<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Exertional rhabdomyolysis and can you explain it in depth? [/INST] Exertional rhabdomyolysis (ER) is the breakdown of muscle from extreme physical exertion. It is one of many types of rhabdomyolysis that can occur, and because of this, the exact prevalence and incidence are unclear.

Cause
ER is more likely to occur when strenuous exercise is performed under high temperatures and humidity. Poor hydration levels before, during, and after strenuous bouts of exercise have also been reported to lead to ER. This condition and its signs and symptoms are not well known amongst the sport and fitness community and because of this it is believed that the incidence is greater but highly underreported.Risks that lead to ER include exercise in hot and humid conditions, improper hydration, inadequate recovery between bouts of exercise, intense physical training, and inadequate fitness levels for beginning high-intensity workouts. Eccentric contraction of muscles can result in ER more often than concentric contraction.  Dehydration is one of the biggest factors that can give almost immediate feedback from the body by producing very dark-colored urine.

Mechanism
Anatomy
Exertional rhabdomyolysis results from damage to the intercellular proteins inside the sarcolemma. Myosin and actin break down in the sarcomeres when ATP is no longer available due to injury to the sarcoplasmic reticulum. Damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to power the cell properly. Reduction in ATP production impairs the cells ability to extract calcium from the muscle cell.  The ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax.  The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream.

Physiology
Rhabdomyolysis causes the myosin and actin to degenerate into smaller proteins that travel into the circulatory system. The body reacts by increasing intracellular swelling to the injured tissue to send repair cells to the area. This allows creatine kinase and myoglobin to be flushed from the tissue where it travels in the blood until reaching the kidneys. In addition to the proteins released, large quantities of ions such as intracellular potassium, sodium, and chloride find their way into the circulatory system. Intracellular potassium ion has deleterious effects on the hearts ability to generate action potentials leading to cardiac arrhythmias.  Consequently, this can affect peripheral and central perfusion which in turn can affect all major organ systems in the body.When the protein reaches the kidneys it causes a strain on the anatomical structures reducing its effectiveness as a filter for the body. The protein acts as a dam as it forms into tight aggregates when it enters the renal tubules. In addition, the increased intracellular calcium has greater time to bind due to the blockage allowing for renal calculi to form. As a result this causes urine output to decrease allowing for the uric acid to build up inside the organ. The increased acid concentration allows the iron from the aggregate protein to be released into the surrounding renal tissue. Iron then strips away molecular bonds of the surrounding tissue which eventually will lead to kidney failure if the tissue damage is too great.

Mechanical consideration
Muscle degeneration from rhabdomyolysis destroys the myosin and actin filaments in the affected tissue. This initiates the bodys natural reaction to increasing perfusion to the area allowing for an influx of specialized cells to repair the injury. However, the swelling increases the intracellular pressure beyond normal limits. As the pressure builds in the muscle tissue, the surrounding tissue is crushed against the underlying tissue and bone. This is known as compartment syndrome which leads to greater death of the surrounding muscle tissue around the injury.  As the muscle dies this will cause pain to radiate from the affected area into the compartmentalized tissue. A loss of range of motion from swelling will also be seen in the affected limb. Along with muscle strength weakness associated with the muscles involved from loss of filament interaction.

Dehydration is a common risk factor for exertional rhabdomyolysis because it causes a reduction of plasma volume during exertion. This leads to a reduction of blood flow through the vascular system which inhibits blood vessel constriction.

Diagnosis
Exertional rhabdomyolysis, the exercise-induced muscle breakdown that results in muscle pain/soreness, is commonly diagnosed using the urine myoglobin test accompanied by high levels of creatine kinase (CK). Myoglobin is the protein released into the bloodstream when skeletal muscle is broken down. The urine test simply examines whether myoglobin is present or absent. When results are positive the urine normally obtains a dark, brown color followed by serum CK level evaluation to determine the severity of muscle damage. Elevated levels of serum CK greater than 5,000 U/L that are not caused by myocardial infarction, brain injury or disease, generally indicate serious muscle damage confirming the diagnosis of ER.
Urine is often a dark "cola" color as a result of the excretion of muscle cell components.

Prevention
Military data suggest that the risk of exertional rhabdomyolysis can be lowered by engaging in prolonged lower-intensity exercise, as opposed to high-intensity exercise over a shorter time period.  In all athletic programs, three features should be present: (1) emphasizing prolonged lower-intensity exercise, as opposed to repetitive max intensity exercises; (2) adequate rest periods and a high-carbohydrate diet, to replenish glycogen stores; and (3) proper hydration, to enhance renal clearance of myoglobin. Also, exercise in above-average temperature and humidity can increase risk for ER. ER can be avoided by gradually increasing intensity during new exercise regimens, properly hydrating, acclimatization, and avoidance of diuretics during times of strenuous activity.

Treatment
After ER is diagnosed, treatment is applied to 1) avoid renal dysfunction and 2) alleviate symptoms. This should be followed by recommended rehabilitation program, exercise prescription (ExRx). Treatment involves extensive hydration normally done through IV fluid replacement with administration of normal saline until CK levels reduce to a maximum of 1,000 U/L </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Proteus syndrome and can you explain it in depth? [/INST] Proteus syndrome is a rare disorder with a genetic background that can cause tissue overgrowth involving all three embryonic lineages. Patients with Proteus syndrome tend to have an increased risk of embryonic tumor development. The clinical and radiographic symptoms of Proteus syndrome are highly variable, as are its orthopedic manifestations.Only a few more than 200 cases have been confirmed worldwide, with estimates that about 120 people are currently alive with the condition. As attenuated forms of the disease may exist, there could be many people with Proteus syndrome who remain undiagnosed. Those most readily diagnosed are also the most severely disfigured.
The syndrome is named after the Greek sea-god Proteus, who could change his shape. The condition appears to have been first described in the American medical literature by Samia Temtamy and John Rogers in 1976. American pathologist Michael Cohen described it in 1979.

Signs and symptoms
Proteus syndrome causes an overgrowth of skin, bones, muscles, fatty tissues, and blood and lymphatic vessels. Proteus syndrome is a progressive condition wherein children are usually born without any obvious deformities. Tumors of skin and bone growths appear as they age typically in early childhood. The musculoskeletal manifestations are cardinal for the diagnosis of Proteus syndrome. The severity and locations of these various asymmetrical growths vary greatly but typically the skull, one or more limbs, and soles of the feet will be affected. There is a risk of premature death in affected individuals due to deep vein thrombosis and pulmonary embolism caused by the vessel malformations that are associated with this disorder. Because of carrying excess weight and enlarged limbs, arthritis and muscle pain may also be symptoms. Further risks may occur due to the mass of extra tissue.The disorder itself does not uniformly cause learning impairments: the distribution of intelligence deficits among those with Proteus syndrome appears higher than that of the general population, although this is difficult to determine with statistical significance. In addition, the presence of visible deformity may have a negative effect on the social experiences of the affected individual, causing cognitive and social deficits.Affected individuals are at increased risk for developing certain tumors including unilateral ovarian cystadenomas, testicular tumors, meningiomas, and monomorphic adenomas of the parotid gland.Hemimegalencephaly is often found to be associated.

Orthopaedic features
The musculoskeletal manifestations of Proteus syndrome are frequent and recognizable. Patients tend to demonstrate a unique pattern of skeletal abnormalities. The orthopaedic features are usually bilateral, asymmetrical, progressive and involving all four limbs and spine. Affected patients usually have localized periarticular limb distortions, limb length discrepancy, and spine deformity. Patients with Proteus syndrome can have regular bone configuration and contours despite the bone enlargement. Patients can also exhibit deformation of the skull in the form of dolichocephaly or elongated skull and facial abnormalities. Because of the rarity of the syndrome and the variability of signs, the orthopaedic management should be individualized.

Genetics
In 2011 researchers determined the cause of Proteus syndrome. In 26 of 29 patients who met strict clinical criteria for the disorder, Lindhurst et al. identified an activating mutation in AKT1 kinase in a mosaic state gene.Previous research had suggested the condition linked to PTEN on chromosome 10, while other research pointed to chromosome 16. Prior to the findings regarding AKT1 in 2011, other researchers expressed doubt regarding the involvement of PTEN or GPC3, which codes for glypican 3 and may play a role in regulating cell division and growth regulation.

Diagnosis
Differential diagnosis
Macrodystrophia lipomatosa
Fibrolipomatous hamartoma
Neurofibromatosis type 1
Klippel–Trénaunay syndrome
Parkes Weber syndrome
Sotos syndrome
Hemangiomas

Classification
Many sources classify Proteus syndrome to be a type of nevus syndrome </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Geotrichosis and can you explain it in depth? [/INST] Geotrichosis is a mycosis caused by Geotrichum candidum.: 311

Human colonization and disease
Geotrichum candidum is also a frequent member of the human microbiome, notably associated with skin, sputum and feces where it occurs in 25-30% of specimens. The fungus can cause an infection known as geotrichosis, affecting the oral, bronchial, skin and bronchopulmonary epithelia. The inoculum may arise from endogenous or exogenous sources.In 1847 Bennett described Geotrichum candidum causing a superinfection in the tuberculous cavity. Bennett was able to differentiate infection by Geotrichum candidum from candidiasis, and diagnose the first case of geotrichosis. Other early medical case reports in 1916 and 1928 also described lung infections. Most cases affect the bronchopulmonary tree, although other sites can be involved, such as oral mucosa and vagina. Skin and gut infections are also known. Reported cases of geotrichosis have been characterized with symptoms of chronic or acute bronchitis. Exogenous geotrichosis may arise from contact with contaminated soil, fruits or dairy products.
Pulmonary geotrichosis is the most frequent form of geotrichosis. The symptoms appear to be secondary symptoms of tuberculosis. This includes symptoms such as light, thick, grey sputum, which in some cases may be blood-tinged. Patients often have a cough that produces clear or yellow sputum. Another symptom of pulmonary geotrichosis includes fine to medium rales. Patients may develop fever, rapid pulse and leukocytosis. The condition appears chronic with the presence of a little debilitation and fever. There is no chest pain and occasional wheezing can occur.
Bronchial geotrichosis does not involve the lung instead the disease persists within the bronchial. Geotrichum candidum grows in the lumen of the bronchi. The disease is characterized as an endobronchial infection. Bronchial geotrichosis is similar to the allergic reaction of aspergillosis. Symptoms include prominent chronic cough, gelatinous sputum, lack of fever and medium to coarse rales. Patients with the bronchial condition their pulse and respiration are rarely elevated. Fine mottling may be present in the middle or basilar pulmonary region. Colonization of the bronchi can be associated with Candida albicans and usually occur with patients with chronic obstructive lung disease.
Oral and vaginal geotrichosis is similar to thrush in its appearances and was often confused with this infection. The difference between oral and vaginal geotrichosis can be determined using microscope analysis. The infected area forms a white plaque and patients usually report burning sensation in the affected areas. The vaginal geotrichosis is more common in pregnant women and is often associated with vaginitis.
Gastrointestinal geotrichosis is enterocolitis associated with glutamic therapy. The symptoms usually stop once the glutamic therapy is discontinued. Establishment of the etiology of the fungi is difficult since G. candidum is found within the gut normal flora. The difference between normal gut flora form and the disease causing form is the production of toxins.
Cutaneous geotrichosis has two different types of variants which include superficial and deep infection. The superficial form the infection occurs on skin folds including submammary, inguinal, perianal and interdigital folds. The deep form develops nodules, tumours and ulcers on legs, face and hands. Geotrichosis can cause a cystic lesion appears as soft tissue on the skin.

Diagnosis
Laboratory culture
The diagnoses of geotrichosis cannot be determined without using culture or microscopic measurements. The laboratory diagnosis of geotrichosis involves collected fungi samples areas of infections without contamination. Scraping of the mouth lesions and the ulcers can provide a sample of G. candidum. Samples can also be collected from pus and mucus can be obtained from the feces. Sputum can be searched for the mucoid-like white flakes for further examination. Culturing the cylindrical barrel-shaped or elliptical fungi in considerable numbers in oral lesions is an indicator that a patient may have geotrichosis. Under the microscope the fungi appears yeast-like and septate branching hyphae that can be broken down into chains or individual arthrospores. Arthrospores appear rectangular with flat or rounded ends. Under the microscope the arthroconidia size range from 6-12μm x 3-6μm. Arthroconidia and coarse true hyphae can be observed can be observed under the microscope. Another identification method for G. candidum is selective isolation method. A selection isolation method based on the fungi tolerance to novobiocin and carbon dioxide can determine if G. candidum is the cause of illness.

Diagnostic imaging
X-rays can be used to examine the lung tissue, however it can not be used to positively diagnose geotrichosis. X-rays may show cavitation that is located the walls of the lungs tissues. The lung tissue resemble the early signs of tuberculosis. The results of an x-ray examination of pulmonary geotrichosis presents smooth, dense patchy infiltrations and some cavities. Bronchial geotrichosis shows peribronchial thickening with fine mottling may be present on middle or basilar pulmonary fields </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Acrogeria and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Giant axonal neuropathy and can you explain it in depth? [/INST] Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sesamoiditis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Baboon syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Larsen syndrome and can you explain it in depth? [/INST] Larsen syndrome (LS) is a congenital disorder discovered in 1950 by Larsen and associates when they observed dislocation of the large joints and face anomalies in six of their patients.  Patients with Larsen syndrome normally present with a variety of symptoms, including congenital anterior dislocation of the knees, dislocation of the hips and elbows, flattened facial appearance, prominent foreheads, and depressed nasal bridges.  Larsen syndrome can also cause a variety of cardiovascular and orthopedic abnormalities.  This rare disorder is caused by a genetic defect in the gene encoding filamin B, a cytoplasmic protein that is important in regulating the structure and activity of the cytoskeleton.  The gene that influences the emergence of Larsen syndrome is found in chromosome region, 3p21.1-14.1, a region containing human type VII collagen gene.  Larsen syndrome has recently been described as a mesenchyme disorder that affects the connective tissue of an individual.  Autosomal dominant and recessive forms of the disorder have been reported, although most cases are autosomal dominant. Reports have found that in Western societies, Larsen syndrome can be found in one in every 100,000 births, but this is most likely an underestimate because the disorder is frequently unrecognized or misdiagnosed.

Signs and symptoms
Common symptoms
Symptoms are related to defects in connective tissue.

Congenital anterior dislocation of the knees
Dislocation of hips and shoulders
Flattened facial appearance
Prominent forehead
Depressed nasal bridge
Club foot
Cervical kyphosis

Cardiac anomalies
Cardiac defects are similar to those associated with Marfans syndrome, a disorder of the connective tissue.

Elongation of aorta
Bicuspid aortic valve
Subaortic stenosis
Mitral valve prolapse with mitral regurgitation
Atrial septal defect
Patent ductus arteriosus
Tricuspid valve prolapse
Aortic dissection and aneurysm
Aneurysm of ductus arteriosus

Other reported symptoms
These symptoms were found in rare cases of Larsen syndrome.
Cataracts
Cleft palate
Extra bones of wrist
Malocclusion
Microdontia and hypodontia
Complete agenesis of anus
Bifid uterus
Bifid tongue

Causes
Mutations in gene encoding filamin B
Filamins are cytoplasmic proteins that regulate the structure and activity of the cytoskeleton.  These proteins serve as scaffolds on which intracellular signaling and protein trafficking are organized. Filamin B has been found to be expressed in human growth plate chondrocytes, which are especially important in vertebrae segmentation and skeleton morphogenesis.  Genetic analysis of patients with Larsen syndrome has found the syndrome is caused by missense mutations in the gene that codes for filamin B.  These mutations cause an accelerated rate of apoptosis in the epiphyseal growth plates of individuals with the mutation.  The defects can cause short stature and other symptoms associated with Larsen syndrome.

Localization
Genetic analysis has found that a gene linked to Larsen syndrome, LAR1, is strongly linked to chromosome 3p markers.  The locus of this gene is found in a region defined distally by D3S1581 and proximally by D3S1600.  This location can be mapped to chromosome region 3p21.1-14.1.  Human type VII collagen gene is found within this region in chromosome region 3p21.1.  It is reasonable to believe that the joint abnormalities and cardiac anomalies associated with Larsen syndrome are related to the fact that the human type VII collagen gene is found within the same chromosome region as the LAR1 gene.

Genetics
Both autosomal dominant and recessive forms of Larsen syndrome have been reported.  The former is significantly more common than the latter </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Liebenberg syndrome and can you explain it in depth? [/INST] Liebenberg syndrome is a rare autosomal genetic disease that involves a deletion mutation upstream of the PITX1 gene, which is one thats responsible for the bodys organization, specifically in forming lower limbs. In animal studies, when this deletion was introduced to developing birds, their wing buds were noted to take on limb-like structures.The condition was first described by Dr. F. Liebenberg in 1973 while he followed multiple generations of a South African family, but it has since been noticed in other family lineages across the world.

Symptoms and signs
People who are affected by Liebenberg Syndrome suffer from three main symptoms:
Dysplasia (improper formation) of the bony components of the elbow
Abnormal shape of carpal bones
Brachydactyly, a symptom where the fingers and toes are shorter than normal.

Phenotype
People with Liebenberg Syndrome have normal overall body structure. Their morphological differences are in both of their distal humeri, elbows, hands and wrists. The elbows are enlarged with abnormally large olecranons and radial heads. Patients have relatively fixed elbow positions and are therefore unable to pronate or supinate their forearms. Their wrists are also limited in their active movements and have very prominent ulnar sides of the joints. The fingers adopt toe-like structures. Brachydactyly and camptodactyly occur; fingers are short and abnormally bent. These changes in finger shape result in small club shaped appendages. Motion is reduced in all digital joints of the hand.

Genetics
Liebenberg Syndrome follows an autosomal dominant mode of inheritance, whereby heterozygotes with this mutation express the disease phenotype.
It is caused by a heterozygous mutation to chromosome 5. It involves the inappropriate enhancement of the PITX1 gene due to genetic deletions and chromosome translocations.PITX1 is a homeobox gene which are genes that regulate proper body structure development. This PT1X gene encodes a transcription factor expressed in hind limbs </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tolosa–Hunt syndrome and can you explain it in depth? [/INST] Tolosa–Hunt syndrome is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies).In 2004, the International Headache Society provided a definition of the diagnostic criteria which included granuloma.

Signs and symptoms
Symptoms are usually limited to one side of the head, and in most cases the individual affected will experience intense, sharp pain and paralysis of muscles around the eye. Symptoms may subside without medical intervention, yet recur without a noticeable pattern.In addition, affected individuals may experience paralysis of various facial nerves and drooping of the upper eyelid (ptosis) </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Familial thoracic aortic aneurysm and aortic dissection and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pagetoid reticulosis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Smokers melanosis and can you explain it in depth? [/INST] Smokers melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, cheeks or palate  as well as in larynx. It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation.The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deep, some of the toxic substances due to the UV-light damage to the cells, are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and keratinocytes together protect the tissue, with melanin serving as a toxic defence and cleaning agent.
In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, cleaning the mucosa from different toxic chemicals penetrating the epithelium. Besides chemicals in tobacco  also antimalaria-drugs cause an oral pigmentation. Smokers melanosis is like the genetic melanin pigmentations, a defence-system in action.
The microscope shows smokers melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans". They are produced by the dendritic, octopus-like melanocytes, seen between the epithelial cells situated closest to the epithelium/connective tissue border.In tobacco-users the melanocytes are stimulated to produce melanin granules and to distribute them out to the surrounding epithelial cells for further transport to the mucosal surface, like the mechanism in melanin-pigmented skin.
Small amounts of melanin-like granules together with other electron-dense particles can also be seen within large melanosome complexes in the underlying connective tissue. If the granules derive from the epithelium,  a phenomenon known as melanin incontinence, is not known. In Caucasians these granules are not expected to influence on the clinically observed degree of smokers melanosis.

Causes
Smoking or the use of nicotine-containing drugs is the cause to Smokers melanosis,. Also tar-components (benzopyrenes) are known to stimulate melanocytes to melanin production, and other unknown toxic agents in tobacco may also be the cause.  These chemical agents have a polycyclic, chain-like structure.  Environmental tobacco smoke from parents is causing smokers melanosis in their children    Swedish snuff causes a small elevation of oral melanin pigmented individuals from 3.0% to 4.7%. Nicotine tablets have shown to stimulate to melanin pigmentation of the oral mucosa.

Treatment and prognosis
Lesions usually disappear between 3 months to 3 years for those who stop smoking.  Smokers melanosis is a benign, normal physiological reaction, and does not develop into cancer </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Atrichia with papular lesions and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Childhood granulomatous periorificial dermatitis and can you explain it in depth? [/INST] Childhood granulomatous periorificial dermatitis (CGPD), is a rare benign granulomatous skin disease of unknown cause. The disorder was first described in 1970 by Gianotti in a case series of five children. CGPD is more common in boys than girls.

Signs and symptoms
CGPD is characterized by the presence of small, raised, dome-shaped, flesh-colored or yellow-brown papules primarily distributed around the mouth, eyes, and nose. Affected children may also have papules on the ears, eyelids, cheeks, forehead, and nose. CGPD skin lesions rarely affect areas of the skin other than the face.

Cause
The cause of CGPD is unknown.

Diagnosis
The approach to diagnosing CGPD is controversial. Certain dermatologists suggest that ruling out infectious and allergic causes of similar skin eruptions and a skin biopsy demonstrating features consistent with CGPD is adequate for diagnosis. In contrast, other dermatologists advocate for performing a complete history and physical examination and obtaining laboratories and appropriate imaging to rule out cutaneous sarcoidosis. On microscopy, non-tuberculous granulomas with surrounding lymphocytes clustered around hair follicles may be seen; additionally, infiltrates of epithelioid macrophages, lymphocytes, and giant cells may also be seen.Several conditions exhibit skin findings similar to those of CGPD. These conditions include perioral dermatitis, acne vulgaris, granulomatous rosacea, contact dermatitis, folliculitis, atopic dermatitis, cheilitis, medication-induced acneiform eruptions, lupus miliaris disseminatus faciei, benign cephalic histiocytosis, granulosis rubra nasi, xanthomas, zinc deficiency, glucagonoma, cutaneous sarcoidosis, and scabies.

Treatment
Treatment recommendations for CGPD vary and may include observation without treatment, stopping the use of topical corticosteroids, and the use of topical or oral antibiotics as well as isotretinoin. Topical antibiotics such as metronidazole and erythromycin have been used for CGPD. Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. Trimethoprim/sulfamethoxazole has also been used. The use of oral systemic antibiotics is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children.The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others saw incomplete resolution or prolonged symptoms </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cylindroma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Renovascular hypertension and can you explain it in depth? [/INST] Renovascular hypertension is a condition in which high blood pressure is caused by the kidneys hormonal response to narrowing of the arteries supplying the kidneys. When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.

Signs and symptoms
Symptoms of renovascular hypertension include the following:
High blood pressure (early age)
Kidney dysfunction
Narrowing of arteries elsewhere in the body
Pulmonary edema

Cause
The cause of renovascular hypertension is consistent with any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: diabetes, high cholesterol and advanced age, also of importance is that a unilateral
condition is sufficient to cause renovascular hypertension.

Pathogenesis
The pathogenesis of renovascular hypertension involves the narrowing of the arteries supplying the kidneys which causes a low perfusion pressure that is detected by the juxtaglomerular apparatus (via the macula densa cells, which act as baroreceptors; located on the afferent arteriole wall). This leads to renin secretion that causes the angiotensinogen conversion to angiotensin I. Angiotensin I then proceeds to the lung where it is converted to angiotensin II via angiotensin converting enzyme (ACE).In most people fibromuscular dysplasia or atherosclerosis is the reason for the occlusion of a renal artery which ultimately leads to this condition.

Diagnosis
The diagnosis for renovascular hypertension is done by:
Blood test (for renal function)
Urinary test (tests for microalbuminuria)
Serology (to exclude systemic lupus erythematosus )
Lipid profile
Urinalysis (to exclude presence of red blood cells)

Treatment
In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.

Prognosis
The prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore, those who also have renal dysfunction have a higher mortality risk.
However, the majority of renovascular diseases can be improved with surgery.

See also
Fibromuscular dysplasia
Hypertensive nephropathy
Kidney failure
Renal artery stenosis

References
Further reading
Advances in Renal Hypertension Research and Treatment: 2012 Edition: ScholarlyPaper. ScholarlyEditions. 2012-12-26. ISBN 9781481636018.
Textor, Stephen C. (2009). "Current Approaches to Renovascular Hypertension". Medical Clinics of North America </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Mantleoma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Boutonneuse fever and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is List of phobias and can you explain it in depth? [/INST] The English suffixes -phobia, -phobic, -phobe (from Greek φόβος phobos, "fear") occur in technical usage in psychiatry to construct words that describe irrational, abnormal, unwarranted, persistent, or disabling fear as a mental disorder (e.g. agoraphobia), in chemistry to describe chemical aversions (e.g. hydrophobic), in biology to describe organisms that dislike certain conditions (e.g. acidophobia), and in medicine to describe hypersensitivity to a stimulus, usually sensory (e.g. photophobia). In common usage, they also form words that describe dislike or hatred of a particular thing or subject (e.g. homophobia). The suffix is antonymic to -phil-.
For more information on the psychiatric side, including how psychiatry groups phobias such as agoraphobia, social phobia, or simple phobia, see phobia. The following lists include words ending in -phobia, and include fears that have acquired names. In some cases, the naming of phobias has become a word game, of notable example being a 1998 humorous article published by BBC News. In some cases, a word ending in -phobia may have an antonym with the suffix -phil-, e.g. Germanophobe/Germanophile.
Many -phobia lists circulate on the Internet, with words collected from indiscriminate sources, often copying each other. Also, a number of psychiatric websites exist that at the first glance cover a huge number of phobias, but in fact use a standard text to fit any phobia and reuse it for all unusual phobias by merely changing the name. Sometimes it leads to bizarre results, such as suggestions to cure "prostitute phobia". Such practice is known as content spamming and is used to attract search engines.
An article published in 1897 in American Journal of Psychology noted "the absurd tendency to give Greek names to objects feared (which, as Arndt says, would give us such terms as klopsophobia – fear of thieves, triakaidekaphobia – fear of the number 13....)".

Psychological conditions
Specialists may prefer to avoid the suffix -phobia and use more descriptive terms such as personality disorders, anxiety disorders, and avoidant personality disorder. Terms should strictly have a Greek prefix although many are irregularly formed with Latin or even English prefixes. Many use inaccurate or imprecise prefixes, such as aerophobia (fear of air) for fear of flying.

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Cultural prejudices and discrimination
Ethnic prejudices and discrimination
The suffix -phobia is used to coin terms that denote a particular anti-ethnic or anti-demographic sentiment, such as Americanophobia, Europhobia, Francophobia, Hispanophobia, and Indophobia. Often a synonym with the prefix "anti-" already exists (e.g. Polonophobia vs. anti-Polonism). Anti-religious sentiments are expressed in terms such as Christianophobia and Islamophobia.

Medical conditions
Cultural phenomena
-phobia in the natural sciences
In the natural sciences, words with the suffix -phobia/-phobic generally describe a predisposition for avoidance and/or exclusion. For antonyms, see here

Jocular and fictional phobias
Aibohphobia – a humorous term for the fear of palindromes, which is a palindrome itself. The term is a piece of computer humor entered into the 1981 The Devils DP Dictionary.
Anatidaephobia – the fictional fear that one is being watched by a duck. The word comes from the name of the family Anatidae, and was used in Gary Larsons The Far Side.
Anoraknophobia – a portmanteau of "anorak" and "arachnophobia". It was used in the Wallace and Gromit comic book Anoraknophobia. Also the title of an album by Marillion.
Arachibutyrophobia – fear of peanut butter sticking to the roof of the mouth, from Latin arachis "peanut" and butyrum "butter". The word is used by Charles M. Schulz in a 1982 installment of his Peanuts comic strip, and by Peter ODonnell in his 1985 Modesty Blaise adventure novel Dead Mans Handle.
Charlophobia – the fictional fear of any person named Charlotte or Charlie, mentioned in the comedic book A Duck is Watching Me: Strange and Unusual Phobias (2014), by Bernie Hobbs. The phobia was created to mock name bias, a form of discrimination studied by researchers at the University of California, Berkeley and the University of Chicago.
Hippopotomonstrosesquipedaliophobia – fear of long words, from the root word sesquipedalophobia combined with monstrum and hippopotamus. This was mentioned on the first episode of Brainiac Series Five as a Tickles Teaser.
Keanuphobia – fear of Keanu Reeves, portrayed in the Dean Koontz book, False Memory, where a woman has an irrational fear of Reeves and has to see her psychiatrist, Mark Ahriman, each week, unaware that she only has the fear in the first place because Ahriman implanted it via hypnotic suggestion to amuse himself </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Intracranial pressure and can you explain it in depth? [/INST] Intracranial pressure (ICP) is the pressure exerted by fluids such as cerebrospinal fluid (CSF) inside the skull and on the brain tissue. ICP is measured in millimeters of mercury (mmHg) and at rest, is normally 7–15 mmHg for a supine adult. The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF.
Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (which is induced by contraction of the diaphragm and abdominal wall muscles, the latter of which also increases intra-abdominal pressure), the valsalva maneuver, and communication with the vasculature (venous and arterial systems).
Intracranial hypertension (IH), also called increased ICP (IICP) or raised intracranial pressure (RICP), is elevation of the pressure in the cranium. ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.

Signs and symptoms of raised intracranial pressure
In general, symptoms and signs that suggest a rise in ICP include headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain, and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache that may wake the person up. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours, and cerebral edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing, or bending and progressively worsens over time. There may also be personality or behavioral changes.In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and Cushings triad. Cushings triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern. In children, a low heart rate is especially suggestive of high ICP.Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Biots respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged.As a rule, patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–50 mmHg does CPP and cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death.In infants and small children, the effects of ICP differ because their cranial sutures have not closed. In infants, the fontanels, or soft spots on the head where the skull bones have not yet fused, bulge when ICP gets too high. ICP correlates with intraocular pressure (IOP) but seems to lack the accuracy necessary for close management of intracranial pressure in the acute posttraumatic period.Papilledema, or the swelling of the optic disc, can be a reliable sign that ICP is elevated. Unlike other conditions that may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected.

Causes of abnormal intracranial pressure
Increased ICP
Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

Mass effect such as brain tumor, infarction with edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.
Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
Increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
Obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold–Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger women)
CraniosynostosisOne of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure. ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. It is a cause of reflex bradycardia.

Low ICP
Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity. More commonly, decreased ICP is the result of lumbar puncture or other medical procedures involving the brain or spinal cord. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. Often, the syndrome is self-limiting, especially if it is the result of a medical procedure.If persistent intracranial hypotension is the result of a lumbar puncture, a "blood patch" may be applied to seal the site of CSF leakage. Various medical treatments have been proposed; only the intravenous administration of caffeine and theophylline has shown to be particularly useful.

Pathophysiology
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP − ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The bodys response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus.

Monro–Kellie hypothesis
The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis.The Monro–Kellie hypothesis states that the cranial compartment is inelastic and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. *This concept only applies to adults, as the presence of fontanelles and open suture lines in infants that have not yet fused means there is potential for a change in size and intracranial volume.
The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.

Diagnosis
The most definitive way of measuring the intracranial pressure is with transducers placed within the brain. A catheter can be surgically inserted into one of the brains lateral ventricles and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICPs. This type of drain is known as an external ventricular drain (EVD). This is rarely required outside brain injury and brain surgery settings.In situations when only small amounts of CSF are to be drained to reduce ICPs (e.g. in IIH), drainage of CSF via lumbar puncture can be used as a treatment. Non-invasive measurement of intracranial pressure is being studied.

Treatment
The treatment for ICP depends on the cause. In addition to management of the underlying causes, major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma.For long-term or chronic forms of raised ICP, especially idiopathic intracranial hypertension (IIH), a specific type of diuretic medication (acetazolamide) is used. In cases of confirmed brain neoplasm, dexamethasone is given to decrease ICP. Although the exact mechanism is unknown, current research shows that dexamethasone is capable of decreasing peritumoral water content and local tissue pressure to decrease ICP.

Ventilation
In people who have high ICP due to an acute injury, it is particularly important to ensure adequate airway, breathing, and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise. Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilating blood vessels and exacerbating the problem. Conversely, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a person with a ventilator or bag valve mask can temporarily reduce ICP. Hyperventilation was formerly a part of the standard treatment of traumatic brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used. Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels were returned to normal too quickly. Hyperventilation is still used if ICP is resistant to other methods of control, or there are signs of brain herniation, because the damage herniation can cause is so severe that it may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck in trauma patients, and this may also increase the ICP. Sandbags may be used to further limit neck movement.

Medication
In the hospital, the blood pressure can be increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling. Since hypertension is the bodys way of forcing blood into the brain, medical professionals do not normally interfere with it when it is found in a person with a head injury. When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.If there is an intact blood–brain barrier, osmotherapy (mannitol or hypertonic saline) may be used to decrease ICP.It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes.Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure. Analgesia and sedation are used to reduce agitation and metabolic needs of the brain, but these medications may cause low blood pressure and other side effects. Thus if full sedation alone is ineffective, people may be paralyzed with drugs such as atracurium. Paralysis allows the cerebral veins to drain more easily, but can mask signs of seizures, and the drugs can have other harmful effects. Paralysing drugs are only introduced if patients are fully sedated (this is essentially the same as a general anaesthetic)

Surgery
Craniotomies are holes drilled in the skull with the help of cranial drills to remove intracranial hematomas or relieve pressure from parts of the brain. As raised ICPs may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICPs.A drastic treatment for increased ICP is decompressive craniectomy, in which a part of the skull is removed and the dura mater is expanded to allow the brain to swell without crushing it or causing herniation </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Primordial cyst and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Acne cosmetica and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Anterior interosseous syndrome and can you explain it in depth? [/INST] Anterior interosseous syndrome  is a medical condition in which damage to the anterior interosseous nerve (AIN), a distal motor and sensory branch of the median nerve, classically with severe weakness of the pincer movement of the thumb and index finger, and can cause transient pain in the wrist (the terminal, sensory branch of the AIN innervates the bones of the carpal tunnel).
Most cases of AIN syndrome are now thought to be due to a transient neuritis, although compression of the AIN in the forearm is a risk, such as pressure on the forearm from immobilization after shoulder surgery.  Trauma to the median nerve or around the proximal median nerve have also been reported as causes of AIN syndrome.
Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome.  Although the exact etiology is unknown, there is evidence that it is caused by an immune-mediated response that can follow other illnesses, such as pneumonia or severe viral illness.
Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome.  While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset.  Other retrospective studies have concluded that there is no difference in outcome in surgically versus nonsurgically treated patients.  The role of surgery in AIN syndrome remains controversial.  Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) or fascial compression, and persistent symptoms beyond 1 year of conservative treatment.

Symptoms and signs
Patients may experience poorly localised, transient pain in the wrist, i.e. where the sensory branch of the AIN is mapped in the brain. The pain is sometimes referred into the cubital fossa and elbow pain has been reported as being a primary complaint.
The characteristic severe impairment of the pincer movement of the thumb and index finger is most striking.

Clinical signs
In a pure lesion of the anterior interosseous nerve there is weakness of the long flexor muscle of the thumb (Flexor pollicis longus), the deep flexor muscles of the index  and middle fingers (Flexor digitorum profundus I & II), and the pronator quadratus muscle.There is no sensory deficit since the anterior interosseous nerve has no cutaneous branch to skin, but there is a large sensory branch to the volar carpus, and transient wrist pain may be experienced.

Causes
Injuries of the forearm with compression of the nerve from swelling is the most common cause: examples include supracondylar fractures, often associated with haemorrhage into the deep musculature; injury secondary to open reduction of a forearm fracture; or dislocation of the elbow.Direct trauma from a penetrating injury such as a stab wound is a possible cause for the syndrome.Fibrous bands or Arcuate ligament~arcuate (curved) ligaments may entrap the median as well as the anterior interosseous nerve, in which case a patient may experience hand numbness as well as wrist pain.Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis.Anterior interosseous nerve entrapment or compression injury remains a difficult clinical diagnosis because it is mainly a motor nerve problem, and the syndrome is often mistaken for index finger and/or thumb tendon injury.

Anatomy
The anterior interosseous nerve is a branch of the median nerve, with a large sensory branch to the wrist bones, which arises just below the elbow. It passes distally, anteriorly along the interosseous membrane and innervates flexor pollicis longus, flexor digitorum profundus to index and middle finger as well as pronator quadratus, and supplies sensory feedback from the wrist bones, i.e </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pancoast tumor and can you explain it in depth? [/INST] A Pancoast tumor is a tumor of the apex of the lung. It is a type of lung cancer defined primarily by its location situated at the top end of either the right or left lung. It typically spreads to nearby tissues such as the ribs and vertebrae. Most Pancoast tumors are non-small-cell lung cancers.
The growing tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, vagus nerve, or, characteristically, compression of a sympathetic ganglion (the stellate ganglion), resulting in a range of symptoms known as Horners syndrome.
Pancoast tumors are named for Henry Pancoast, an American radiologist, who described them in 1924 and 1932.

Signs and symptoms
Aside from constitutional symptoms of cancer such as malaise, fever, weight loss and fatigue, Pancoast tumor can include a complete Horners syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid), and pseudoenophthalmos (as a result of the ptosis). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand with a symptomatology typical of thoracic outlet syndrome. The tumor can also compress the recurrent laryngeal nerve and from this a hoarse voice and "bovine" (non-explosive) cough may occur.In superior vena cava syndrome, obstruction of the superior vena cava by a tumor (mass effect) causes facial swelling cyanosis and dilatation of the veins of the head and neck.A Pancoast tumor is an apical tumor that is typically found in conjunction with a history of smoking tobacco </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Developmental coordination disorder and can you explain it in depth? [/INST] Developmental coordination disorder (DCD), also known as developmental motor coordination disorder, developmental dyspraxia or simply dyspraxia, is a neurodevelopmental disorder characterized by impaired coordination of physical movements as a result of brain messages not being accurately transmitted to the body. Deficits in fine or gross motor skills movements  interfere with activities of daily living. It is often described as disorder in skill acquisition, where the learning and execution of coordinated motor skills is substantially below that expected given the individuals chronological age. Difficulties may present as clumsiness, slowness and inaccuracy of performance of motor skills (e.g., catching objects, using cutlery, handwriting, riding a bike, use of tools or participating in team sports or swimming). It is also often accompanied by difficulty with organisation and/or problems with attention, working memory and time management.
A diagnosis of DCD is reached only in the absence of other neurological impairments such as cerebral palsy, multiple sclerosis, or Parkinsons disease. Onset of the condition is in early childhood and is lifelong. It is thought to affect about 5% of the population.

Signs and symptoms
The World Health Organisation (WHO) recognise DCD as a condition, and have published  their definition in the International Classification of Diseases. This describes DCD as:

6A04 Developmental motor coordination disorderDevelopmental motor coordination disorder is characterised by a significant delay in the acquisition of gross and fine motor skills and impairment in the execution of coordinated motor skills that manifest in clumsiness, slowness, or inaccuracy of motor performance. Coordinated motor skills are substantially below that expected given the individuals chronological age and level of intellectual functioning. Onset of coordinated motor skills difficulties occurs during the developmental period and is typically apparent from early childhood. Coordinated motor skills difficulties cause significant and persistent limitations in functioning (e.g., in activities of daily living, school work, and vocational and leisure activities). Difficulties with coordinated motor skills are not solely attributable to a Disease of the Nervous System, Disease of the Musculoskeletal System or Connective Tissue, sensory impairment, and not better explained by a Disorder of Intellectual Development.

The American Psychiatric Association (APA)s Diagnostic and Statistical Manual, DSM-5 classifies Developmental Coordination Disorder (DCD) as a discrete motor disorder under the broader heading of neurodevelopmental disorders. It is often described as a disorder in skill acquisition or motor learning, where the learning and execution of coordinated motor skills is substantially below that expected given the individuals chronological age. Various areas of development can be affected by DCD and these may persist into adulthood.In children, DCD may exhibit as delays in early development of sitting, crawling, walking; poor ability or difficulties with childhood activities such as running, jumping, hopping, catching, sports and swimming; slowness; frequent tripping and bruising; poor handwriting skills; difficulties with self care; difficulties with skills such as using cutlery or tying shoelaces; poor spatial understanding; difficulty following instructions; poor time management; and often losing objects.In adulthood, in addition to a childhood history as above, the condition may manifest as a difficulty learning new motor skills or applying skills in a different or busy environment, poor organisation and time management skills, missed deadlines and lateness for appointments (or earliness as a coping strategy), and awkward pauses before answering in conversation. There is often a history of underachievement in education or the workplace. Although skills can be acquired, such as neat handwriting, handwriting speed will then be much lower than expected. DCD has no cure. Often various coping strategies are developed, and these can be enhanced through occupational therapy, psychomotor therapy, physiotherapy, speech therapy, or psychological training.
Evidence from research and clinical practice indicates that DCD is not just a physical disorder, and there may be deficits in executive functions, behavioural organisation and emotional regulation that extend beyond the motor impairments and which are independent of diagnoses of co-morbidities. In addition to the physical or motor impairments, developmental coordination disorder is associated with problems with memory, especially working memory. This typically results in difficulty remembering instructions, difficulty organizing ones time and remembering deadlines, increased propensity to lose things or problems carrying out tasks which require remembering several steps in sequence (such as cooking). Whilst most of the general population experience these problems to some extent, they have a much more significant impact on the lives of dyspraxic people. However, many dyspraxics have excellent long-term memories, despite poor short-term memory. Many dyspraxics benefit from working in a structured environment, as repeating the same routine minimises difficulty with time-management and allows them to commit procedures to long-term memory.
People with developmental coordination disorder sometimes have difficulty moderating the amount of sensory information that their body is constantly sending them, so as a result these dyspraxics may be prone to sensory overload and panic attacks.Moderate to extreme difficulty doing physical tasks is experienced by some people with dyspraxia, and fatigue is common because so much energy is expended trying to execute physical movements correctly. Some dyspraxics have hypotonia, low muscle tone, which can also detrimentally affect balance.

Gross motor control
Whole body movement and motor coordination issues mean that major developmental targets including walking, running, climbing and jumping can be affected. The difficulties vary from person to person and can include the following:

Fine motor control
Fine-motor problems can cause difficulty with a wide variety of other tasks such as using a knife and fork, fastening buttons and shoelaces, cooking, brushing teeth, styling hair, shaving, applying cosmetics, opening jars and packets, locking and unlocking doors, and doing housework.
Difficulties with fine motor co-ordination lead to problems with handwriting,
Problems associated with this area may include:

Developmental verbal dyspraxia
Developmental verbal dyspraxia (DVD) is a type of ideational dyspraxia, causing speech and language impairments. This is the favoured term in the UK; however, it is also sometimes referred to as articulatory dyspraxia, and in the United States the usual term is childhood apraxia of speech (CAS).Key problems include:

Associated disorders and secondary consequences
People who have developmental coordination disorder may also have one or more of these co-morbid conditions:

However, a person with DCD is unlikely to have all of these conditions. The pattern of difficulty varies widely from person to person; an area of major weakness for one dyspraxic can be an area of strength or gift for another. For example, while some dyspraxics have difficulty with reading and spelling due to dyslexia, or with numeracy due to dyscalculia, others may have brilliant reading and spelling or mathematical abilities. Co-morbidity between ADHD and DCD is particularly high; the overlap between the two disorders is believed to be about 50% (approximately half of people with DCD have ADHD, and approximately half of people with ADHD have DCD).

Sensory processing disorder
Sensory processing disorder (SPD) concerns having oversensitivity or undersensitivity to physical stimuli, such as touch, light, sound, and smell. This may manifest itself as an inability to tolerate certain textures such as sandpaper or certain fabrics such as wool, oral intolerance of excessively textured food (commonly known as picky eating), being touched by another individual (in the case of touch oversensitivity) or it may require the consistent use of sunglasses outdoors since sunlight may be intense enough to cause discomfort to a dyspraxic person (in the case of light oversensitivity). An aversion to loud music and naturally loud environments (such as clubs and bars) is typical behavior of individuals with dyspraxia who have auditory oversensitivity, while only being comfortable in unusually warm or cold environments is typical of a dyspraxic with temperature oversensitivity. Undersensitivity to stimuli may also cause problems, as individuals do not receive the sensory input they need to understand where their bodies are in space. This can make it even more challenging to complete tasks. Dyspraxics who are undersensitive to pain may injure themselves without realising it. Some dyspraxics may be oversensitive to some stimuli and undersensitive to others.

Developmental Language Disorder
Developmental Language Disorder (DLD) research has found that students with developmental coordination disorder and normal language skills still experience learning difficulties despite relative strengths in language. This means that, for students with developmental coordination disorder, their working memory abilities determine their learning difficulties. Any strength in language that they have is not able to sufficiently support their learning.Students with developmental coordination disorder struggle most in visual-spatial memory. When compared to their peers without motor difficulties, students with developmental coordination disorder are seven times more likely than typically developing students to achieve very poor scores in visual-spatial memory. As a result of this working memory impairment, students with developmental coordination disorder have learning deficits as well.

Psychological and social consequences
Psychological domain: Children with DCD may struggle with lower self-efficacy and lower self-perceived competence in peer and social relations. Some demonstrate greater aggressiveness and hyperactivity.Social domain: Children may be more vulnerable to social rejection and bullying, possibly resulting in higher levels of loneliness.

Diagnosis
Assessments for developmental coordination disorder typically require a developmental history, detailing ages at which significant developmental milestones, such as crawling and walking, occurred. Motor skills screening includes activities designed to indicate developmental coordination disorder, including balancing, physical sequencing, touch sensitivity, and variations on walking activities.The American Psychiatric Association has four primary inclusive diagnostic criteria for determining if a child has developmental coordination disorder.
The criteria are as follows:

Motor coordination will be greatly reduced, although the intelligence of the child is normal for the age.
The difficulties the child experiences with motor coordination or planning interfere with the childs daily life.
The difficulties with coordination are not due to any other medical condition
If the child does also experience comorbidities such as intellectual or other developmental disability; motor coordination is still disproportionally affected.

Screening tests
Currently there is no single "gold standard" assessment test for DCD. Various screening tests may be used, including the following.

A baseline motor assessment establishes the starting point for developmental intervention programs. Comparing children to normal rates of development may help to establish areas of significant difficulty.
However, research in the British Journal of Special Education has shown that knowledge is severely limited in many who should be trained to recognise and respond to various difficulties, including developmental coordination disorder, dyslexia and deficits in attention, motor control and perception (DAMP). The earlier that difficulties are noted and timely assessments occur, the quicker intervention can begin. A teacher or GP could miss a diagnosis if they are only applying a cursory knowledge.

"Teachers will not be able to recognise or accommodate the child with learning difficulties in class if their knowledge is limited. Similarly GPs will find it difficult to detect and appropriately refer children with learning difficulties."
A diagnosis of DCD is reached only in the absence of other neurological impairments such as cerebral palsy, multiple sclerosis, or Parkinsons disease.

Classification
Developmental coordination disorder is classified in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as a motor disorder, in the category of neurodevelopmental disorders.

Prevalence
The exact proportion of people with the disorder is unknown since the disorder can be difficult to detect due to a lack of specific laboratory tests, thus making diagnosis of the condition one of elimination of all other possible causes/diseases. Approximately 5–6% of children and adults are affected by this condition. and approximately 2% are severely affected.DCD is a lifelong neurological condition that is expected to be as common in males as it is in females. Currently however, the diagnosis criteria favours males which results in over 80% of males being diagnosed before the age of 16 compared to only 22% for females.

Management
There is no cure for the condition. Instead, it is managed through therapy. Physical therapy or occupational therapy can help those living with the condition.
Some people with the condition find it helpful to find alternative ways of carrying out tasks or organizing themselves, such as typing on a laptop instead of writing by hand, or using diaries and calendars to keep organized. A review completed in 2017 by Cochrane of task-oriented interventions for DCD resulted in inconsistent findings and a call for further research and randomized controlled trials.

Co-occuring conditions
DCD is know to co-occur with other Neurodevelopmental Disorders. Most commonly, Attention Deficit Hyperactivity Disorder (ADHD) co-occurs in an estimated 50% of cases, but other co-occurring conditions are Autistic Spectrum Disorder (ASD), Developmental Speech and Language Disorder and Developmental Learning Disorder.

History
Collier first described developmental coordination disorder as "congenital maladroitness". A. Jean Ayres referred to developmental coordination disorder as a disorder of sensory integration in 1972, while in 1975 Sasson Gubbay, MD, called it the "clumsy child syndrome". Developmental coordination disorder has also been called "minimal brain dysfunction", although the two latter names are no longer in use.
Other names include developmental apraxia, disorder of attention and motor perception (DAMP) dyspraxia, developmental dyspraxia, "motor learning difficulties", perceptuo-motor dysfunction, and sensorimotor dysfunction.The World Health Organization currently lists developmental coordination disorder as "Specific Developmental Disorder of Motor Function".

In popular culture
Helen Burns, a character from Charlotte Brontes Jane Eyre, is alleged to have been based on the authors dyspraxic elder sister Maria Bronte.
Ryan Sinclair, a companion of the Doctor in the BBC science fiction television programme Doctor Who, has the disorder. The character debuted in 2018.

Notable cases
People who have publicly stated they have been diagnosed with developmental coordination disorder include:

Harry Potter actor Daniel Radcliffe,
photographer David Bailey,
model Cara Delevingne,
singer Florence Welch,
UK politician Emma Lewell-Buck,
Rugby Union player Ellis Genge,
actor Will Poulter,
singer Mel B,
actor Olive Gray,
author Holly Smale,
games critic John "TotalBiscuit" Bain,
musician Toyah Willcox
English comedian Harriet Kemsley.

See also
References
Sources
Further reading
Polatajko H, Fox M, Missiuna C (1995). "An International Consensus on Children with Developmental Coordination Disorder". Canadian Journal of Occupational Therapy. 62 (1): 3–6. doi:10.1177/000841749506200101. S2CID 75856620.
Mandich A, Polatajko HJ (November 2003) </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Retinal migraine and can you explain it in depth? [/INST] Retinal migraine is a retinal disease often accompanied by migraine headache and typically affects only one eye. It is caused by ischaemia or vascular spasm in or behind the affected eye.
The terms "retinal migraine" and "ocular migraine" are often confused with "visual migraine", which is a far-more-common symptom of vision loss, resulting from the aura phase of migraine with aura. The aura phase of migraine can occur with or without a headache. Ocular or retinal migraines happen in the eye, so only affect the vision in that eye, while visual migraines occur in the brain, so affect the vision in both eyes together. Visual migraines result from cortical spreading depression and are also commonly termed scintillating scotoma.

Symptoms
Retinal migraine is associated with transient monocular visual loss (scotoma) in one eye lasting less than one hour </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Subungual hematoma and can you explain it in depth? [/INST] A subungual hematoma is a collection of blood (hematoma) underneath a toenail or fingernail. It can be extremely painful for an injury of its size, although otherwise it is not a serious medical condition.

Nature
A laceration of the nail bed causes bleeding into the constricted area underneath the hard nail plate.  The blood pools under the nail, giving a reddish, brownish, blueish, or grey/blackish discoloration. The blood puts pressure to the nailbed causing pain which can be throbbing in quality and disappears when the pressure on the nail bed is relieved.Subungual hematomas typically heal without incident, though infection may occur. The pressure of the blood blister may cause separation of nail plate from the nail bed (onycholysis), but the nail should not be pulled off, as this can cause scarring of the nailbed and deformed nails. Nail discolouration may last some months.The nail plate may also become thicker and more brittle as a result of the injury (onychochauxis). The deformed nail plate will gradually grow out and be replaced by new, normal-appearing nail plate in several months time. Infrequently, the nail may become painful and require surgical drainage.

Causes
The condition is caused by a traumatic injury, such as slamming a finger in a door, or from sports activities, especially those involving sudden accelerations, such as soccer, basketball, and tennis,  or going downhill, such as running or hiking rugged terrain, and ill-fitting footwear.: 52, 135 Repeatedly thrusting the toes against a shoes toe box can cause a subungual hematoma called joggers toe, runners toe, or black toenail. In a marathon, several percent of runners may be affected. Wearing footwear which fits helps prevent runners toe.If the shoe is too loose on the midfoot, the foot can slide forwards in the shoe, especially when going downhill. This may jam the toes into the end of the toebox. If the foot is sliding forwards because the shoe is too loose around the midfoot, it may be restrained by lacing the shoe carefully, or placing bulky padding between the tongue and the lacing, or by wrapping a strap in a figure-eight around the foot and ankle (image).: 86–87, 128, 142  Excessively tight or uneven fit around the midfoot may, however, cause tendon problems.: 125 Separately, if there is not enough space around the toes, the toes will also hit the toebox repeatedly. Feet become longer and wider when weight is put on them, because the arches flatten, and the toes also splay and bend.: p15, 18, 72–73  At the end of a long journey on foot, the arches flatten, the metatarsals spread, and the foot swells more than after a short one.: 52  The toes also need vertical space; a toe cap which is low enough to press on the top of the toe may also cause bruising under the nail, especially if the toe cap is stiff </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Myelomalacia and can you explain it in depth? [/INST] Myelomalacia is a pathological term referring to the softening of the spinal cord. Possible causes of myelomalacia include cervical myelopathy, hemorrhagic infarction, or acute injury, such as that caused by intervertebral disc extrusion.In advanced stages, this disorder causes flaccid paraplegia  (impairment of motor function in lower extremities), total areflexia  (below normal or absence of reflexes) of the pelvic limbs and anus, loss of deep pain perception caudal (toward the coccyx, or tail) to the site of spinal cord injury, muscular atrophy (wasting away of muscle tissue), depressed mental state, and respiratory difficulty due to intercostal  (muscles that run between the ribs) and diaphragmatic paralysis. Gradual cranial migration of the neurological deficits (problems relating to the nervous system), is known as ascending syndrome and is said to be a typical feature of diffuse myelomalacia. Although clinical signs of myelomalacia are observed within the onset (start) of paraplegia, sometimes they may become evident only in the post-operative period, or even days after the onset of paraplegia. Death from myelomalacia may occur as a result of respiratory paralysis when the ascending lesion  (abnormal damaged tissue) reaches the motor nuclei of the phrenic nerves (nerves between the C3-C5 region of the spine) in the cervical (neck) region.

Classification
Myelomalacia affects the neurological functions in the spinal cord. Once breached, the ramification of the damage directly affects the motor functions of the body. Because the central nervous system is affected, the condition is classified under the neurological field of study.

Spinal Cord Injury
When myelomalacia occurs, the damage done to the spinal cord may range from minimal to extensive. The spinal cord and the brain work together, making them the key components of the central nervous system. Damage to this system affects specific functions of the body, primarily relating to the function of muscles. The areas most commonly injured include the cervical vertebrae (C1-C7), and the lumbar spine (L1-L5).

Symptoms
The onset of myelomalacia may be so subtle that it is overlooked. Depending on the extent of the spinal cord injury, the symptoms may vary. In some cases, the symptom may be as common as hypertension. Though every case is different, several cases reported loss of motor functions in the extremities, areflexia or sudden jerks of the limbs, loss of pain perception, or even paralysis; all of which are possible indicators of a damaged and softened spinal cord. In the most severe cases, paralysis of the respiratory system manifests in death.

Cause
The most common way the disorder occurs is from a result of hemorrhaging (bleeding within) or inadequate blood supply to the spinal cord, making it weak and susceptible to damage.Because myelomalacia involves a damaged spinal cord, it may occur in any individual. Those most at risk are the geriatric population due to weaker bone density. Once the spinal injury has occurred, one of two things may happen. Firstly, hemorrhaging within the spinal cord may cause compression, which damages the spinal cord even further. Another consequence of myelomalacia is improper circulation of blood to the area damaged, resulting in  further damage to the spinal cord.

Sport Athletes
Due to extensive physical contact and activity, many athletes become victim to myelomalacia </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Arteritic anterior ischemic optic neuropathy and can you explain it in depth? [/INST] Arteritic anterior ischemic optic neuropathy (AAION or arteritic AION) is the cause of vision loss that occurs in temporal arteritis (aka giant-cell arteritis). Temporal arteritis is an inflammatory disease of medium-sized blood vessels that happens especially with advancing age. AAION occurs in about 15-20 percent of patients with temporal arteritis. Damage to the blood vessels supplying the optic nerves leads to insufficient blood supply (ischemia) to the nerve and subsequent optic nerve fiber death. Most cases of AAION result in nearly complete vision loss first to one eye. If the temporal arteritis is left untreated, the fellow eye will likely suffer vision loss as well within 1–2 weeks. Arteritic AION falls under the general category of anterior ischemic optic neuropathy, which also includes non-arteritic AION. AION is considered an eye emergency, immediate treatment is essential to rescue remaining vision.
An exhaustive review article published in March 2009 described the latest information on arteritic and non-arteritic ischemic optic neuropathy, both anterior (A-AION and NA-AION) and posterior (A-PION, NA-PION, and surgical).

Symptoms
There are several constitutional symptoms of temporal arteritis that may aid in diagnosis of AAION such as jaw claudication (spasms of the jaw muscle), scalp tenderness, unintentional weight loss, fatigue, myalgias and loss of appetite </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is 3q29 microdeletion syndrome and can you explain it in depth? [/INST] 3q29 microdeletion syndrome is a rare genetic disorder resulting from the deletion of a segment of chromosome 3.  This syndrome was first described in 2005.

Presentation
The clinical phenotype of 3q29 microdeletion syndrome is variable. Clinical features can include mild to moderate intellectual disability with mildly dysmorphic facial features (long and narrow face, short philtrum and a high nasal bridge) </s>