms of thyroid overactivity, such as  weight loss ,  a fast or irregular heart rate ,  tremor , and  perspiration ; [ 1 ] [ 2 ]  but such symptoms occur in only half of all cases. [ 5 ]  The most common type of hyperthyroidism,  Graves' disease , may additionally cause eye problems ( Graves' ophthalmopathy ) and skin changes of the legs ( pretibial myxedema ). [ 6 ]  Thyroid disease may also cause muscle weakness in the form of  thyrotoxic myopathy , but this is constant rather than episodic. [ 5 ]


Genetic mutations in the L-type calcium channel α1-subunit (Ca v 1.1) have been described in Southern Chinese with TPP. The mutations are located in a different part of the gene from those described in the related condition  familial periodic paralysis . In TPP, the mutations described are  single-nucleotide polymorphisms  located in the  hormone response element  responsive to thyroid hormone, implying that  transcription  of the gene and production of ion channels may be altered by increased thyroid hormone levels. Furthermore, mutations have been reported in the genes coding for  potassium voltage-gated channel, Shaw-related subfamily, member 4  (K v 3.4) and  sodium channel protein type 4 subunit alpha  (Na 4 1.4). [ 1 ]


Of people with TPP, 33% from various populations were demonstrated to have mutations in  KCNJ18 , the gene coding for K ir 2.6, an  inward-rectifier potassium ion channel . This gene, too, harbors a thyroid response element. [ 3 ]


Certain forms of  human leukocyte antigen  (HLA)—especially B46, DR9, DQB1*0303, A2, Bw22, AW19, B17, and DRW8—are more common in TPP. Linkage to particular forms of HLA, which plays a central role in the  immune response , might imply an immune system cause, but it is uncertain whether this directly causes TPP or whether it increases the susceptibility to Graves' disease, a known  autoimmune disease . [ 1 ]


The most common underlying form of thyroid disease associated with TPP is Graves' disease, a syndrome due to an  autoimmune reaction  that leads to overproduction of thyroid hormone. [ 6 ]  TPP has also been described in people with other thyroid problems such as  thyroiditis ,  toxic nodular goiter ,  toxic adenoma ,  TSH -producing  pituitary adenoma , excessive ingestion of  thyroxine  or  iodine , [ 1 ]  and  amiodarone -induced hyperthyroidism. [ 2 ]


The muscle weakness and increased risk of irregular heart beat in TPP result from markedly reduced levels of potassium in the bloodstream. Potassium is not in fact lost from the body, but increased  Na + /K + -ATPase  activity (the  enzyme  that moves potassium into cells and keeps  sodium  in the blood) leads to shift of potassium into tissues, and depletes the circulation. In other types of potassium derangement, the  acid-base balance  is usually disturbed, with  metabolic alkalosis  and  metabolic acidosis  often being present. In TPP, these disturbances are generally absent. Hypokalemia leads to  hyperpolarization  of  muscle cells , making the  neuromuscular junction  less responsive to normal nerve impulses and leading to decreased contractility of the muscles. [ 1 ]


It is not clear how the described genetic defects increase the Na + /K + -ATPase activity, but it is suspected that the enzyme becomes more active due to increased thyroid hormone levels. Hyperthyroidism increases the levels of  catecholamines  (such as  adrenaline ) in the blood, increasing Na + /K + -ATPase activity. [ 5 ]  The enzyme activity is then increased further by the precipitating causes. For instance, increased carbohydrate intake leads to increased  insulin  levels; this is known to activate Na + /K + -ATPase. Once the precipitant is removed, the enzyme activity returns to normal levels. [ 1 ]  It has been postulated that  male hormones  increase Na + /K + -ATPase activity, and that this explains why males are at a higher risk of TPP despite thyroid disease being more common in females. [ 2 ]


TPP is regarded as a model for related conditions, known as "channelopathies", which have been linked with mutations in ion channels; the majority of these conditions occurs episodically. [ 3 ]


Hypokalemia  (low blood  potassium  levels) commonly occurs during attacks; levels below 3.0 mmol/L are typically encountered.  Magnesium  and  phosphate  levels are often found to be decreased.  Creatine kinase  levels are elevated in two-thirds of cases, usually due to a degree of muscle injury; severe elevations suggestive of  rhabdomyolysis  (muscle tissue destruction) are rare. [ 1 ] [ 2 ]   Electrocardiography  (ECG/EKG) may show  tachycardia  (a fast heart rate) due to the thyroid disease, abnormalities due to cardiac arrhythmia ( atrial fibrillation ,  ventricular tachycardia ), and conduction changes associated with hypokalemia (U waves, QRS widening, QT prolongation, and T wave flattening). [ 2 ]   Electromyography  shows changes similar to those encountered in  myopathies  (muscle diseases), with a reduced amplitude of the  compound muscle action potentials  (CMAPs); [ 4 ]  they resolve when treatment has commenced. [ 1 ]


TPP is distinguished from other forms of periodic paralysis (especially  hypokalemic periodic paralysis ) with  thyroid function tests  on the blood. These are normal in the other forms, and in  thyrotoxicosis  the levels of  thyroxine  and  triiodothyronine  are elevated, with resultant suppression of TSH production by the  pituitary gland . [ 1 ] [ 6 ]  Various other investigations are usually performed to separate the different causes of  hyperthyroidism . [ 6 ]


In the acute phase of an attack, administration of  potassium  will quickly restore muscle strength and prevent complications. However, caution is advised as the total amount of potassium in the body is not decreased, and it is possible for potassium levels to overshoot ("rebound  hyperkalemia "); slow infusions of potassium chloride are therefore recommended while other treatment is commenced. [ 1 ]


The effects of excess thyroid hormone typically respond to the administration of a non-selective  beta blocker , such as  propranolol  (as most of the symptoms are driven by increased levels of adrenaline and its effect on the  β-adrenergic receptors ). Subsequent attacks may be prevented by avoiding known precipitants, such as high salt or carbohydrate intake, until the thyroid disease has been adequately treated. [ 1 ]


Treatment of the thyroid disease usually leads to resolution of the paralytic attacks. Depending on the nature of the disease, the treatment may consist of  thyrostatics  (drugs that reduce production of thyroid hormone),  radioiodine , or occasionally thyroid surgery. [ 1 ] [ 2 ]


TPP occurs predominantly in  males  of Chinese, Japanese, Vietnamese, Filipino, and Korean descent, [ 1 ]  as well as  Thais , [ 3 ]  with much lower rates in people of other ethnicities. [ 1 ]  In Chinese and Japanese people with hyperthyroidism, 1.8–1.9% experience TPP. This is in contrast to North America, where studies report a rate of 0.1–0.2%. [ 1 ] [ 2 ]   Native Americans , who share a genetic background with East Asians, are at an increased risk. [ 1 ]


The typical age of onset is 20–40. It is unknown why males are predominantly affected, with rates in males being 17- to 70-fold those in females, despite thyroid overactivity being much more common in women. [ 1 ] [ 2 ]


After several case reports in the 18th and 19th centuries, periodic paralysis was first described in full by the German neurologist  Karl Friedrich Otto Westphal  (1833–1890) in 1885. [ 7 ] [ 8 ]  In 1926 the Japanese physician Tetsushiro Shinosaki, from  Fukuoka , observed the high rate of thyroid disease in Japanese people with periodic paralysis. [ 9 ] [ 10 ]  The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the  Mayo Clinic ; they described the condition in a patient with features of  Graves' disease . [ 2 ] [ 10 ]  In 1937 periodic paralysis was linked with hypokalemia, as well as precipitation of attacks with glucose and insulin. [ 11 ] [ 12 ]  This phenomenon has been used as a diagnostic test. [ 12 ]


In 1974 it was discovered that  propranolol  could prevent attacks. [ 13 ]  The concept of channelopathies and the link with specific ion channel mutations emerged at the end of the 20th century. [ 1 ] [ 3 ] [ 4 ]


Weakness  is a  symptom  of many different medical conditions. [ 1 ]  The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including  muscular dystrophy  and  inflammatory myopathy . It occurs in  neuromuscular junction  disorders, such as  myasthenia gravis . [ citation needed ]


Muscle cells work by detecting a  flow  of electrical impulses from the  brain , which signals them to  contract  through the release of  calcium  by the  sarcoplasmic reticulum . Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers. [ 2 ]


Substrates  within the muscle generally serve to power muscular contractions. They include molecules such as  adenosine triphosphate  (ATP),  glycogen  and  creatine phosphate . ATP binds to the  myosin  head and causes the 'ratchetting' that results in contraction according to the  sliding filament model . Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from  adenosine diphosphate  (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of  glucose , used to generate energy quickly once intramuscular creatine stores are exhausted, producing  lactic acid  as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation felt when people exhaust their oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce  pyruvate  in the liver, which is known as the  Cori cycle . [ citation needed ]


Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so. [ citation needed ]


In some conditions, such as  myasthenia gravis , muscle strength is normal when resting, but  true weakness  occurs after the muscle has been subjected to exercise. This is also true for some cases of  Myalgic encephalomyelitis/chronic fatigue syndrome , where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions. [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ]


Asthenia  or  asthaenia  ( Greek :  ἀσθένεια , literally  lack of strength  but also  disease ) is a medical term referring to a condition in which the body lacks or has lost strength either as a whole or in any of its parts. It is a poorly defined condition that can include true or primary  muscle weakness  or perceived muscle weakness. [ 10 ]  For perceived muscle weakness, asthenia has been described as the feeling of weak or tired muscles in the absence of muscle weakness, that is the muscle can generate a normal amount of force but it is perceived as requiring more effort. [ 11 ] [ 12 ]


General asthenia occurs in many chronic wasting diseases (such as tuberculosis and cancer), sleep disorders or chronic disorders of the heart, lungs or kidneys, and is probably most marked in diseases of the adrenal gland. Asthenia may be limited to certain  organs  or systems of organs, as in  asthenopia , characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as  Ritonavir  (a  protease inhibitor  used in  HIV  treatment).  [ 13 ]


Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness. [ citation needed ]


Myasthenia or myasthaenia (my- from  Greek :  μυο  meaning "muscle" + -asthenia [ ἀσθένεια ] meaning "weakness"), or simply muscle weakness, is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in  neuromuscular diseases , such as myasthenia gravis. Perceived muscle weakness occurs in diseases such as sleep disorders, and depression. [ 11 ]


Muscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work. [ 14 ] [ 15 ]  Neuromuscular fatigue can be either central or peripheral. [ citation needed ]


The central fatigue is generally described in terms of a reduction in the  neural  drive or nerve-based motor command to working muscles that results in a decline in the force output. [ 16 ] [ 17 ] [ 18 ]   It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. [ 19 ] [ 20 ]  The exact mechanisms of central fatigue are unknown, though there has been considerable interest in the role of  serotonergic  pathways. [ 21 ] [ 22 ] [ 23 ]


For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice  strength trainers , the muscle's ability to generate force is most strongly limited by nerve's ability to sustain a  high-frequency signal . After an extended period of maximum contraction, the nerve's signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply 'stop listening' and gradually cease to move, often  lengthening . As there is insufficient stress on the muscles and tendons, there will often be no  delayed onset muscle soreness  following the workout.  Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force.  It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic  hypertrophy  and metabolic fatigue becomes the factor limiting contractile force.


Peripheral muscle fatigue during physical work is considered [ by whom? ]  an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national [ where? ]  average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal  aerobic metabolism , generally results in the accumulation of  lactic acid  and other  acidic  anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy. [ 24 ]


Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the  myocytes . This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca 2+  to stimulate  actin  and  myosin  to contract.


Writer's cramp  or  focal hand dystonia  ( FHD ) is an  idiopathic   movement disorder  of adult onset, characterized by abnormal posturing and movement of the hand and/or forearm during tasks requiring skilled hand use, such as writing. [ 1 ] [ 2 ]  Overcontraction of affected muscles,  cocontraction  of  agonist and antagonist pairs , and activation of muscles inappropriate to a task all impair use of the affected hand. [ 3 ]


Writer's cramp is a task-specific  focal dystonia  of the hand. [ 4 ]  'Focal' refers to the symptoms being limited to one location (the hand in this case), and 'task-specific' means that symptoms first occur only when the individual engages in a particular activity. Writer's cramp first affects an individual by interfering with their ability to write, especially for prolonged periods of time. [ 2 ]


Epidemiologic  studies report a prevalence of 7–69 per million population for writer's cramp, [ 5 ]  which explains its recognition as a  rare disease , like all other forms of  dystonia . [ 6 ]


Onset usually occurs between the ages of 30 and 50 years and often starts with a feeling of tension in fingers and forearms that interferes with writing fluency. [ 7 ]


More specifically, early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, dropped items and a noticeable increase in dropped or chipped dishes), cramping pain with sustained use and trembling. Significant muscle pain and cramping may result from very minor exertions like holding a book and turning pages. It may become difficult to find a comfortable position for arms and legs with even the minor exertions associated with holding arms crossed causing significant pain similar to restless leg syndrome. Affected persons may notice trembling in the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt and heard while lying down, and the constant movement to avoid pain may result in the grinding and wearing down of teeth, or symptoms similar to  TMD . The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping. Patients may also present with varying degree of disability and symptoms, such as experiencing more difficulty writing down-stroke as compared to writing upstroke. [ 2 ]


Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears under load). The symptoms worsen significantly with use, especially in the case of focal dystonia, and a "mirror effect" is often observed in other body parts: use of the right hand may cause pain and cramping in that hand as well as in the other hand and legs that were not being used. Stress, anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms. [ citation needed ]


Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty concentrating, blurred vision, digestive problems and short temper. People with dystonia may also become depressed and find great difficulty adapting their activities and livelihood to a progressing disability. Side effects from treatment and medications can also present challenges in normal activities.


In some cases, symptoms may progress and then plateau for years, or stop progressing entirely. The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued use may make symptoms progress more rapidly. In others, the symptoms may progress to total disability, making some of the more risky forms of treatment worth considering in the future. [ citation needed ]


Although the cause of writer's cramp is not well known, it was historically believed to be the result of excessive fine motor activity, possibly complicated by a tense or otherwise inappropriate writing technique. [ 8 ]   More recently, Karin Rosenkranz et al. have suggested that this is not necessarily the case. [ 9 ]


Recent studies point out that there appears to be a  genetic  component to focal hand dystonia (FHD). In fact, up to 20% of those with writer's cramp have a family member with some form of dystonia. [ 7 ]


Musician's cramp (a similar focal dystonia which affects less than 1% of instrumentalists [ 10 ] ) has historically been grouped together with writer's cramp because of this and their common task-specificity. Rosenkranz et al. have more recently identified significant differences between the two populations, however. [ 9 ]   No matter exactly how it arises, researchers generally agree that these types of focal dystonia are the result of a  basal ganglia  and/or  sensorimotor cortex  malfunction in the brain. [ citation needed ]


Although dystonias may be induced by chemical exposure/ingestion, brain injury, or hereditary/genetic predisposition, the task-specific focal dystonias such as writer's cramp are a unique challenge to diagnose and treat. Some cases may respond to chemical injections - botulinum toxin (botox) is often cited, though it is not helpful in all cases. [ 2 ] [ 11 ]  Behavioral retraining attempts may include writing devices, switching hands, occupational therapy, biofeedback, constraint-induced motion therapy, and others. Some writing instruments allow variations of pressure application for use. None of these are effective in all cases, however. The work of Dr.  Joaquin Farias  has shown that  proprioceptive stimulation can induce  neuroplasticity , making it possible for patients to recover substantial function that was lost from focal dystonia. [ 12 ]


Anticholinergics  such as   Artane  can be prescribed for off-label use, as some patients have had success. [ 13 ]


Creutzfeldt–Jakob disease


The  epitrochleoanconeus muscle  ( anconeous epitrochlearis muscle ,  anconeus-epitrochlearis  or  anconeus sextus ) is a small  accessory muscle  of the  arm  which runs from the back of the inner condyle of the  humerus  over the  ulnar nerve  to the  olecranon . The average prevalence of this muscle is 14.2% in healthy individuals. [ 1 ]


The epitrochleoanconeus is a short striated muscle which originates on the posterior surface of the medial epicondyle of the humerus. The muscle runs over the ulnar nerve, forms an arch over the  cubital tunnel  and inserts on the olecranon. It is innervated by the ulnar nerve.


There are cases where there is no structure at all bridging the space occupied by the epitrochleoanconeus. [ 2 ]  The muscle tends to be hypertrophied when associated with  cubital tunnel syndrome . [ 1 ]


The presence of the epitrochleoanconeus muscle can lead to ulnar neuropathy, or cubital tunnel syndrome, due to compression of the ulnar nerve. [ 3 ] [ 4 ] [ 5 ]  The absence of epitrochleoanconeus muscle or Osborne's ligament can increase the chances of ulnar nerve dislocation. [ 2 ]


While there were previous identifications of the epitrochleoanconeus in animal studies, under a variety of names, Gruber (1866) seems to offer the first extensive comparative study involving the epitrochleoanconeus in man. [ 6 ]  This was shortly followed by several accounts by Wood describing his identification of the muscle during a series of dissections in humans along with comparative studies in other animals. [ 7 ] [ 8 ]


In animals with a discrete developed epitrochleoanconeus the muscle acts as an  adductor  of the olecranon and a  supinator  of the forearm. [ 9 ]  A variety of names have been given to this muscle in different species including flexor antebrachii ulnaris, epitrochleo-cubitalis and entepicondylo-ulnaris. The epitrochleoanconius is common amongst  tetrapods  being found in  reptiles ,  amphibians ,  mammals  and  birds . [ 10 ]


The epitrochleoanconeus is found widely amongst mammals having been characterised in the mid 19th century in a variety of species including  two-toed sloth ,  duck billed platypus  and  echidna . Galton (1874) gave an overview of the several species characterised at that point and noted that at least 15 species had been figured with the muscle in  Cuvier 's "Anatomie comparée" of 1855 but that the muscle was given a wide variety of aliases and was not shown in many species where it should have been seen. [ 9 ]  The muscle is common in lower primates but has been lost as a discrete muscle in apes, although it has reoccurred in chimpanzees. [ 9 ] [ 11 ]


This article incorporates text in the  public domain  from  page 448  of the 20th edition of   Gray's Anatomy   (1918)


Extensor digitorum brevis manus  is an extra or  accessory muscle  on the backside (dorsum) of the  hand . It was first described by Albinus in 1758. [ 1 ]  The muscles lies in the fourth extensor compartment of the  wrist , and is relatively rare. [ 2 ]   It has a prevalence of 4% in the general population according to a meta-analysis. [ 3 ]  This muscle is commonly misdiagnosed as a ganglion cyst, synovial nodule or  cyst . [ 4 ] [ 5 ] [ 6 ]


The extensor digitorum brevis manus usually originates from the dorsal aspect (backside) of the wrist, either from the joint capsule, the distal end (the most distant end) of the radius, the metacarpal, or from the  radiocarpal ligament  in the area of the fourth extensor compartment. [ 3 ]  Many variations of the muscle have been described in the literature. It could have up to four tendons with a single tendon inserting to the index or the middle finger being the two most common variations. [ 7 ]  At the insertion the tendon of the extensor digitorum brevis manus often joins the  extensor indicis proprius , [ 3 ]  although it also occurs when the extensor indicis proprius is absent. It was also reported to coexist with the  extensor medii proprius , another anatomical variation in the extensor compartment of the hand. [ 8 ]  The muscle is supplied the  posterior interosseous nerve  and posterior branch of the  anterior interosseous artery .


The extensor digitorum brevis manus was found to be present in 4% of the population, and there was no correlation between gender, side or ancestry. [ 2 ]  it inserted to the index finger and the middle finger in 77% and 23% of the cases, respectively. [ 2 ]  It occurred bilaterally in 26% the total cases.


At some point during the  embryonic development , the precursor extensor mass differentiates into three layers: radial, superficial, and deep. [ 9 ]  The extensor digitorum brevis manus may have been originated from the deep layer, a typical location where most of the variations take place. [ 2 ]  Some authors believe that this muscle may represent a failure of proximal migration of ulnocarpal elements of the extensor muscle mass in humans. [ 8 ] [ 10 ]


It extends the index or the middle finger. It is believed to be a substitute for the extension of the index finger when the extensor indicis proprius is absent.


Only a few clinical cases have been reported among more than 300 clinical and cadaveric dissections. [ 11 ]  This implies that the presence of this muscle is usually asymptomatic, although the extensor digitorum brevis manus might cause a painful  swelling  which can potentially be misdiagnosed as other  pathology  such as synovial cyst and  lipoma . [ 4 ] [ 5 ] [ 6 ]


The  rectus sternalis muscle  is an  anatomical variation  that lies in front of the sternal end of the  pectoralis major  parallel to the margin of the  sternum . The sternalis muscle may be a variation of the pectoralis major or of the  rectus abdominis .


The sternalis is a  muscle  that runs along the anterior aspect of the body of the sternum. It lies superficially and parallel to the sternum. Its origin and insertion are variable. The sternalis muscle often originates from the upper part of the sternum and can display varying insertions such as the  pectoral fascia ,  lower ribs ,  costal cartilages ,  rectus sheath , aponeurosis of the  abdominal external oblique muscle . [ 1 ] [ 2 ] [ 3 ]  There is still a great deal of disagreement about its  innervation  and its embryonic origin. [ 1 ]


In a review, [ 4 ]  it was reported that the muscle was innervated by the external or internal thoracic nerves in 55% of the cases, by the  intercostal nerves  in 43% of the cases, while the remaining cases were supplied by both nerves. [ 4 ]  However, innervation by the pectoral nerves has also been reported. [ 5 ]  This appears to indicate that the sternalis is not always derived from the same embryonic origin. [ 6 ]


Cadaveric studies showed that the sternalis muscle has a mean prevalence of around 7.8% in the population, [ 7 ]  with a slightly higher incidence in females. [ 1 ]  The prevalence ranges from 0.5% to 23.5%, depending on the subpopulation [ 8 ] —   it has been proposed that the possible reason for the sizable range could be the fact of the existence of small, ill-defined, or tendinous fibres which may or may not be accepted as being a
sternalis muscle. [ 9 ]


A 2014 study [ 8 ]  classified the sternalis into three types depending on morphology.


Type I, the single head and single belly was seen in the majority of reported cases (58.5%), type II in 18.1%, and type III in 23.4%. [ 8 ]


In addition to the above classification, triple-bellied/double-headed sternalis has also been reported. [ 10 ]


There is no apparent physiological function of the sternalis muscle. [ 11 ]  However, there are many theories for a function. It may function as a  proprioceptive  sensor for thoracic wall movements. [ 12 ]  It may also take part in the movement of the  shoulder joint  or have an additional role in elevation of the chest wall. [ 13 ]


The presence of the sternalis is asymptomatic [ 1 ]  but aesthetic complaints have been reported as it was reported to cause chest  asymmetry  or deviation of the nipple-areola complex. [ 1 ] [ 14 ]  The presence of the sternalis may cause alterations in the  electrocardiogram [ 15 ]  or confusion in  mammography . [ 16 ]  However, there is a potential benefit of the muscle as it can be used as a flap in a  reconstructive surgery  of the head and neck and the anterior chest wall. [ 14 ]


The sternalis was first reported by Carbolius in 1604 and the name was first given by Turner in 1867. [ 17 ]  Different terminologies have been given to the sternalis due to its highly varied morphology and the disagreement on its embryonic origin. The sternalis was referred to as the  rectus sternalis,   sternalis brutorum, musculus sternalis, episternalis, parasternalis, presternalis, rectus sterni, rectus thoracis, rectus thoracicus superficialis, superficial rectus abdominis, japonicas, and thoracicus  depending on studies . [ 7 ] [ 17 ]


A  saccade  ( / s ə ˈ k ɑː d /   sə- KAHD ;  French:   [sakad] ;  French  for 'jerk') is a quick, simultaneous movement of both  eyes  between two or more phases of focal points in the same direction. [ 1 ]  In contrast, in  smooth-pursuit movements , the eyes move smoothly instead of in jumps; it could be associated with a shift in frequency of an emitted signal [ clarification needed ]  or a movement of a body part or device. [ 2 ]  Controlled cortically by the  frontal eye fields  (FEF), or subcortically by the  superior colliculus , saccades serve as a mechanism for focal points, rapid eye movement, and the fast phase of  optokinetic nystagmus . [ 1 ]  The word appears to have been coined in the 1880s by French ophthalmologist  Émile Javal , who used a mirror on one side of a page to observe eye movement in  silent reading , and found that it involves a succession of discontinuous individual movements. [ 3 ]


Humans and many organisms do not look at a scene in steadiness; instead, the eyes move around, locating interesting parts of the scene and building up a three-dimensional 'map' corresponding to the scene (as opposed to the graphical map of  avians , which often relies upon detection of angular movement on the retina). [ citation needed ]


When scanning immediate surroundings or reading, human eyes make saccadic movements and stop several times, moving very quickly between each stop. The speed of movement during each saccade cannot be controlled; the eyes move as fast as they are able. [ 4 ]  One reason for the saccadic movement of the human eye is that the central part of the  retina —known as the  fovea —which provides the high-resolution portion of vision is very small in humans, only about 1–2 degrees of vision, but it plays a critical role in resolving objects. [ 5 ]  By moving the eye so that small parts of a scene can be sensed with greater  resolution , body resources can be used more efficiently. [ how? ]


Saccades are one of the fastest movements produced by the human eye ( blinks  may reach even higher peak velocities). The peak  angular speed  of the eye during a saccade reaches up to 700°/s in humans for great saccades (25° of visual angle); in some monkeys, peak speed can reach 1000°/s. [ 6 ]  Saccades to an unexpected stimulus normally take about 200 milliseconds (ms) to initiate, and then last from about 20–200 ms, depending on their amplitude (20–30 ms is typical in language reading). Under certain laboratory circumstances, the latency of, or reaction time to, saccade production can be cut nearly in half (express saccades). These saccades are generated by a neuronal mechanism that bypasses time-consuming circuits and activates the eye muscles more directly. [ 7 ] [ 8 ]   Specific pre-target oscillatory ( alpha rhythms ) and transient activities occurring in posterior-lateral  parietal cortex  and  occipital cortex  also characterize express saccades. [ 9 ]


To achieve such high speeds, there are specialized oculomotor burst neurons in the brainstem that wire into the ocular motor neuron. The burst neurons implement  bang-bang control : they are either completely inhibited, or firing at its full rate of ~1000 Hz. [ 10 ]  Since the motion of the eye is essentially a linear system, bang-bang control minimizes travel time. [ 11 ]  After a saccade, a constant force is required to hold the position against elastic force, thus resulting in a pulse-step control. [ 12 ]


The amplitude of a saccade is the angular distance the eye travels during the movement. For amplitudes up to 15 or 20°, the velocity of a saccade linearly depends on the amplitude (the so-called  saccadic main sequence , [ 13 ]  a term borrowed from  astrophysics ; see Figure). For amplitudes larger than 20°, the peak velocity starts to plateau [ 13 ]  (nonlinearly) toward the maximum velocity attainable by the eye at around 60°.  For instance, a 10° amplitude is associated with a velocity of 300°/s, and 30° is associated with 500°/s. [ 14 ]  Therefore, for larger amplitude ranges, the main sequence can best be modeled by an inverse  power law  function. [ 15 ]


The high peak velocities and the main sequence relationship can also be used to distinguish  micro- /saccades from other  eye movements  (like  ocular tremor ,  ocular drift , and  smooth pursuit ). Velocity-based  algorithms  are a common  approach for saccade detection in  eye tracking . [ 16 ] [ 17 ] [ 18 ]  Although, depending on the demands on timing accuracy, acceleration-based methods are more precise. [ 19 ]


Saccades may rotate the eyes in any direction to relocate gaze direction (the direction of sight that corresponds to the fovea), but normally saccades do not rotate the eyes torsionally. (Torsion is clockwise or counterclockwise rotation around the line of sight when the eye is at its central primary position; defined this way,  Listing's law  says that, when the head is motionless, torsion is kept at zero.)


Head-fixed saccades can have amplitudes of up to 90° (from one edge of the oculomotor range to the other), but in normal conditions saccades are far smaller, and any shift of gaze larger than about 20° is accompanied by a head movement. During such gaze saccades, first, the eye produces a saccade to get gaze on target, whereas the head follows more slowly and the  vestibulo-ocular reflex  (VOR) causes the eyes to roll back in the head to keep gaze on the target. Since the VOR can actually rotate the eyes around the line of sight, combined eye and head movements do not always obey  Listing's law . [ 20 ]


The rotational inertia of the eye is negligible compared to the elastic and viscous force.


Saccades can be categorized by intended goal in four ways: [ 21 ]


As referenced to above, it is also useful to categorize saccades by latency (time between go-signal and movement onset). In this case the categorization is binary: Either a given saccade is an  express saccade  or it is not. The latency cut-off is approximately ~200 ms; any longer than this is outside the express saccade range. [ 7 ] [ 8 ]


Microsaccades  are a related type of  fixational eye movement  that are small, jerk-like, involuntary  eye movements , similar to miniature versions of voluntary saccades. They typically occur during visual  fixation , not only in humans, but also in animals with  foveal  vision (primates, cats, etc.). Microsaccade amplitudes vary from 2 to 120  arcminutes .


When exploring the visual environment with the gaze, humans make two to three fixations a second. Each fixation involves binocularly coordinated movements of the eyes to acquire the new target in three dimensions: horizontal and vertical, but also in-depth. In literature it has been shown how an upward or a vertical saccade is generally accompanied by a divergence of the eyes, while a downward saccade is accompanied by a convergence. [ 22 ]  The amount of this  intra-saccadic   vergence  has a strong functional significance for the effectiveness of binocular vision. [ 23 ]  When making an upward saccade, the eyes diverged to be aligned with the most probable uncrossed disparity in that part of the visual field. On the other way around, when making a downward saccade, the eyes converged to enable alignment with crossed disparity in that part of the field. The phenomenon can be interpreted as an adaptation of rapid binocular eye movements to the statistics of the 3D environment, in order to minimize the need for corrective vergence movements at the end of saccades.


Saccadic oscillations not fitting the normal function are a deviation from a healthy or normal condition.  Nystagmus  is characterized by the combination of 'slow phases', which usually take the eye off the point of regard, interspersed with saccade-like "quick phases" that serve to bring the eye back on target. Pathological slow phases may be due to either an imbalance in the  vestibular system  or damage to the  brainstem  "neural integrator" that normally holds the eyes in place. [ citation needed ]  On the other hand,  opsoclonus  or  ocular flutter  are composed purely of fast-phase saccadic eye movements. Without the use of objective recording techniques, it may be very difficult to distinguish between these conditions. [ medical citation needed ]


Eye movement measurements are also used to investigate psychiatric disorders. For example,  ADHD  is characterized by an increase of antisaccade errors and an increase in delays for visually guided saccade. [ 21 ]  Various pathological conditions also alter microsaccades and other  fixational eye movements . [ 24 ] [ 25 ]


Paroxysmal eye–head movements, termed aberrant gaze saccades, are an early symptom of  GLUT1 deficiency syndrome  in infancy. [ 26 ] [ non-primary source needed ]


When the brain is led to believe that the saccades it is generating are too large or too small (by an experimental manipulation in which a saccade-target steps backward or forward contingent on the eye movement made to acquire it), saccade amplitude gradually decreases (or increases), an adaptation (also termed  gain adaptation ) widely seen as a simple form of motor learning, possibly driven by an effort to correct visual error. This effect was first observed in humans with ocular muscle palsy. [ 27 ]  In these cases, it was noticed that the patients would make hypometric (small) saccades with the affected eye, and that they were able to correct these errors over time. This led to the realization that visual or retinal error (the difference between the post-saccadic point of regard and the target position) played a role in the homeostatic regulation of saccade amplitude. Since then, much scientific research has been devoted to various experiments employing saccade adaptation. [ 28 ]


Saccadic eye movement allows the mind to read quickly, but it comes with its disadvantages. It can cause the mind to skip over words because it does not see them as important to the sentence, and the mind completely leaves it from the sentence or it replaces it with the wrong word. This can be seen in " Paris in the the Spring ". This is a common psychological test, where the mind will often skip the second "the", especially when there is a line break in between the two.


When speaking, the mind plans what will be said before it is said. Sometimes the mind is not able to plan in advance and the speech is rushed out. This is why there are errors like mispronunciation, stuttering, and unplanned pauses. The same thing happens when reading. The mind does not always know what will come next. This is another reason that the second "the" can be missed. [ 29 ]


It is a common but false belief that during the saccade, no information is passed through the optic nerve to the brain. Whereas low spatial frequencies (the 'fuzzier' parts) are attenuated, higher spatial frequencies (an image's fine details) that would otherwise be blurred by the eye movement remain unaffected.  This phenomenon, known as  saccadic masking  or  saccadic suppression , is known to begin prior to saccadic eye movements in every primate species studied, implying neurological reasons for the effect rather than simply the image's motion blur. [ 30 ]   This phenomenon leads to the so-called stopped-clock illusion, or  chronostasis .


A person may observe the saccadic masking effect by standing in front of a mirror and looking from one eye to the next (and vice versa).  The subject will not experience any movement of the eyes or any evidence that the optic nerve has momentarily ceased transmitting. Due to saccadic masking, the eye/brain system not only hides the eye movements from the individual but also hides the evidence that anything has been hidden. Of course, a second observer watching the experiment will see the subject's eyes moving back and forth. The function's main purpose is to prevent an otherwise significant smearing of the image. [ 14 ]  (You can experience your eye saccade movements by using your cellphone's front-facing camera as a mirror, hold the cellphone screen a couple of inches away from your face as you saccade from one eye to the other—the cellphone's signal processing delay allows you to see the end of the saccade movement.)


When a visual stimulus is seen before a saccade, subjects are still able to make another saccade back to that image, even if it is no longer visible. This shows that the brain is somehow able to take into account the intervening eye movement. It is thought that the brain does this by temporarily recording a copy of the command for the eye movement, and comparing this to the remembered image of the target. This is called spatial updating. Neurophysiologists, having recorded from cortical areas for saccades during spatial updating, have found that memory-related signals get remapped during each saccade. [ citation needed ]


It is also thought that perceptual memory is updated during saccades so that information gathered across fixations can be compared and synthesized. However, the entire visual image is not updated during each saccade. Some scientists believe that this is the same as visual working memory, but as in spatial updating the eye movement has to be accounted for. The process of retaining information across a saccade is called trans-saccadic memory, and the process of integrating information from more than one fixation is called trans-saccadic integration.


Saccades are a widespread phenomenon across animals with image-forming visual systems. They have been observed in animals across three  phyla , including animals that do not have a  fovea  (most vertebrates do) and animals that cannot move their eyes independently of their head (such as insects). [ 31 ]  Therefore, while saccades serve in humans and other primates to increase the effective visual resolution of a scene, there must be additional reasons for the behavior. The most frequently suggested of these reasons is to avoid blurring of the image, which would occur if the response time of a  photoreceptor cell  is longer than the time a given portion of the image is stimulating that photoreceptor as the image drifts across the eye.


In birds, saccadic eye movements serve a further function.  The  avian retina  is highly developed. It is thicker than the  mammalian retina , has a higher metabolic activity, and has less  vasculature  obstruction, for greater visual acuity. [ 32 ]  Because of this, the retinal cells must obtain nutrients via diffusion through the  choroid  and from the  vitreous humor . [ 33 ]  The  pecten  is a specialised structure in the avian retina. It is a highly vascular structure that projects into the vitreous humor. Experiments show that, during saccadic eye oscillations (which occupy up to 12% of avian viewing time), the  pecten oculi  acts as an agitator, propelling perfusate (natural lubricants) toward the retina. Thus, in birds, saccadic eye movements appear to be important in retinal nutrition and  cellular respiration . [ 34 ]


The  frontal eye fields  ( FEF ) are a region located in the  frontal cortex , more specifically in  Brodmann area 8  or BA8, [ 1 ]  of the primate  brain . In humans, it can be more accurately said to lie in a region around the intersection of the  middle frontal gyrus  with the  precentral gyrus , consisting of a frontal and parietal portion. [ 2 ]  The FEF is responsible for  saccadic eye movements  for the purpose of visual field perception and awareness, as well as for voluntary eye movement. The FEF communicates with extraocular muscles indirectly via the  paramedian pontine reticular formation . Destruction of the FEF causes deviation of the eyes to the ipsilateral side.


The cortical area called frontal eye field (FEF) plays an important role in the control of visual attention and eye movements. [ 3 ]  Electrical stimulation in the FEF elicits saccadic eye movements. The FEF have a topographic structure and represents saccade targets in  retinotopic  coordinates. [ 4 ]


The frontal eye field is reported to be activated during the initiation of  eye movements , such as voluntary  saccades [ 5 ]  and  pursuit eye movements . [ 6 ]  There is also evidence that it plays a role in purely sensory processing and that it belongs to a “fast brain” system through a  superior colliculus  –  medial dorsal nucleus  – FEF ascending pathway. [ 7 ]


In humans, its earliest activations in regard to visual stimuli occur at 45 ms with activations related to changes in visual stimuli within 45–60 ms (these are comparable with response times in the  primary visual cortex ). [ 7 ]
This fast brain pathway also provides auditory input at even shorter times starting at 24 ms and being affected by auditory characteristics at 30–60 ms. [ 7 ]


The FEF constitutes together with the  supplementary eye fields  (SEF), the  intraparietal sulcus  (IPS) and the   superior colliculus  (SC) one of the most important brain areas involved in the generation and control of eye movements, particularly in the direction contralateral to the frontal eye fields' location. In addition, FEF has an important role in the covert allocation of spatial attention through its reciprocal connectivity with visual cortex. [ 8 ]


Unilateral irritative stimulation of a FEF, such as a frontal seizure causes  conjugate gaze  contralateral to the stimulation. Conversely, a unilateral destructive lesion of the FEF causes conjugate gaze towards the lesion.


Paris in the the Spring  is a phrase often used in an informal  psychological test . The phrase "Paris in the the Spring" is written with an extra "the". A subject is asked to read the text, and will often jump to conclusions and fail to notice the extra "the", especially when there is a line break between the two  the s. [ 1 ]


The second ‘the’ is skipped because of  saccades , jerky movements that eyes make when looking around. The brain counteracts these movements by steadying them and making everything appear smooth. While the brain is using saccadic movements to read, it searches for the most important words and skips over the less important ones, and fills them in using the words around it and what the brain sees when it quickly skips over it. For instance, in ‘Paris in the   the Spring’, the eyes will read Paris and quickly move ahead to Spring, and just glance over ‘in the   the’, leading the mind to completely disregard the second ‘the’. [ 2 ]


This  psychology -related article is a  stub . You can help Wikipedia by  expanding it .


Supplementary eye field  ( SEF ) is the name for the anatomical area of the dorsal medial  frontal lobe  of the primate  cerebral cortex  that is indirectly involved in the control of  saccadic   eye movements . Evidence for a supplementary eye field was first shown by Schlag, and Schlag-Rey. [ 1 ]  Current research strives to explore the SEF's contribution to visual search and its role in visual  salience . [ 2 ] [ 3 ]  The SEF constitutes together with the   frontal eye fields (FEF) , the  intraparietal sulcus  (IPS), and the   superior colliculus  (SC) one of the most important brain areas involved in the generation and control of eye movements, particularly in the direction contralateral to their location. [ 2 ] [ 4 ]  Its precise function is not yet fully known. [ 2 ]  Neural recordings in the SEF show signals related to both vision and saccades somewhat like the frontal eye fields and  superior colliculus , but currently most investigators think that the SEF has a special role in high level aspects of saccade control, like complex spatial transformations, [ 5 ]  learned transformations, [ 6 ]  and executive cognitive functions. [ 7 ] [ 8 ]


In 1874,  David Ferrier , a Scottish neurologist first described the  frontal eye fields (FEF) . He noted that unilateral electrical stimulation of the frontal lobe of macaque monkeys caused "turning of the eyes and head to the opposite side"  (Fig. 2) . [ 9 ]  The brain area allotted to the FEF by Ferrier's original map was actually quite large and also encompassed the area which we now call the SEF. A century's worth of experimental findings following Ferrier's work have led to shrinking the FEF's size. [ 10 ]


During the 1950s,  surgical treatment of epileptic patients  was being conducted. Neurosurgeons were removing lesions and other parts of the brain thought to be involved in causing the patient's seizures.
Treatment of these epileptic patients lead to the discovery of many new brain areas by observant neurosurgeons concerned with the post-surgical implications of removing sections of the brain. Through electrical stimulation studies an area called the  supplementary motor area (SMA)  was observed and documented by the neurosurgeon  Wilder Penfield  in 1950. [ 11 ] [ 12 ]  As Penfield had noted the induction of gaze shifts by stimulation of the rostral part of the SMA, another eye field's existence was postulated.


In 1987, the SEF was finally characterized by Schlag and Schlag-Rey as an area where low intensity electrical stimulation could evoke saccades, similar to the FEF. It was named as such to complement the SMA's name. [ 1 ]


The eye field originally defined by Ferrier's map of the frontal cortex extended medially to the dorsal surface of the brain  (Fig. 2) . [ 9 ]  But the FEF proper has since shrunk into the rostral back of the  arcuate sulcus   (Fig. 1) . [ 10 ]  Experimenters have since established that the FEF and SEF are two separate and distinct brain areas responsible for saccade initiation through cerebral blood flow, and subdural electrode array studies. [ 11 ] [ 13 ] [ 14 ] [ 15 ]


In humans, the SEF is located in the rostral  supplementary motor area  (SMA). [ 16 ]  It is located in   Brodmann area 6 (BA6)  which corresponds to  area F7 , the premotor cortex. [ 17 ]  Based on  single unit recording  and  microstimulation  it has been established that the SEF is caudally contiguous with the parts of the SMA which represent orofacial, and forelimb movements. [ 1 ] [ 18 ]


The FEF is located in  Brodmann area 8  which is just anterior to the premotor cortex (BA6)  (Fig. 3) . [ 19 ]


As opposed to the FEF, the SEF plays an indirect but executive role in saccade initiation. For example, the activity of SEF neurons is not sufficient to control saccade initiation in macaque monkeys performing  stop signal go/no-go tasks . [ 3 ]  In this kind of task a trained monkey is to make a particular response (in this case move its eyes, or produce a saccade) to a stimulus on a screen such as a flashing dot. For the go-task, the monkey is to look at the dot. But for the no-go task, the go signal will appear and be followed by the no-go signal, testing whether the saccade initiation can be inhibited. [ 20 ]


In other words, the SEF does not immediately  or directly contribute to saccade initiation. But, the SEF is thought to improve saccade production by using prior knowledge of anticipated task requirements to influence saccadic eye movements. It does so by balancing gaze holding and gaze shifting actions, yielding a modest improvement in performance in stop signal tasks by delaying saccade initiation when necessary. [ 2 ] [ 3 ]  It can be thought that the  FEF  does the driving part of saccade initiation, while the SEF acts as a backseat passenger, advising the driver as to what to do based on past insights. The SEF has recently been found to encode reward prediction error, suggesting that the SEF may actively evaluate decisions based on a value system on an occulomotor basis, independent of other brain regions. [ 21 ]


The visual system is sensitive to sudden change. [ 22 ]  If something distracting occurs while a person is performing a task—reading a newspaper, for example—this immediately captures one's attention. [ 23 ] [ 24 ] [ 25 ]  This sudden shift can be a distraction but it has been also thought to be a reflex of great importance as identifying and reacting to environmental changes quickly (when needed) can be imperative to survival. [ 24 ] [ 26 ] [ 27 ] [ 28 ] [ 29 ]  Saccadic latency, the time delay between the appearance of a target and the initiation of a saccade,  is an important parameter for learning which occulomotor neurons and structures of the brain play what specific roles in saccade initiation. [ 30 ] [ 31 ]  There is much research being conducted on the role of SEF in determining visually salient objects and occurrences, using saccadic latency as the parameter of interest. [ 2 ] [ 26 ] [ 32 ] [ 33 ] [ 34 ]


SEF activity has been found to govern decisions in smooth pursuit but not the decision itself. [ 35 ]


The SEF responds to auditory stimuli as well as visual stimuli. [ 20 ]  Visual responses from the SEF happen later and are much weaker than that observed in the FEF, though. SEF neurons also exhibit non-retinal modulation including anticipation and reward prediction. [ 3 ] [ 36 ]


The SEF was defined by the Schlags as a region where low currents (<50μA) evoke saccades. It is still found using this characterization as well as the known neighboring anatomy  (Fig. 1) . [ 1 ] [ 10 ]


SEF research is conducted mainly in monkey models. Typically trained  rhesus macaque  monkeys are used and surgically implanted with recording chambers. In this fashion,  spike  and  local field potential (LFP)  data can be acquired from SEF neurons, using  microelectrodes  in the recording chamber. Eye movements can also be monitored using eye-tracking camera equipment. [ 2 ]


Experiments obviously vary, but to give an example: the monkey might be made to partake in a color visual search task, sitting in front of a computer screen. The monkey would look at a point on the screen which would change from filled in to open at the same time which a colored point of "opposite" color appears on the screen. The monkey would be rewarded for looking at a new spot—"for making a single saccade"—within 2000 ms and then fixating on the spot for 500 ms. Varied tasks such as these are used and data is analyzed to determine the SEF's role in saccade initiation, visual saliency, etc. [ 2 ] [ 3 ]


The  triangles of the neck  describe the divisions created by the major muscles in the region.


The side of the  neck  presents a somewhat quadrilateral outline, limited, above, by the lower border of the body of the  mandible , and an imaginary line extending from the angle of the mandible to the  mastoid process ; below, by the upper border of the  clavicle ; in front, by the middle line of the neck; behind, by the anterior margin of the  trapezius .


This space is subdivided into two large triangles by  sternocleidomastoid , which passes obliquely across the neck, from the  sternum  and  clavicle  below, to the  mastoid process  and  occipital bone  above.


The triangular space in front of this muscle is called the  anterior triangle of the neck ; and that behind it, the  posterior triangle of the neck .


The anterior triangle is further divided into  muscular ,  carotid ,  submandibular  and  submental  and the posterior into  occipital  and  subclavian  triangles. [ 1 ]


The use of the divisions described as the triangles of the neck permit the effective communication of the location of palpable masses located in the neck between healthcare professionals.


The common swellings anterior of the midline are:


This article incorporates text in the  public domain  from  page 563  of the 20th edition of   Gray's Anatomy   (1918)


The  anterior triangle  is a region of the  neck .


The triangle is inverted with its apex inferior to its base which is under the chin. [ 1 ]


Investing fascia  covers the roof of the triangle while  visceral fascia  covers the floor.


Muscles:


2 Bellies of digastric


Stylohyoid: by the facial nerve, by a branch from that to the posterior belly of digastric.


Mylohyoid: by its own nerve, a branch of the inferior alveolar (from the mandibular division of trigeminal nerve), which arises just before the parent nerve enters the mandibular foramen, pierces the sphenomandibular ligament, and runs forward on the inferior surface of the mylohyoid, supplying it and the anterior belly of the digastric.


Geniohyoid: by a branch from the hypoglossal nerve consisting of fibres from the C1 nerve.


Sternohyoid, omohyoid, sternothyroid are supplied by ansa cervicalis.


Thyrohyoid: by a branch of hypoglossal nerve but the fibres are all 'hitch-hiking' from C1.


This space is subdivided into four smaller triangles by the  digastricus  above, and the superior belly of the  omohyoideus .


These smaller triangles are named:


The  carotid triangle  (or  superior carotid triangle ) is a portion of the  anterior triangle of the neck .


It is bounded:


The roof is formed by:


The floor is formed by (parts of) the:


Superficial to the  carotid sheath  lies the  hypoglossal nerve , and  ansa cervicalis  of the  cervical plexus .


The  hypoglossal nerve  crosses both the internal and external carotids, curving around the origin of the  occipital artery .


Within the sheath, between the artery and vein, and behind both, is the  vagus nerve ; behind the sheath, the  sympathetic trunk .


On the lateral side of the vessels, the  accessory nerve  runs for a short distance before it pierces the  Sternocleidomastoideus ; and on the medial side of the  external carotid , just below the  hyoid bone , the internal branch of the  superior laryngeal nerve  may be seen; and, still more inferiorly, the external branch of the same nerve.


The superior portion of the larynx and inferior portion of the pharynx are also found in the anterior portion part of this space.


This article incorporates text in the  public domain  from  page 564  of the 20th edition of   Gray's Anatomy   (1918)


The  inferior carotid triangle  (or  muscular triangle ), is bounded, in front, by the median line of the neck from the  hyoid bone  to the  sternum ; behind, by the anterior margin of the  sternocleidomastoid ; above, by the superior belly of the  omohyoid .


It is covered by the integument, superficial fascia,  platysma , and deep fascia, ramifying in which are some of the branches of the supraclavicular nerves.


Beneath these superficial structures are the  sternohyoid  and  sternothyroid , which, together with the anterior margin of the  sternocleidomastoid , conceal the lower part of the  common carotid artery .


This vessel is enclosed within its sheath, together with the  internal jugular vein  and  vagus nerve ; the vein lies lateral to the artery on the right side of the neck, but overlaps it below on the left side; the nerve lies between the artery and vein, on a plane posterior to both.


In front of the sheath are a few descending filaments from the  ansa cervicalis ; behind the sheath are the  inferior thyroid artery , the  recurrent nerve , and the  sympathetic trunk ; and on its medial side, the  esophagus , the  trachea , the  thyroid gland , and the lower part of the  larynx .


By cutting into the upper part of this space, and slightly displacing the sternocleidomastoid, the common carotid artery may be tied below the omohyoid.


The  occipital triangle , the larger division of the posterior triangle, is bounded, in front, by the  Sternocleidomastoideus ; behind, by the  Trapezius ; below, by the  Omohyoideus .


Its floor is formed from above downward by the  Splenius capitis ,  Levator scapulæ , and the  Scalenus medius  and posterior.


It is covered by the skin, the superficial and deep fasciæ, and by the  Platysma  below.


The  accessory nerve  is directed obliquely across the space from the  Sternocleidomastoideus , which it pierces, to the under surface of the  Trapezius ; below, the  supraclavicular nerves  and the  transverse cervical vessels  and the upper part of the  brachial plexus  cross the space.


The roof of this triangle is formed by the cutaneous nerves of cervical plexus and the external jugular vein and platysma muscle.


A chain of  lymph glands  is also found running along the posterior border of the  Sternocleidomastoideus , from the mastoid process to the root of the  neck .


This article incorporates text in the  public domain  from  page 565  of the 20th edition of   Gray's Anatomy   (1918)


The  posterior triangle  (or  lateral cervical region ) is a region of the  neck .


The posterior triangle has the following boundaries: [ 1 ]


Apex:  Union of the  sternocleidomastoid  and the  trapezius  muscles at the  superior nuchal line  of the  occipital bone


Anteriorly:  Posterior border of the  sternocleidomastoideus


Posteriorly:  Anterior border of the  trapezius


Inferiorly:  Middle one third of the  clavicle


Roof:  Investing layer of the  deep cervical fascia


Floor:  (From superior to inferior)


1) M. semispinalis capitis


2) M. splenius capitis


3) M. levator scapulae


4) M. scalenus posterior


5) M. scalenus medius


The posterior triangle is crossed, about 2.5 cm above the clavicle, by the inferior belly of the  omohyoid muscle , which divides the space into two triangles:


A) Nerves and plexuses:


B) Vessels:


C) Lymph nodes:


D) Muscles:


The accessory nerve (CN XI) is particularly vulnerable to damage during lymph node biopsy. Damage results in an inability to shrug the shoulders or raise the arm above the head, particularly due to compromised  trapezius muscle  innervation.


The  external jugular vein 's superficial location within the posterior triangle also makes it vulnerable to injury.


The  subclavian triangle  (or  supraclavicular triangle ,  omoclavicular triangle ,  Ho's triangle ), the smaller division of the posterior triangle, is bounded, above, by the inferior belly of the  omohyoideus ; below, by the  clavicle ; its base is formed by the posterior border of the  sternocleidomastoideus .


Its floor is formed by the first rib with the first digitation of the  serratus anterior .


The size of the subclavian triangle varies with the extent of attachment of the clavicular portions of the  Sternocleidomastoideus  and  Trapezius , and also with the height at which the  Omohyoideus  crosses the neck.


Its height also varies according to the position of the arm, being diminished by raising the limb, on account of the ascent of the clavicle, and increased by drawing the arm downward, when that bone is depressed.


This space is covered by the integument, the superficial and deep fasciæ and the  platysma , and crossed by the supraclavicular nerves.


Just above the level of the clavicle, the third portion of the  subclavian artery  curves lateralward and downward from the lateral margin of the  scalenus anterior , across the first  rib , to the  axilla , and this is the situation most commonly chosen for  ligaturing  the vessel.


Sometimes this vessel rises as high as 4 cm. above the clavicle; occasionally, it passes in front of the Scalenus anterior, or pierces the fibers of that muscle.


The subclavian vein lies behind the clavicle, and is not usually seen in this space; but in some cases it rises as high as the artery, and has even been seen to pass with that vessel behind the Scalenus anterior.


The  brachial plexus  of nerves lies above the artery, and in close contact with it. Passing transversely behind the clavicle are the  transverse scapular vessels ; and traversing its upper angle in the same direction, the  transverse cervical artery  and vein.


The  external jugular vein  runs vertically downward behind the posterior border of the Sternocleidomastoideus, to terminate in the  subclavian vein ; it receives the transverse cervical and transverse scapular veins, which form a plexus in front of the artery, and occasionally a small vein which crosses the  clavicle  from the  cephalic .


The small nerve to the subclavius also crosses this triangle about its middle, and some  lymph glands  are usually found in the space.


Enlarged nodes in this triangle irrespective of size are categorized at N3 in the TNM classification for nasopharyngeal carcinoma.


The  submandibular triangle  (or  submaxillary   or  digastric triangle ) corresponds to the region of the neck immediately beneath the body of the  mandible .


It is bounded: [ 1 ]


It is covered by the  integument ,  superficial fascia ,  Platysma , and deep fascia, ramifying in which are branches of the  facial nerve  and ascending filaments of the  cutaneous cervical nerve .


Its floor is formed by the  Mylohyoideus  anteriorly, and by the  hyoglossus  posteriorly.


It is divided into an anterior and a posterior part by the  stylomandibular ligament . [ citation needed ]


The anterior part contains the  submandibular gland , superficial to which is the  anterior facial vein , while imbedded in the gland is the  facial artery  and its glandular branches.


Beneath the gland, on the surface of the  Mylohyoideus , are the  submental artery  and the  mylohyoid artery  and nerve.


The posterior part of this triangle contains the external carotid artery, ascending deeply in the substance of the  parotid gland


This vessel lies here in front of, and superficial to, the external carotid, being crossed by the  facial nerve , and gives off in its course the  posterior auricular ,  superficial temporal , and  internal maxillary  branches: more deeply are the  internal carotid , the  internal jugular vein , and the  vagus nerve , separated from the external carotid by the  Styloglossus  and  Stylopharyngeus , and the  hypoglossal nerve


The following summarizes the important structures found in the submandibular triangle:


The  submental triangle  (or  suprahyoid triangle ) is a division of the  anterior triangle of the neck .


It is limited to:


It contains one or two  lymph glands , the  submental lymph nodes  (three or four in number) and Submental veins and commencement of  anterior jugular veins.


(The contents of the triangle actually lie in the superficial fascia over the roof of submental triangle)


This article incorporates text in the  public domain  from  page 565  of the 20th edition of   Gray's Anatomy   (1918) , Page 88 of Textbook of Anatomy; head, neck and brain by Vishram Singh


The  suboccipital triangle  is a region of the  neck  bounded by the following three muscles of the  suboccipital group of muscles :


(Rectus capitis posterior minor is also in this region but does not form part of the triangle)


It is covered by a layer of dense fibro-fatty tissue, situated beneath the  semispinalis capitis .


The floor is formed by the  posterior atlantooccipital membrane , and the  posterior arch  of the  atlas .


In the deep groove on the upper surface of the posterior arch of the atlas are the  vertebral artery  and the first cervical or  suboccipital nerve .


In the past, the vertebral artery was accessed here in order to conduct  angiography  of the  circle of Willis . Presently, formal angiography of the circle of Willis is performed via catheter angiography, with access usually being acquired at the common femoral artery. Alternatively, a computed tomographic angiogram or magnetic resonance angiogram is performed.


1) Third part of  vertebral artery
2) Dorsal ramus of nerve C1- suboccipital nerve
3)  Suboccipital venous plexus


The purpose of these muscles is to provide fine motor function in movements of the head. The actions of  trapezius ,  sternocleidomastoid  and other larger muscles that move the head are refined by the relatively small suboccipital triangle muscles.


This article incorporates text in the  public domain  from  page 402  of the 20th edition of   Gray's Anatomy   (1918)


The  supraclavicular fossa  is an indentation (fossa) immediately above the  clavicle .


In  terminologia anatomica , it is divided into  fossa supraclavicularis major  and  fossa supraclavicularis minor


Fullness in the supraclavicular fossa can be a sign of upper extremity  deep venous thrombosis .


Exploration of the spinal cord and meninges in situ
										 Cauda equina, conus medullaris and filum terminale
										The lumbar part of the spinal cord has been exposed. The conus medullaris ends at the level of the arch of the second lumbar vertebra.

														 1
						.
					 Posterior lateral cutaneous branch of thoracic nerve XII  2
						.
					 Posterior intertransverse muscle  3
						.
					 Arch of lumbar vertebra I (cut across)  4
						.
					 Lateral intertransverse muscle  5
						.
					 Mamillary processs lumbar vertebra II  6
						.
					 Posterior branch of lumbar nerve I  7
						.
					 Dorsal iliocostal muscle  8
						.
					 Spinous process lumbar vertebra II (partly resected)  9
						.
					 Joint capsule of intervertebral articulation  10
						.
					 Dorsal root thoracic nerve XII  11
						.
					 Denticulate ligament  12
						.
					 Lumbar enlargement  13
						.
					 Latissimus dorsi muscle (cut across)  14
						.
					 Cauda equina  15
						.
					 Longissimus dorsi muscle  16
						.
					 Superior articular surface lumbar vertebra II  17
						.
					 Conus medullaris  18
						.
					 Filum terminale


Exploration of the spinal cord and meninges in situ
										 Arachnoid membrane covering cauda equina
										The dura has been cut away in such a manner that the arachnoid membrane remains intact. The filum terminale (15) appears as a white strand deep to the arachnoid. An extensive subarachnoid space surrounds nerve roots which form the cauda equina.

														 1
						.
					 Mamillary process of lumbar vertebra III  2
						.
					 Inferior articular process lumbar vertebra II  3
						.
					 Dorsal iliocostal muscle  4
						.
					 Arch of lumbar vertebra IV  5
						.
					 Lumbodorsal fascia  6
						.
					 Ligamentum flavum  7
						.
					 Epidural space and cut margin of dura  8
						.
					 Fibrous attachment of dura to sacrum  9
						.
					 Cystic enlargement of dura covering roots of second sacral nerve (note resorption of neighboring bone)  10
						.
					 Gluteus maximus muscle  11
						.
					 Spinous process lumbar vertebra II  12
						.
					 Branch lumbar artery  13
						.
					 Dura mater  14
						.
					 Arachnoid  15
						.
					 Filum terminale (beneath arachnoid)  16
						.
					 Root sacral nerve II  17
						.
					 Level at which spinal subarachnoid space terminates  18
						.
					 Filum spinal dura mater


Exploration of the spinal cord and meninges in situ
										 Lumbar region; dura covering cauda equina
										The arches of the third, fourth and fifth lumbar vertebrae and the upper two sacral segments have been resected. Epidural fat has been removed to expose segmentally arranged veins (15). Several fibrous strands (10) pass from the lower part of the dura to the sacrum.

														 1
						.
					 Postero-lateral cutaneous branch of thoracic nerve XII  2
						.
					 Spinous process lumbar vertebra II  3
						.
					 Inferior articular process lumbar vertebra II  4
						.
					 Longissimus dorsi muscle  5
						.
					 Dorsal iliocostal muscle  6
						.
					 Lumbodorsal fascia  7
						.
					 Multifidus muscle (cut across near origin from mammillary process)  8
						.
					 Superficial Fascia  9
						.
					 Dura mater  10
						.
					 Fibrous strands attaching dura to sacrum  11
						.
					 Gluteus maximus muscle  12
						.
					 Fascia of latissimus dorsi muscle  13
						.
					 Aponeurosis of latissimus dorsi muscle  14
						.
					 Layer of fascia beneath lumbodorsal fascia  15
						.
					 Internal vertebral venous plexus  16
						.
					 Arch of lumbar vertebra III (cut across)  17
						.
					 Arch of lumbar vertebra IV (cut across)  18
						.
					 Arch of lumbar vertebra V (cut across)  19
						.
					 Arch of sacrum (cut across)  20
						.
					 Root sacral nerve I  21
						.
					 Filum of spinal dura mater (coccygeal nerve roots accompany this band)


Exploration of the spinal cord and meninges in situ
										 Roots and ganglion of 10th thoracic nerve
										The articular processes of the tenth and eleventh thoracic vertebrae have been cut away on the right side to reveal the lateral course of the 10th thoracic spinal roots. Subarachnoid spaces extend only a millimeter or two along the anterior and posterior roots after they pierce the dura mater. A narrow bridge of dura intervenes between the motor and sensory roots. A mass of plexiform veins was removed from the intervertebral foramen.

														 1
						.
					 Thoracic part spinal cord  2
						.
					 Internal vertebral venous plexus  3
						.
					 Superior articular surface thoracic vertebra XI  4
						.
					 External posterior spinal vein  5
						.
					 Vein within arch of 11th thoracic vertebra  6
						.
					 Levator costarum muscle  7
						.
					 Ligamentum flavum  8
						.
					 Superior articular process thoracic vertebra XII  9
						.
					 Superior articular process thoracic vertebra X  10
						.
					 Dura mater  11
						.
					 Dorsal root thoracic nerve X  12
						.
					 Spinal branch of intercostal artery (anterior root of nerve lies just above this)  13
						.
					 Spinal ganglion thoracic nerve X  14
						.
					 Posterior branch of thoracic nerve X  15
						.
					 Transverse process thoracic vertebra XI  16
						.
					 Longissimus dorsi muscle  17
						.
					 Ligamentum intertransversarium  18
						.
					 Inferior articular process thoracic vertebra XI


Exploration of the spinal cord and meninges in situ
										 Epidural plexus of veins, upper thoracic region

														 1
						.
					 Semispinalis capitis muscle (reflected)  2
						.
					 Dura mater  3
						.
					 Splenius cervicis muscle (reflected)  4
						.
					 Internal vertebral venous plexus  5
						.
					 Rhomboid major muscle (cut across)  6
						.
					 Dorsal iliocostal muscle  7
						.
					 Trapezius muscle (cut across)  8
						.
					 Posterior funiculus spinal cord  9
						.
					 Dorsal root cervical nerve VII  10
						.
					 Arch of thoracic vertebra I (cut across)  11
						.
					 Superior posterior serratus muscle  12
						.
					 Longissimus dorsi muscle


Exploration of the spinal cord and meninges in situ
										 Epidural space in thoracic region
										The epidural space lying deep to the 5th, 6th, 7th and 8th thoracic vertebrae has been exposed. A window has been cut through the dura to expose the subdural space with the arachnoid membrane in its depths. The subdural space appears unduly large due to the collapse of the underlying arachnoid.

														 1
						.
					 Longissimus dorsi muscle (cut across)  2
						.
					 Lateral cutaneous branch of posterior brach of thoracic nerve V  3
						.
					 Dorsal iliocostal muscle  4
						.
					 Transverse process thoracic vertebrae VI  5
						.
					 Levator costarum muscle  6
						.
					 Intertransverse ligament  7
						.
					 Dorsal root thoracic nerve VII  8
						.
					 Thoracic part spinal cord  9
						.
					 Posterior costotransverse ligament  10
						.
					 Arch of thoracic vertebra VIII  11
						.
					 Dorsal semispinalis muscle  12
						.
					 Arch of thoracic vertebra V (partly resected)  13
						.
					 Lumbodorsal fascia  14
						.
					 Fat within epidural space  15
						.
					 Internal vertebral venous plexus  16
						.
					 Longissimus dorsi muscle  17
						.
					 Branch of intercostal artery  18
						.
					 Dura mater  19
						.
					 Ligamentum flavum (cut across)


Exploration of the spinal cord and meninges in situ
										 General view of spinal cord; meninges removed
										The vertebral arches have been cut away with the exception of the left half of the second lumbar arch and spine (16). This spine serves as a land-mark in the close-up studies of the lumbar region which follow and is a guide to the location of the termination of the spinal cord.

														 1
						.
					 Cervical part spinal cord  2
						.
					 Thoracic part spinal cord  3
						.
					 Lumbar part spinal cord (lower pointer on conus medullaris)  4
						.
					 Dorsal root cervical nerve II  5
						.
					 Semispinalis capitis muscle (reflected)  6
						.
					 Splenius capitis and cervicis muscles (reflected)  7
						.
					 Trapezius muscle (cut across)  8
						.
					 Levator scapulae muscle  9
						.
					 Scapular-vertebral margin  10
						.
					 Cut surface of vertebral arch  11
						.
					 Trapezius muscle (cut across)  12
						.
					 Levator costarum muscle  13
						.
					 Dorsal iliocostal muscle  14
						.
					 Longissimus dorsi muscle  15
						.
					 Latissimus dorsi muscle  16
						.
					 Spinous process lumbar vertebra II  17
						.
					 Cauda equina  18
						.
					 Parts of longissimus dorsi muscle  19
						.
					 Subarachnoid space (lumbar cistern)  20
						.
					 Filum of dura mater


Exploration of the spinal cord and meninges in situ
										 Orientation view; areas of subsequent close-up views indicated
										The spinal meninges have been exposed in the cervical region (A), thoracic region (B) and lumbosacral region (C). These areas are the subject of separate study in the following views of this series.

														 1
						.
					 Cerebellum and occipital bone (cut across)  2
						.
					 Arachnoid covering cervical part of spinal cord  3
						.
					 Splenius capitis and cervicis muscles (reflected)  4
						.
					 Spinous process cervical vertebra VI  5
						.
					 Trapezius muscle (cut across)  6
						.
					 Posterior superior serratus muscle (cut across)  7
						.
					 Lumbodorsal fascia (partially removed)  8
						.
					 Position of scapular-vertebral margin  9
						.
					 Rhomboid major muscle (cut across)  10
						.
					 Dura mater covering thoracic part spinal cord  11
						.
					 Transverse process thoracic vertebra VII  12
						.
					 Spinous process thoracic vertebra VIII  13
						.
					 Longissimus dorsi muscle (cut across)  14
						.
					 Dorsal iliocostal muscle  15
						.
					 Latissimus dorsi muscle  16
						.
					 Spinous process lumbar vertebra II  17
						.
					 Lumbodorsal fascia (partially cut away)  18
						.
					 Arachnoid covering cauda equina (dura mater removed)  19
						.
					 Sacrum (arches resected)  20
						.
					 Gluteus maximus muscle