<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 Scoliosis and can you explain it in depth? [/INST] Scoliosis is a condition in which a persons spine has a sideways curve. The curve is usually "S"- or "C"-shaped over three dimensions. In some, the degree of curve is stable, while in others, it increases over time. Mild scoliosis does not typically cause problems, but more severe cases can affect breathing and movement. Pain is usually present in adults, and can worsen with age.The cause of most cases is unknown, but it is believed to involve a combination of genetic and environmental factors. Risk factors include other affected family members. It can also occur due to another condition such as muscle spasms, cerebral palsy, Marfan syndrome, and tumors such as neurofibromatosis. Diagnosis is confirmed with X-rays. Scoliosis is typically classified as either structural in which the curve is fixed, or functional in which the underlying spine is normal.Treatment depends on the degree of curve, location, and cause. Minor curves may simply be watched periodically. Treatments may include bracing, specific exercises, posture checking, and surgery. The brace must be fitted to the person and used daily until growing stops. Specific exercises, such as exercises that focus on the core, may be used to try to decrease the risk of worsening. They may be done alone or along with other treatments such as bracing. Evidence that chiropractic manipulation, dietary supplements, or exercises can prevent the condition from worsening is weak. However, exercise is still recommended due to its other health benefits.Scoliosis occurs in about 3% of people. It most commonly develops between the ages of ten and twenty. Females typically are more severely affected than males with a ratio of 4:1. The term is from Ancient Greek: σκολίωσις, romanized: skoliosis which means "a bending".

Signs and symptoms
Symptoms associated with scoliosis can include:
Pain in the back, shoulders, neck, ribs and buttock pain nearest the bottom of the back
Respiratory or cardiac problems in severe cases
Constipation due to curvature causing "tightening" of the stomach, intestines, etc.
Limited mobility secondary to pain or functional limitation in adults mostly when twisting the torso.The signs of scoliosis can include:

Uneven musculature on one side of the spine
Rib prominence or a prominent shoulder blade, caused by rotation of the rib cage in thoracic scoliosis
Uneven hips, arms, or leg lengths
Slow nerve action
Uneven posture
Heart and lung problems in severe cases
Calcium deposits in the cartilage endplate and sometimes in the disc itself

Course
People who have reached skeletal maturity are less likely to have a worsening case. Some severe cases of scoliosis can lead to diminishing lung capacity, pressure exerted on the heart, and restricted physical activities.Recent longitudinal studies reveal that the most common form of the condition, late-onset idiopathic scoliosis, causes little physical impairment other than back pain and cosmetic concerns, even when untreated, with mortality rates similar to the general population. Older beliefs that untreated idiopathic scoliosis necessarily progresses into severe (cardiopulmonary) disability by old age have been refuted by later studies.

Causes
The many causes of scoliosis include neuromuscular problems and inherited diseases or conditions caused by the environment.An estimated 65% of scoliosis cases are idiopathic, about 15% are congenital, and about 10% are secondary to a neuromuscular disease.About 38% of variance in scoliosis risk is due to genetic factors, and 62% is due to the environment. The genetics are likely complex, however, given the inconsistent inheritance and discordance among monozygotic twins. The specific genes that contribute to development of scoliosis have not been conclusively identified. At least one gene, CHD7, has been associated with the idiopathic form of scoliosis.
Several candidate gene studies have found associations between idiopathic scoliosis and genes mediating bone formation, bone metabolism, and connective tissue structure. Several genome-wide studies have identified a number of loci as significantly linked to idiopathic scoliosis. In 2006, idiopathic scoliosis was linked with three microsatellite polymorphisms in the MATN1 gene (encoding for matrilin 1, cartilage matrix protein). Fifty-three single nucleotide polymorphism markers in the DNA that are significantly associated with adolescent idiopathic scoliosis were identified through a genome-wide association study.Adolescent idiopathic scoliosis has no clear causal agent, and is generally believed to be multifactorial; leading to "progressive functional limitations" for individuals. Research suggests that Posterior Spinal Fusion (PSF) can be used to correct the more severe deformities caused by adolescent idiopathic scoliosis. Such procedures can result in a return to physical activity in about 6 months, which is very promising, although minimal back pain is still to be expected in the most severe cases. The prevalence of scoliosis is 1% to 2% among adolescents, but the likelihood of progression among adolescents with a Cobb angle less than 20° is about 10% to 20%.Congenital scoliosis can be attributed to a malformation of the spine during weeks three to six in utero due to a failure of formation, a failure of segmentation, or a combination of stimuli. Incomplete and abnormal segmentation results in an abnormally shaped vertebra, at times fused to a normal vertebra or unilaterally fused vertebrae, leading to the abnormal lateral curvature of the spine.

Resulting from other conditions
Secondary scoliosis due to neuropathic and myopathic conditions can lead to a loss of muscular support for the spinal column so that the spinal column is pulled in abnormal directions. Some conditions which may cause secondary scoliosis include muscular dystrophy, spinal muscular atrophy, poliomyelitis, cerebral palsy, spinal cord trauma, and myotonia. Scoliosis often presents itself, or worsens, during an adolescents growth spurt and is more often diagnosed in females than males.Scoliosis associated with known syndromes is often subclassified as "syndromic scoliosis". Scoliosis can be associated with amniotic band syndrome, Arnold–Chiari malformation, Charcot–Marie–Tooth disease, cerebral palsy, congenital diaphragmatic hernia, connective tissue disorders, muscular dystrophy, familial dysautonomia, CHARGE syndrome, Ehlers–Danlos syndrome (hyperflexibility, "floppy baby" syndrome, and other variants of the condition), fragile X syndrome, Friedreichs ataxia, hemihypertrophy, Loeys–Dietz syndrome, Marfan syndrome, nail–patella syndrome, neurofibromatosis, osteogenesis imperfecta, Prader–Willi syndrome, proteus syndrome, spina bifida, spinal muscular atrophy, syringomyelia, and pectus carinatum.Another form of secondary scoliosis is degenerative scoliosis, also known as de novo scoliosis, which develops later in life secondary to degenerative (may or may not be associated with aging) changes. This is a type of deformity that starts and progresses because of the collapse of the vertebral column in an asymmetrical manner. As bones start to become weaker and the ligaments and discs located in the spine become worn as a result of age-related changes, the spine begins to curve.

Diagnosis
People who initially present with scoliosis undergo a physical examination to determine whether the deformity has an underlying cause and to exclude the possibility of the underlying condition more serious than simple scoliosis.The persons gait is assessed, with an exam for signs of other abnormalities (e.g., spina bifida as evidenced by a dimple, hairy patch, lipoma, or hemangioma).  A thorough neurological examination is also performed, the skin for café au lait spots, indicative of neurofibromatosis, the feet for cavovarus deformity, abdominal reflexes and muscle tone for spasticity.When a person can cooperate, they are asked to bend forward as far as possible. This is known as the Adams forward bend test and is often performed on school students. If a prominence is noted, then scoliosis is a possibility and an X-ray may be done to confirm the diagnosis.
As an alternative, a scoliometer may be used to diagnose the condition.When scoliosis is suspected, weight-bearing, full-spine AP/coronal (front-back view) and lateral/sagittal (side view) X-rays are usually taken to assess the scoliosis curves and the kyphosis and lordosis, as these can also be affected in individuals with scoliosis. Full-length standing spine X-rays are the standard method for evaluating the severity and progression of scoliosis, and whether it is congenital or idiopathic in nature. In growing individuals, serial radiographs are obtained at 3- to 12-month intervals to follow curve progression, and, in some instances, MRI investigation is warranted to look at the spinal cord. An average scoliosis patient has been in contact with around 50-300mGy of radiation due to these radiographs during this time period. The standard method for assessing the curvature quantitatively is measuring the Cobb angle, which is the angle between two lines, drawn perpendicular to the upper endplate of the uppermost vertebra involved and the lower endplate of the lowest vertebra involved. For people with two curves, Cobb angles are followed for both curves. In some people, lateral-bending X-rays are obtained to assess the flexibility of the curves or the primary and compensatory curves.Congenital and idiopathic scoliosis that develops before the age of 10 is referred to as early-onset scoliosis. Progressive idiopathic early-onset scoliosis can be a life-threatening condition with negative effects on pulmonary function. Scoliosis that develops after 10 is referred to as adolescent idiopathic scoliosis. Screening adolescents without symptoms for scoliosis is of unclear benefit.

Definition
Scoliosis is defined as a three-dimensional deviation in the axis of a persons spine. Most instances, including The Scoliosis Research Society, define scoliosis as a Cobb angle of more than 10° to the right or left as the examiner faces the person, i.e. in the coronal plane.Scoliosis has been described as a biomechanical deformity, the progression of which depends on asymmetric forces otherwise known as the Hueter-Volkmann Law.

Management
Scoliosis curves do not straighten out on their own. Many children have slight curves that do not need treatment. In these cases, the children grow up to lead normal body posture by itself, even though their small curves never go away. If the patient has a larger curve and they are still growing, it is important to monitor the curve for change by periodic examination and standing x-rays as needed. The rise in spinal abnormalities require examination by an orthopaedic surgeon to determine if active treatment is needed.The traditional medical management of scoliosis is complex and is determined by the severity of the curvature and skeletal maturity, which together help predict the likelihood of progression.
The conventional options for children and adolescents are:
Observation
Bracing
Surgery
Physical Therapy. Evidence suggests use of scoliosis specific exercises might prevent the progression of the curve along with possible bracing and surgery avoidance.For adults, treatment usually focuses on relieving any pain:
Pain medication
Posture checking
Bracing
SurgeryTreatment for idiopathic scoliosis also depends upon the severity of the curvature, the spines potential for further growth, and the risk that the curvature will progress. Mild scoliosis (less than 30° deviation) and moderate scoliosis (30–45°) can typically be treated conservatively with bracing in conjunction with scoliosis-specific exercises. Severe curvatures that rapidly progress may require surgery with spinal rod placement and spinal fusion. In all cases, early intervention offers the best results.A specific type of physical therapy may be useful. Evidence to support their use however is weak. Low quality evidence suggests scoliosis-specific exercises (SSE) may be more effective than electrostimulation. Evidence for the Schroth method is insufficient to support its use. Significant improvement in function, vertebral angles and trunk asymmetries have been recorded following the implementation of Schroth method in terms of conservative management of scoliosis. Some other forms of exercises interventions have been lately used in the clinical practice for therapeutic management of scoliosis such as global postural reeducation and the Klapp method.

Bracing
Bracing is normally done when the person has bone growth remaining and is, in general, implemented to hold the curve and prevent it from progressing to the point where surgery is recommended. In some cases with juveniles, bracing has reduced curves significantly, going from a 40° (of the curve, mentioned in length above) out of the brace to 18°. Braces are sometimes prescribed for adults to relieve pain related to scoliosis. Bracing involves fitting the person with a device that covers the torso; in some cases, it extends to the neck (example being the Milwaukee Brace).

The most commonly used brace is a TLSO, such as a Boston brace, a corset-like an appliance that fits from armpits to hips and is custom-made from fiberglass or plastic. It is typically recommended to be worn 22–23 hours a day, and applies pressure on the curves in the spine. The effectiveness of the brace depends on not only brace design and orthotist skill, but also peoples compliance and amount of wear per day.
An alternative form of brace is a nighttime only brace, that are worn only at night whilst the child sleeps, which overcorrect the deformity. Whilst nighttime braces are more convenient for children and families, it is unknown if the effectiveness of the brace is as good as conventional braces, therefore the UK government have funded a large clinical trial to resolve this uncertainty; called the BASIS study.  The BASIS study is ongoing throughout the UK in all of the leading UK childrens hospitals that treat scoliosis, with families encouraged to take part.
Indications for bracing: people who are still growing who present with Cobb angles less than 20° should be closely monitored. People who are still growing who present with Cobb angles of 20 to 29° should be braced according to the risk of progression by considering age, Cobb angle increase over a six-month period, Risser sign, and clinical presentation. People who are still growing who present with Cobb angles greater than 30° should be braced. However, these are guidelines and not every person will fit into this table.
For example, a person who is still growing with a 17° Cobb angle and significant thoracic rotation or flatback could be considered for nighttime bracing. On the opposite end of the growth spectrum, a 29° Cobb angle and a Risser sign three or four might not need to be braced because the potential for progression is reduced. The Scoliosis Research Societys recommendations for bracing include curves progressing to larger than 25°, curves presenting between 30 and 45°, Risser sign 0, 1, or 2 (an X-ray measurement of a pelvic growth area), and less than six months from the onset of menses in girls.Scoliosis braces are usually comfortable, especially when well designed and well fitted, also after the 7- to 10-day break-in period. A well fitted and functioning scoliosis brace provides comfort when it is supporting the deformity and redirecting the body into a more corrected and normal physiological position.Evidence supports that bracing prevents worsening of disease, but whether it changes quality of life, appearance, or back pain is unclear.

Surgery
Surgery is usually recommended by orthopedists for curves with a high likelihood of progression (i.e., greater than 45 to 50° of magnitude), curves that would be cosmetically unacceptable as an adult, curves in people with spina bifida and cerebral palsy that interfere with sitting and care, and curves that affect physiological functions such as breathing.Surgery is indicated by the Society on Scoliosis Orthopaedic and Rehabilitation Treatment (SOSORT) at 45 to 50° and by the Scoliosis Research Society (SRS) at a Cobb angle of 45°. SOSORT uses the 45 to 50° threshold as a result of the well-documented, plus or minus 5° measurement error that can occur while measuring Cobb angles.Surgeons who are specialized in spine surgery perform surgery for scoliosis. To completely straighten a scoliotic spine is usually impossible, but for the most part, significant corrections are achieved.The two main types of surgery are:
Anterior fusion: This surgical approach is through an incision at the side of the chest wall.
Posterior fusion: This surgical approach is through an incision on the back and involves the use of metal instrumentation to correct the curve.One or both of these surgical procedures may be needed. The surgery may be done in one or two stages and, on average, takes four to eight hours.
A new tethering procedure (anterior vertebral body tethering) may be appropriate for some patients.

Prognosis
A 50-year follow-up study published in the Journal of the American Medical Association (2003) asserted the lifelong physical health, including cardiopulmonary and neurological functions, and mental health of people with idiopathic scoliosis are comparable to those of the general population. Scoliosis that interferes with normal systemic functions is "exceptional" and "rare", and "untreated [scoliosis] people had similar death rates and were just as functional and likely to lead productive lives 50 years after diagnosis as people with normal spines." In an earlier University of Iowa follow-up study, 91% of people with idiopathic scoliosis displayed normal pulmonary function, and their life expectancy was 2% less than that of the general population. Later (2006-) studies corroborate these findings, adding that they are "reassuring for the adult patient who has adolescent onset idiopathic scoliosis in approximately the 50–70° range." These modern landmark studies supersede earlier studies (e.g. Mankin-Graham-Schauk 1964) that did implicate moderate idiopathic scoliosis in impaired pulmonary function.Generally, the prognosis of scoliosis depends on the likelihood of progression. The general rules of progression are larger curves carry a higher risk of progression than smaller curves, and thoracic and double primary curves carry a higher risk of progression than single lumbar or thoracolumbar curves. In addition, people not having yet reached skeletal maturity have a higher likelihood of progression (i.e., if the person has not yet completed the adolescent growth spurt).

Epidemiology
Scoliosis affects 2–3% of the United States population, which is equivalent to about five to nine million cases. A scoliosis spinal column curve of 10° or less affects 1.5% to 3% of individuals. The age of onset is usually between 10 years and 15 years (can occur at a younger age) in children and adolescents, making up to 85% of those diagnosed. This is seen to be due to rapid growth spurts occurring at puberty when spinal development is most relenting to genetic and environmental influences. Because female adolescents undergo growth spurts before postural musculoskeletal maturity, scoliosis is more prevalent among females.Although fewer cases are present today using Cobb angle analysis for diagnosis, scoliosis remains a prevailing condition, appearing in otherwise healthy children. Despite the fact that scoliosis is a disfigurement of the spine, it has been shown to influence the pneumonic function, balance while standing and stride execution of kids with scoliosis. The impacts of backpack carriage on these three side effects have been broadly researched. Incidence of idiopathic scoliosis (IS) stops after puberty when skeletal maturity is reached, however, further curvature may proceed during late adulthood due to vertebral osteoporosis and weakened musculature.

History
Ever since the condition was discovered by the Greek physician Hippocrates, a cure has been sought. Treatments such as bracing and the insertion of rods into the spine were employed during the 1900s. In the mid-20th century, new treatments and improved screening methods have been developed to reduce the progression of scoliosis in patients and alleviate their associated pain. School children were during this period believed to develop poor posture as a result of working at their desks, and many were diagnosed with scoliosis. It was also considered to be caused by tuberculosis or poliomyelitis, diseases that were successfully managed using vaccines and antibiotics.The American orthopaedic surgeon Alfred Shands Jr. discovered that two percent of patients had non-disease related scoliosis, later termed idiopathic scoliosis, or the "cancer of orthopaedic surgery". These patients were treated with questionable remedies. A theory at the time—now discredited—was that the condition needed to be detected early to halt its progression, and so some schools made screening for scoliosis mandatory. Measurements of shoulder height, leg length and spinal curvature were made, and the ability to bend forwards, along with body posture, was tested, but students were sometimes misdiagnosed because of their poor posture.An early treatment was the Milwaukee brace, a rigid contraption of metal rods attached to a plastic or leather girdle, designed to straighten the spine. Because of the constant pressure applied to the spine, the brace was uncomfortable. It caused jaw and muscle pain, skin irritation, as well as low self-esteem.

Surgery
In 1962, the American orthopaedic surgeon Paul Harrington introduced a metal spinal system of instrumentation that assisted with straightening the spine, as well as holding it rigid while fusion took place. The now obsolete Harrington rod operated on a ratchet system, attached by hooks to the spine at the top and bottom of the curvature that when cranked would distract—or straighten—the curve. The Harrington rod obviates the need for prolonged casting, allowing patients greater mobility in the postoperative period and significantly reducing the quality of life burden of fusion surgery. The Harrington rod was the precursor to most modern spinal instrumentation systems. A major shortcoming was that it failed to produce a posture wherein the skull would be in proper alignment with the pelvis, and it did not address rotational deformity. As the person aged, there would be increased wear and tear, early onset arthritis, disc degeneration, muscular stiffness, and acute pain. "Flatback" became the medical name for a related complication, especially for those who had lumbar scoliosis.In the 1960s, the gold standard for idiopathic scoliosis was a posterior approach using a single Harrington rod. Post-operative recovery involved bed rest, casts, and braces. Poor results became apparent over time.In the 1970s, an improved technique was developed using two rods and wires attached at each level of the spine. This segmented instrumentation system allowed patients to become mobile soon after surgery.In the 1980s, Cotrel-Dubousset instrumentation improved fixation and addressed sagittal imbalance and rotational defects unresolved by the Harrington rod system. This technique used multiple hooks with rods to give stronger fixation in three dimensions, usually eliminating the need for postoperative bracing.

Evolution
There are links between human spinal morphology, bipedality, and scoliosis which suggest an evolutionary basis for the condition. Scoliosis has not been found in chimpanzees or gorillas. Thus, it has been hypothesized that scoliosis may actually be related to humans morphological differences from these apes. Other apes have a shorter and less mobile lower spine than humans. Some of the lumbar vertebrae in Pan are "captured", meaning that they are held fast between the ilium bones of the pelvis. Compared to humans, Old World monkeys have far larger erector spinae muscles, which are the muscles which hold the spine steady. These factors make the lumbar spine of most primates less flexible and far less likely to deviate than those of humans. While this may explicitly relate only to lumbar scolioses, small imbalances in the lumbar spine could precipitate thoracic problems as well.Scoliosis may be a byproduct of strong selection for bipedalism. For a bipedal stance, a highly mobile, elongated lower spine is very beneficial </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 Expressive language disorder and can you explain it in depth? [/INST] Expressive language disorder is a communication disorder in which there are difficulties with verbal and written expression. It is a specific language impairment characterized by an ability to use expressive spoken language that is markedly below the appropriate level for the mental age, but with a language comprehension that is within normal limits. There can be problems with vocabulary, producing complex sentences, and remembering words, and there may or may not be abnormalities in articulation.Careful diagnosis is also important because "atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems".

Models of language production
Willem Levelt outlined the currently accepted theory of speech production. Words are produced after the concept waiting to be produced is conceptualized, related words are selected, encoded and the sound waves of speech are produced.

Association with language networks
There is also a lot of debate about whether specific language impairments, such as expressive language disorder, are caused by deficits in grammar or by a deficit in processing language information. However, an alternative hypothesis to the cause of SLIs has been posited, called the Procedural Deficit Hypothesis. The Procedural Deficit Hypothesis opines that we can explain language impairments due to abnormal development of brain structures that are involved in procedural memory, our memories that remember how to perform different cognitive and motor tasks. The procedural memory system is associated with basal-ganglia circuits in the frontal lobe and further investigation of this particular hypothesis could aid in the development of a clinical neurological picture of what the underlying causes of SLI are.

Scientific studies of speech and language
Some of the earliest neuroscientific discoveries were related to the discovery that damage to certain areas of the brain related to impairments in language, such as the discovery of Wernickes area and Brocas area. Lesions in these parts of the brain impair language comprehension and language production, respectively. Paul Broca was the first to note that the left hemisphere of the brain appeared to be localized for language function, particularly for right handed patients. Modern neuroscientific research has verified this, though language may be lateralizaed to the right hemisphere in some right-handed individuals.

Developmental verbal dyspraxia
In 1990, it was reported that the several generations of the KE family had developmental verbal dyspraxia and orofacial praxis that were inherited in a typical autosomal dominant pattern. Further analysis traced this inheritance pattern back to mutations in the FOXP2 genes. These studies have allowed scientists to begin to investigate how changes to one gene can alter human communication.
FOXP2 is the first gene that has been identified that is specifically linked to speech and language production. Mutant alleles of the normal FOXP2 gene have been found to be the cause of severe speech impairments.

Specific language impairment
Neuroimaging techniques, such as structural and functional MRI, found no significant differences between individuals with SLI and normal controls. However, more subtle and sophisticated techniques, such as voxel-based morphometry studies have allowed researchers to identify bilateral abnormalities in neural volume in areas of the brain associated with motor functions, such as the caudate nucleus, in the affected members of the KE family when compared to the unaffected family members. This volume reduction showed a high correlation between reduced volume and tests of oral praxis, supporting the idea that odd development of the caudate nucleus is related to the problems in motor control observed in the KE family.Due to the vague nature of the diagnosis of expressive language disorder, there is little specific scientific research that we can currently locate. A larger body of research exists around neuroscientific studies with children diagnosed with a specific language impairment (SLI). fMRI studies have shown that children with SLI have a significantly smaller left hemispheric pars triangularis (Brocas area) and asymmetry of dominance of language structures, as opposed to the more typical left hemisphere dominance. Scientists are beginning to elucidate differences in activation patterns in children with SLIs using neuroimaging techniques to capture brain activity while performing different cognitive tasks. A major observation is lack of left hemisphere lateralization in major language structures such as the inferior frontal gyrus-opercularis, inferior frontal gyrus-triangularis, supramarginal gyrus and superior temporal gyrus. The same study reported hypoactivation and hyper activation of other brain regions - the supramarginal junction and anterior insula, respectively. Other in-depth imaging studies report finding previously undiagnosed lesions in the brains of children with well-characterized developmental language development. Together, these findings strongly suggest that language impairments are the result of an underlying neurological defect in an area of the brain related to language.
Studies looking at long-term outcomes for individuals with specific language impairments such as expressive language disorder track these individuals from childhood to adulthood. As Whitehouse and his colleagues  suggest, "When childhood language problems persist into adulthood, they can have far reaching consequences in terms of academic, social and vocational outcomes." These researchers found that children diagnosed with an SLI would have persistent problems with language and are more likely to pursue vocational training rather than university, thereby avoiding professions requiring high levels of literacy. A lower socioeconomic status was also noted by adults who were diagnosed with an SLI as a child. Whitehouse  also reported that these adults had more difficulties in establishing friendships, most likely due to a decreased ability to express themselves socially.

Current educational interventions for students with an SLI
Specific language impairments are often secondary characteristics of other disorders such as autism spectrum disorder and attention deficit hyperactivity disorder. In these cases, issues with speech and language are often not treated specifically, but rather attention is given to the primary complaint. Due to the high correlation of an SLI with other disorders, it is difficult to tell the difference between "pure SLI" or language impairments due to the presence of another disorder.

See also
Auditory processing disorder
Speech-Language Pathology
Mixed receptive-expressive language disorder

References
Further reading
Bacon C, Rappold GA (November 2012). "The distinct and overlapping phenotypic spectra of FOXP1 and FOXP2 in cognitive disorders". Hum. Genet. 131 (11): 1687–98. doi:10.1007/s00439-012-1193-z. PMC 3470686. PMID 22736078.
Bearzotti F, Tavano A, Fabbro F (June 2007). "Development of orofacial praxis of children from 4 to 8 years of age". Percept mot Skills. 104 (3 Pt 2): 1355–66. doi:10.2466/pms.104.4.1355-1366. PMID 17879670. S2CID 11775613.
Caulfield MB, Fischel JE, DeBaryshe BD, Whitehurst GJ (April 1989). "Behavioral correlates of developmental expressive language disorder". J Abnorm Child Psychol. 17 (2): 187–201. doi:10.1007/bf00913793 </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 Acral nevus 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 Sialectasis 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 Retrobulbar bleeding 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 Dermatographic urticaria and can you explain it in depth? [/INST] Dermatographic urticaria is a skin disorder and one of the most common types of urticaria, affecting 2–5% of the population.

Signs and symptoms
The condition manifests as an allergic-like reaction, causing a warm red wheal to appear on the skin. As it is often the result of scratches, involving contact with other materials, it can be confused with an allergic reaction, when in fact it is the act of being scratched that causes a wheal to appear. These wheals are a subset of urticaria (hives), and appear within minutes, in some cases accompanied by itching. The first outbreak of urticaria can lead to other reactions on body parts not directly stimulated, scraped, or scratched. In a normal case, the swelling will decrease without treatment within 15–30 minutes, but, in extreme cases, itchy red welts may last anywhere from a few hours to days.

Causes
Symptoms are thought to be the result of histamine being released by mast cells on the surface of the skin. Despite the lack of antigens, histamine causes the skin to swell in affected areas </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 Lumbar vertebrae and can you explain it in depth? [/INST] The lumbar vertebrae are, in human anatomy, the five vertebrae between the rib cage and the pelvis. They are the largest segments of the vertebral column and are characterized by the absence of the foramen transversarium within the transverse process (since it is only found in the cervical region) and by the absence of facets on the sides of the body (as found only in the thoracic region). They are designated L1 to L5, starting at the top.  The lumbar vertebrae help support the weight of the body, and permit movement.

Human anatomy
General characteristics
The adjacent figure depicts the general characteristics of the first through fourth lumbar vertebrae.  The fifth vertebra contains certain peculiarities, which are detailed below.
As with other vertebrae, each lumbar vertebra consists of a vertebral body and a vertebral arch.  The vertebral arch, consisting of a pair of pedicles and a pair of laminae, encloses the vertebral foramen (opening) and supports seven processes.

Body
The vertebral body of each lumbar vertebra is kidney shaped, wider from side to side than from front to back, and a little thicker in front than in back. It is flattened or slightly concave above and below, concave behind, and deeply constricted in front and at the sides.

Arch
The pedicles are very strong, directed backward from the upper part of the vertebral body; consequently, the inferior vertebral notches are of considerable depth. The pedicles change in morphology from the upper lumbar to the lower lumbar. They increase in sagittal width from 9 mm to up to 18 mm at L5. They increase in angulation in the axial plane from 10 degrees to 20 degrees by L5. The pedicle is sometimes used as a portal of entrance into the vertebral body for fixation with pedicle screws or for placement of bone cement as with kyphoplasty or vertebroplasty.
The laminae are broad, short, and strong. They form the posterior portion of the vertebral arch. In the upper lumbar region the lamina are taller than wide but in the lower lumbar vertebra the lamina are wider than tall. The lamina connects the spinous process to the pedicles.
The vertebral foramen within the arch is triangular, larger than the thoracic vertebrae, but smaller than in the cervical vertebrae.

Processes
The spinous process is thick, broad, and somewhat quadrilateral; it projects backward and ends in a rough, uneven border, thickest below where it is occasionally notched.The superior and inferior articular processes are well-defined, projecting respectively upward and downward from the junctions of pedicles and laminae. The facets on the superior processes are concave, and look backward and medialward; those on the inferior are convex, and are directed forward and lateralward. The former are wider apart than the latter since in the articulated column, the inferior articular processes are embraced by the superior processes of the subjacent vertebra.The transverse processes are long and slender. They are horizontal in the upper three lumbar vertebrae and incline a little upward in the lower two. In the upper three vertebrae they arise from the junctions of the pedicles and laminae, but in the lower two they are set farther forward and spring from the pedicles and posterior parts of the vertebral bodies. They are situated in front of the articular processes instead of behind them as in the thoracic vertebrae, and are homologous with the ribs.Three portions or tubercles can be noticed in a transverse process of a lower lumbar vertebrae: the lateral or costiform process, the mammillary process, and the accessory process. The costiform is lateral, the mammillary is superior (cranial), and the accessory is inferior (caudal). The mammillary is connected in the lumbar region with the back part of the superior articular process. The accessory process is situated at the back part of the base of the transverse process </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 Infantile myofibromatosis and can you explain it in depth? [/INST] Infantile myofibromatosis (IMF) is a rare tumor found in 1 in 150,000 to 1 in 400,000 live births. It is nonetheless the most common tumor derived from fibrous connective tissue that occurs primarily in infants and young children. IMF tumors are benign in the sense that they do not metastasize to distant tissues although when occurring in the viscera, i.e. internal organs, carry guarded to poor prognoses and can be life-threatening, particularly in newborns and young infants.IMF tumors occur in three clinical patterns: 1) solitary IMF tumors (also called myofibromas) which often regress spontaneously and rarely cause serious issues; 2) multiple tumors (no viscera involvement) which consists of numerous (i.e. dozens to >100) IMF lesions most of which are located in the skin, subcutaneous tissues, and non-visceral but not visceral organs, may regress spontaneously, and rarely cause serious issues; and 3) multiple tumors (with viscera involvement) (also called generalized myofibromatosis) which rarely regress spontaneously and consist of numerous IMF lesions in non-visceral tissues plus one or more visceral tumors that may be life-threatening.A minority of infantile myofibromatosis tumors present in individuals with a strong family history of the disease. These familial cases are associated with mutations in either the PDGFRB or NOTCH3 gene. However, most IMF cases have no family history of the disease but nonetheless have PDGFRB gene mutations in their tumor cells; these mutations are similar to those occurring in the familial PDGFRB gene mutations. Regardless of these genetic variations, all IMF tumors consist of bland-appearing, benign (i.e. non-malignant) myofibroblasts, i.e. cells that blend a variable set of features seen in fibroblasts, the most common cell type in connective tissue, with a variable set of features seen in smooth muscle cells.Treatment of IMF tumors depends upon the tumor numbers, locations, and genetic abnormalities found in each individual and often include more than one therapeutic regimen. Individuals with solitary tumors are usually treated by observation with the expectation that many of these tumors will regress spontaneiously. Single tumors located in vital areas (e.g. intracranial tumors) and tumors that do not regress over suitable observation periods are often treated by surgical removal. Multiple tumors (with viscera involvement) and surgically inaccessible life-threatening IMF tumors have been treated with one or a combination of chemotherapy drugs, radiation therapy or, in tumors with certain PDGFRB gene mutations, drugs directed specifically against this mutated genes protein product.

Presentation
IMF tumors are usually painless, well-encapsulated, rubbery to hard, and freely movable-to-fixed masses. They may be evident at birth in up to 60% of cases but generally go undetected until they are diagnosed in the first year of life, uncommonly in older infants and young (<10 years/old) children, or rarely in older children and adults (one individual was diagnosed with IMF at 85 years of age). The tumors may be flesh-colored papules or nodules; plaques (i.e. flat-topped papules that are equal to or greater than 10 mm in largest diameter); pedunculated, calcified masses; or ulcerated, necrotic masses. Most of these tumors are <1 cm in diameter but can be much larger, e.g. 5.2 cm in diameter. At least 9 IMF cases described in the English literature were diagnosed in fetuses based on the findings of fetal spectrogram and/or magnetic resonance imaging. IMF tumors in the viscera or deep tissues may present with serious or life-threatening signs and symptoms of organ and/or deep tissue damage due to these tumors space-filling and pressuring effects.Some individuals with IMF present with a family history of IMF tumors. To date (2021), 20 families have been reported to carry various germline (i.e. inherited) mutations in one of their two PDGFRB genes. All of these mutations were gain of function mutations (i.e. the mutant genes product is overactive) and inherited in an autosomal dominant manner with incomplete penetrance. Among 36 identified familial carriers of these mutant genes, 4 had no history of IMF, 3 had developed a solitary IMF, 29 had developed multiple tumors (no viscera involvement) or multiple tumors (with viscera involvement) IMF, and 2 had died. Most of these individuals were diagnosed with IMF in their infancy or early childhood. Subsequent studies have found that up to 70% of individuals with IMF and no family history of the disease also carry mutations in one of their two PDGFRB genes in the cells of their tumor tissues. These mutations are somatic mutations (i.e. non-inherited mutations developing only after conception) that are identical or similar to those seen in familial cases. The familial and non-familial mutated PDGFRB genes produce highly overactive platelet-derived growth factor receptor beta (i.e. PDGFβ receptor) proteins that contribute to the development and/or progression of IMF.A mutation in one of the two NOTCH3 genes has been reported to occur in a single family with autosomal dominant inheritance of IMF: 9 of this familys members had IMF plus the mutation while 7 of its members did not have IMF or the mutation. Since the mutated NOTCH3 gene in this family produces an overactive neurogenic locus notch homolog protein 3 product that in cell culture studies increases the expression of the PDGFRB genes product, the PDGFβ receptor, this NOTCH3 mutation may promote the development and/or progression of IMF in a manner similar to PDGFRB mutant genes, i.e. by increasing the number and therefore overall activity of the PDGFβ receptor. Further studies are needed to define NOTCH3 gene mutations frequency of occurrence in, and contribution to the development of, IMF.

Solitary IMF tumors
Solitary IMF tumors represent 50 to 74% of all IMF cases. These tumors commonly present with a mass that infiltrates the surrounding tissue in the head and neck areas (e.g. in the ethmoid sinus/maxillary sinus, infratemporal fossa, tongue, hard palate, behind an ear, or temporal bone); less commonly in other sites such as the scapula/axilla area, lower back, or soft tissue/bone in the lower leg; and also less commonly in visceral organs such as the pancreas, spleen, lung, or heart. Solitary IMF tumors often (i.e. 25 to 61% of cases in different studies) regress spontaneously.

Multiple tumors (no viscera involvement)
Multiple tumors (no viscera involvement) typically occur as dozens to hundreds of mostly small tumors located in various areas such as the skin, muscles, and frontal eye socket, These tumors do not involve visceral organs, often take a benign course, and may regress spontaneously.

Multiple tumors (with viscera involvement)
Multiple tumors (with viscera involvement) typically occur as dozens to hundreds of tumors located in the same sites as multiple tumors (no viscera involvement) but also occur in one or more visceral organs such as those in the gastrointestinal tract and upper respiratory tract and/or the heart, liver, cerebellum, rectum, parietal cortex of brain, and lung. This form of IMF, particularly in cases with tumors involving the gastrointestinal tract, heart, and/or lung, has a far higher morbidity and mortality than the other forms with death occurring in infants during the first weeks to 4 months of life in 30–70% of cases Death is typically due to a tumors compression of vital organs or tissues (e.g. blood vessels). However, there are uncommon cases of multiple tumors (with viscera involvement) that were not associated with serious symptoms, were observed without treatment, and over time showed spontaneous regressions of all or almost all of their tumors.

Pathology
Microscopic histopathologic analyses of IMF tumor tissues commonly show repeated patterns of a central zone consisting of spindle-shaped cells lining capillaries and round-to-oval cells arranged around prominent "antler-shaped" vascular spaces all of which are surrounded by a peripheral zone of clustered smooth muscle-like cells. The relative proportions of the two zones can vary within different areas of a tumor and between tumors. Immunohistochemical analyses indicate that the spindle-shaped cells strongly express smooth muscle actin, calponin, and, less commonly, desmin proteins.

Gene abnormalities
Familial IMF
Twenty families with inherited IMF have been shown to have mutations in one of their two PDGFRB genes. The PDGFRB gene is located in band 32 on the long (or "q") arm of chromosome 5. Of the 20 families with PDGFRB gene mutations, 15 carried a p.Arg561Cys mutation. This mutation substitutes the amino acid Arg, i.e. arginine, for the amino acid cystine at the 561st amino acid position as numbered starting at the N-terminus of the genes product protein, the PDGFβ receptor. Four of the remaining families carried either a p.Pro560Leu (Pro=proline, Leu=leucine); p.Arg561Ser (Ser=serine); p. Lys567Glu (Lys=lysine, Glu=glutamate); or p.Pro660Thr (Thr=threonine) mutation in this protein. The NOTCH3 gene (located in band 13.12 on the short (or "p") arm of chromosome 19) mutation in the carrier family was p. Leu1519Pro. The p.Arg561Cys, p.Pro560Leu, p.Arg561Ser, and p. Lys567Glu mutations are regarded as contributing to the development and/or progression of IMF while the p.Pro660Thr PDGFRB gene mutation and the p. Leu1519Pro NOTCH3 p. Leu1519Pro gene mutation require further study to determine more clearly their clinical significances.

Non-familial IMF
Somatic PDGFRB gene mutations have been found in 29% of individuals with solitary IMF tumors and 68% of individuals with multiple tumors (with viscera involvement) plus multiple tumors (no visceral involvement) IMF. In about 50% of these cases, these somatic mutations were the same as those found in familial IMF with the remaining cases having mutations in other sites of the gene. These other somatic mutation sites included 2 cases of p.Asp850Val (Asp=aspartate, Val=valine), 2 case of p.Asn666Lys (Asn=asparagine, Lys=lysine), and concurrent double mutations p.Arg561Cyt plus Asp666Lys in one case and p.Trp566Arg (Trp=tryptophan) plus AspN666Lys in another case. Three cases had more complex mutations involving multiple gene sites with two of them having the p.Asn666Lys mutation gene in combination with other mutations.

PDGFRB gene
The PDGFRB gene product, the PDGFβ receptor, is normally highly expressed in fibroblasts and other cells of mesenchymal origin including vascular smooth muscle cells. When activated, the PDGFβ receptors tyrosine kinase stimulates cell signaling proteins such as phosphatidylinositol-3 kinase, STAT proteins, phospholipase Cγ, and GRB2 which in turn promote their parent cells to grow, proliferate, and survive for abnormally prolonged times. The PDGFβ receptor gene is a proto-oncogene, i.e. a normal gene that when mutated could form a cancer-causing oncoprotein. Studies show that the PDGFRB mutant proteins in IMF are constitutively overactive and that the tyrosine kinase inhibitor imatinib blocks the activity of the p.Arg561Cys and p.Asn666Lys mutants as well as the p.Arg561Cyt plus Asp666Lys and p.Trp566Arg plus AspN666Lys double mutants but not the p.Asp850Val mutant. Two other tyrosine kinase inhibitors, dasatinib and ponatinib, do inhibit the p.Asp850Val mutants tyrosine kinase activity. Limited initial studies suggest that these inhibitors are useful in treating severe cases of IMF.

Diagnosis
Based on their clinical presentation and gross appearance IMF tumors can be confused with a wide range of benign and malignant papular, nodular, and tumorous lesions particular in cases which involve multiple tumors. However, the presence of two zone histopathology, family history of disease, and presence of the above cited PDGFRB gene mutations are almost always definitive indicators of IMF. IMF and the classic form of mesoblastic nephroma have been suggested to be the same disease because of their very similar histopathology. However, mesoblastic nephroma tumor cells, unlike IMF tumor cells, express cyclin D1 and Beta-catenin proteins and therefore likely have a very different cellular origin than IMF tumors. Infantile digital fibromatosis, a tumor that develops primarily in the fingers and toes, had been regarded as a type of IMF. However its tumors have a distinctly different clinical presentation and histopathology than IMF. The World Health Organization (2020) redefined infantile digital fibromatosis as a benign tumor in the in the category of benign fibroblastic and myofibroblastic tumors and therefore different than IMF.

Treatment and prognosis
There are no controlled studies to define the optimal treatment(s) for IMF. The following give the currently widely used and recommended treatments along with the result of these treatments for the three categories of the IMF tumors.

Solitary IMF tumors
Solitary IMF tumors typically grow slowly, produce few or no symptoms, and often regress spontaneously within 18 to 24 months of diagnosis. A watchful waiting strategy is commonly used for these tumors. Visceral solitary IMF tumors that cause significant tissue injury, are located in vital areas, and/or are life-threatening have been treated by surgical excision or, if surgery is deemed inappropriate, are treated with drugs and/or radiation therapy as indicated in the following section on multiple tumors (with visceral involvement). Surgical excision has also be used if the diagnosis of the tumor is in doubt. In rare cases, aggressive IMF tumors have recurred after regressing and required further observation and/or treatment. Overall, the prognosis in almost all cases of solitary IMF is good to excellent.

Multiple tumors (no viscera involvement)
Multiple tumors (no viscera involvement) also may regress spontaneously and carry a good to excellent prognosis even when they invade local tissues. However, neonates presenting with multiple IMF tumors should undergo a through examination including medical imaging tests to determine the extent of their disease, particularly with respect to determining if a visceral tumor(s) is present and therefore that the proper diagnosis is multiple tumors (with viscera involvement) </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 Lichen sclerosus and can you explain it in depth? [/INST] Lichen sclerosus (LS) is a chronic, inflammatory skin disease of unknown cause which can affect any body part of any person but has a strong preference for the genitals (penis, vulva) and is also known as balanitis xerotica obliterans (BXO) when it affects the penis. Lichen sclerosus is not contagious. There is a well-documented increase of skin cancer risk in LS, potentially improvable with treatment. LS in adult age women is normally incurable, but improvable with treatment, and often gets progressively worse if not treated properly. Most males with mild or intermediate disease restricted to prepuce or glans can be cured by either medical or surgical treatment.

Signs and symptoms
LS can occur without symptoms. White patches on the LS body area, itching, pain, dyspareunia (in genital LS), easier bruising, cracking, tearing and peeling, and hyperkeratosis are common symptoms in both men and women. In women, the condition most commonly occurs on the vulva and around the anus with ivory-white elevations that may be flat and glistening.In males, the disease may take the form of whitish patches on the foreskin and its narrowing (preputial stenosis), forming an "indurated ring", which can make retraction more difficult or impossible (phimosis). In addition there can be lesions, white patches or reddening on the glans. In contrast to women, anal involvement is less frequent. Meatal stenosis, making it more difficult or even impossible to urinate, may also occur.On the non-genital skin, the disease may manifest as porcelain-white spots with small visible plugs inside the orifices of hair follicles or sweat glands on the surface. Thinning of the skin may also occur.

Psychological effect
Distress due to the discomfort and pain of lichen sclerosus is normal, as are concerns with self-esteem and sex. Counseling can help.According to the National Vulvodynia Association, which also supports women with lichen sclerosus, vulvo-vaginal conditions can cause feelings of isolation, hopelessness, low self-image, and much more. Some women are unable to continue working or have sexual relations and may be limited in other physical activities. Depression, anxiety, and even anger are all normal responses to the ongoing pain LS patients experience.

Pathophysiology
Although it is not clear what causes LS, several theories have been postulated. Lichen sclerosus is not contagious; it cannot be caught from another person.Several risk factors have been proposed, including autoimmune diseases, infections and genetic predisposition. There is evidence that LS can be associated with thyroid disease.

Genetic
Lichen sclerosus may have a genetic component. A high correlation of lichen sclerosus has been reported between twins and between family members.

Autoimmunity
Autoimmunity is a process in which the body fails to recognize itself and therefore attacks its own cells and tissue. Specific antibodies have been found in LS. Furthermore, there seems to be a higher prevalence of other autoimmune diseases such as diabetes mellitus type 1, vitiligo, alopecia areata, and thyroid disease.

Infection
Both bacterial as well as viral pathogens have been implicated in the etiology of LS. A disease that is similar to LS, acrodermatitis chronica atrophicans is caused by the spirochete Borrelia burgdorferi. Viral involvement of HPV and hepatitis C are also suspected.
A link with Lyme disease is shown by the presence of Borrelia burgdorferi in LSA biopsy tissue.

Hormones
Since LS in females is primarily found in women with a low estrogen state (prepubertal and postmenopausal women), hormonal influences were postulated. To date though, very little evidence has been found to support this theory.

Local skin changes
Some findings suggest that LS can be initiated through scarring or radiation, although these findings were sporadic and very uncommon.

Diagnosis
The disease often goes undiagnosed for several years, as it is sometimes not recognized and misdiagnosed as thrush or other problems and not correctly diagnosed until the patient is referred to a specialist when the problem does not clear up.A biopsy of the affected skin can be done to confirm diagnosis. When a biopsy is done, hyperkeratosis, atrophic epidermis, sclerosis of dermis and lymphocyte activity in dermis are histological findings associated with LS. The biopsies are also checked for signs of dysplasia.It has been noted that clinical diagnosis of BXO can be "almost unmistakable," though there are other dermatologic conditions such as lichen planus, localized scleroderma, leukoplakia, vitiligo, and the cutaneous rash of Lyme disease can have a similar appearance.

Treatment
Main treatment
There is no definitive cure for LS. Behavior change is part of treatment. The patient should minimize or preferably stop scratching LS-affected skin. Any scratching, stress or damage to the skin can worsen the disease. Scratching has been theorized to increase cancer risks. Furthermore, the patient should wear comfortable clothes and avoid tight clothing, as it is a major factor in the severity of symptoms in some cases.Topically applied corticosteroids to the LS-affected skin are the first-line treatment for lichen sclerosus in women and men, with strong evidence showing that they are "safe and effective" when appropriately applied, even over long courses of treatment, rarely causing serious adverse effects. They improve or suppress all symptoms for some time, which highly varies across patients, until it is required to use them again. Methylprednisolone aceponate has been used as a safe and effective corticosteroid for mild and moderate cases. For severe cases, it has been theorized that mometasone furoate might be safer and more effective than clobetasol. Recent studies have shown that topical calcineurin inhibitors such as tacrolimus can have an effect similar to corticosteroids, but its effects on cancer risks in LS are not conclusively known. Based on limited evidence, a 2011 Cochrane review concluded that clobetasol propionate, mometasone furoate, and pimecrolimus (calcineurin inhibitor) all are effective therapies in treating genital lichen sclerosus. However, randomized-controlled trials are needed to further identify the optimal potency and regimen of topical corticosteroids and assess the duration of remission and/or the prevention of flares patients experience with these topical therapies.Continuous usage of appropriate doses of topical corticosteroids is required to ensure symptoms stay relieved over the patients life time. If continuously used, corticosteroids have been suggested to minimize the risk of cancer in various studies. In a prospective longitudinal cohort study of 507 women throughout 6 years, cancer occurred for 4.7% of patients who were only "partially compliant" with corticosteroid treatment, while it occurred in 0% of cases where they were "fully compliant". In a second study, of 129 patients, cancer occurred in 11% of patients, none of which were fully compliant with corticosteroid treatment. Both these studies however also said that a corticosteroid as powerful as clobetasol is not necessary in most cases. In a prospective study of 83 patients, throughout 20 years, 8 patients developed cancer. 6 already had cancer at presentation and had not had treatment, while the other 2 were not taking corticosteroids often enough. In all three studies, every single cancer case observed occurred in patients who werent taking corticosteroids as often as the study recommended.Continuous, abundant usage of emollients topically applied to the LS-affected skin is recommended to improve symptoms. They can supplement but not replace corticosteroid therapy. They can be used much more frequently than corticosteroids due to the extreme rarity of serious adverse effects. Appropriate lubrication should be used every time before and during sex in genital LS in order to avoid pain and worsening the disease. Some oils such as olive oil and coconut oil can be used to accomplish both the emollient and sexual lubrication function.In males, it has been reported that circumcision can have positive effects, but does not necessarily prevent further flares of the disease and does not protect against the possibility of cancer. Circumcision does not prevent or cure LS; in fact, "balanitis xerotica obliterans" in men was first reported as a condition affecting a set of circumcised men, by Stühmer in 1928.

Other treatments
Carbon dioxide laser treatment is safe and effective, and it improves symptoms over a long time, but it does not lower cancer risks.
Platelet-rich plasma was reported to be effective in one study, producing large improvements in the patients quality of life, with an average IGA improvement of 2.04 and DLQI improvement of 7.73.

Prognosis
The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.
Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".

Epidemiology
There is a bimodal age distribution in the incidence of LS in women. It occurs in females with an average age of diagnosis of 7.6 years in girls and 60 years old in women. The average age of diagnosis in boys is 9–11 years old.In men, the most common age of incidence is 21–30.

History
In 1875, Weir reported what was possible vulvar or oral LS as "ichthyosis." In 1885, Breisky described kraurosis vulvae. In 1887, Hallopeau described a series of extragenital cases of LS. In 1892, Darier formally described the classic histopathology of LS. In 1900 the concept was formed that scleroderma and LS are closely related, which continues to this day. In 1901, pediatric LS was described. From 1913 to present, the concept that scleroderma is not closely related to LS also was formed. In 1920, Taussig established vulvectomy as the treatment of choice for kraurosis vulvae, a premalignant condition. In 1927, Kyrle defined LS ("white spot disease") as an entity sui generis. In 1928, Stühmer described balanitis xerotica obliterans as a postcircumcision phenomenon. In 1936, retinoids (vitamin A) were used in LS. In 1945, testosterone was used in genital LS. In 1961, the use of corticosteroids started </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 Frontal lobe disorder and can you explain it in depth? [/INST] Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe that occurs due to disease or frontal lobe injury. The frontal lobe of the brain plays a key role in executive functions such as motivation, planning, social behaviour, and speech production. Frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, neurodegenerative diseases, Neurodevelopmental disorders, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical signs and symptoms, use of simple screening tests, and specialist neurological testing.

Signs and symptoms
The signs and symptoms of frontal lobe disorder can be indicated by dysexecutive syndrome which consists of a number of symptoms which tend to occur together. Broadly speaking, these symptoms fall into three main categories; cognitive (movement and speech), emotional or behavioral. Although many of these symptoms regularly co-occur, it is common to encounter patients who have several, but not all of these symptoms. This is one reason why some researchers are beginning to argue that dysexecutive syndrome is not the best term to describe these various symptoms. The fact that many of the dysexecutive syndrome symptoms can occur alone has led some researchers to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research on frontal cortex areas suggests that executive functions may be more discrete than was previously thought.
Signs/symptoms can be divided as follows:

Causes
The causes of frontal lobe disorders can be closed head injury. An example of this can be from an accident, which can cause damage to the orbitofrontal cortex area of the brain.Cerebrovascular disease may cause a stroke in the frontal lobe. Tumours such as meningiomas may present with a frontal lobe syndrome. Frontal lobe impairment is also a feature of Alzheimers disease, and frontotemporal dementia.

Pathogenesis
The pathogenesis of frontal lobe disorders entails various pathologies, some are as follows:

Anatomy and functions
The frontal lobe contains the precentral gyrus and prefrontal cortex and, by some conventions, the orbitofrontal cortex. These three areas are represented in both the left and the right cerebral hemispheres. The precentral gyrus or primary motor cortex is concerned with the planning, initiation and control of fine motor movements dorsolateral to each hemisphere. The dorsolateral part of the frontal lobe is concerned with planning, strategy formation, and other executive functions. The prefrontal cortex in the left hemisphere is involved with verbal memory while the prefrontal cortex in the right hemisphere is involved in spatial memory. The left frontal operculum region of the prefrontal cortex, or Brocas area, is responsible for expressive language, i.e. language production. The orbitofrontal cortex is concerned with response inhibition, impulse control, and social behaviour.

Diagnosis
The diagnosis of frontal lobe disorder can be divided into the following three categories:

Clinical historyFrontal lobe disorders may be recognized through a sudden and dramatic change in a persons personality, for example with loss of social awareness, disinhibition, emotional instability, irritability or impulsiveness. Alternatively, the disorder may become apparent because of mood changes such as depression, anxiety or apathy.
ExaminationOn mental state examination a person with frontal lobe damage may show speech problems, with reduced verbal fluency. Typically the person is lacking in insight and judgment, but does not have marked cognitive abnormalities or memory impairment (as measured for example by the mini-mental state examination). With more severe impairment there may be echolalia or mutism. Neurological examination may show primitive reflexes (also known as frontal release signs) such as the grasp reflex. Akinesia (lack of spontaneous movement) will be present in more severe and advanced cases.
Further investigationA range of neuropsychological tests are available for clarifying the nature and extent of frontal lobe dysfunction. For example, concept formation and ability to shift mental sets can be measured with the Wisconsin Card Sorting Test, planning can be assessed with the Mazes subtest of the WISC. Frontotemporal dementia shows up as atrophy of the frontal cortex on MRI. Frontal impairment due to head injuries, tumours or cerebrovascular disease will also appear on brain imaging.

Treatment
In terms of treatment for frontal lobe disorder, there is none, general supportive care is given, also some level of supervision could be needed. The prognosis will depend on the cause of the disorder, of course. A possible complication is that individuals with severe injuries may be disabled, such that, a caregiver may be unrecognizable to the person. Another aspect of treatment of frontal lobe disorder is speech therapy. This type of therapy might help individuals with symptoms that are associated with aphasia and dysarthria.

History
Phineas Gage, who sustained a severe frontal lobe injury in 1848, has been called a case of dysexecutive syndrome. Gages psychological changes are almost always exaggerated – of the symptoms listed, the only ones Gage can be said to have exhibited are "anger and frustration", slight memory impairment, and "difficulty in planning".

See also
Attention
Cognitive neuropsychology
Dysexecutive syndrome
Executive functions
Frontal lobe
Gourmand syndrome
Klüver–Bucy syndrome
Phineas Gage
Working memory

References
Further reading
Paradiso, S (1999). "Frontal lobe syndrome reassessed: comparison of patients with lateral or medial frontal brain damage". Journal of Neurology, Neurosurgery, and Psychiatry. 67 (5): 664–7. doi:10.1136/jnnp.67.5.664 </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 Android fat distribution and can you explain it in depth? [/INST] Android fat distribution describes the distribution of human adipose tissue mainly around the trunk and upper body, in areas such as the abdomen, chest, shoulder and nape of the neck. This pattern may lead to an "apple”-shaped body or central obesity, and is more common in males than in females. Thus, the android fat distribution of men is about 48.6%, which is 10.3% higher than that of premenopausal women. In other cases, an ovoid shape forms, which does not differentiate between men and women. Generally, during early adulthood, females tend to have a more peripheral fat distribution such that their fat is evenly distributed over their body. However, it has been found that as females age, bear children and approach menopause, this distribution shifts towards the android pattern of fat distribution, resulting in a 42.1% increase in android body fat distribution in postmenopausal women. This could potentially provide evolutionary advantages such as lowering a womans center of gravity making her more stable when carrying offspring.Android fat distribution is contrasted with gynoid fat distribution, whereby fat around the hips, thighs, and bottom results in a “pear”-shaped body.
Jean Vague, a physician from Marseilles, France, was one of the first individuals to bring to attention the increased risk of developing certain diseases (e.g., diabetes and gout) in individuals with an android distribution compared to a gynoid distribution.  There are other health consequences beyond these, including psychological consequences.

Biology
Android fat is readily mobilized by deficits in energy balance. It is stored in different depots to gynoid fat.Android fat cells are mostly visceral - they are large, deposited deep under the skin and are highly metabolically active. The hormones they secrete have direct access to the liver. The presence of fat in the trunk and upper body in males is facilitated by testosterone. Testosterone circulation causes fat cells to deposit around the abdominal and gluteofemoral region, whereas in women oestrogen circulation leads to fat deposits around areas such as thighs, breasts and buttocks. Therefore, measuring a persons oestrogen to testosterone ratio can reveal their predicted gynoid to android fat distribution. Android fat develops as a back-up source of energy when the male body is experiencing an imbalance, whereas gynoid fat develops after puberty, in order to better prepare the body for supporting a potential infant.
50% of the variance in abdominal fat mass observed in humans is due to genetic factors The cellular characteristics of adipose tissue in android and [gynoid] obese women are different. Android type have larger fat (hypertrophy) cells whereas gynoid type have increased number of fat cells (hyperplasia). This allows for hypertrophic obesity and hyperplastic obesity. Two different receptors, alpha and beta fat cell receptors, vary in their ability to facilitate or inhibit fat mobilization. Alpha-receptors are predominately in the lower body thus more abundant in gynoid patterns and Beta-receptors are predominantly in the upper body and so more abundant in android patterns.

Causes
Hormonal disorders or fluctuations can lead to the formation of a lot of visceral fat and a protruding abdomen. Medications such as protease inhibitors that are used to treat HIV and AIDS also form visceral fat. Android fat can be controlled with proper diet and exercise. A poor diet with lack of exercise is likely to increase android fat level.

Health consequences
Differences in body fat distribution are found to be associated with high blood pressure, high triglyceride, lower high-density lipoprotein (HDL) cholesterol levels and high fasting and post-oral glucose insulin levels The android, or male pattern, fat distribution has been associated with a higher incidence of coronary artery disease, in addition to an increase in resistance to insulin in both obese children and adolescents. Studies have also related central abdominal obesity (indicated via increased waist–hip ratio) with increases in peripheral fasting insulin levels.Android fat is also associated with a change in pressor response in circulation. Specifically, in response to stress in a subject with central obesity the cardiac output dependent pressor response is shifted toward a generalised rise in peripheral resistance with an associated decrease in cardiac output.There are differences in android and gynoid fat distribution among individuals, which relates to various health issues among individuals. Android body fat distribution is related to high cardiovascular disease and mortality rate. People with android obesity have higher hematocrit and red blood cell count and higher blood viscosity than people with gynoid obesity. Blood pressure is also higher in those with android obesity which leads to cardiovascular disease.Women who are infertile and have polycystic ovary syndrome show high amounts of android fat tissue. In contrast, patients with anorexia nervosa have increased gynoid fat percentage  Women normally have small amounts of androgen, however when the amount is too high they develop male psychological characteristics and male physical characteristics of muscle mass, structure and function and an android adipose tissue distribution. Women who have high amounts of androgen and thus an increase tendency for android fat distribution are in the lowest quintiles of levels of sex-hormone-binding globulin and more are at high risks of ill health associated with android fat High levels of android fat have been associated with obesity  and diseases caused by insulin insensitivity, such as diabetes. Insulin responsiveness is dependent on adipose cell size. The larger the adipose cell size the less sensitive the insulin. Diabetes is more likely to occur in obese women with android fat distribution and hypertrophic fat cells. It is not just general obesity that is a consequence of android fat distribution but also other health consequences. There are connections between high android fat distributions and the severity of diseases such as acute pancreatitis - where the higher the levels of android fat are, the more severe the pancreatitis can be.
An increase in android fat distribution is positively correlated with foot pain and disability associated with foot pain. Foot pain is reported to be the second most common musculoskeletal symptom in children who are obese. Even adults who are overweight and obese report foot pain to be a common problem.

Psychological consequences
Body fat can impact on an individual mentally, for example high levels of android fat have been linked to poor mental wellbeing, including anxiety, depression and body confidence issues. On the reverse, psychological aspects can impact on body fat distribution too, for example women classed as being more extraverted tend to have less android body fat.

Waist–hip ratio
See gynoid fat distribution
Central obesity is measured as increase by waist circumference or waist–hip ratio. Increase in waist circumference > 102 cm (40 in.) in males and > 88 cm (35 in.) in females. However increase in abdominal circumference may be due to increasing in subcutaneous or visceral fat, and it is the visceral fat which increases the risk of coronary diseases. The visceral fat can be estimated with the help of MRI and CT scan.
In females, measures of Waist to Hip ratio have been observed as an evolutionary sign of attractiveness and reproductive success. A females waist being smaller than her hips by a ratio of 0.7 is considered most attractive as it indicated readiness to give birth to offspring, and overall health to ensure survival of offspring. Waist to hip ratio is determined by an individuals proportions of android fat and gynoid fat. A small waist to hip ratio indicates less android fat, high waist to hip ratios indicate high levels of android fat.As  WHR is associated with a womans pregnancy rate, it has been found that a high waist-to-hip ratio can impair pregnancy, thus a health consequence of high android fat levels is its interference with the success of pregnancy and in-vitro fertilisation. Body fat distribution is also related to the sex ratio of offspring. Women with large waists (a high WHR)  tend to have an android fat distribution caused by a specific hormone profile, that is, having higher levels of androgens. This leads to such women having more sons.

Liposuction
Liposuction is a medical procedure used to remove fat from the body, common areas being around the abdomen, thighs and buttocks. Liposuction does not improve an individuals health or insulin sensitivity  and is therefore considered a cosmetic surgery.  liposuction improves quality of life in everyday activities and issues regarding ones psychological state or social life after liposuction are less serious. It has been found that abdominal exercise alone cannot reduce android fat around the trunk and abdomen  so liposuction is often a short term solution.
As liposuction can lower a persons waist–hip ratio by removing fat from locations where android fat accumulates, it can give the appearance of a more attractive body shape, and imitate an indication of reproductive health. Another method of reducing android fat is Laparoscopic Adjustable Gastric Banding which has been found to significantly reduce overall android fat percentages in obese individuals.

Individual differences
Cultural differences
Cultural differences in the distribution of android fat have been observed in several studies </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 Myxoid liposarcoma 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 Muscular dystrophy and can you explain it in depth? [/INST] Muscular dystrophies (MD) are a genetically and clinically heterogeneous group of rare neuromuscular diseases that cause progressive weakness and breakdown of skeletal muscles over time. The disorders differ as to which muscles are primarily affected, the degree of weakness, how fast they worsen, and when symptoms begin. Some types are also associated with problems in other organs.Over 30 different disorders are classified as muscular dystrophies. Of those, Duchenne muscular dystrophy (DMD) accounts for approximately 50% of cases and affects males beginning around the age of four. Other relatively common muscular dystrophies include Becker muscular dystrophy, facioscapulohumeral muscular dystrophy, and myotonic dystrophy, whereas limb–girdle muscular dystrophy and congenital muscular dystrophy are themselves groups of several – usually ultrarare – genetic disorders.
Muscular dystrophies are caused by mutations in genes, usually those involved in making muscle proteins. These mutations are either inherited from parents or may occur spontaneously during early development. Muscular dystrophies may be X-linked recessive, autosomal recessive, or autosomal dominant. Diagnosis often involves blood tests and genetic testing.There is no cure for any disorder from the muscular dystrophy group. Several drugs designed to address the root cause are under development, including gene therapy (Microdystrophin), and antisense drugs (Ataluren, Eteplirsen etc.).  Other medications used include corticosteroids (Deflazacort), calcium channel blockers (Diltiazem) to slow skeletal and cardiac muscle degeneration, anticonvulsants to control seizures and some muscle activity, and immunosuppressants (Vamorolone) to delay damage to dying muscle cells. Physical therapy, braces, and corrective surgery may help with some symptoms while assisted ventilation may be required in those with weakness of breathing muscles.Outcomes depend on the specific type of disorder. Many affected people will eventually become unable to walk and Duchenne muscular dystrophy in particular is associated with shortened life expectancy.
Muscular dystrophy was first described in the 1830s by Charles Bell. The word "dystrophy" comes from the Greek dys, meaning "no, un-" and troph- meaning "nourish".

Signs and symptoms
The signs and symptoms consistent with muscular dystrophy are:

Causes
The majority of muscular dystrophies are inherited; the different muscular dystrophies follow various inheritance patterns (X-linked, autosomal recessive or autosomal dominant). In a small percentage of patients, the disorder may have been caused by a de novo (spontaneous) mutation.

Diagnosis
The diagnosis of muscular dystrophy is based on the results of muscle biopsy, increased creatine phosphokinase (CpK3), electromyography, and genetic testing. A physical examination and the patients medical history will help the doctor determine the type of muscular dystrophy. Specific muscle groups are affected by different types of muscular dystrophy.

Classification
Management
Currently, there is no cure for muscular dystrophy. In terms of management, physical therapy, occupational therapy, orthotic intervention (e.g., ankle-foot orthosis), speech therapy, and respiratory therapy may be helpful. Low intensity corticosteroids such as prednisone, and deflazacort may help to maintain muscle tone. Orthoses (orthopedic appliances used for support) and corrective orthopedic surgery may be needed to improve the quality of life in some cases. The cardiac problems that occur with Emery–Dreifuss muscular dystrophy (EDMD) and myotonic muscular dystrophy may require a pacemaker. The myotonia (delayed relaxation of a muscle after a strong contraction) occurring in myotonic muscular dystrophy may be treated with medications such as quinine.Occupational therapy assists the individual with MD to engage in activities of daily living (such as self-feeding and self-care activities) and leisure activities at the most independent level possible. This may be achieved with use of adaptive equipment or the use of energy-conservation techniques.  Occupational therapy may implement changes to a persons environment, both at home or work, to increase the individuals function and accessibility; furthermore, it addresses psychosocial changes and cognitive decline which may accompany MD, and provides support and education about the disease to the family and individual.

Prognosis
Prognosis depends on the individual form of muscular dystrophy. Some dystrophies cause progressive weakness and loss of muscle function, which may result in severe physical disability and a life-threatening deterioration of respiratory muscles or heart. Other dystrophies do not affect life expectancy and only cause relatively mild impairment.

History
In the 1860s, descriptions of boys who grew progressively weaker, lost the ability to walk, and died at an early age became more prominent in medical journals. In the following decade, French neurologist Guillaume Duchenne gave a comprehensive account of the most common and severe form of the disease, which now carries his name – Duchenne MD.

Society and culture
In 1966 in the US and Canada, Jerry Lewis and the Muscular Dystrophy Association (MDA) began the annual Labor Day telecast The Jerry Lewis Telethon, significant in raising awareness of muscular dystrophy in North America. Disability rights advocates, however, have criticized the telethon for portraying those living with the disease as deserving pity rather than respect.On December 18, 2001, the MD CARE Act was signed into law in the US; it amends the Public Health Service Act to provide research for the various muscular dystrophies. This law also established the Muscular Dystrophy Coordinating Committee to help focus research efforts through a coherent research strategy.

See also
References
Further reading
De Los Angeles Beytía, Maria; Vry, Julia; Kirschner, Janbernd (2012). "Drug treatment of Duchenne musculardystrophy: available evidence and perspectives" </s>