<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 MELAS syndrome and can you explain it in depth? [/INST] Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the family of mitochondrial diseases, which also include MIDD (maternally inherited diabetes and deafness,  MERRF syndrome, and Lebers hereditary optic neuropathy. It was first characterized under this name in 1984. A feature of these diseases is that they are caused by defects in the mitochondrial genome which is inherited purely from the female parent. The most common MELAS mutation is mitochondrial mutation, mtDNA, referred to as m.3243A>G.

Signs and symptoms
MELAS is a condition that affects many of the bodys systems, particularly the brain and nervous system (encephalo-) and muscles (myopathy). In most cases, the signs and symptoms of this disorder appear in childhood following a period of normal development. Children with MELAS often have normal early psychomotor development until the onset of symptoms between 2 and 10 years old. Though less common, infantile onset may occur and may present as failure to thrive, growth retardation and progressive deafness. Onset in older children typically presents as recurrent attacks of a migraine-like headache, anorexia, vomiting, and seizures. Children with MELAS are also frequently found to have short stature.Most people with MELAS have a buildup of lactic acid in their bodies, a condition called lactic acidosis. Increased acidity in the blood can lead to vomiting, abdominal pain, extreme tiredness (fatigue), muscle weakness, loss of bowel control, and difficulty breathing. Less commonly, people with MELAS may experience involuntary muscle spasms (myoclonus), impaired muscle coordination (ataxia), hearing loss, heart and kidney problems, diabetes, epilepsy, and hormonal imbalances.

Differential diagnosis
The presentation of some cases is similar to that of Kearns–Sayre syndrome.Myoclonus epilepsy associated with ragged red fibers (MERRF) may be confused with MELAS as they both involve seizures, mental deterioration, and myopathy with ragged red fibers on biopsy. MERRF patients may also have hearing loss, visual disturbance secondary to optic atrophy, and short stature. The characteristic myoclonic seizure in MERRF may help to narrow diagnosis, but genetic testing should be considered to distinguish the two conditions.Leigh syndrome may also present with progressive neurological deterioration, seizures, and vomiting mainly in young children.

Genetics
MELAS is mostly caused by mutations in the genes in mitochondrial DNA, but it can also be caused by mutations in the nuclear DNA.

NADH dehydrogenase
Some of the genes (MT-ND1, MT-ND5) affected in MELAS encode proteins that are part of NADH dehydrogenase (also called complex I) in mitochondria, that helps convert oxygen and simple sugars to energy.

Transfer RNAs
Other genes (MT-TH, MT-TL1, and MT-TV) encode mitochondrial specific transfer RNAs (tRNAs).Mutations in MT-TL1 cause more than 80 percent of all cases of MELAS. They impair the ability of mitochondria to make proteins, use oxygen, and produce energy. Researchers have not determined how changes in mitochondrial DNA lead to the specific signs and symptoms of MELAS. They continue to investigate the effects of mitochondrial gene mutations in different tissues, particularly in the brain.

Inheritance
This condition is inherited in a mitochondrial pattern, which is also known as maternal inheritance and heteroplasmy. This pattern of inheritance applies to genes contained in mitochondrial DNA. Because egg cells, but not sperm cells, contribute mitochondria to the developing embryo, only females pass mitochondrial conditions to their children. Mitochondrial disorders can appear in every generation of a family and can affect both males and females, but fathers do not pass mitochondrial traits to their children. In most cases, people with MELAS inherit an altered mitochondrial gene from their mother. Less commonly, the disorder results from a new mutation in a mitochondrial gene and occurs in people with no family history of MELAS.

Diagnosis
MRI: Multifocal infarct-like cortical areas in different stages of ischemic evolution, areas that do not conform to any known vascular territory. Initial lesions often occur in the occipital or parietal lobes with eventual involvement of the cerebellum, cerebral cortex, basal ganglia, and thalamus.Lactate levels are often elevated in serum and cerebrospinal fluid. MR spectroscopy may show an elevated lactate peak in affected and even unaffected brain areas. Muscle biopsy shows ragged red fibers. However, genetic evaluation should be done first, which eliminates the need for muscle biopsy in most cases. Diagnosis may be molecular or clinical:
Stroke-like episodes before or after 40 years old
Encephalopathy with seizures or dementia
Blood lactic acidosis* or ragged red fibers on muscle biopsyDue to mitochondrial heteroplasmy, urine and blood testing is preferable to blood alone. PCR and ARMS-PCR are commonly used, reliable, rapid, and cost-effective techniques for the diagnosis of MELAS.Hearing loss and mitochondrial diabetes are common features. Eyes may have a distinctive speckled pigment in the retina, referred to as a maculopathy. Family members may present differently.

Treatment
There is no curative treatment. The disease remains progressive and fatal.Patients are managed according to what areas of the body are affected at a particular time. Enzymes, amino acids, antioxidants and vitamins have been used. Treatment for MELAS currently is 1 </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 Procedure 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 Browns syndrome and can you explain it in depth? [/INST] Browns syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose). Harold W. Brown first described the disorder in 1950 and initially named it the "superior oblique tendon sheath syndrome".

Presentation
A simple definition of the syndrome is "limited elevation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye.Harold W. Brown characterized the syndrome in many ways such as:
Limited elevation in the eye when head is straight up
Eyes point out in a straight up gaze (divergence in up gaze)
Widening of the eyelids in the affected eye on adduction
Head tilts backwards (compensatory chin elevation to avoid double vision)
Near normal elevation in abductionHe concluded that all of these features of Brown syndrome were due to the shortening or tightening of the anterior superior oblique tendon. Because this syndrome can be acquired or occur at random and has spontaneous resolution, Brown hypothesized one major truth for this disorder — that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral (on the same side) inferior oblique muscle and secondary to a permanent shortening.After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of Browns Syndrome. The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic.

Causes
Browns syndrome can be divided in two categories based on the restriction of movement on the eye itself and how it affects the eye excluding the movement:
Congenital (present at birth) Browns syndrome results from structural anomalies other than a short tendon sheath but other fibrous adhesions may be present around the trochlear area.
Acquired cases arise from trauma, surgery, sinusitis and inflammation of the superior oblique tendon sheath in rheumatoid arthritis. Orbital floor fractures may trap the orbital tissue in such a way as to simulate Browns syndrome </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Headache and can you explain it in depth? [/INST] Headache is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.Headaches can occur as a result of many conditions. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society, which classifies it into more than 150 types of primary and secondary headaches. Causes of headaches may include dehydration; fatigue; sleep deprivation; stress; the effects of medications (overuse) and recreational drugs, including withdrawal; viral infections; loud noises; head injury; rapid ingestion of a very cold food or beverage; and dental or sinus issues (such as sinusitis).Treatment of a headache depends on the underlying cause, but commonly involves pain medication (especially in case of migraine or cluster headache). A headache is one of the most commonly experienced of all physical discomforts.About half of adults have a headache in a given year. Tension headaches are the most common, affecting about 1.6 billion people (21.8% of the population) followed by migraine headaches which affect about 848 million (11.7%).

Causes
There are more than 200 types of headaches. Some are harmless and some are life-threatening. The description of the headache and findings on neurological examination, determine whether additional tests are needed and what treatment is best.Headaches are broadly classified as "primary" or "secondary". Primary headaches are benign, recurrent headaches not caused by underlying disease or structural problems. For example, migraine is a type of primary headache. While primary headaches may cause significant daily pain and disability, they are not dangerous from a physiological point of view. Secondary headaches are caused by an underlying disease, like an infection, head injury, vascular disorders, brain bleed, stomach irritation, or tumors. Secondary headaches can be dangerous. Certain "red flags" or warning signs indicate a secondary headache may be dangerous.

Primary
Ninety percent of all headaches are primary headaches. Primary headaches usually first start when people are between 20 and 40 years old. The most common types of primary headaches are migraines and tension-type headaches. They have different characteristics. Migraines typically present with pulsing head pain, nausea, photophobia (sensitivity to light) and phonophobia (sensitivity to sound). Tension-type headaches usually present with non-pulsing "bandlike" pressure on both sides of the head, not accompanied by other symptoms. Such kind of headaches maybe further classified into-episodic and chronic tension type headaches Other very rare types of primary headaches include:
cluster headaches: short episodes (15–180 minutes) of severe pain, usually around one eye, with autonomic symptoms (tearing, red eye, nasal congestion) which occur at the same time every day. Cluster headaches can be treated with triptans and prevented with prednisone, ergotamine or lithium.
trigeminal neuralgia or occipital neuralgia: shooting face pain
hemicrania continua: continuous unilateral pain with episodes of severe pain. Hemicrania continua can be relieved by the medication indomethacin.
primary stabbing headache: recurrent episodes of stabbing "ice pick pain" or "jabs and jolts" for 1 second to several minutes without autonomic symptoms (tearing, red eye, nasal congestion). These headaches can be treated with indomethacin.
primary cough headache: starts suddenly and lasts for several minutes after coughing, sneezing or straining (anything that may increase pressure in the head). Serious causes (see secondary headaches red flag section) must be ruled out before a diagnosis of "benign" primary cough headache can be made.
primary exertional headache: throbbing, pulsatile pain which starts during or after exercising, lasting for 5 minutes to 24 hours. The mechanism behind these headaches is unclear, possibly due to straining causing veins in the head to dilate, causing pain. These headaches can be prevented by not exercising too strenuously and can be treated with medications such as indomethacin.
primary sex headache: dull, bilateral headache that starts during sexual activity and becomes much worse during orgasm. These headaches are thought to be due to lower pressure in the head during sex. It is important to realize that headaches that begin during orgasm may be due to a subarachnoid hemorrhage, so serious causes must be ruled out first. These headaches are treated by advising the person to stop sex if they develop a headache. Medications such as propranolol and diltiazem can also be helpful.
hypnic headache: a moderate-severe headache that starts a few hours after falling asleep and lasts 15–30 minutes. The headache may recur several times during the night. Hypnic headaches are usually in older women. They may be treated with lithium.

Secondary
Headaches may be caused by problems elsewhere in the head or neck. Some of these are not harmful, such as cervicogenic headache (pain arising from the neck muscles). The excessive use of painkillers can paradoxically cause worsening painkiller headaches.More serious causes of secondary headaches include the following:
meningitis: inflammation of the meninges which presents with fever and meningismus, or stiff neck
bleeding inside the brain (intracranial hemorrhage)
subarachnoid hemorrhage (acute, severe headache, stiff neck without fever)
ruptured aneurysm, arteriovenous malformation, intraparenchymal hemorrhage (headache only)
brain tumor: dull headache, worse with exertion and change in position, accompanied by nausea and vomiting. Often, the person will have nausea and vomiting for weeks before the headache starts.
temporal arteritis: inflammatory disease of arteries common in the elderly (average age 70) with fever, headache, weight loss, jaw claudication, tender vessels by the temples, polymyalgia rheumatica
acute closed-angle glaucoma (increased pressure in the eyeball): a headache that starts with eye pain, blurry vision, associated with nausea and vomiting. On physical exam, the person will have red eyes and a fixed, mid-dilated pupil.
Post-ictal headaches: Headaches that happen after a convulsion or other type of seizure, as part of the period after the seizure (the post-ictal state)Gastrointestinal disorders may cause headaches, including Helicobacter pylori infection, celiac disease, non-celiac gluten sensitivity, irritable bowel syndrome, inflammatory bowel disease, gastroparesis, and hepatobiliary disorders. The treatment of the gastrointestinal disorders may lead to a remission or improvement of headaches.Migraine headaches are also associated with Cyclic Vomiting Syndrome (CVS). CVS is characterized by episodes of severe vomiting, and often occur alongside symptoms similar to those of migraine headaches (photophobia, abdominal pain, etc.).

Pathophysiology
The brain itself is not sensitive to pain, because it lacks pain receptors. However, several areas of the head and neck do have pain receptors and can thus sense pain. These include the extracranial arteries, middle meningeal artery, large veins, venous sinuses, cranial and spinal nerves, head and neck muscles, the meninges, falx cerebri, parts of the brainstem, eyes, ears, teeth, and lining of the mouth. Pial arteries, rather than pial veins are responsible for pain production.Headaches often result from traction to or irritation of the meninges and blood vessels. The pain receptors may be stimulated by head trauma or tumors and cause headaches. Blood vessel spasms, dilated blood vessels, inflammation or infection of meninges and muscular tension can also stimulate pain receptors. Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signalling that a part of the body hurts.Primary headaches are more difficult to understand than secondary headaches. The exact mechanisms which cause migraines, tension headaches and cluster headaches are not known. There have been different hypotheses over time that attempt to explain what happens in the brain to cause these headaches.Migraines are currently thought to be caused by dysfunction of the nerves in the brain. Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted.  Studies have shown migraine head pain is not accompanied by extracranial vasodilation, but rather only has some mild intracranial vasodilation.Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression followed by a period of depressed activity. Some people think headaches are caused by the activation of sensory nerves which release peptides or serotonin, causing inflammation in arteries, dura and  meninges and also cause some vasodilation. Triptans, medications that treat migraines, block serotonin receptors and constrict blood vessels.People who are more susceptible to experiencing migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pills or are prescribed hormone replacement therapy.Tension headaches are thought to be caused by activation of peripheral nerves in the head and neck muscles.Cluster headaches involve overactivation of the trigeminal nerve and hypothalamus in the brain, but the exact cause is unknown.

Diagnosis
Most headaches can be diagnosed by the clinical history alone. If the symptoms described by the person sound dangerous, further testing with neuroimaging or lumbar puncture may be necessary. Electroencephalography (EEG) is not useful for headache diagnosis.The first step to diagnosing a headache is to determine if the headache is old or new. A "new headache" can be a headache that has started recently, or a chronic headache that has changed character. For example, if a person has chronic weekly headaches with pressure on both sides of his head, and then develops a sudden severe throbbing headache on one side of his head, they have a new headache.

Red flags
It can be challenging to differentiate between low-risk, benign headaches and high-risk, dangerous headaches since symptoms are often similar. Headaches that are possibly dangerous require further lab tests and imaging to diagnose.The American College for Emergency Physicians published criteria for low-risk headaches. They are as follows:
age younger than 30 years
features typical of primary headache
history of similar headache
no abnormal findings on neurologic exam
no concerning change in normal headache pattern
no high-risk comorbid conditions (for example, HIV)
no new concerning history or physical examination findingsA number of characteristics make it more likely that the headache is due to potentially dangerous secondary causes which may be life-threatening or cause long-term damage. These "red flag" symptoms mean that a headache warrants further investigation with neuroimaging and lab tests.In general, people complaining of their "first" or "worst" headache warrant imaging and further workup. People with progressively worsening headache also warrant imaging, as they may have a mass or a bleed that is gradually growing, pressing on surrounding structures and causing worsening pain. People with neurological findings on exam, such as weakness, also need further workup.The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache:
Systemic symptoms (fever or weight loss)
Systemic disease (HIV infection, malignancy)
Neurologic symptoms or signs
Onset sudden (thunderclap headache)
Onset after age 40 years
Previous headache history (first, worst, or different headache)Other red flag symptoms include:

Old headaches
Old headaches are usually primary headaches and are not dangerous. They are most often caused by migraines or tension headaches. Migraines are often unilateral, pulsing headaches accompanied by nausea or vomiting. There may be an aura (visual symptoms, numbness or tingling) 30–60 minutes before the headache, warning the person of a headache. Migraines may also not have auras. Tension-type headaches usually have bilateral "bandlike" pressure on both sides of the head usually without nausea or vomiting. However, some symptoms from both headache groups may overlap. It is important to distinguish between the two because the treatments are different.
The mnemonic POUND helps distinguish between migraines and tension-type headaches. POUND stands for:
One review article found that if 4–5 of the POUND characteristics are present, a migraine is 24 times as likely a diagnosis than a tension-type headache (likelihood ratio 24). If 3 characteristics of POUND are present, migraine is 3 times more likely a diagnosis than tension type headache (likelihood ratio 3). If only 2 POUND characteristics are present, tension-type headaches are 60% more likely (likelihood ratio 0.41). Another study found the following factors independently each increase the chance of migraine over tension-type headache: nausea, photophobia, phonophobia, exacerbation by physical activity, unilateral, throbbing quality, chocolate as a headache trigger, and cheese as a headache trigger.Cluster headaches are relatively rare (1 in 1000 people) and are more common in men than women. They present with sudden onset explosive pain around one eye and are accompanied by autonomic symptoms (tearing, runny nose and red eye).Temporomandibular jaw pain (chronic pain in the jaw joint), and cervicogenic headache (headache caused by pain in muscles of the neck) are also possible diagnoses.For chronic, unexplained headaches, keeping a headache diary can be useful for tracking symptoms and identifying triggers, such as association with menstrual cycle, exercise and food. While mobile electronic diaries for smartphones are becoming increasingly common, a recent review found most are developed with a lack of evidence base and scientific expertise.

New headaches
New headaches are more likely to be dangerous secondary headaches. They can, however, simply be the first presentation of a chronic headache syndrome, like migraine or tension-type headaches.One recommended diagnostic approach is as follows. If any urgent red flags are present such as visual loss, new seizures, new weakness, new confusion, further workup with imaging and possibly a lumbar puncture should be done (see red flags section for more details). If the headache is sudden onset (thunderclap headache), a computed tomography test to look for a brain bleed (subarachnoid hemorrhage) should be done. If the CT scan does not show a bleed, a lumbar puncture should be done to look for blood in the CSF, as the CT scan can be falsely negative and subarachnoid hemorrhages can be fatal. If there are signs of infection such as fever, rash, or stiff neck, a lumbar puncture to look for meningitis should be considered. If there is jaw claudication and scalp tenderness in an older person, a temporal artery biopsy to look for temporal arteritis should be performed and immediate treatment should be started.

Neuroimaging
Old headaches
The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered.

New headaches
All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the persons headaches.The American College of Radiology recommends the following imaging tests for different specific situations:

Lumbar puncture
A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first.

Classification
Headaches are most thoroughly classified by the International Headache Societys International Classification of Headache Disorders (ICHD), which published the second edition in 2004. The third edition of the International Headache Classification was published in 2013 in a beta version ahead of the final version. This classification is accepted by the WHO.Other classification systems exist.  One of the first published attempts was in 1951. The US National Institutes of Health developed a classification system in 1962.

ICHD-2
The International Classification of Headache Disorders (ICHD) is an in-depth hierarchical classification of headaches published by the International Headache Society. It contains explicit (operational) diagnostic criteria for headache disorders. The first version of the classification, ICHD-1, was published in 1988. The current revision, ICHD-2, was published in 2004. The classification uses numeric codes. The top, one-digit diagnostic level includes 14 headache groups. The first four of these are classified as primary headaches, groups 5-12 as secondary headaches, cranial neuralgia, central and primary facial pain and other headaches for the last two groups.The ICHD-2 classification defines migraines, tension-types headaches, cluster headache and other trigeminal autonomic headache as the main types of primary headaches. Also, according to the same classification, stabbing headaches and headaches due to cough, exertion and sexual activity (sexual headache) are classified as primary headaches. The daily-persistent headaches along with the hypnic headache and thunderclap headaches are considered primary headaches as well.Secondary headaches are classified based on their cause and not on their symptoms. According to the ICHD-2 classification, the main types of secondary headaches include those that are due to head or neck trauma such as whiplash injury, intracranial hematoma, post craniotomy or other head or neck injury. Headaches caused by cranial or cervical vascular disorders such as ischemic stroke and transient ischemic attack, non-traumatic intracranial hemorrhage, vascular malformations or arteritis are also defined as secondary headaches. This type of headache may also be caused by cerebral venous thrombosis or different intracranial vascular disorders. Other secondary headaches are those due to intracranial disorders that are not vascular such as low or high pressure of the cerebrospinal fluid pressure, non-infectious inflammatory disease, intracranial neoplasm, epileptic seizure or other types of disorders or diseases that are intracranial but that are not associated with the vasculature of the central nervous system.ICHD-2 classifies headaches that are caused by the ingestion of a certain substance or by its withdrawal as secondary headaches as well. This type of headache may result from the overuse of some medications or exposure to some substances. HIV/AIDS, intracranial infections and systemic infections may also cause secondary headaches. The ICHD-2 system of classification includes the headaches associated with homeostasis disorders in the category of secondary headaches. This means that headaches caused by dialysis, high blood pressure, hypothyroidism, cephalalgia and even fasting are considered secondary headaches. Secondary headaches, according to the same classification system, can also be due to the injury of any of the facial structures including teeth, jaws, or temporomandibular joint. Headaches caused by psychiatric disorders such as somatization or psychotic disorders are also classified as secondary headaches.The ICHD-2 classification puts cranial neuralgias and other types of neuralgia in a different category. According to this system, there are 19 types of neuralgias and headaches due to different central causes of facial pain. Moreover, the ICHD-2 includes a category that contains all the headaches that cannot be classified.Although the ICHD-2 is the most complete headache classification there is and it includes frequency in the diagnostic criteria of some types of headaches (primarily primary headaches), it does not specifically code frequency or severity which are left at the discretion of the examiner.

NIH
The NIH classification consists of brief definitions of a limited number of headaches.The NIH system of classification is more succinct and only describes five categories of headaches. In this case, primary headaches are those that do not show organic or structural causes. According to this classification, primary headaches can only be vascular, myogenic, cervicogenic, traction, and inflammatory.

Management
Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit.

Migraines
Migraine can be somewhat improved by lifestyle changes, but most people require medicines to control their symptoms. Medications are either to prevent getting migraines, or to reduce symptoms once a migraine starts.Preventive medications are generally recommended when people have more than four attacks of migraine per month, headaches last longer than 12 hours or the headaches are very disabling. Possible therapies include beta blockers, antidepressants, anticonvulsants and NSAIDs. The type of preventive medicine is usually chosen based on the other symptoms the person has. For example, if the person also has depression, an antidepressant is a good choice.Abortive therapies for migraines may be oral, if the migraine is mild to moderate, or may require stronger medicine given intravenously or intramuscularly. Mild to moderate headaches should first be treated with acetaminophen (paracetamol) or NSAIDs, like ibuprofen. If accompanied by nausea or vomiting, an antiemetic such as metoclopramide (Reglan) can be given orally or rectally. Moderate to severe attacks should be treated first with an oral triptan, a medication that mimics serotonin (an agonist) and causes mild vasoconstriction. If accompanied by nausea and vomiting, parenteral (through a needle in the skin) triptans and antiemetics can be given.Sphenopalatine ganglion block (SPG block, also known nasal ganglion block or pterygopalatine ganglion blocks) can abort and prevent migraines, tension headaches and cluster headaches. It was originally described by American ENT surgeon Greenfield Sluder in 1908. Both blocks and neurostimulation have been studied as treatment for headaches.Several complementary and alternative strategies can help with migraines. The American Academy of Neurology guidelines for migraine treatment in 2000 stated relaxation training, electromyographic feedback and cognitive behavioral therapy may be considered for migraine treatment, along with medications.

Tension-type headaches
Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen, aspirin), or acetaminophen. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches.

Cluster headaches
Abortive therapy for cluster headaches includes subcutaneous sumatriptan (injected under the skin) and triptan nasal sprays. High flow oxygen therapy also helps with relief.For people with extended periods of cluster headaches, preventive therapy can be necessary. Verapamil is recommended as first line treatment. Lithium can also be useful. For people with shorter bouts, a short course of prednisone (10 days) can be helpful. Ergotamine is useful if given 1–2 hours before an attack.

Secondary headaches
Treatment of secondary headaches involves treating the underlying cause. For example, a person with meningitis will require antibiotics. A person with a brain tumor may require surgery, chemotherapy or brain radiation.

Neuromodulation
Peripheral neuromodulation has tentative benefits in primary headaches including cluster headaches and chronic migraine. How it may work is still being looked into.

Epidemiology
Literature reviews find that approximately 64–77% of adults have had a headache at some point in their lives.  During each year, on average, 46–53% of people have headaches. However, the prevalence of headache varies widely depending on how the survey was conducted, with studies finding lifetime prevalence of as low as 8% to as high as 96%.  Most of these headaches are not dangerous. Only approximately 1–5% of people who seek emergency treatment for headaches have a serious underlying cause.More than 90% of headaches are primary headaches. Most of these primary headaches are tension headaches. Most people with tension headaches have "episodic" tension headaches that come and go. Only 3.3% of adults have chronic tension headaches, with headaches for more than 15 days in a month.Approximately 12–18% of people in the world have migraines. More women than men experience migraines. In Europe and North America, 5–9% of men experience migraines, while 12–25% of women experience migraines.Cluster headaches are relatively uncommon. They affect only 1–3 per thousand people in the world. Cluster headaches affect approximately three times as many men as women.

History
The first recorded classification system was published by Aretaeus of Cappadocia, a medical scholar of Greco-Roman antiquity. He made a distinction between three different types of headache: i) cephalalgia, by which he indicates a shortlisting, mild headache; ii) cephalea, referring to a chronic type of headache; and iii) heterochromia, a paroxysmal headache on one side of the head.
Another classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories.

Children
In general, children experience the same types of headaches as adults do, but their symptoms may be slightly different. The diagnostic approach to headaches in children is similar to that of adults. However, young children may not be able to verbalize pain well. If a young child is fussy, they may have a headache.Approximately 1% of emergency department visits for children are for headache. Most of these headaches are not dangerous. The most common type of headache seen in pediatric emergency rooms is headache caused by a cold (28.5%). Other headaches diagnosed in the emergency department include post-traumatic headache (20%), headache related to a problem with a ventriculoperitoneal shunt (a device put into the brain to remove excess CSF and reduce pressure in the brain) (11.5%) and migraine (8.5%). The most common serious headaches found in children include brain bleeds (subdural hematoma, epidural hematoma), brain abscesses, meningitis and ventriculoperitoneal shunt malfunction </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 Viral cardiomyopathy 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 Argyll Robertson pupil and can you explain it in depth? [/INST] Argyll Robertson pupils (AR pupils) are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not react). They are a highly specific sign of neurosyphilis; however, Argyll Robertson pupils may also be a sign of diabetic neuropathy. In general, pupils that accommodate but do not react are said to show light-near dissociation (i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation/convergence).AR pupils are extremely uncommon in the developed world.  There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult.

Pathophysiology
The two different types of near response are caused by different underlying disease processes.  Adies pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear, but is believed to be the result of bilateral damage to the pretectal nuclei in the midbrain. Studies have failed to demonstrate a focal localising lesion. Research has implicated the rostral midbrain in the vicinity of the cerebral aqueduct of the third ventricle as the most likely region of damage. A lesion in this area would involve efferent pupillary fibres on the dorsal aspect of the Edinger-Westphal nucleus (associated with the response to light) while sparing the fibres associated with the response to near, which lie slightly more ventrally.
The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time.  The older literature on AR pupils did not report the details of pupillary constriction (brisk vs. tonic) that are necessary to distinguish AR pupils from tonic pupils. Tonic pupils can occur in neurosyphilis.  It is not known whether neurosyphilis itself (infection by Treponema pallidum) can cause tonic pupils, or whether tonic pupils in syphilis simply reflect a coexisting peripheral neuropathy.
Thompson and Kardon summarize the present view:

The evidence supports a midbrain cause of the AR pupil, provided one follows Loewenfeld’s definition of the AR pupil as small pupils that react very poorly to light and yet seem to retain a normal pupillary near response that is definitely not tonic.To settle the question of whether the AR pupil is of central or peripheral origin, it will be necessary to perform iris transillumination (or a magnified slit-lamp examination) in a substantial  number of patients who have a pupillary light-near dissociation (with and without tonicity of the near reaction), perhaps in many parts of the world.

Parinaud syndrome
A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome.  This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react."  The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction.
Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome.  It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions.
The condition is diagnosed clinically by a physician.

Treatment
There is no definite treatment, but, because syphilis may be an underlying cause, it should be treated.
However, because this sign is associated with neurosyphilis, it should be treated with crystalline penicillin 24 mU intravenous per day for 10 to 14 days. If the patient is allergic to penicillin, they should undergo desensitization and then be treated.

History
Argyll Robertson pupils were named after Douglas Argyll Robertson (1837–1909), a Scottish ophthalmologist and surgeon who described the condition in the mid-1860s in the context of neurosyphilis.
In the early 20th century, William John Adie described a second type of pupil that could "accommodate but not react".  Adies tonic pupil is usually associated with a benign peripheral neuropathy (Adie syndrome), not with syphilis.When penicillin became widely available in the 1940s, the prevalence of AR pupils (which develop only after decades of untreated infection) decreased dramatically.  AR pupils are now quite rare.  A patient whose pupil “accommodates but does not react” almost always has a tonic pupil, not an AR pupil.
In the 1950s, Loewenfeld distinguished between the two types of pupils by carefully observing the exact way in which the pupils constrict with near vision.  The near response in AR pupils is brisk and immediate </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 Hypernasal speech and can you explain it in depth? [/INST] Hypernasal speech is a disorder that causes abnormal resonance in a humans voice due to increased airflow through the nose during speech. It is caused by an open nasal cavity resulting from an incomplete closure of the soft palate and/or velopharyngeal sphincter. In normal speech, nasality is referred to as nasalization and is a linguistic category that can apply to vowels or consonants in a specific language. The primary underlying physical variable determining the degree of nasality in normal speech is the opening and closing of a velopharyngeal passage way between the oral vocal tract and the nasal vocal tract.  In the normal vocal tract anatomy, this opening is controlled by lowering and raising the velum or soft palate, to open or close, respectively, the velopharyngeal passageway.

Anatomy
The palate comprises two parts, the hard palate (palatum durum) and the soft palate (palatum molle), which is connected to the uvula. The movements of the soft palate and the uvula are made possible by the velopharyngeal sphincter. During speech or swallowing, the soft palate lifts against the back throat wall to close the nasal cavity. When producing nasal consonants (such as "m", "n", and "ng"), the soft palate remains relaxed, thereby enabling the air to go through the nose.
The Eustachian tube, which opens near the velopharyngeal sphincter, connects the middle ear and nasal pharynx. Normally, the tube ensures aeration and drainage (of secretions) of the middle ear. Narrow and closed at rest, it opens during swallowing and yawning, controlled by the tensor veli palatini and the levator veli palatini (muscles of the soft palate). Children with a cleft palate have difficulties controlling these muscles and thus are unable to open the Eustachian tube. Secretions accumulate in the middle ear when the tube remains dysfunctional over a long period of time, which cause hearing loss and middle ear infections. Ultimately, hearing loss can lead to impaired speech and language development.

Causes
The general term for disorders of the velopharyngeal valve is velopharyngeal dysfunction (VPD). It includes three subterms: velopharyngeal insufficiency, velopharyngeal inadequacy, and velopharyngeal mislearning.

Velopharyngeal insufficiency can be caused by an anatomical abnormality of the throat. It occurs in children with a history of cleft palate or submucous cleft, who have short or otherwise abnormal vela. Velopharyngeal insufficiency can also occur after adenoidectomy.
Velopharyngeal incompetence is a defective closure of the velopharyngeal valve due to its lack of speed and precision. It is caused by a neurologic disorder or injury (e.g. cerebral palsy or traumatic brain injury).
Sometimes children present no abnormalities yet still have hypernasal speech: this can be due to velopharyngeal mislearning, indicating that the child has been imitating or has never learned how to use the valve correctly.

Diagnosis
There are several methods for diagnosing hypernasality.

A speech therapist listens to and records the child while analysing perceptual speech. In hypernasality, the child cannot produce oral sounds (vowels and consonants) correctly. Only the nasal sounds can be correctly produced. A hearing test is also desirable.
A mirror is held beneath the nose while the child pronounces the vowels. Nasal air escape, and thus hypernasality, is indicated if the mirror fogs up.
A pressure-flow technique is used to measure velopharyngeal orifice area during the speech. The patient must be at least three to four years old.
A video nasopharyngeal endoscopy observes velopharyngeal function, movements of the soft palate, and pharyngeal walls. It utilises a very small scope placed in the back of the nasal cavity. The doctor will then ask the child to say a few words. The patient must be at least three to four years old to ensure cooperation.
A cinefluoroscopy gives dynamic visualisation and can easier be applied to younger children, though it has the disadvantage of exposing the patient to radiation.
A nasometer calculates the ratio of nasality. The patient wears a headset, where the oral and nasal cavities are separated by a plate. On both sides of the plate are microphones. The ratio calculated by the nasometer indicates the amount of nasality, with a higher ratio indicating more nasality.

Effects on Speech
Hypernasality is generally segmented into so-called resonance effects in vowels and some voiced or sonorant consonants and the effects of excess nasal airflow during those consonants requiring a buildup of oral air pressure, such as stop consonants (as /p/) or sibilants (as /s/).  The latter nasal airflow problem is termed nasal emission, and acts to prevent the buildup of air pressure and thus prevent the normal production of the consonant.  In testing for resonance effects without the aid of technology, speech pathologists are asked to rate the speech by listening to a recorded sentence or paragraph, though there is much variability in such subjective ratings, for at least two reasons. First, the acoustic effect of a given velopharyngeal opening varies greatly depending on the degree of occlusion of the nasal passageways.  (This is the reason why a stuffy nose from an allergy or cold will sound more nasal than when the nose is clear.)  Secondly, for many persons with hypernasal speech, especially hearing impaired, there are also mispronunciations of the articulation of the vowels.  It is extremely difficult to separate the acoustic effects of hypernasality from the acoustic effects of mispronounced vowels (examples).  Of course, in speech training of the hearing impaired, there is little possibility of making nasality judgments aurally, and holding a finger to the side of the nose, to feel voice frequency vibration, is sometimes recommended.

Treatment
Speech therapy
In cases of muscle weakness or cleft palate, special exercises can help to strengthen the soft palate muscles with the ultimate aim of decreasing airflow through the nose and thereby increasing intelligibility. Intelligibility requires the ability to close the nasal cavity, as all English sounds, except the nasal sounds "m" [m], "n" [n], and "ng" [ŋ], have airflow only through the mouth. Normally, by age three, a child can raise the muscles of the soft palate to close to nasal cavity.
Without the use of a technological aid, nasal emission is sometimes judged by listening for any turbulence that may be produced by the nasal airflow, as when there is a small velopharyngeal opening and there is some degree of mucous in the opening.  More directly, methods recommended include looking for the fogging of a mirror held near the nares or listening through a tube, the other end of which is held in or near a nares opening.There have been many attempts to use technological augmentation more than a mirror or tube to aid the speech pathologist or provide meaningful feedback to the person attempting to correct their hypernasality.  Among the more successful of these attempts, the incompleteness of velopharyngeal closure during vowels and sonorants that causes nasal resonance can be estimated and displayed for evaluation or biofeedback in speech training through the nasalance of the voice, with nasalance defined as a ratio of acoustic energy at the nostrils to that at the mouth, with some form of acoustic separation present between the mouth and nose.  In the nasalance measurement system sold by WEVOSYS, the acoustic separation is provided by a mask-tube system, nasalance measurement system sold by Kay-Pentax, the acoustic separation is provided by a solid flat partition held against the upper lip, while in the system sold by Glottal Enterprises the acoustic separation can be by either a solid flat partition or a two-chamber mask.However, devices for measuring nasalance do not measure nasal emission during pressure consonants.  Because of this, a means for measuring the degree of velopharyngeal closure in consonants is also needed.  A commercially available device for making such measurements is the Perci-Sar system from Microtronics. The Nasality Visualization System from Glottal Enterprises allows both the measurement of Nasal Emission and Nasalance. In the presence of a cleft palate, either of these systems can be helpful in evaluating the need for an appliance or surgical intervention to close the cleft or the success of an appliance or a surgical attempt to close the cleft.

Exercises
If a child finds it difficult to blow, pinching the nose can help regulate airflow. The child should then practice speech sounds without pinching the nose.
These exercises only work as treatments if hypernasality is small. Severe deviations should be treated surgically.

CPAP
There is insufficient evidence to support the use of traditional non-speech oral motor exercises can reduce hypernasality. Velopharyngeal closure patterns and their underlying neuromotor control may differ for speech and nonspeech activities. Therefore, the increase in velar movement through blowing, sucking, and swallowing may not transfer to speech tasks. Thus, hypernasality remains while individual speak. Kuehn proposed a new way of treatment by using a CPAP machine during speech tasks. The positive pressure provided by a CPAP machine provides resistance to strengthen velopharyngeal muscles. With nasal mask in place, an individual is asked to produce VNCV syllables and short sentences. It is believed that CPAP therapy can increase both muscle endurance as well as strength because it overloads the levator veli palatini muscle and involves a regimen with a large number of repetitions of velar elevation. Research findings proved that patients with hypernasality due to flaccid dysarthria, TBI or cleft palate do eliminate hypernasality after receiving this training program.

Surgery
The two main surgical techniques for correcting the aberrations the soft palate present in hypernasality are the posterior pharyngeal flap and the sphincter pharyngoplasty. After surgical interventions, speech therapy is necessary to learn how to control the newly constructed flaps.

Posterior pharyngeal flap
Posterior pharyngeal flap surgery is mostly used for vertical clefts of the soft palate. The surgeon cuts through the upper layers of the back of the throat, creating a small square of tissue </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 Sister and can you explain it in depth? [/INST] A sister is a woman or a girl who shares one or more parents with another individual; a female sibling. The male counterpart is a brother. Although the term typically refers to a familial relationship, it is sometimes used endearingly to refer to non-familial relationships. A full sister is a first degree relative.

Overview
The English word sister comes from Old Norse systir which itself derives from Proto-Germanic *swestēr,  both of which have the same meaning, i.e. sister. Some studies have found that sisters display more traits indicating jealousy around their siblings than their male counterparts, brothers. In some cultures, sisters are afforded a role of being under the protection by male siblings, especially older brothers from issues ranging from bullies or sexual advances by womanizers. In some quarters the term sister has gradually broadened its colloquial meaning to include individuals stipulating kinship. In response, in order to avoid equivocation, some publishers prefer the usage of female sibling over sister. Males with a twin sister sometimes view her as their female alter ego, or what they would have been like, if they had two X chromosomes. A study in Perth Australia found that girls having only youngers brothers resulted in a chastity effect, losing their virginity on average more than a year later than average </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 Monocytosis 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 Plica syndrome and can you explain it in depth? [/INST] Plica syndrome is a condition that occurs when a plica (a vestigial extension of the protective synovial capsule of usually the knee) becomes irritated, enlarged, or inflamed.

Cause
This inflammation is typically caused by the plica being caught on the femur, or pinched between the femur and the patella </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 Disorder 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 Tinea manuum and can you explain it in depth? [/INST] Tinea manuum is a fungal infection of the hand, mostly a type of dermatophytosis, often part of two feet-one hand syndrome. There is diffuse scaling on the palms or back of usually one hand and the palmer creases appear more prominent. When both hands are affected, the rash looks different on each hand, with palmer creases appearing whitish if the infection has been present for a long time. It can be itchy and look slightly raised. Nails may also be affected.The most common cause is Trichophyton rubrum. The infection can result from touching another area of the body with a fungal infection such as athletes foot or fungal infection of groin, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors include diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet. Pet owners and farmworkers are also at higher risk. Machine operators, mechanics, gas/electricity workers and people who work with chemicals have also been reported to be at greater risk.Diagnosis is by visualization, direct microscopy and culture. Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole taken by mouth might be options.It occurs worldwide. One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male,

Signs and symptoms
There is usually an itch, with generalised dry flaky thick skin of the palm of a hand. Frequently, one hand is affected, but it can be in both </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 Pantothenate kinase-associated neurodegeneration and can you explain it in depth? [/INST] Pantothenate kinase-associated neurodegeneration (PKAN), formerly called Hallervorden–Spatz syndrome, is a genetic degenerative disease of the brain that can lead to parkinsonism, dystonia, dementia, and ultimately death. Neurodegeneration in PKAN is accompanied by an excess of iron that progressively builds up in the brain.
PKAN is caused by loss of function of the enzyme PANK2, due to bi-allelic genetic mutations. It follows autosomal recessive inheritance. This enzyme is the first step in the pathway converting vitamin B5 into coenzyme A. There are currently no treatments that modify disease progress, though there are a number of medications and therapies that can help improve symptoms and there is active research into treatments.

Signs and symptoms
Symptoms typically begin in childhood and are progressive, often resulting in death by early adulthood. Symptoms of PKAN begin before middle childhood, and most often are noticed before ten years of age. Symptoms include:
dystonia (repetitive uncontrollable muscle contractions that may cause jerking or twisting of certain muscle groups)
dysphagia & dysarthria due to muscle groups involved in speech being involved
rigidity/stiffness of limbs
tremor
writhing movements
dementia
spasticity
weakness
seizures (rare)
toe walking
retinitis pigmentosa, another degenerative disease that affects the individuals retina, often causing alteration of retinal color and progressive deterioration of the retina at first causing night blindness and later resulting in a complete loss of vision.25% of individuals experience an uncharacteristic form of PKAN that develops post-10 years of age and follows a slower, more gradual pace of deterioration than those pre-10 years of age. These individuals face significant speech deficits as well as psychiatric and behavioral disturbances.Being a progressive, degenerative nerve illness, PKAN leads to early immobility and often death by early adulthood. Death occurs prematurely due to infections such as pneumonia, and the disease in itself is technically not life limiting.

Genetics
PKAN is an autosomal recessive disorder. Both the parents of an affected child must be heterozygous carriers for the disease and therefore must carry one mutant allele. As it is an autosomal disorder, those heterozygous for the disorder may not display any atypical characteristics that are considered suggestive of the disorder, however there have been reported cases of compound heterozygosity in which heterozygous individuals do develop the classic form of the disease.The disorder is caused by a mutant PANK2 gene located at the chromosomal locus: 20p13-p12.3. PANK2 is responsible for coding the protein Pantothenate kinase 2. PANK2 encodes the enzyme pantothenate kinase, and mutations in the gene lead to an inborn error of vitamin B5 (pantothenate) metabolism. Vitamin B5 is required for the production of coenzyme A in cells. Disruption of this enzyme affects energy and lipid metabolism and may lead to accumulation of potentially harmful compounds in the brain, including iron.PANK2 encodes a 1.85Kb transcript which is derived from seven exons covering a total distance of approximately 3.5Mb of genomic DNA. The PANK2 gene also encodes a 50.5-kDaprotein that is a functional pantothenate kinase, an essential regulatory enzyme in coenzyme A (CoA) biosynthesis, and catalyzing the phosphorylation of pantothenate (vitamin B5), N-pantothenoyl-cysteine, and pantetheine (OMIM).
Mutant PANK2 gene coded proteins are often caused by null or missense mutations most notably a 7bp deletion in the PANK2 gene coding sequence.This disorder has been reported in specific communities based on intra-community marriages where both parents of the child are carrying the same mutation. One of the communities reported is Agrawal (Agarwal) Community mainly based in Northern Part of India. The known mutation in Agarwal community is pathogenic mutation 1c.215_216insA in PANK2 gene. This is also coded as chr20:3870292-3870293insA by some labs. It results in a frameshift and premature truncation of the protein 47 amino acids downstream to codon 183 (p.Arg183GlufsTer47; ENST00000316562).

Diagnosis
A neurological examination would show evidence of muscle rigidity; weakness; and abnormal postures, movements, and tremors. If other family members are also affected, this may help determine the diagnosis. Genetic tests can confirm an abnormal gene causing the disease. However, this test is not yet widely available. Other movement disorders and diseases must be ruled out. Individuals exhibiting any of the above listed symptoms are often tested using MRI (Magnetic Resonance Imaging) for a number of neuro-related disorders. An MRI usually shows iron deposits in the basal ganglia. Development of diagnostic criteria continues in the hope of further separating PKAN from other forms of neurodegenerative diseases featuring NBIA.

Neuropathology
Microscopic features of PKAN include high levels of iron in the globus pallidus and the pars reticulata of substantia nigra, evident as a characteristic rust-brown discoloration in a pattern called the eye-of-the-tiger sign; lipofuscin and neuromelanin concentrated in the iron-accumulating areas; oval, nonnucleated structures representing swollen axons whose cytoplasm swells with vacuoles, referred to as spheroids, axon schollen, or neuroaxonal dystrophy; and Lewy bodies.

Treatment
Phosphopantothenate has been shown to treat PKAN in a human, and also in a mouse model of the disease. Pantethine (a precursor of pantetheine) has been studied and shown to be effective in a mouse and in a fruit fly model of the disease.

Prognosis
Survival rates for those diagnosed with typical PKAN, and left untreated is 11.18 years with a standard deviation of 7.8 years. A study reporting good outcomes in a single patient with late onset PKAN has been performed.

Epidemiology
Prevalence data regarding this disorder remains incomplete, however it is estimated that anywhere between 1 in 1,000,000 to 3 in 1,000,000 individuals will be affected by this disorder (based upon observed cases in a population), but once again this is only an estimate as the disease is so rare it is difficult to statistically and accurately ascertain.

History
PKAN was first described by Hallervorden and Spatz (1922). Their discovery was brought about by a diagnosis of a family of 12 in which five sisters exhibited progressively increasing dementia and dysarthria. Autopsies revealed brown discolorations in different areas of the brain (particularly of interest were the globus pallidus and substantia nigra regions). Further investigation and description was brought about by Meyer (1958) who diagnosed 30 separate cases of PKAN. Meyer(1958) was followed by Elejalde et al. (1978) who described 5 affected family members and hypothesized that the disorder originated in central Europe, backing up his hypothesis with clinical and genetic analysis. Further investigation and insights were provided by Malmstrom-Groth and Kristensson (1982) and Jankovic et al. (1985).Diagnosis of PKAN hit a milestone with the availability of MRIs, as well as the in-depth descriptions of those MRIs provided by Littrup and Gebarski (1985), Tanfani et al. (1987), Sethi et al </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 Activity 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 Thoracic cavity 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 Trichorrhexis nodosa 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 Alcohol dependence and can you explain it in depth? [/INST] Alcohol dependence is a previous (DSM-IV and ICD-10) psychiatric diagnosis in which an individual is physically or psychologically dependent upon alcohol (also chemically known as ethanol).
In 2013, it was reclassified as alcohol use disorder in DSM-5, which combined alcohol dependence and alcohol abuse into this diagnosis.

Definition
Diagnosis
DSM: Alcohol dependence
According to the DSM-IV criteria for alcohol dependence, at least three out of seven of the following criteria must be manifest during a 12-month period:

Tolerance
Withdrawal symptoms or clinically defined alcohol withdrawal syndrome
Use in larger amounts or for longer periods than intended
Persistent desire or unsuccessful efforts to cut down on alcohol use
Time is spent obtaining alcohol or recovering from effects
Social, occupational and recreational pursuits are given up or reduced because of alcohol use
Use is continued despite knowledge of alcohol-related harm (physical or psychological)

Other alcohol-related disorders
Because only 3 of the 7 DSM-IV criteria for alcohol dependence are required, not all patients meet the same criteria and therefore not all have the same symptoms and problems related to drinking. Not everyone with alcohol dependence, therefore, experiences physiological dependence. Alcohol dependence is differentiated from alcohol abuse by the presence of symptoms such as tolerance and withdrawal. Both alcohol dependence and alcohol abuse are sometimes referred to by the less specific term alcoholism. However, many definitions of alcoholism exist, and only some are compatible with alcohol abuse. There are two major differences between alcohol dependence and alcoholism as generally accepted by the medical community.

Alcohol dependence refers to an entity in which only alcohol is the involved addictive agent. Alcoholism refers to an entity in which alcohol or any cross-tolerant addictive agent is involved.
In alcohol dependence, reduction of alcohol, as defined within DSM-IV, can be attained by learning to control the use of alcohol. That is, a client can be offered a social learning approach that helps them to cope with external pressures by re-learning their pattern of drinking alcohol. In alcoholism, patients are generally not presumed to be in remission unless they are abstinent from alcohol.The following elements are the template for which the degree of dependence is judged:

Narrowing of the drinking repertoire.
Increased salience of the need for alcohol over competing needs and responsibilities.
An acquired tolerance to alcohol.
Withdrawal symptoms.
Relief or avoidance of withdrawal symptoms by further drinking.
Subjective awareness of compulsion to drink.
Reinstatement after abstinence.

Screening
AUDIT has replaced older screening tools such as CAGE but there are many shorter alcohol screening tools, mostly derived from the AUDIT. The Severity of Alcohol Dependence Questionnaire (SAD-Q) is a more specific twenty-item inventory for assessing the presence and severity of alcohol dependence.

AUDIT
The Alcohol Use Disorders Identification Test (AUDIT) is considered the most accurate alcohol screening tool for identifying potential alcohol misuse, including dependence. It was developed by the World Health Organisation, designed initially for use in primary healthcare settings with supporting guidance.

CAGE
The CAGE questionnaire, the name of which is an acronym of its four questions, is a widely used method of screening for alcoholism.

Online version of the CAGE questionnaire

SADQ
The Severity of Alcohol Dependence Questionnaire (SADQ or SAD-Q) is a 20 item clinical screening tool designed to measure the presence and level of alcohol dependence.

Withdrawal
Withdrawals from alcohol dependence is a common side effect that occurs when a person with the dependency stops drinking abruptly or even cuts back on their drinking after a prolonged period of indulgence. Withdrawal from alcohol dependence can vary from mild, moderate to severe, depending on several factors such as: how long the person has been drinking, are they a binge drinker, do they relapse chronically, how much do they drink daily. All these factors can vary from one person to the next depending on psychological, environmental, and biological factors. Some common withdrawal side effects are as listed:

Mild
Nausea
Vomiting
Rapid heartbeat
Elevated blood pressure
Fatigue
Body aches / tremors
Anxiety / Irritability / Depression
Fuzzy brain
Issues with sleeping

Severe
Vomiting
Hypertensive crisis
Seizures / Tremors
Delusions / Hallucinations
Dehydration
Fever
Chills / Shakes
Extreme mood lability
Mental pandemonium
Little to no appetiteThe spectrum of alcohol withdrawal symptoms range from such minor symptoms as insomnia and tremulousness to severe complications such as withdrawal seizures and delirium tremens. Alcohol withdrawal syndrome can be very tricky to diagnose, due to other preliminary conditions that may exist from individual to individual.

Treatment
Treatments for alcohol dependence can be separated into two groups, those directed towards severely alcohol-dependent people, and those focused for those at risk of becoming dependent on alcohol.  Treatment for alcohol dependence often involves utilizing relapse prevention, support groups, psychotherapy, and setting short-term goals. The Twelve-Step Program is also a popular faith-based process used by those wishing to recover from alcohol dependence.The ultimate goal when it comes to treating alcohol dependence or as the DSM-5 now calls it alcohol use disorder, is to help with establishing abstinence from drinking. There are several other benefits that come along with treatment. For some, it is reconnecting with themselves and obtaining self-esteem and confidence, a healthier lifestyle (physically and mentally), creating new relationships with other like-minded people as well as rekindling or mending old relationships if possible. The treatment process consists typically of two parts short-term and long-term. First, there is the path to abstinence and/or recovery. There are several reasons why someone with alcohol use disorder or alcohol dependency would seek treatment. This can either be a personal reason or because of law enforcement. There is a series of different levels of treatment processes depending on the severity subtype. Some would or could benefit from medication treatment with psychosocial treatment, while others could just benefit from psychosocial treatment. Listed below are different some different types of treatments that are used with treating alcohol dependency/alcohol use disorder depending on several factors that vary from person to person.

Types of treatments:

Withdrawals (no medication aid needed)
Withdrawals (depending on severity of symptoms, could be accompanied with supervision by medical personal and medication)
Psychosocial treatment (counseling, CBT, psychoeducation, assertive community treatment)
Alcoholics Anonymous
Inpatient or outpatient programs
Social services (case management)
Al-Anon/Alateen

Epidemiology
About 12% of American adults have had an alcohol dependence problem at some time in their life. In the UK the NHS estimates that around 9% of men and 4% of UK women show signs of alcohol dependence.

History
The term alcohol dependence has replaced alcoholism as a term in order that individuals do not internalize the idea of cure and disease, but can approach alcohol as a chemical they may depend upon to cope with outside pressures.
The contemporary definition of alcohol dependence is still based upon early research.  There has been considerable scientific effort over the past several decades to identify and understand the core features of alcohol dependence. This work began in 1976, when the British psychiatrist Griffith Edwards and his American colleague Milton M </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 Sputum and can you explain it in depth? [/INST] Sputum is mucus that is coughed up from the lower airways (the trachea and bronchi). In medicine, sputum samples are usually used for a naked eye examination, microbiological investigation of respiratory infections and cytological investigations of respiratory systems. It is crucial that the specimen does not include any mucoid material from the nose or oral cavity.
A naked eye exam of the sputum can be done at home by a patient in order to note the various colors (see below). Any hint of yellow or green color (pus) suggests an airway infection (but does not indicate the type of organism causing it). Such color hints are best detected when the sputum is viewed on a very white background such as white paper, a white pot or a white sink surface. The more intense the yellow color, the more likely it is a caused by an infection (bronchitis, bronchopneumonia or pneumonia).
Having green, yellow, or thickened phlegm (sputum) does not always indicate the presence of an infection. Also, if an infection is present, the color of the phlegm (sputum) does not determine whether a virus, a bacterium or another pathogen has caused it. Simple allergies can also cause changes in the color of the mucus.

Description
The best sputum samples contain very little saliva, as saliva contaminates the sample with oral bacteria. This is especially true for samples for laboratory testing in cytology or microbiology. Specimen adequacy is assessed by the laboratory technologists by examining a Gram stain or cytology stain of the sputum. More than 25 squamous epithelial cells at low power magnification exam under the microscope strongly suggest salivary contamination </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 Congenital heart defect and can you explain it in depth? [/INST] A congenital heart defect (CHD), also known as a congenital heart anomaly and congenital heart disease, is a defect in the structure of the heart or great vessels that is present at birth. A congenital heart defect is classed as a cardiovascular disease. Signs and symptoms depend on the specific type of defect. Symptoms can vary from none to life-threatening. When present, symptoms may include rapid breathing, bluish skin (cyanosis), poor weight gain, and feeling tired. CHD does not cause chest pain. Most congenital heart defects are not associated with other diseases. A complication of CHD is heart failure.The cause of a congenital heart defect is often unknown. Risk factors include certain infections during pregnancy such as rubella, use of certain medications or drugs such as alcohol or tobacco, parents being closely related, or poor nutritional status or obesity in the mother. Having a parent with a congenital heart defect is also a risk factor. A number of genetic conditions are associated with heart defects, including Down syndrome, Turner syndrome, and Marfan syndrome. Congenital heart defects are divided into two main groups: cyanotic heart defects and non-cyanotic heart defects, depending on whether the child has the potential to turn bluish in color. The defects may involve the interior walls of the heart, the heart valves, or the large blood vessels that lead to and from the heart.Congenital heart defects are partly preventable through rubella vaccination, the adding of iodine to salt, and the adding of folic acid to certain food products. Some defects do not need treatment. Others may be effectively treated with catheter based procedures or heart surgery. Occasionally a number of operations may be needed, or a heart transplant may be required. With appropriate treatment, outcomes are generally good, even with complex problems.Congenital heart defects are the most common birth defect. In 2015, they were present in 48.9 million people globally. They affect between 4 and 75 per 1,000 live births, depending upon how they are diagnosed. In about 6 to 19 per 1,000 they cause a moderate to severe degree of problems. Congenital heart defects are the leading cause of birth defect-related deaths: in 2015, they resulted in 303,300 deaths, down from 366,000 deaths in 1990.

Signs and symptoms
Signs and symptoms are related to type and severity of the heart defect. Symptoms frequently present early in life, but it is possible for some CHDs to go undetected throughout life. Some children have no signs while others may exhibit shortness of breath, cyanosis, fainting, heart murmur, under-development of limbs and muscles, poor feeding or growth, or respiratory infections. Congenital heart defects cause abnormal heart structure resulting in production of certain sounds called heart murmur. These can sometimes be detected by auscultation; however, not all heart murmurs are caused by congenital heart defects.

Associated conditions
Congenital heart defects are associated with an increased incidence of seven other specific medical conditions, together being called the VACTERL association:
V — Vertebral anomalies
A — Anal atresia
C — Cardiovascular anomalies
T  — Tracheoesophageal fistula
E — Esophageal atresia
R — Renal (Kidney) and/or radial anomalies
L — Limb defectsVentricular septal defect (VSD), atrial septal defects, and tetralogy of Fallot are the most common congenital heart defects seen in the VACTERL association. Less common defects in the association are truncus arteriosus and transposition of the great arteries.

Causes
The cause of congenital heart disease may be genetic, environmental, or a combination of both.

Genetic
Genetic mutations, often sporadic, represent the largest known cause of congenital heart defects. They are described in the table below.

Molecular pathways
The genes regulating the complex developmental sequence have only been partly elucidated. Some genes are associated with specific defects. A number of genes have been associated with cardiac manifestations. Mutations of a heart muscle protein, α-myosin heavy chain (MYH6) are associated with atrial septal defects. Several proteins that interact with MYH6 are also associated with cardiac defects. The transcription factor GATA4 forms a complex with the TBX5 which interacts with MYH6. Another factor, the homeobox (developmental) gene, NKX2-5 also interacts with MYH6. Mutations of all these proteins are associated with both atrial and ventricular septal defects; In addition, NKX2-5 is associated with defects in the electrical conduction of the heart and TBX5 is related to the Holt–Oram syndrome which includes electrical conduction defects and abnormalities of the upper limb. The Wnt signaling co-factors BCL9, BCL9L and PYGO might be part of this molecular pathways, as when their genes are mutated, this causes phenotypes similar to the features present in Holt-Oram syndrome. Another T-box gene, TBX1, is involved in velo-cardio-facial syndrome DiGeorge syndrome, the most common deletion which has extensive symptoms including defects of the cardiac outflow tract including tetralogy of Fallot.
The notch signaling pathway, a regulatory mechanism for cell growth and differentiation, plays broad roles in several aspects of cardiac development. Notch elements are involved in determination of the right and left sides of the body plan, so the directional folding of the heart tube can be impacted. Notch signaling is involved early in the formation of the endocardial cushions and continues to be active as the develop into the septa and valves. It is also involved in the development of the ventricular wall and the connection of the outflow tract to the great vessels. Mutations in the gene for one of the notch ligands, Jagged1, are identified in the majority of examined cases of arteriohepatic dysplasia (Alagille syndrome), characterized by defects of the great vessels (pulmonary artery stenosis), heart (tetralogy of Fallot in 13% of cases), liver, eyes, face, and bones. Though less than 1% of all cases, where no defects are found in the Jagged1 gene, defects are found in Notch2 gene. In 10% of cases, no mutation is found in either gene. For another member of the gene family, mutations in the Notch1 gene are associated with bicuspid aortic valve, a valve with two leaflets instead of three. Notch1 is also associated with calcification of the aortic valve, the third most common cause of heart disease in adults.Mutations of a cell regulatory mechanism, the Ras/MAPK pathway are responsible for a variety of syndromes, including Noonan syndrome, LEOPARD syndrome, Costello syndrome and cardiofaciocutaneous syndrome in which there is cardiac involvement. While the conditions listed are known genetic causes, there are likely many other genes which are more subtle. It is known that the risk for congenital heart defects is higher when there is a close relative with one.

Environmental
Known environmental factors include certain infections during pregnancy such as rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus). Alcohol exposure in the father also appears to increase the risk of congenital heart defects.Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both pre-pregnancy folate deficiency and diabetes have been implicated in some studies.

Mechanism
There is a complex sequence of events that result in a well formed heart at birth and disruption of any portion may result in a defect. The orderly timing of cell growth, cell migration, and programmed cell death ("apoptosis") has been studied extensively and the genes that control the process are being elucidated.
Around day 15 of development, the cells that will become the heart exist in two horseshoe shaped bands of the middle tissue layer (mesoderm), and some cells migrate from a portion of the outer layer (ectoderm), the neural crest, which is the source of a variety of cells found throughout the body. On day 19 of development, a pair of vascular elements, the "endocardial tubes", form. The tubes fuse when cells between then undergo programmed death and cells from the first heart field migrate to the tube, and form a ring of heart cells (myocytes) around it by day 21. On day 22, the heart begins to beat and by day 24, blood is circulating.At day 22, the circulatory system is bilaterally symmetrical with paired vessels on each side and the heart consisting of a simple tube located in the midline of the body layout. The portions that will become the atria and will be located closest to the head are the most distant from the head. From days 23 through 28, the heart tube folds and twists, with the future ventricles moving left of center (the ultimate location of the heart) and the atria moving towards the head.On day 28, areas of tissue in the heart tube begin to expand inwards; after about two weeks, these expansions, the membranous "septum primum" and the muscular "endocardial cushions", fuse to form the four chambers of the heart. A failure to fuse properly will result in a defect that may allow blood to leak between chambers.  After this happens, cells that have migrated from the neural crest begin to divide the bulbus cordis, the main outflow tract is divided in two by the growth a spiraling septum, becoming the great vessels—the ascending segment of the aorta and the pulmonary trunk. If the separation is incomplete, the result is a "persistent truncus arteriosus". The vessels may be reversed ("transposition of the great vessels"). The two halves of the split tract must migrate into the correct positions over the appropriate ventricles. A failure may result in some blood flowing into the wrong vessel (e.g.overriding aorta). The four-chambered heart and the great vessels have features required for fetal growth. The lungs are unexpanded and cannot accommodate the full circulatory volume. Two structures exist to shunt blood flow away from the lungs. Cells in part of the septum primum die creating a hole while muscle cells, the "septum secundum", grow along the right atrial side the septum primum, except for one region, leaving a gap through which blood can pass from the right artium to the left atrium, the foramen ovale. A small vessel, the ductus arteriosus allows blood from the pulmonary artery to pass to the aorta.

Changes at birth
The ductus arteriosus stays open because of circulating factors including prostaglandins. The foramen ovale stays open because of the flow of blood from the right atrium to the left atrium. As the lungs expand, blood flows easily through the lungs and the membranous portion of the foramen ovale (the septum primum) flops over the muscular portion (the septum secundum). If the closure is incomplete, the result is a patent foramen ovale. The two flaps may fuse, but many adults have a foramen ovale that stays closed only because of the pressure difference between the atria.

Theories
Rokitansky (1875) explained congenital heart defects as breaks in heart development at various ontogenesis stages. Spitzer (1923) treats them as returns to one of the phylogenesis stages. Krimski (1963), synthesizing two previous points of view, considered congenital heart diseases as a stop of development at the certain stage of ontogenesis, corresponding to this or that stage of the phylogenesis. Hence these theories can explain feminine and neutral types of defects only.

Diagnosis
Many congenital heart defects can be diagnosed prenatally by fetal echocardiography. This is a test which can be done during the second trimester of pregnancy, when the woman is about 18–24 weeks pregnant. It can be an abdominal ultrasound or transvaginal ultrasound.If a baby is born with cyanotic heart disease, the diagnosis is usually made shortly after birth due to the blue colour of their skin (called cyanosis).If a baby is born with a septal defect or an obstruction defect, often their symptoms are only noticeable after several months or sometimes even after many years.

Classification
A number of classification systems exist for congenital heart defects. In 2000 the International Congenital Heart Surgery Nomenclature was developed to provide a generic classification system.

Hypoplasia
Hypoplasia can affect the heart, typically resulting in the underdevelopment of the right ventricle or the left ventricle. This causes only one side of the heart to be capable of pumping blood to the body and lungs effectively. Hypoplasia of the heart is rare but is the most serious form of CHD. It is called hypoplastic left heart syndrome when it affects the left side of the heart and hypoplastic right heart syndrome when it affects the right side of the heart. In both conditions, the presence of a patent ductus arteriosus (and, when hypoplasia affects the right side of the heart, a patent foramen ovale) is vital to the infants ability to survive until emergency heart surgery can be performed, since without these pathways blood cannot circulate to the body (or lungs, depending on which side of the heart is defective). Hypoplasia of the heart is generally a cyanotic heart defect.

Obstructive defects
Obstructive defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common defects include pulmonic stenosis, aortic stenosis, and coarctation of the aorta, with other types such as bicuspid aortic valve stenosis and subaortic stenosis being comparatively rare. Any narrowing or blockage can cause heart enlargement or hypertension.

Septal defects
The septum is a wall of tissue which separates the left heart from the right heart. Defects in the interatrial septum or the interventricular septum allow blood to flow from the left side of the heart to the right, reducing the hearts efficiency. Ventricular septal defects are collectively the most common type of CHD, although approximately 30% of adults have a type of atrial septal defect called probe patent foramen ovale.

Cyanotic defects
Cyanotic heart defects are called such because they result in cyanosis, a bluish-grey discoloration of the skin due to a lack of oxygen in the body. Such defects include persistent truncus arteriosus, total anomalous pulmonary venous connection, tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia.

Defects
Aortic stenosis
Arrhythmogenic right ventricular cardiomyopathy
Atrial septal defect (ASD)
Atrioventricular septal defect (AVSD)
Bicuspid aortic valve
Cardiomyopathy
Complete heart block (CHB)
Dextrocardia
Double inlet left ventricle (DILV)
Double outlet right ventricle (DORV)
Ebsteins anomaly
Early Repolarization Syndrome
Hypoplastic left heart syndrome (HLHS)
Hypoplastic right heart syndrome (HRHS)
Mitral stenosis
Myocardial bridge
Persistent truncus arteriosus
Pulmonary atresia
Pulmonary stenosis
Rhabdomyomas (Tumors of the Heart)
Transposition of the great vessels
dextro-Transposition of the great arteries (d-TGA)
levo-Transposition of the great arteries (l-TGA)
Tricuspid atresia
Ventricular septal defect (VSD)
Wolff–Parkinson–White syndrome (WPW)Some conditions affect the great vessels or other vessels in close proximity to the heart, but not the heart itself, but are often classified as congenital heart defects.
Coarctation of the aorta (CoA)
Double aortic arch, aberrant subclavian artery, and other malformations of the great arteries
Interrupted aortic arch (IAA)
Patent ductus arteriosus (PDA)
Scimitar syndrome (SS)
Partial anomalous pulmonary venous connection (PAPVC)
Total anomalous pulmonary venous connection (TAPVC)Some constellations of multiple defects are commonly found together.
Tetralogy of Fallot (ToF)
Pentalogy of Cantrell
Shones syndrome/ Shones complex / Shones anomaly

Treatment
CHD may require surgery and medications. Medications include diuretics, which aid the body in eliminating water, salts, and digoxin for strengthening the contraction of the heart </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 Levocardia and can you explain it in depth? [/INST]  </s>