<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 Macrocephaly and can you explain it in depth? [/INST] Macrocephaly is a condition in which circumference of the human head is abnormally large. It may be pathological or harmless, and can be a familial genetic characteristic. People diagnosed with macrocephaly will receive further medical tests to determine whether the syndrome is accompanied by particular disorders. Those with benign or familial macrocephaly are considered to have megalencephaly.

Causes
Many people with abnormally large heads or large skulls are healthy, but macrocephaly may be pathological. Pathologic macrocephaly may be due to megalencephaly (enlarged brain), hydrocephalus (abnormally increased cerebrospinal fluid), cranial hyperostosis (bone overgrowth), and other conditions. Pathologic macrocephaly is called "syndromic", when it is associated with any other noteworthy condition, and "nonsyndromic" otherwise. Pathologic macrocephaly may be caused by congenital anatomic abnormalities, genetic conditions, or by environmental events.Many genetic conditions are associated with macrocephaly, including familial macrocephaly related to the holgate gene, autism, PTEN mutations such as Cowden disease, neurofibromatosis type 1, and tuberous sclerosis; overgrowth syndromes such as Sotos syndrome (cerebral gigantism), Weaver syndrome, Simpson–Golabi–Behmel syndrome (bulldog syndrome), and macrocephaly-capillary malformation (M-CMTC) syndrome; neurocardiofacial-cutaneous syndromes such as Noonan syndrome, Costello syndrome, Gorlin syndrome, (also known as Basal Cell Nevus Syndrome) and cardiofaciocutaneous syndrome; Fragile X syndrome; leukodystrophies (brain white matter degeneration) such as Alexander disease, Canavan disease, and megalencephalic leukoencephalopathy with subcortical cysts; and glutaric aciduria type 1 and D-2-hydroxyglutaric aciduria.At one end of the genetic spectrum, duplications of chromosomes have been found to be related to autism and macrocephaly; at the other end, deletions of chromosomes have been found to be related to schizophrenia and microcephaly.Environmental events associated with macrocephaly include infection, neonatal intraventricular hemorrhage (bleeding within the infant brain), subdural hematoma (bleeding beneath the outer lining of the brain), subdural effusion (collection of fluid beneath the outer lining of the brain), and arachnoid cysts (cysts on the brain surface).In research, cranial height or brain imaging may be used to determine intracranial volume more accurately.
Below is a list of causes of macrocephaly from Swaimans Pediatric Neurology: Principles and Practice noted in The Little Black Book of Neurology:

Hydrocephalus
Noncommunicating
Arnold–Chiari malformation
Aqueductal stenosis
X-linked hydrocephalus with stenosis of the aqueduct of Sylvius (HSAS) syndrome (L1CAM)
Dandy–Walker malformation
Galenic vein aneurysm or malformation
Neoplasms, supratentorial, and infratentorial
Arachnoid cyst, infratentorial
Holoprosencephaly with dorsal interhemispheric sac

Communicating
External or extraventricular obstructive hydrocephalus (dilated subarachnoid space)

Arachnoid cyst, supratentorial
Meningeal fibrosis/obstruction
Postinflammatory
Posthemorrhagic
Neoplastic infiltration

Vascular
Arteriovenous malformation
Intracranial hemorrhage
Dural sinus thrombosis

Choroid plexus papilloma
Neurocutaneous syndromes
Incontinentia pigmenti

Destructive lesions
Hydranencephaly
Porencephaly

Familial, autosomal-dominant, autosomal-recessive, X-linked
Subdural fluid
Hematoma
Hygroma
Empyema

Brain edema (toxic-metabolic)
Intoxication
Lead
Vitamin A
Tetracycline
Endocrine (hypoparathyroidism, hypoadrenocorticism)
Galactosemia
Idiopathic (pseudotumorcerebri)

Thick skull or scalp (hyperostosis)
Familial variation
Anemia
Osteoporosis, severe precocious autosomal-recessive osteoporosis (CLCN7, TCIRG1)
Pycnodysostosis (CTSK)
Craniometaphyseal dysplasia (ANKH)
Craniodiaphyseal dysplasia
Pyle dysplasia
Sclerosteosis (SOST)
Juvenile Paget disease
Idiopathic hyperphosphatasia
Familial osteoectasia
Osteogenesis imperfecta
Rickets
Cleidocranial dysostosis
Hyperostosis corticalis generalisata (van Buchem disease)
Proteus syndrome

Megalencephaly and hemimegalencephaly
Diagnosis
Macrocephaly is customarily diagnosed if head circumference is greater than two standard deviations (SDs) above the mean </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 Visual release hallucinations and can you explain it in depth? [/INST] Visual release hallucinations, also known as Charles Bonnet syndrome or CBS, are a type of psychophysical visual disturbance in which a person with partial or severe blindness experiences visual hallucinations.
First described by Charles Bonnet in 1760, the term Charles Bonnet syndrome was first introduced into English-speaking psychiatry in 1982.  A related type of hallucination that also occurs with lack of visual input is the closed-eye hallucination.

Signs and symptoms
People with significant vision loss may have vivid recurrent visual hallucinations (fictive visual percepts). One characteristic of these hallucinations is that they usually are "lilliputian" (hallucinations in which the characters or objects are smaller than normal). Depending on the content, visual hallucinations can be classified as either simple or complex. Simple visual hallucinations are commonly characterized by shapes, photopsias, and grid-like patterns. Complex visual hallucinations consist of highly detailed representations of people and objects. The most common hallucination is of faces or cartoons. Sufferers understand that the hallucinations are not real, and the hallucinations are only visual, that is, they do not occur in any other senses (such as hearing, smell or taste). Visual hallucinations generally appear when the eyes are open, fading once the visual gaze shifts. It is widely claimed that sensory deprivation is instrumental in the progression of CBS. During episodes of inactivity, hallucinations are more likely to occur. The majority of those suffering from CBS describe the duration of hallucinations to continue for up to a few minutes, multiple times a day or week.Even though people of all ages may be afflicted by Charles Bonnet syndrome, those within the age range of 70 to 80 are primarily affected. Among older adults (> 65 years) with significant vision loss, the prevalence of Charles Bonnet syndrome has been reported to be between 10% and 40%; a 2008 Australian study found the prevalence to be 17.5%. Two Asian studies, however, report a much lower prevalence. The high incidence of underreporting this disorder is the greatest hindrance to determining the exact prevalence. Underreporting is thought to be a result of sufferers being afraid to discuss the symptoms out of fear that they will be labeled of unsound mind.

Pathophysiology
There is no general consensus on the definition of CBS. Predominant factors correlated with CBS are a decrease of visual acuity, visual field loss, and elderly age. While characteristic features of visual hallucinations are not specifically linked to the anatomical site of the ocular injury, they usually match to the location of visual loss. The most commonly accepted theory for Charles Bonnet Syndrome proposes that extreme visual impairment promotes sensory deafferentation, leading to disinhibition, thus resulting in sudden neural firings of the visual cortical regions. A few studies record that visual hallucinations are likely to be concentrated in the blind regions. Functional magnetic resonance imaging (fMRI) of Charles Bonnet Syndrome patients displays a relationship between visual hallucinations and activity in the ventral occipital lobe. A connection between age-related macular degeneration (AMD) and colored visual hallucinations has been presented. Color vision signals travel through the parvocellular layers of the lateral geniculate nucleus (LGN), later transmitting down the color regions of the ventral visual pathway. Due to cone photoreceptor damage located in the macula, there is a significant reduction of visual input to the visual association cortex, stirring endogenous activation in the color areas and thus leading to colored hallucinations. Patients with CBS alongside macular degeneration exhibit hyperactivity in the color areas of the visual association cortex (as shown in fMRIs). Those who have significant ocular disease yet maintain visual acuity may still be susceptible to CBS.The Deep Boltzmann Machine (DBM) is a way of utilizing an undirected probabilistic process in a neural framework. Researchers argue that the DBM has the ability to model features of cortical learning, perception, and the visual cortex (the locus of visual hallucinations). Compelling evidence details the role homeostatic operations in the cortex play in regards to stabilizing neuronal activity. By using the DBM, researchers show that when sensory input is absent, neuron excitability is influenced, thus potentially triggering complex hallucinations.

A short-term change in the levels of feedforward and feedback flows of information may intensely affect the presence of hallucinations. In periods of drowsiness, CBS related hallucinations are more prone to arise. Disrupting cortical homeostatic processes after vision has been lost may prevent or setback the emergence of hallucinations. At varying stages of the cortical grading, acetylcholine (ACh) may impact the balance of thalamic and intracortical inputs as well as the balance in between bottom-up and top-down. Particularly in CBS, a shortage of acetylcholine at cortical locations should correspond to the onset of hallucinations.The syndrome can also develop after bilateral optic nerve damage due to methyl alcohol poisoning.

Diagnosis
A variety of disciplines including optometry, ophthalmology, geriatric medicine, psychiatry, and neurology play a part in securing the diagnosis of CBS. Since CBS is not commonly recognized by all clinicians, it oftentimes goes misdiagnosed and identified as psychosis, delirium, or dementia. As a result of this, it is estimated that almost 60% of CBS patients hesitate to notify their physicians. By focusing on the specific type of visual hallucination, one may find an accurate diagnosis. If a patient presents symptoms indicative of Charles Bonnet syndrome, basic laboratory examinations like metabolic panel and blood count tests, as well as neuroimaging, may aid in an accurate diagnosis.

Prognosis
There is no treatment of proven effectiveness for CBS. For those experiencing CBS, knowing that they are suffering from this syndrome and not a mental illness seems to be the most comforting treatment so far, as it improves their ability to cope with the hallucinations. As time passes from the initial onset of visual hallucinations, studies show that around 60% of those living with CBS feel that visual hallucinations have no effect on their lives, 33% of people feel that the hallucinations are disruptive to their lives, and 7% of people even find pleasure in the hallucinations.A large proportion of those suffering from CBS develop the visual hallucinations as vision begins to deteriorate and stop hallucinating once vision is entirely gone. Complex hallucinations may progress over time if the primary loss of vision is due to damage of the early cortical areas. If activation of the early cortical areas is suppressed when CBS symptoms have already been exhibited, hallucinations may temporarily terminate. Also, interrupting vision for a short time by closing the eyes or blinking may be helpful.It is possible for a stressful life event to alter the disposition of hallucinatory experiences as well as the emotional experiences (from unconcerning to concerning) in CBS. As expressed in some patients, an interplay between CBS and an acute or post-traumatic stress disorder may exist. The role that trauma plays in CBS may affect how and when a hallucinatory episode is triggered.

History
The disease was first noted by the Swiss naturalist Charles Bonnet, who described the condition in 1760. He documented it in his 90-year-old grandfather who was nearly blind from cataracts in both eyes. After Bonnet’s grandfather received bilateral cataract surgery, his vision evolved from slightly better to complete deterioration over time. It was around this period that his visual hallucinations started. His hallucinations consisted of perceptions of men, women, birds, carriages, buildings, tapestries, physically impossible circumstances and scaffolding patterns. Even though his health was in good shape and he had an absence of any psychiatric disorders, the source of the hallucinations remained unknown. At forty years old, Charles Bonnet himself suffered from an unrevealed cause of severe vision loss and experienced the hallucinations.In 1936, Jean Lhermitte and Julian de Ajuriaguerra, concluded that visual hallucinations consist of thalamic lesions as well as ocular pathology.In 1967, French-Swiss neurologist, Georges de Morsier, coined the term Charles Bonnet Syndrome in Bonnets honor. De Morsier’s description of CBS implies a concentrated neurodegeneration, usually occurring in the elderly with typical cognition. In psychiatric literature, the most commonly accepted interpretation of CBS is that of Gold and Rabins’ </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 Epiploic appendagitis and can you explain it in depth? [/INST] Epiploic appendagitis (EA) is an uncommon, benign, self-limiting inflammatory process of the epiploic appendices. Other, older terms for the process include appendicitis epiploica and appendagitis, but these terms are used less now in order to avoid confusion with acute appendicitis.
Epiploic appendices are small, fat-filled sacs or finger-like projections along the surface of the upper and lower colon and rectum. They may become acutely inflamed as a result of torsion (twisting) or venous thrombosis. The inflammation causes pain, often described as sharp or stabbing, located on the left, right, or central regions of the abdomen. There is sometimes nausea and vomiting. The symptoms may mimic those of acute appendicitis, diverticulitis, or cholecystitis. The pain is characteristically intense during/after defecation or micturition (espec. in the sigmoid type) due to the effect of traction on the pedicle of the lesion caused by straining and emptying of the bowel and bladder.  Initial lab studies are usually normal. EA is usually diagnosed incidentally on CT scan which is performed to exclude more serious conditions.
Although it is self-limiting, epiploic appendagitis can cause severe pain and discomfort. It is usually thought to be best treated with an anti-inflammatory and a moderate to severe pain medication (depending on the case) as needed. Surgery is not recommended in nearly all cases.  Sand and colleagues, however, recommend laparoscopic surgery to excise the inflamed appendage in most cases in order to prevent recurrence.

Signs and symptoms
The condition commonly occurs in patients in their 40s and 50s predominantly in men. Epiploic appendagitis is normally misdiagnosed in most patients. Epiploic appendagitis presents with an acute onset of pain, commonly in the left lower quadrant the symptoms often lead to a misdiagnosis for diverticulitis. Diverticulitis manifests with evenly distributed lower abdominal pain accompanied with nausea, fever, and leukocytosis. Patients with acute epiploic appendagitis do not normally report a change in bowel habits, while a small number may have constipation or diarrhea.

Peritoneal loose body
It is rare however possible for epiploic appendagitis to result in a peritoneal loose body. Peritoneal loose body is a free floating mass of dead fibrous tissue surrounded by several layers of calcification (deposit of calcium salts). The loose body is the result of torsed, infarcted or detached epiploic appendages that eventually become fibrotic (inflammation and scarring) masses. If the loose body becomes large enough it can cause urinary retention (inability to empty bladder) or bowel obstructions.

Background
Epiploic appendages are also called appendices epiploicae. The appendages themselves are 50–100 appendages that are oriented in two rows anterior and posterior. The appendages are parallel to the superficial section of the taenia coli. Furthermore, the appendages are between 0.5 and 5 cm long, each appendage is attached with one or two arterioles and a venule within vascular stalks attached to the colon. Torsion (twisting or wrenching motion) of the appendages can cause ischemia which can cause painful symptoms that mimic other conditions such as diverticulitis, and appendicitis; however, it is rare. The pain associated with the inflamed appendages is located in the left and sometimes in the right lower abdominal quadrant. Diagnosis of epiploic appendagitis can be challenging due to its infrequency.

Diagnosis
Epiploic appendagitis is more common in patients older than 40 years of age; however, it can occur at any age. "The reported ages range from 12 to 82 years. Men are slightly more affected than woman."  Patients with epiploic appendicitis describe having a localized, strong, non-migratory sharp pain after eating. Patients generally have tender abdomens as a symptom. Symptoms do not include fever, vomiting, or leukocytosis. The pain is typically located in the right or left lower abdominal quadrant. When there is pain in the right lower quadrant, it can mimic appendicitis; however, it more commonly mimics diverticulitis, with pain present on the left side.

Differential diagnosis
There are several conditions that mimic the symptoms of epiploic appendicitis.
Omental infarction: Omental infarction is uncommon reason for acute abdomen. It is similar to acute appendicitis. The pain is of a few days duration centering in the right lower or upper quadrant. Imaging is required to obtain an accurate diagnosis due to the common misdiagnosis of omental infarction as appendicitis or cholecystitis. Omental infarction occurs commonly in pediatric patients approximately 15 percent of cases. The most frequent cause of non- torsion related omental infarction is due to trauma as well as thrombosis or the omental veins. The predisposition for omental infarction includes obesity, strenuous activity, congestive heart failure, digitalis administration, recent abdominal surgery and trauma. "The typical CT findings are a solitary large non-enhancing omental mass with heterogeneous attenuation, which is most often located in the right lower quadrant, deep to the rectus abdominis muscle and either anterior to the transverse colon or anteromedial to the ascending colon". Omental Infarction can be difficult to differentiate from diverticulitis however omental infarction is not normally attributed with bowel wall thickening. It is rare that the colonic wall will be thickened due to spread of the inflammation from the omentum (a fold of peritoneum connecting or supporting abdominal structures) to the tenia omentalis of the colon.Diverticulitis: Diverticulitis normally happens in older patients than in epiploic appendagitis. The two inflammatory conditions are quite indistinguishable based on physical manifestations. Patients with diverticulitis will present with nausea, vomiting, fever, elevated leukocyte count rebound tenderness, and will have more extensive lower abdominal pain than patients with epiploic appendagitis. Additionally inflammation from diverticulitis may spread to the epiploic appendages making it difficult to diagnose, for inflammation of the appendices epiploicae may be resultant to other inflammatory conditions in the colonic wall and surrounding mesocolon.

Radiologic evaluation
Ultrasound and CT scans are the normal means of positive diagnosis of Epiploic Appendagitis </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 Psoriatic arthritis and can you explain it in depth? [/INST] Psoriatic arthritis is a long-term inflammatory arthritis that occurs in people affected by the autoimmune disease psoriasis. The classic feature of psoriatic arthritis is swelling of entire fingers and toes with a sausage-like appearance. This often happens in association with changes to the nails such as small depressions in the nail (pitting), thickening of the nails, and detachment of the nail from the nailbed. Skin changes consistent with psoriasis (e.g., red, scaly, and itchy plaques) frequently occur before the onset of psoriatic arthritis but psoriatic arthritis can precede the rash in 15% of affected individuals.   It is classified as a type of seronegative spondyloarthropathy.
Genetics are thought to be strongly involved in the development of psoriatic arthritis. Obesity and certain forms of psoriasis are thought to increase the risk.Psoriatic arthritis affects up to 30% of people with psoriasis and occurs in both children and adults. Approximately 40–50% of individuals with psoriatic arthritis have the HLA-B27 genotype. The condition is less common in people of Asian or African descent and affects men and women equally.

Signs and symptoms
Pain, swelling, or stiffness in one or more joints is commonly present in psoriatic arthritis. Psoriatic arthritis is inflammatory, and affected joints are generally red or warm to the touch. Asymmetrical oligoarthritis, defined as inflammation affecting two to four joints during the first six months of disease, is present in 70% of cases. However, in 15% of cases, the  arthritis is symmetrical.  The joints of the hand that is involved in psoriasis are the proximal interphalangeal (PIP), the distal interphalangeal (DIP), the metacarpophalangeal (MCP), and the wrist. Involvement of the distal interphalangeal joints (DIP) is a characteristic feature and is present in 15% of cases.
In addition to affecting the joints of the hands and wrists, psoriatic arthritis may affect the fingers, nails, and skin. Sausage-like swelling in the fingers or toes, known as dactylitis, may occur. Psoriasis can also cause changes to the nails, such as pitting or separation from the nail bed, onycholysis, hyperkeratosis under the nails, and horizontal ridging. Psoriasis classically presents with scaly skin lesions, which are most commonly seen over extensor surfaces such as the scalp, natal cleft and umbilicus.
In psoriatic arthritis, pain can occur in the area of the sacrum (the lower back, above the tailbone), as a result of sacroiliitis or spondylitis, which is present  in 40% of cases. Pain  can occur in and around the feet and ankles, especially enthesitis in the Achilles tendon (inflammation of the Achilles tendon where it inserts into the bone) or plantar fasciitis in the sole of the foot.Along with the above-noted pain and inflammation, there is extreme exhaustion that does not go away with adequate rest. The exhaustion may last for days or weeks without abatement.  Psoriatic arthritis may remain mild or may progress to more destructive joint disease. Periods of active disease, or flares, will typically alternate with periods of remission. In severe forms, psoriatic arthritis may progress to arthritis mutilans which on X-ray gives a "pencil-in-cup" appearance.Because prolonged inflammation can lead to joint damage, early diagnosis and treatment to slow or prevent joint damage is recommended.

Causes
The exact causes are not yet known, however silica dust exposure has been identified in Australia and a number of genetic associations have been identified in a genome-wide association study of psoriasis and psoriatic arthritis including HLA-B27.

Diagnosis
There is no definitive test to diagnose psoriatic arthritis. Symptoms of psoriatic arthritis may closely resemble other diseases, including rheumatoid arthritis. A rheumatologist (a physician specializing in autoimmune diseases) may use physical examinations, health history, blood tests and x-rays to accurately diagnose psoriatic arthritis.
Factors that contribute to a diagnosis of psoriatic arthritis include the following:

Psoriasis in the patient, or a family history of psoriasis or psoriatic arthritis.
A negative test result for rheumatoid factor, a blood factor associated with rheumatoid arthritis.
Arthritis symptoms in the distal Interphalangeal articulations of hand (the joints closest to the tips of the fingers). This is not typical of rheumatoid arthritis.
Ridging or pitting of fingernails or toenails (onycholysis), which is associated with psoriasis and psoriatic arthritis.
Radiologic images demonstrating degenerative joint changes.Other symptoms that are more typical of psoriatic arthritis than other forms of arthritis include enthesitis (inflammation in the Achilles tendon (at the back of the heel) or the plantar fascia (bottom of the feet)), and dactylitis (sausage-like swelling of the fingers or toes).

Differential diagnosis
Several conditions can mimic the clinical presentation of psoriatic arthritis including rheumatoid arthritis, osteoarthritis, reactive arthritis, gouty arthritis, systemic lupus erythematosus, and inflammatory bowel disease-associated arthritis. In contrast to psoriatic arthritis, rheumatoid arthritis tends to affect the proximal joints (e.g., the metacarpophalangeal joints), involves a greater number of joints than psoriatic arthritis, and affect them symmetrically. Involvement of the spinal joints is more suggestive of psoriatic arthritis than rheumatoid arthritis. Osteoarthritis shares certain clinical features with psoriatic arthritis such as its tendency to affect multiple distal joints in an asymmetric pattern. Unlike psoriatic arthritis, osteoarthritis does not typically involve inflammation of the sacroiliac joint. Psoriatic arthritis sometimes affects only one joint and is sometimes confused for gout or pseudogout when this happens.

Classification
There are five main types of psoriatic arthritis:
Oligoarticular: This type affects around 70% of patients and is generally mild.  This type does not occur in the same joints on both sides of the body and usually only involves fewer than 3 joints.
Polyarticular: This type accounts for around 25% of cases, and affects five or more joints on both sides of the body simultaneously.  This type is most similar to rheumatoid arthritis and is disabling in around 50% of all cases.
Arthritis mutilans (M07.1): Affects less than 5% of patients and is a severe, deforming and destructive arthritis.  This condition can progress over months or years causing severe joint damage.  Arthritis mutilans has also been called chronic absorptive arthritis, and may be seen in rheumatoid arthritis as well.
Spondyloarthritis (M07.2): This type is characterized by stiffness of the neck or the sacroiliac joint of the spine, but can also affect the hands and feet, in a similar fashion to symmetric arthritis.
Distal interphalangeal predominant (M07.0): This type of psoriatic arthritis is found in about 5% of patients, and is characterized by inflammation and stiffness in the joints nearest to the ends of the fingers and toes.  Nail changes are often marked.

Treatments
The underlying process in psoriatic arthritis is inflammation; therefore, treatments are directed at reducing and controlling inflammation. Milder cases of psoriatic arthritis may be treated with NSAIDs alone; however, there is a trend toward earlier use of disease-modifying antirheumatic drugs or biological response modifiers to prevent irreversible joint destruction.

Nonsteroidal anti-inflammatory drugs
Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen, followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding. Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk reduction in gastrointestinal ulcers and bleeding complications compared to traditional NSAIDs, but carry an increased rate of cardiovascular events such as myocardial infarction (MI) or heart attack, and stroke. Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys.

Disease-modifying antirheumatic drugs
These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. According to a recent Cochrane review, low dose oral methotrexate was slightly more effective than placebos. Immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

Biological response modifiers
A new class of therapeutics called biological response modifiers or biologics has been developed using recombinant DNA technology. Biologic medications are derived from living cells cultured in a laboratory. Unlike traditional DMARDS that affect the entire immune system, biologics target specific parts of the immune system. They are given by injection or intravenous (IV) infusion.
Biologics prescribed for psoriatic arthritis are TNF-α inhibitors, including infliximab, etanercept, golimumab, certolizumab pegol and adalimumab, as well as the IL-12/IL-23 inhibitor ustekinumab, and the IL-17a inhibitor secukinumab. Recently, the Jak inhibitor, tofacitinib (Xeljanz), was approved for the use in active psoriatic arthritis.Biologics may increase the risk of minor and serious infections. More rarely, they may be associated with nervous system disorders, blood disorders or certain types of cancer.

Phosphodiesterase-4 inhibitors
A first-in-class treatment option for the management of psoriatic arthritis is apremilast; a small molecule phosphodiesterase-4 inhibitor approved for use by the FDA in 2014 </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 Visceroptosis and can you explain it in depth? [/INST] Visceroptosis is a prolapse or a sinking of the abdominal viscera (internal organs) below their natural position. "Ptosis" being the defining term, any or all of the organs may be displaced downward. When only the intestines are involved, the condition is known as enteroptosis. When the stomach is found below its normal position, the term gastroptosis is used. The condition exists in all degrees of severity and may not give rise to any adverse symptoms.
Generally, when adverse symptoms are associated with the condition, however, there may be loss of appetite, heartburn, nervous indigestion, constipation, diarrhea, abdominal distention, headache, vertigo, emaciation, and loss of sleep. Any or all of these symptoms may be present.
The condition may be brought about by loss of muscular tone, particularly of the abdominal muscles, with relaxation of the ligaments that typically hold the viscera in place. Tightlacing has been held to be a cause as well. Corsets to reduce the circumference of womens waists have been used to enable fashionable styles occurring during several historical periods, such as the late 1800s and early 1900s, when these symptoms were described for treatment by physicians </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 Lamellar ichthyosis and can you explain it in depth? [/INST] Lamellar ichthyosis, also known as ichthyosis lamellaris and nonbullous congenital ichthyosis, is a rare inherited skin disorder, affecting around 1 in 600,000 people.

Presentation
Affected babies are born in a collodion membrane, a shiny, waxy-appearing outer layer to the skin. This is shed  10–14 days after birth, revealing the main symptom of the disease, extensive scaling of the skin caused by hyperkeratosis.
With increasing age, the scaling tends to be concentrated around joints in areas such as the groin, the armpits, the inside of the elbow and the neck. The scales often tile the skin and may resemble fish scales.

Collodion baby
In medicine, the term collodion baby applies to newborns who appear to have an extra layer of skin (known as a collodion membrane) that has a collodion-like quality. It is a descriptive term, not a specific diagnosis or disorder (as such, it is a syndrome).

Appearance and treatment at birth
The appearance is often described as a shiny film looking like a layer of Vaseline. The eyelids and mouth may have the appearance of being forced open due to the tightness of the skin. There can be associated eversion of the eyelids (ectropion).
Collodion babies can have severe medical consequences, mainly because the baby can lose heat and fluid through the abnormal skin. This can lead to hypothermia and dehydration. Strategies to prevent these problems are the use of emollients or nursing the baby in a humidified incubator. There is also an increased risk of skin infection and mechanical compression, leading to problems like limb ischemia. There is also a risk of intoxication by cutaneous absorption of topical products, for example salicylate intoxication (similar to aspirin overdose) due to keratolytics.The condition is not thought to be painful or in itself distressing to the child. Nursing usually takes place in a neonatal intensive care unit, and good intensive care seems to have improved the prognosis markedly </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 Myxobolus cerebralis and can you explain it in depth? [/INST] Myxobolus cerebralis is a myxosporean parasite of salmonids (salmon, trout, and their allies) that causes whirling disease in farmed salmon and trout and also in wild fish populations. It was first described in rainbow trout in Germany a century ago, but its range has spread and it has appeared in most of Europe (including Russia), the United States, South Africa, Canada and other countries. In the 1980s, M. cerebralis was found to require a tubificid oligochaete (a kind of segmented worm) to complete its life cycle. The parasite infects its hosts with its cells after piercing them with polar filaments ejected from nematocyst-like capsules.
Whirling disease affects juvenile fish (fingerlings and fry) and causes skeletal deformation and neurological damage. Fish "whirl" forward in an awkward, corkscrew-like pattern instead of swimming normally, find feeding difficult, and are more vulnerable to predators. The mortality rate is high for fingerlings, up to 90% of infected populations, and those that do survive are deformed by the parasites residing in their cartilage and bone. They act as a reservoir for the parasite, which is released into water following the fishs death. M. cerebralis is one of the most economically important myxozoans in fish, as well as one of the most pathogenic. It was the first myxosporean whose pathology and symptoms were described scientifically. The parasite is not transmissible to humans.

Taxonomy
The taxonomy and naming of both M. cerebralis, and of myxozoans in general, have complicated histories. It was originally thought to infect fish brains (hence the specific epithet cerebralis) and nervous systems, though it soon was found to primarily infect cartilage and skeletal tissue. Attempts to change the name to Myxobolus chondrophagus, which would more accurately describe the organism, failed because of nomenclature rules. Later, the organisms previously called Triactinomyxon dubium and T. gyrosalmo (class Actinosporea) were found to be, in fact, triactinomyxon stages of M. cerebralis, the life cycle of which was expanded to include the triactinomyxon stage. Similarly, other actinosporeans were folded into the life cycles of various myxosporeans.Today, the myxozoans, previously thought to be multicellular protozoans, are considered animals by most scientists, though their status has not officially changed. Recent molecular studies suggest they are related to Bilateria or Cnidaria, with Cnidaria being closer morphologically because both groups have extrusive filaments. Bilateria were somewhat closer in some genetic studies, but those were found to have used samples that were contaminated by material from the host organism, and a 2015 study confirms they are cnidarians.

Morphology
M. cerebralis has many diverse stages ranging from single cells to relatively large spores, not all of which have been studied in detail.

Triactinomyxon stage
The stages that infect fish, called triactinomyxon spores, are made of a single style that is about 150 micrometers (μm) long and three processes or "tails", each about 200 micrometers long. A sporoplasm packet at the end of the style contains 64 germ cells surrounded by a cellular envelope. There are also three polar capsules, each of which contains a coiled polar filament between 170 and 180 μm long. Polar filaments in both this stage and in the myxospore stage (see picture above) rapidly shoot into the body of the host, creating an opening through which the sporoplasm can enter.

Sporoplasm stage
Upon contact with fish hosts and firing of the polar capsules, the sporoplasm contained within the central style of the triactinomyxon migrates into the epithelium or gut lining. Firstly, this sporoplasm undergoes mitosis to produce more amoeboid cells, which migrate into deeper tissue layers, to reach the cerebral cartilage.

Myxosporean stage
Myxospores, which develop from sporogonic cell stages inside fish hosts, are lenticular. They have a diameter of about 10 micrometers and are made of six cells. Two of these cells form polar capsules, two merge to form a binucleate sporoplasm, and two form protective valves. Myxospores are infective to oligochaetes, and are found among the remains of digested fish cartilage. They are often difficult to distinguish from related species because of morphological similarities across genera. Though M. cerebralis is the only myxosporean ever found in salmonid cartilage, other visually similar species may be present in the skin, nervous system, or muscle.

Life cycle
Myxobolus cerebralis has a two-host life cycle involving a salmonid fish and a tubificid oligochaete. So far, the only worm known to be susceptible to M. cerebralis infection is Tubifex tubifex, though what scientists currently call T. tubifex may in fact be more than one species. First, myxospores are ingested by tubificid worms. In the gut lumen of the worm, the spores extrude their polar capsules and attach to the gut epithelium by polar filaments. The shell valves then open along the suture line and the binucleate germ cell penetrates between the intestinal epithelial cells of the worm. This cell multiplies, producing many amoeboid cells by an asexual cell fission process called merogony. As a result of the multiplication process, the intercellular space of the epithelial cells in more than 10 neighbouring worm segments may become infected.Around 60–90 days postinfection, sexual cell stages of the parasite undergo sporogenesis, and develop into pansporocysts, each of which contains eight triactinomyxon-stage spores. These spores are released from the oligochaete anus into the water. Alternatively, a fish can become infected by eating an infected oligochaete. Infected tubificids can release triactinomyxons for at least a year. The triactinomyxon spores are carried by the water currents, where they can infect a salmonid through the skin. Penetration of the fish by these spores takes only a few seconds. Within five minutes, a sac of germ cells called a sporoplasm has entered the fish epidermis, and within a few hours, the sporoplasm splits into individual cells that will spread through the fish.Within the fish, both intracellular and extracellular stages reproduce in its cartilage by asexual endogeny, meaning new cells grow from within old cells. The final stage within the fish is the creation of the myxospore, which is formed by sporogony. They are released into the environment when the fish decomposes or is eaten. Some recent research indicates some fish may expel viable myxospores while still alive.Myxospores are extremely tough: "it was shown that Myxobolus cerebralis spores can tolerate freezing at −20°C for at least 3 months, aging in mud at 13°C for at least 5 months, and passage through the guts of northern pike Esox lucius or mallards Anas platyrhynchos without loss of infectivity" to worms. Triactinomyxons are much shorter-lived, surviving 34 days or less, depending on temperature.

Pathology
M. cerebralis infections have been reported from a wide range of salmonid species: eight species of "Atlantic" salmonids, Salmo; four species of "Pacific" salmonids, Oncorhynchus; four species of char, Salvelinus; the grayling, Thymallus thymallus; and the huchen, Hucho hucho. M. cerebralis causes damage to its fish hosts through attachment of triactinomyxon spores and the migrations of various stages through tissues and along nerves, as well as by digesting cartilage. The fishs tail may darken, but aside from lesions on cartilage, internal organs generally appear healthy. Other symptoms include skeletal deformities and "whirling" behavior (tail-chasing) in young fish, which was thought to have been caused by a loss of equilibrium, but is actually caused by damage to the spinal cord and lower brain stem. Experiments have shown that fish can kill Myxobolus in their skin (possibly using antibodies), but that the fish do not attack the parasites once they have migrated to the central nervous system. This response varies from species to species.In T. tubifex, the release of triactinomyxon spores from the intestinal wall damages the worms mucosa; this may happen thousands of times in a single worm, and is believed to impair nutrient absorption. Spores are released from the worm almost exclusively when the temperature is between 10 °C and 15 °C, so fish in warmer or cooler waters are less likely to be infected, and infection rates vary seasonally.

Susceptibility
Fish size, age, concentration of triactinomyxon spores, and water temperature all affect infection rates in fish, as does the species of the fish in question. The disease has the most impact on fish less than five months old because their skeletons have not ossified. This makes young fish more susceptible to deformities and provides M. cerebralis more cartilage on which to feed. In one study of seven species of many strains, brook trout and rainbow trout (except one strain) were far more heavily affected by M. cerebralis after two hours of exposure than other species were, while bull trout, Chinook salmon, brown trout, and Arctic grayling were least severely affected. While brown trout may harbor the parasite, they typically do not show any symptoms, and this species may have been M. cerebralis original host. This lack of symptoms in brown trout meant that the parasite was only discovered after nonnative rainbow trouts were introduced in Europe.

Diagnosis
Moderate or heavy clinical infection of fish with whirling disease can be presumptively diagnosed on the basis of changes in behavior and appearance about 35 to 80 days after initial infection, though "injury or deficiency in dietary tryptophan and ascorbic acid can evoke similar signs", so conclusive diagnosis may require finding myxospores in the fishs cartilage. In heavy infections, only examining cartilage microscopically may be necessary to find spores. In less severe infections, the most common test involves digestion of the cranial cartilage with the proteases pepsin and trypsin (pepsin-trypsin digest—PTD) before looking for spores. The head and other tissues can be further examined using histopathology to confirm whether the location and morphology of the spores matches what is known for M. cerebralis. Serological identification of spores in tissue sections using an antibody raised against the spores is also possible. Parasite identity can also be confirmed using polymerase chain reaction to amplify the 415 base pair 18S rRNA gene from M. cerebralis. Fish should be screened at the life stage most susceptible to the parasites, with particular focus on fish in aquaculture units.

Impact
Although originally a mild pathogen of Salmo trutta in central Europe and other salmonids in northeast Asia, the introduction of the rainbow trout (Oncorhynchus mykiss) has greatly increased the impact of this parasite. Having no innate immunity to M. cerebralis, rainbow trout are particularly susceptible, and can release so many spores that even more resistant species in the same area, such as S. trutta, can become overloaded with parasites and incur 80%–90% mortalities. Where M. cerebralis has become well-established, it has caused decline or even elimination of whole cohorts of fish.

Impact in Europe
The impact of M. cerebralis in Europe is somewhat lessened because the species is endemic to this region, giving native fish stocks a degree of immunity. Rainbow trout, the most susceptible species to this parasite, are not native to Europe; successfully reproducing feral populations are rare, so few wild rainbow trout are young enough to be susceptible to infection. On the other hand, they are widely reared for restocking sport-fishing waters and for aquaculture, where this parasite has its greatest impact. Hatching and rearing methods designed to prevent infection of rainbow trout fry have proved successful in Europe. These techniques include hatching eggs in spore-free water and rearing fry to the "ossification" stage in tanks or raceways. These methods give particular attention to the quality of water sources to guard against spore introduction during water exchanges. Fry are moved to earthen ponds only once they are considered to be clinically resistant to the parasite, after skeletal ossification occurs.

Impact in New Zealand
M. cerebralis was first found in New Zealand in 1971. The parasite has only been found in rivers in the South Island, away from the most important aquaculture sites. Additionally, salmonid species commercially aquacultured in New Zealand have low susceptibility to whirling disease, and the parasite has also not been shown to affect native salmonids. An important indirect effect of the parasites presence is quarantine restriction placed on exports of salmon products to Australia.

Impact in the United States
M. cerebralis was first recorded in North America in 1956 in Pennsylvania, having been introduced via infected trout imported from Europe, and has spread steadily south and westwards. Until the 1990s, whirling disease was considered a manageable problem affecting rainbow trout in hatcheries. However, it has recently become established in natural waters of the Rocky Mountain states (Colorado, Wyoming, Utah, Montana, Idaho, New Mexico), where it is causing heavy mortalities in several sportfishing rivers. Some streams in the western United States have lost 90% of their trout. In addition, whirling disease threatens recreational fishing, which is important for the tourism industry, a key component of the economies of some U.S. western states. For example, "the Montana Whirling Disease Task Force estimated trout fishing generated US $300,000,000 in recreational expenditures in Montana alone". Making matters worse, some of the fish species that M. cerebralis infects (bull trout, cutthroat trout, and steelhead) are already threatened or endangered, and the parasite could worsen their already precarious situations. For reasons that are poorly understood, but probably have to do with environmental conditions, the impact on infected fish has been greatest in Colorado and Montana, and least in California, Michigan, and New York.

Impact in Canada
Whirling disease was first detected in fish in Johnson Lake in Banff National Park in May, 2016. CFIA Labs confirmed in August and Parks Canada announced the outbreak August 23, 2016. Although it was first discovered in Banff, it is not necessarily where the disease originated and spread. The Government of Alberta is currently sampling and testing fish in 6 different watersheds (Peace River, Athabasca, North Saskatchewan, Red Deer, Bow and Oldman) to see where the disease has spread. Initial sample fish were collected in 2016, and are currently being processed by the Government of Alberta and CFIA labs. Since testing began, it has been detected in the Upper Bow River, and in May 2017 it was confirmed that whirling disease had also been detected in the Oldman River Basin. The declaration does not mean that every susceptible finfish population within the Bow and Oldman River watersheds are infected with the disease.As a result of the new declaration, a domestic movement permit will be required from the CFIA for susceptible species and end uses identified in the Domestic Movement Control Program, the vector Tubifex tubifex, the disease causing agent Myxobolus cerebralis, and/or related things out of the infected and buffer areas of Alberta. Recreational and sport fishing, including fishing led by a professional guide, will not require a CFIA permit.

Prevention and control
Some biologists have attempted to disarm triactinomyxon spores by making them fire prematurely. In the laboratory, only extreme acidity or basicity, moderate to high concentrations of salts, or electric current caused premature filament discharge; neurochemicals, cnidarian chemosensitizers, and trout mucus were ineffective, as were anesthetized or dead fish. If spores could be disarmed, they would be unable to infect fish, but further research is needed to find an effective treatment.Some strains of fish are more resistant than others, even within species; using resistant strains may help reduce the incidence and severity of whirling disease in aquaculture </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 Sclerema neonatorum 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 Chorea and can you explain it in depth? [/INST] Chorea (or choreia, occasionally) is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias. The term chorea is derived from the Ancient Greek: χορεία ("dance"; see choreia), as the quick movements of the feet or hands are comparable to dancing.
The term hemichorea refers to chorea of one side of the body, such as chorea of one arm but not both (analogous to hemiballismus).

Presentation
Chorea is characterized by brief, semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next. These dance-like movements of chorea often occur with athetosis, which adds twisting and writhing movements. Walking may become difficult, and include odd postures and leg movements. Unlike ataxia, which affects the quality of voluntary movements, or Parkinsonism, which is a hindrance of voluntary movements, the movements of chorea and ballism occur on their own, without conscious effort. Thus, chorea is said to be a hyperkinetic movement disorder. When chorea is serious, slight movements will become thrashing motions; this form of severe chorea is referred to as ballism, or ballismus.

Causes
Huntingtons disease
Huntingtons disease is a neurodegenerative disease and most common inherited cause of chorea </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 Visual impairment and can you explain it in depth? [/INST] Visual impairment, also known as vision impairment, is a medical definition primarily measured based on an individuals better eye visual acuity; in the absence of treatment such as correctable eyewear, assistive devices, and medical treatment– visual impairment may cause the individual difficulties with normal daily tasks including reading and walking. Low vision is a functional definition of visual impairment that is chronic, uncorrectable with treatment or correctable lenses, and impacts daily living. As such low vision can be used as a disability metric and varies based on an individuals experience, environmental demands, accommodations, and access to services. The American Academy of Ophthalmology defines visual impairment as the best-corrected visual acuity of less than 20/40 in the better eye, and the World Health Organization defines it as a presenting acuity of less than 6/12 in the better eye. The term blindness is used for complete or nearly complete vision loss. In addition to the various permanent conditions, fleeting temporary vision impairment, amaurosis fugax, may occur, and may indicate serious medical problems.
The most common causes of visual impairment globally are uncorrected refractive errors (43%), cataracts (33%), and glaucoma (2%). Refractive errors include near-sightedness, far-sightedness, presbyopia, and astigmatism. Cataracts are the most common cause of blindness. Other disorders that may cause visual problems include age-related macular degeneration, diabetic retinopathy, corneal clouding, childhood blindness, and a number of infections. Visual impairment can also be caused by problems in the brain due to stroke, premature birth, or trauma, among others. These cases are known as cortical visual impairment. Screening for vision problems in children may improve future vision and educational achievement. Screening adults without symptoms is of uncertain benefit. Diagnosis is by an eye exam.The World Health Organization (WHO) estimates that 80% of visual impairment is either preventable or curable with treatment. This includes cataracts, the infections river blindness and trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness. Many people with significant visual impairment benefit from vision rehabilitation, changes in their environment, and assistive devices.As of 2015 there were 940 million people with some degree of vision loss. 246 million had low vision and 39 million were blind. The majority of people with poor vision are in the developing world and are over the age of 50 years. Rates of visual impairment have decreased since the 1990s. Visual impairments have considerable economic costs both directly due to the cost of treatment and indirectly due to decreased ability to work.

Classification
In 2010, the WHO definition for visual impairment was changed and now follows the ICD-11. The previous definition which used "best corrected visual acuity" was changed to "presenting visual acuity". This change was made as newer studies showed that best-corrected vision overlooks a larger proportion of the population who has visual impairment due to uncorrected refractive errors, and/or lack of access to medical or surgical treatment.Distance vision impairment:

Category 0: No or mild visual impairment –presenting visual acuity better than 6/18
Category 1: Moderate visual impairment –presenting visual acuity worse than 6/18 and better than 6/60
Category 2: Severe visual impairment –presenting visual acuity worse than 6/60 and better than 3/60
Category 3: Blindness –presenting visual acuity worse than 3/60 and better than 1/60
Category 4: Blindness—presenting visual acuity worse than 1/60 with light perception
Category 5: Blindness—irreversible blindness with no light perceptionNear vision impairment:

Near visual acuity worse than N6 or M.08 at 40 cm.

United Kingdom
Severely sight impaired

Defined as having central visual acuity of less than 3/60 with normal fields of vision, or gross visual field restriction.
Unable to see at 3 metres (10 ft) what the normally sighted person sees at 60 metres (200 ft).Sight impaired

Able to see at 3 metres (10 ft), but not at 6 metres (20 ft), what the normally sighted person sees at 60 metres (200 ft)
Less severe visual impairment is not captured by registration data, and its prevalence is difficult to quantifyLow vision

A visual acuity of less than 6/18 but greater than 3/60.
Not eligible to drive and may have difficulty recognising faces across a street, watching television, or choosing clean, unstained, co-ordinated clothing.In the UK, the Certificate of Vision Impairment (CVI) is used to certify patients as severely sight impaired or sight impaired. The accompanying guidance for clinical staff states: "The National Assistance Act 1948 states that a person can be certified as severely sight impaired if they are so blind as to be unable to perform any work for which eye sight is essential". Certification is based on whether a person can do any work for which eyesight is essential, not just one particular job (such as their job before becoming blind).In practice, the definition depends on individuals visual acuity and the extent to which their field of vision is restricted. The Department of Health identifies three groups of people who may be classified as severely visually impaired.
Those below 3/60 (equivalent to 20/400 in US notation) Snellen (most people below 3/60 are severely sight impaired).
Those better than 3/60 but below 6/60 Snellen (people who have a very contracted field of vision only).
Those 6/60 Snellen or above (people in this group who have a contracted field of vision especially if the contraction is in the lower part of the field).The Department of Health also state that a person is more likely to be classified as severely visually impaired if their eyesight has failed recently or if they are an older individual, both groups being perceived as less able to adapt to their vision loss.

United States
In the United States, any person with vision that cannot be corrected to better than 20/200 in the best eye, or who has 20 degrees (diameter) or less of visual field remaining, is considered legally blind or eligible for disability classification and possible inclusion in certain government sponsored programs.
In the United States, the terms partially sighted, low vision, legally blind and totally blind are used by schools, colleges, and other educational institutions to describe students with visual impairments. They are defined as follows:

Partially sighted indicates some type of visual problem, with a need of person to receive special education in some cases.
Low vision generally refers to a severe visual impairment, not necessarily limited to distance vision. Low vision applies to all individuals with sight who are unable to read the newspaper at a normal viewing distance, even with the aid of eyeglasses or contact lenses. They use a combination of vision and other senses to learn, although they may require adaptations in lighting or the size of print, and, sometimes, braille.
Legally blind indicates that a person has less than 20/200 vision in the better eye after best correction (contact lenses or glasses), or a field of vision of less than 20 degrees in the better eye.
Totally blind students learn via braille or other non-visual media.In 1934, the American Medical Association adopted the following definition of blindness:

Central visual acuity of 20/200 or less in the better eye with corrective glasses or central visual acuity of more than 20/200 if there is a visual field defect in which the peripheral field is contracted to such an extent that the widest diameter of the visual field subtends an angular distance no greater than 20 degrees in the better eye.
The United States Congress included this definition as part of the Aid to the Blind program in the Social Security Act passed in 1935. In 1972, the Aid to the Blind program and two others combined under Title XVI of the Social Security Act to form the Supplemental Security Income program which states:

An individual shall be considered to be blind for purposes of this title if he has central visual acuity of 20/200 or less in the better eye with the use of a correcting lens. An eye which is accompanied by a limitation in the fields of vision such that the widest diameter of the visual field subtends an angle no greater than 20 degrees shall be considered for purposes of the first sentence of this subsection as having a central visual acuity of 20/200 or less. An individual shall also be considered to be blind for purposes of this title if he is blind as defined under a State plan approved under title X or XVI as in effect for October 1972 and received aid under such plan (on the basis of blindness) for December 1973, so long as he is continuously blind as so defined.

Temporary vision impairment
Vision impairment for a few seconds, or minutes, may occur due to any of a variety of causes, some serious and requiring medical attention.

Health effects
General functioning
Visual impairments may take many forms and be of varying degrees. Visual acuity alone is not always a good predictor of an individuals function. Someone with relatively good acuity (e.g., 20/40) can have difficulty with daily functioning, while someone with worse acuity (e.g., 20/200) may function reasonably well if they have low visual demands. It is also important to note that best-corrected visual acuity differs from presenting visual acuity; a person with a "normal" best corrected acuity can have "poor" presenting acuity (e.g. individual who has uncorrected refractive error). Thus, measuring an individuals general functioning depends on ones situational and contextual factors, as well as access to treatment.The American Medical Association has estimated that the loss of one eye equals 25% impairment of the visual system and 24% impairment of the whole person; total loss of vision in both eyes is considered to be 100% visual impairment and 85% impairment of the whole person.Some people who fall into this category can use their considerable residual vision – their remaining sight – to complete daily tasks without relying on alternative methods. The role of a low vision specialist (optometrist or ophthalmologist) is to maximize the functional level of a patients vision by optical or non-optical means. Primarily, this is by use of magnification in the form of telescopic systems for distance vision and optical or electronic magnification for near tasks.
People with significantly reduced acuity may benefit from training conducted by individuals trained in the provision of technical aids. Low vision rehabilitation professionals, some of whom are connected to an agency for the blind, can provide advice on lighting and contrast to maximize remaining vision. These professionals also have access to non-visual aids, and can instruct patients in their uses.

Mobility
Older adults with visual impairment are at an increased risk of physical inactivity, slower gait speeds, and fear of falls.Physical activity is a useful predictor of overall well-being, and routine physical activity reduces the risk of developing chronic diseases and disability. Older adults with visual impairment (including glaucoma, age-related macular degeneration, and diabetic retinopathy) have decreased physical activity as measured with self-reports and accelerometers. The US National Health and Nutrition Examination Survey (NHANES) showed that people with corrected visual acuity of less than 20/40 spent significantly less time in moderate to vigorous physical activity. Age-related macular degeneration is also associated with a 50% decrease in physical activity–however physical activity is protective against age-related macular degeneration progression.In terms of mobility, those with visual impairment have a slower gait speed than those without visual impairment; however, the rate of decline remains proportional with increasing age in both groups. Additionally, the visually impaired also have greater difficulty walking a quarter mile (400 m) and walking up stairs, as compared to those with normal vision.

Cognitive
Older adults with vision loss are at an increased risk of memory loss, cognitive impairment, and cognitive decline.

Social and psychological
Studies demonstrate an association between older adults with visual impairment and a poor mental health; discrimination was identified as one of the causes of this association. Older adults with visual impairment have a 1.5-fold risk of reporting perceived discrimination and of these individuals, there was a 2-fold risk of loneliness and 4-fold risk of reporting a lower quality of life. Among adults with visual impairment, the prevalence of moderate loneliness is 28.7% (18.2% in general population) and prevalence of severe loneliness is 19.7% (2.7% in general population). The risk of depression and anxiety are also increased in the visually impaired; 32.2% report depressive symptoms (12.01% in general population), and 15.61% report anxiety symptoms (10.69% in general population).The subjects making the most use of rehabilitation instruments, who lived alone, and preserved their own mobility and occupation were the least depressed, with the lowest risk of suicide and the highest level of social integration.
Those with worsening sight and the prognosis of eventual blindness are at comparatively high risk of suicide and thus may be in need of supportive services. Many studies have demonstrated how rapid acceptance of the serious visual impairment has led to a better, more productive compliance with rehabilitation programs. Moreover, psychological distress has been reported to be at its highest when sight loss is not complete, but the prognosis is unfavorable. Therefore, early intervention is imperative for enabling successful psychological adjustment.

Associated conditions
Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy. Blindness in combination with hearing loss is known as deafblindness.
It has been estimated that over half of completely blind people have non-24-hour sleep–wake disorder, a condition in which a persons circadian rhythm, normally slightly longer than 24 hours, is not entrained (synchronized) to the light–dark cycle.

Cause
The most common causes of visual impairment globally in 2010 were:

Refractive error (42%)
Cataract  (33%)
Glaucoma (2%)
Age-related macular degeneration (1%)
Corneal opacification (1%)
Diabetic retinopathy (1%)
Childhood blindness
Trachoma (1%)
Undetermined (18%)The most common causes of blindness worldwide in 2010 were:

Cataracts (51%)
Glaucoma (8%)
Age-related macular degeneration (5%)
Corneal opacification (4%)
Childhood blindness (4%)
Refractive errors (3%)
Trachoma (3%)
Diabetic retinopathy (1%)
Undetermined (21%)About 90% of people who are visually impaired live in the developing world. Age-related macular degeneration, glaucoma, and diabetic retinopathy are the leading causes of blindness in the developed world.Among working-age adults who are newly blind in England and Wales the most common causes in 2010 were:
Hereditary retinal disorders (20.2%)
Diabetic retinopathy (14.4%)
Optic atrophy (14.1%)
Glaucoma (5.9%)
Congenital abnormalities (5.1%)
Disorders of the visual cortex (4.1%)
Cerebrovascular disease (3.2%)
Degeneration of the macula and posterior pole (3.0%)
Myopia (2.8%)
Corneal disorders (2.6%)
Malignant neoplasms of the brain and nervous system (1.5%)
Retinal detachment (1.4%)

Cataracts
Cataracts are the greying or opacity of the crystalline lens, which can be caused in children by intrauterine infections, metabolic disorders, and genetically transmitted syndromes. Cataracts are the leading cause of child and adult blindness that doubles in prevalence with every ten years after the age of 40. Consequently, today cataracts are more common among adults than in children. That is, people face higher chances of developing cataracts as they age. Nonetheless, cataracts tend to have a greater financial and emotional toll upon children as they must undergo expensive diagnosis, long term rehabilitation, and visual assistance. Also, according to the Saudi Journal for Health Sciences, sometimes patients experience irreversible amblyopia after pediatric cataract surgery because the cataracts prevented the normal maturation of vision prior to operation. Despite the great progress in treatment, cataracts remain a global problem in both economically developed and developing countries. At present, with the variant outcomes as well as the unequal access to cataract surgery, the best way to reduce the risk of developing cataracts is to avoid smoking and extensive exposure to sun light (i.e. UV-B rays).

Glaucoma
Glaucoma is an eye disease often characterized by increased pressure within the eye or intraocular pressure (IOP). Glaucoma causes visual field loss as well as severs the optic nerve. Early diagnosis and treatment of glaucoma in patients is imperative because glaucoma is triggered by non-specific levels of IOP. Also, another challenge in accurately diagnosing glaucoma is that the disease has four causes: 1) inflammatory ocular hypertension syndrome (IOHS); 2) severe uveitic angle closure; 3) corticosteroid-induced; and 4) a heterogonous mechanism associated with structural change and chronic inflammation. In addition, often pediatric glaucoma differs greatly in cause and management from the glaucoma developed by adults. Currently, the best sign of pediatric glaucoma is an IOP of 21 mm Hg or greater present within a child. One of the most common causes of pediatric glaucoma is cataract removal surgery, which leads to an incidence rate of about 12.2% among infants and 58.7% among 10-year-olds.

Infections
Childhood blindness can be caused by conditions related to pregnancy, such as congenital rubella syndrome and retinopathy of prematurity. Leprosy and onchocerciasis each blind approximately 1 million individuals in the developing world.
The number of individuals blind from trachoma has decreased in the past 10 years from 6 million to 1.3 million, putting it in seventh place on the list of causes of blindness worldwide.
Central corneal ulceration is also a significant cause of monocular blindness worldwide, accounting for an estimated 850,000 cases of corneal blindness every year in the Indian subcontinent alone. As a result, corneal scarring from all causes is now the fourth greatest cause of global blindness.

Injuries
Eye injuries, most often occurring in people under 30, are the leading cause of monocular blindness (vision loss in one eye) throughout the United States. Injuries and cataracts affect the eye itself, while abnormalities such as optic nerve hypoplasia affect the nerve bundle that sends signals from the eye to the back of the brain, which can lead to decreased visual acuity.
Cortical blindness results from injuries to the occipital lobe of the brain that prevent the brain from correctly receiving or interpreting signals from the optic nerve. Symptoms of cortical blindness vary greatly across individuals and may be more severe in periods of exhaustion or stress. It is common for people with cortical blindness to have poorer vision later in the day.
Blinding has been used as an act of vengeance and torture in some instances, to deprive a person of a major sense by which they can navigate or interact within the world, act fully independently, and be aware of events surrounding them. An example from the classical realm is Oedipus, who gouges out his own eyes after realizing that he fulfilled the awful prophecy spoken of him. Having crushed the Bulgarians, the Byzantine Emperor Basil II blinded as many as 15,000 prisoners taken in the battle, before releasing them. Contemporary examples include the addition of methods such as acid throwing as a form of disfigurement.

Genetic defects
People with albinism often have vision loss to the extent that many are legally blind, though few of them actually cannot see. Leber congenital amaurosis can cause total blindness or severe sight loss from birth or early childhood. Retinitis pigmentosa is characterized by decreased peripheral vision and trouble seeing at night.
Advances in mapping of the human genome have identified other genetic causes of low vision or blindness. Two such examples are Bardet–Biedl syndrome .

Poisoning
Rarely, blindness is caused by the intake of certain chemicals. A well-known example is methanol, which is only mildly toxic and minimally intoxicating, and breaks down into the substances formaldehyde and formic acid which in turn can cause blindness, an array of other health complications, and death. When competing with ethanol for metabolism, ethanol is metabolized first, and the onset of toxicity is delayed. Methanol is commonly found in methylated spirits, denatured ethyl alcohol, to avoid paying taxes on selling ethanol intended for human consumption. Methylated spirits are sometimes used by alcoholics as a desperate and cheap substitute for regular ethanol alcoholic beverages.

Other
Amblyopia: is a category of vision loss or visual impairment that is caused by factors unrelated to refractive errors or coexisting ocular diseases. Amblyopia is the condition when a childs visual systems fail to mature normally because the child either has been born premature, measles, congenital rubella syndrome, vitamin A deficiency, or meningitis. If left untreated during childhood, amblyopia is currently incurable in adulthood because surgical treatment effectiveness changes as a child matures. Consequently, amblyopia is the worlds leading cause of child monocular vision loss, which is the damage or loss of vision in one eye. In the best case scenario, which is very rare, properly treated amblyopia patients can regain 20/40 acuity.
Corneal opacification
Degenerative myopia
Diabetic retinopathy: is one of the manifestation microvascular complications of diabetes, which is characterized by blindness or reduced acuity. That is, diabetic retinopathy describes the retinal and vitreous hemorrhages or retinal capillary blockage caused by the increase of A1C, which a measurement of blood glucose or sugar level. In fact, as A1C increases, people tend to be at greater risk of developing diabetic retinopathy than developing other microvascular complications associated with diabetes (e.g. chronic hyperglycemia, diabetic neuropathy, and diabetic nephropathy). Despite the fact that only 8% of adults 40 years and older experience vision-threatening diabetic retinopathy (e.g. nonproliferative diabetic retinopathy or NPDR and proliferative diabetic retinopathy or PDR), this eye disease accounted for 17% of cases of blindness in 2002.
Retinitis pigmentosa
Retinopathy of prematurity: The most common cause of blindness in infants worldwide. In its most severe form, ROP causes retinal detachment, with attendant visual loss. Treatment is aimed mainly at prevention, via laser or Avastin therapy.
Stargardts disease
Uveitis: is a group of 30 intraocular inflammatory diseases caused by infections, systemic diseases, organ-specific autoimmune processes, cancer or trauma. That is, uveitis refers to a complex category of ocular diseases that can cause blindness if either left untreated or improperly diagnosed. The current challenge of accurately diagnosing uveitis is that often the cause of a specific ocular inflammation is either unknown or multi-layered. Consequently, about 3–10% of those with uveitis in developed countries, and about 25% of those with uveitis in the developing countries, become blind from incorrect diagnosis and from ineffectual prescription of drugs, antibiotics or steroids. In addition, uveitis is a diverse category of eye diseases that are subdivided as granulomatous (or tumorous) or non-granulomatous anterior, intermediate, posterior or pan uveitis. In other words, uveitis diseases tend to be classified by their anatomic location in the eye (e.g. uveal tract, retina, or lens), as well as can create complication that can cause cataracts, glaucoma, retinal damage, age-related macular degeneration or diabetic retinopathy.
Xerophthalmia, often due to vitamin A deficiency, is estimated to affect 5 million children each year; 500,000 develop active corneal involvement, and half of these go blind.

Diagnosis
It is important that people be examined by someone specializing in low vision care prior to other rehabilitation training to rule out potential medical or surgical correction for the problem and to establish a careful baseline refraction and prescription of both normal and low vision glasses and optical aids. Only a doctor is qualified to evaluate visual functioning of a compromised visual system effectively. The American Medical Association provides an approach to evaluating visual loss as it affects an individuals ability to perform activities of daily living.Screening adults who have no symptoms is of uncertain benefit.

Prevention
The World Health Organization estimates that 80% of visual loss is either preventable or curable with treatment. This includes cataracts, onchocerciasis, trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness. The Center for Disease Control and Prevention estimates that half of blindness in the United States is preventable.

Management
Mobility
Many people with serious visual impairments can travel independently, using a wide range of tools and techniques. Orientation and mobility specialists are professionals who are specifically trained to teach people with visual impairments how to travel safely, confidently, and independently in the home and the community. These professionals can also help blind people to practice travelling on specific routes which they may use often, such as the route from ones house to a convenience store. Becoming familiar with an environment or route can make it much easier for a blind person to navigate successfully.
Tools such as the white cane with a red tip – the international symbol of blindness – may also be used to improve mobility. A long cane is used to extend the users range of touch sensation. It is usually swung in a low sweeping motion, across the intended path of travel, to detect obstacles. However, techniques for cane travel can vary depending on the user and/or the situation. Some visually impaired persons do not carry these kinds of canes, opting instead for the shorter, lighter identification (ID) cane. Still others require a support cane. The choice depends on the individuals vision, motivation, and other factors.
A small number of people employ guide dogs to assist in mobility. These dogs are trained to navigate around various obstacles, and to indicate when it becomes necessary to go up or down a step. However, the helpfulness of guide dogs is limited by the inability of dogs to understand complex directions. The human half of the guide dog team does the directing, based upon skills acquired through previous mobility training. In this sense, the handler might be likened to an aircrafts navigator, who must know how to get from one place to another, and the dog to the pilot, who gets them there safely.
GPS devices can also be used as a mobility aid. Such software can assist blind people with orientation and navigation, but it is not a replacement for traditional mobility tools such as white canes and guide dogs.
Some blind people are skilled at echolocating silent objects simply by producing mouth clicks and listening to the returning echoes. It has been shown that blind echolocation experts use what is normally the "visual" part of their brain to process the echoes.Government actions are sometimes taken to make public places more accessible to blind people. Public transportation is freely available to blind people in many cities. Tactile paving and audible traffic signals can make it easier and safer for visually impaired pedestrians to cross streets. In addition to making rules about who can and cannot use a cane, some governments mandate the right-of-way be given to users of white canes or guide dogs.

Reading and magnification
Most visually impaired people who are not totally blind read print, either of a regular size or enlarged by magnification devices. Many also read large-print, which is easier for them to read without such devices. A variety of magnifying glasses, some handheld, and some on desktops, can make reading easier for them.
Others read braille (or the infrequently used Moon type), or rely on talking books and readers or reading machines, which convert printed text to speech or braille. They use computers with special hardware such as scanners and refreshable braille displays as well as software written specifically for the blind, such as optical character recognition applications and screen readers.
Some people access these materials through agencies for the blind, such as the National Library Service for the Blind and Physically Handicapped in the United States, the National Library for the Blind or the RNIB in the United Kingdom.
Closed-circuit televisions, equipment that enlarges and contrasts textual items, are a more high-tech alternative to traditional magnification devices.
There are also over 100 radio reading services throughout the world that provide people with vision impairments with readings from periodicals over the radio. The International Association of Audio Information Services provides links to all of these organizations.

Computers and mobile technology
Access technology such as screen readers, screen magnifiers and refreshable braille displays enable the blind to use mainstream computer applications and mobile phones. The availability of assistive technology is increasing, accompanied by concerted efforts to ensure the accessibility of information technology to all potential users, including the blind. Later versions of Microsoft Windows include an Accessibility Wizard & Magnifier for those with partial vision, and Microsoft Narrator, a simple screen reader. Linux distributions (as live CDs) for the blind include Vinux and Adriane Knoppix, the latter developed in part by Adriane Knopper who has a visual impairment.  macOS and iOS  also come with a built-in screen reader called VoiceOver, while Google TalkBack is built in to most Android devices.
The movement towards greater web accessibility is opening a far wider number of websites to adaptive technology, making the web a more inviting place for visually impaired surfers.
Experimental approaches in sensory substitution are beginning to provide access to arbitrary live views from a camera.
Modified visual output that includes large print and/or clear simple graphics can be of benefit to users with some residual vision.

Other aids and techniques
Blind people may use talking equipment such as thermometers, watches, clocks, scales, calculators, and compasses. They may also enlarge or mark dials on devices such as ovens and thermostats to make them usable. Other techniques used by blind people to assist them in daily activities include:

Adaptations of coins and banknotes so that the value can be determined by touch. For example:
In some currencies, such as the euro, the pound sterling and the Indian rupee, the size of a note increases with its value.
On US coins, pennies and dimes, and nickels and quarters are similar in size. The larger denominations (dimes and quarters) have ridges along the sides (historically used to prevent the "shaving" of precious metals from the coins), which can now be used for identification.
Some currencies banknotes have a tactile feature to indicate denomination. For example, the Canadian currency tactile feature is a system of raised dots in one corner, based on braille cells but not standard braille.
It is also possible to fold notes in different ways to assist recognition.
Labeling and tagging clothing and other personal items
Placing different types of food at different positions on a dinner plate
Marking controls of household appliancesMost people, once they have been visually impaired for long enough, devise their own adaptive strategies in all areas of personal and professional management.
For the blind, there are books in braille, audio-books, and text-to-speech computer programs, machines and e-book readers. Low vision people can make use of these tools as well as large-print reading materials and e-book readers that provide large font sizes.
Computers are important tools of integration for the visually impaired person. They allow, using standard or specific programs, screen magnification and conversion of text into sound or touch (braille line), and are useful for all levels of visual impairment. OCR scanners can, in conjunction with text-to-speech software, read the contents of books and documents aloud via computer. Vendors also build closed-circuit televisions that electronically magnify paper, and even change its contrast and color, for visually impaired users. For more information, consult assistive technology.
In adults with low vision there is no conclusive evidence supporting one form of reading aid over another. In several studies stand-mounted devices allowed faster reading than hand-held or portable optical aids. While electronic aids may allow faster reading for individuals with low vision, portability, ease of use, and affordability must be considered for people.Children with low vision sometimes have reading delays, but do benefit from phonics-based beginning reading instruction methods. Engaging phonics instruction is multisensory, highly motivating, and hands-on. Typically students are first taught the most frequent sounds of the alphabet letters, especially the so-called short vowel sounds, then taught to blend sounds together with three-letter consonant-vowel-consonant words such as cat, red, sit, hot, sun. Hands-on (or kinesthetically appealing) VERY enlarged print materials such as those found in "The Big Collection of Phonics Flipbooks" by Lynn Gordon (Scholastic, 2010) are helpful for teaching word families and blending skills to beginning readers with low vision. Beginning reading instructional materials should focus primarily on the lower-case letters, not the capital letters (even though they are larger) because reading text requires familiarity (mostly) with lower-case letters. Phonics-based beginning reading should also be supplemented with phonemic awareness lessons, writing opportunities, and many read-alouds (literature read to children daily) to stimulate motivation, vocabulary development, concept development, and comprehension skill development. Many children with low vision can be successfully included in regular education environments. Parents may need to be vigilant to ensure that the school provides the teacher and students with appropriate low vision resources, for example technology in the classroom, classroom aide time, modified educational materials, and consultation assistance with low vision experts.

Epidemiology
The WHO estimates that in 2012 there were 285 million visually impaired people in the world, of which 246 million had low vision and 39 million were blind.Of those who are blind 90% live in the developing world. Worldwide for each blind person, an average of 3.4 people have low vision, with country and regional variation ranging from 2.4 to 5.5.By age: Visual impairment is unequally distributed across age groups. More than 82% of all people who are blind are 50 years of age and older, although they represent only 19% of the worlds population. Due to the expected number of years lived in blindness (blind years), childhood blindness remains a significant problem, with an estimated 1.4 million blind children below age 15.
By gender: Available studies consistently indicate that in every region of the world, and at all ages, females have a significantly higher risk of being visually impaired than males.By geography: Visual impairment is not distributed uniformly throughout the world. More than 90% of the worlds visually impaired live in developing countries.Since the estimates of the 1990s, new data based on the 2002 global population show a reduction in the number of people who are blind or visually impaired, and those who are blind from the effects of infectious diseases, but an increase in the number of people who are blind from conditions related to longer life spans.In 1987, it was estimated that 598,000 people in the United States met the legal definition of blindness. Of this number, 58% were over the age of 65. In 1994–1995, 1.3 million Americans reported legal blindness.

Society and culture
Legal definition
To determine which people qualify for special assistance because of their visual disabilities, various governments have specific definitions for legal blindness. In North America and most of Europe, legal blindness is defined as visual acuity (vision) of 20/200 (6/60) or less in the better eye with best correction possible. This means that a legally blind individual would have to stand 20 feet (6.1 m) from an object to see it—with corrective lenses—with the same degree of clarity as a normally sighted person could from 200 feet (61 m). In many areas, people with average acuity who nonetheless have a visual field of less than 20 degrees (the norm being 180 degrees) are also classified as being legally blind.
Approximately fifteen percent of those deemed legally blind, by any measure, have no light or form perception. The rest have some vision, from light perception alone to relatively good acuity. Low vision is sometimes used to describe visual acuities from 20/70 to 20/200.

Literature and art
Antiquity
The Moche people of ancient Peru depicted the blind in their ceramics.In Greek myth, Tiresias was a prophet famous for his clairvoyance. According to one myth, he was blinded by the gods as punishment for revealing their secrets, while another holds that he was blinded as punishment after he saw Athena naked while she was bathing. In the Odyssey, the one-eyed Cyclops Polyphemus captures Odysseus, who blinds Polyphemus to escape. In Norse mythology, Loki tricks the blind god Höðr into killing his brother Baldr, the god of happiness.
The New Testament contains numerous instances of Jesus performing miracles to heal the blind. According to the Gospels, Jesus healed the two blind men of Galilee, the blind man of Bethsaida, the blind man of Jericho and the man who was born blind.
The parable of the blind men and an elephant has crossed between many religious traditions and is part of Jain, Buddhist, Sufi and Hindu lore. In various versions of the tale, a group of blind men (or men in the dark) touch an elephant to learn what it is like. Each one feels a different part, but only one part, such as the side or the tusk. They then compare notes and learn that they are in complete disagreement.
"Three Blind Mice" is a medieval English nursery rhyme about three blind mice whose tails are cut off after chasing the farmers wife. The work is explicitly incongruous, ending with the comment Did you ever see such a sight in your life, As three blind mice?

Modern times
Poet John Milton, who went blind in mid-life, composed "On His Blindness", a sonnet about coping with blindness. The work posits that [those] who best Bear [God]s mild yoke, they serve him best.
The Dutch painter and engraver Rembrandt often depicted scenes from the apocryphal Book of Tobit, which tells the story of a blind patriarch who is healed by his son, Tobias, with the help of the archangel Raphael.Slaver-turned-abolitionist John Newton composed the hymn "Amazing Grace" about a wretch who "once was lost, but now am found, Was blind, but now I see." Blindness, in this sense, is used both metaphorically (to refer to someone who was ignorant but later became knowledgeable) and literally, as a reference to those healed in the Bible. In the later years of his life, Newton himself would go blind.
H. G. Wells story "The Country of the Blind" explores what would happen if a sighted man found himself trapped in a country of blind people to emphasise societys attitude to blind people by turning the situation on its head.
Bob Dylans anti-war song "Blowin in the Wind" twice alludes to metaphorical blindness: How many times can a man turn his head // and pretend that he just doesnt see... How many times must a man look up // Before he can see the sky?
Contemporary fiction contains numerous well-known blind characters. Some of these characters can see by means of devices, such as the Marvel Comics superhero Daredevil, who can see via his super-human hearing acuity, or Star Treks Geordi La Forge, who can see with the aid of a VISOR, a fictional device that transmits optical signals to his brain.

Sports
Blind and partially sighted people participate in sports, such as swimming, snow skiing and athletics. Some sports have been invented or adapted for the blind, such as goalball, association football, cricket, golf, tennis, bowling, and beep baseball. The worldwide authority on sports for the blind is the International Blind Sports Federation. People with vision impairments have participated in the Paralympic Games since the 1976 Toronto summer Paralympics.

Metaphorical uses
The word "blind" (adjective and verb) is often used to signify a lack of knowledge of something. For example, a blind date is a date in which the people involved have not previously met; a blind experiment is one in which information is kept from either the experimenter or the participant to mitigate the placebo effect or observer bias. The expression "blind leading the blind" refers to incapable people leading other incapable people. Being blind to something means not understanding or being aware of it. A "blind spot" is an area where someone cannot see: for example, where a car driver cannot see because parts of his cars bodywork are in the way; metaphorically, a topic on which an individual is unaware of their own biases, and therefore of the resulting distortions of their own judgements (see Bias blind spot).

Research
A 2008 study tested the effect of using gene therapy to help restore the sight of patients with a rare form of inherited blindness, known as Lebers congenital amaurosis or LCA. Lebers Congenital Amaurosis damages the light receptors in the retina and usually begins affecting sight in early childhood, with worsening vision until complete blindness around the age of 30. The study used a common cold virus to deliver a normal version of the gene called RPE65 directly into the eyes of affected patients. All three patients, aged 19, 22 and 25, responded well to the treatment and reported improved vision following the procedure.
Two experimental treatments for retinal problems include a cybernetic replacement and transplant of fetal retinal cells.There is no high-quality evidence on the effect of assistive technologies on educational outcomes and quality of life in children with low vision as of 2015, nor is there evidence on magnifying reading aids in children </s>