Familial dysautonomia is seen almost exclusively in Ashkenazi Jews and is inherited in an autosomal recessive fashion. Both parents must be carriers in order for a child to be affected. The carrier frequency in Jewish individuals of Eastern European (Ashkenazi) ancestry is about 1/30, while the carrier frequency in non-Jewish individuals is unknown. If both parents are carriers, there is a one in four, or 25%, chance with each pregnancy for an affected child. Genetic counseling and genetic testing is recommended for families who may be carriers of familial dysautonomia.

Worldwide, there have been approximately 600 diagnoses recorded since discovery of the disease, with approximately 350 of them still living.

The prognosis of dysautonomia depends on several factors; individuals with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration such as Parkinson's disease or multiple system atrophy have a generally poorer long-term prognosis. Consequently, dysautonomia could be fatal due to pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest.

Autonomic dysfunction symptoms such as orthostatic hypotension, gastroparesis, and gustatory sweating are more frequently identified in mortalities.

Although the brain and spinal cord are surrounded by tough membranes, enclosed in the bones of the skull and spinal vertebrae, and chemically isolated by the blood–brain barrier, they are very susceptible if compromised. Nerves tend to lie deep under the skin but can still become exposed to damage. Individual neurons, and the neural networks and nerves into which they form, are susceptible to electrochemical and structural disruption. Neuroregeneration may occur in the peripheral nervous system and thus overcome or work around injuries to some extent, but it is thought to be rare in the brain and spinal cord.

The specific causes of neurological problems vary, but can include genetic disorders, congenital abnormalities or disorders, infections, lifestyle or environmental health problems including malnutrition, and brain injury, spinal cord injury or nerve injury. The problem may start in another body system that interacts with the nervous system. For example, cerebrovascular disorders involve brain injury due to problems with the blood vessels (cardiovascular system) supplying the brain; autoimmune disorders involve damage caused by the body's own immune system; lysosomal storage diseases such as Niemann-Pick disease can lead to neurological deterioration. The National Institutes of Health recommend considering the evaluation of an underlying celiac disease in people with unexplained neurological symptoms, particularly peripheral neuropathy or ataxia.

In a substantial minority of cases of neurological symptoms, no neural cause can be identified using current testing procedures, and such "idiopathic" conditions can invite different theories about what is occurring.

There is currently no cure for FD and death occurs in 50% of the affected individuals by age 30. There are only two treatment centers, one at New York University Hospital and one at the Sheba Medical Center in Israel. One is being planned for the San Francisco area.

The survival rate and quality of life have increased since the mid-1980s mostly due to a greater understanding of the most dangerous symptoms. At present, FD patients can be expected to function independently if treatment is begun early and major disabilities avoided.

A major issue has been aspiration pneumonia, where food or regurgitated stomach content would be aspirated into the lungs causing infections. Fundoplications (by preventing regurgitation) and gastrostomy tubes (to provide nonoral nutrition) have reduced the frequency of hospitalization.

Other issues which can be treated include FD crises, scoliosis, and various eye conditions due to limited or no tears.

An FD crisis is the body's loss of control of various autonomic nervous system functions including blood pressure, heart rate, and body temperature. Both short-term and chronic periodic high or low blood pressure have consequences and medication is used to stabilize blood pressure.

Dysautonomia may be due to inherited or degenerative neurologic diseases (primary dysautonomia) or it may occur due to injury of the autonomic nervous system from an acquired disorder (secondary dysautonomia). The most common causes of dysautonomia include

In the sympathetic nervous system (SNS), predominant dysautonomia is common along with fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis, raising the possibility that such dysautonomia could be their common clustering underlying pathogenesis.

In addition to sometimes being a symptom of dysautonomia, anxiety can sometimes physically manifest symptoms resembling autonomic dysfunction. A thorough investigation ruling out physiological causes is crucial, but in cases where relevant tests are performed and no causes are found or symptoms do not match any known disorders, a primary anxiety disorder is possible, but should not be presumed. For such patients, the anxiety sensitivity index may have better predictivity for anxiety disorders, while the Beck anxiety inventory may misleadingly suggest anxiety for patients with dysautonomia.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:

- Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.

- Injury to nerves caused by surgery or radiation to the neck.

- Treatment with certain medications, including some drugs used in cancer chemotherapy.

- Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.

- Other chronic illnesses, such as Parkinson's disease, multiple sclerosis and some types of dementia.

- Autonomic neuropathy may also be caused by an abnormal attack by the immune system that occurs as a result of some cancers (paraneoplastic syndrome).

- Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.

- Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.

- Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain-Barre syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.

Primary autonomic failure (also called primary dysautonomia) refers to a category of dysautonomias -- conditions in which the autonomic nervous system does not function properly.

In primary dysautonomias, the autonomic dysfunction occurs as a primary condition (as opposed to resulting from another disease). Autonomic failure is categorized as "primary" when believed to result from a chronic condition characterized by degeneration of the autonomic nervous system, or where autonomic failure is the predominant symptom and its cause is unknown.

Such "primary" dysautonomias are distinguished from secondary dysautonomias, where the dysfunction of the autonomic nervous system is believed to be caused by another disease (e.g. diabetes).

Diseases categorized as primary autonomic failure usually include pure autonomic failure and multiple system atrophy. Many scientists also categorize Parkinson disease and familial dysautonomia as "primary".

The direct cause and pathophysiological basis of RMD is still unknown and can occur in children and adults of perfect or non-perfect health. Rare cases of adult RMD have developed due to head trauma, stress, and herpes encephalitis. Familial cases have been reported suggesting there may be some genetic aspect to the disorder; however, to date, this explanation has not been directly tested. As familial incidence rate is still relatively low, it is believed that behavioral aspects may play a larger role in RMD than family history and genetics. Many sufferers report no family history of the disorder. Another theory suggests that RMD is a learned, self-stimulating behavior to alleviate tension and induce relaxation, similar to tic movements.

An alternative theory suggests that the rhythmic movements help develop the vestibular system in young children, which can partially explain the high prevalence of RMD in infants. It has been seen that children who have underdeveloped vestibular systems benefit from performing RMD-like movements which stimulate the vestibular system

Sleep-related movements are commonly seen in children, especially infants. However, the majority of these movements stop as the child ages. Some 66% of infants of 9-months show RMD-like symptoms compared to only 8% of 4 year olds. The disorder is closely associated to mental retardation or other psychiatric disorders like Autism. More recent studies have shown there is a strong link between prolonged RMD and ADHD

Pharmacological methods of treatment include fludrocortisone, midodrine, somatostatin, erythropoietin, and other vasopressor agents. However, often a patient with pure autonomic failure can mitigate his or her symptoms with far less costly means. Compressing the legs and lower body, through crossing the legs, squatting, or the use of compression stockings can help. Also, ingesting more water than usual can increase blood pressure and relieve some symptoms.

Psycho-organic syndrome is typically diagnosed in individuals following 5–10 years of consistent exposure to chemicals like xylene, toluene, and styrene, which are generally found in paint, plastic and degreasing products.

Patients work and environmental history must be evaluated for exposure to organic chemicals. A traumatic brain injury may also lead to POS.

Consistent intoxication (ie excess use of alcohol and drugs) may also cause a lesion in the brain, eventually leading to POS.

Lyme diseae, the great "new imitator", has been known to mimick depression, scizophreania, depersonazlization disorder, and obsessive-complsive disorder.

Although the cause varies by each individual case, localization of the atrophy in the brain can occur due to aging and without external causes, linked to hereditary.

Prevention includes proper and regular use of Preventive Personal Equipment (PPE) in work environments that involve organic chemicals and limiting alcohol and drug substance intake.

Pure autonomic failure (PAF), also known as Bradbury-Eggleston syndrome or idiopathic orthostatic hypotension, is a form of dysautonomia that first occurs in middle age or later in life; men are affected more often than women.

Many other neurological conditions are associated with acanthocytosis but are not considered 'core' acanthocytosis syndromes. The commonest are:

- Pantothenate kinase-associated neurodegeneration, an autosomal recessive condition caused by mutations in "PANK2".

- Huntington's disease-like syndrome type 2, an autosomal dominant condition caused by mutations in "JPH3" that closely resembles Huntington's disease.

- Bassen-Kornzweig disease, or Bassen-Kornzweig Syndrome (see also History).

- Levine-Critchley syndrome (see History).

- Paroxysmal movement disorders associated with GLUT1 mutations.

- Familial acanthocytosis with paroxysmal exertion-induced dyskinesias and epilepsy (FAPED).

- Some cases of mitochondrial disease.

Environmental dependency syndrome, also called Zelig syndrome or Zelig-like syndrome from the name of the protagonist of Woody Allen's "Zelig", is a syndrome where the affected individual relies on environmental cues in order to accomplish goals or tasks. It is a disorder in personal autonomy that is influenced by individual psychological traits and can be helped through the intervention of other people. For example, adults diagnosed with attention deficit hyperactivity disorder have relied on special coaches to provide cues at appropriate times, helping them to make decisions about how to prioritize and order tasks.

McLeod syndrome is an X-linked recessive disorder caused by mutations in the "XK" gene encoding the Kx blood type antigen, one of the Kell antigens.

Like the other neuroacanthocytosis syndromes, McLeod syndrome causes movement disorder, cognitive impairment and psychiatric symptoms. The particular features of McLeod syndrome are heart problems such as arrhythmia and dilated cardiomyopathy (enlarged heart).

McLeod syndrome is very rare. There are approximately 150 cases of McLeod syndrome worldwide. Because of its X-linked mode of inheritance, it is much more prevalent in males.

This is a form of dysautonomia but differentiated from familial dysautonomia by a lack of familial dysautonomic symptoms such as loss of sense of pain and smell. While L-threo-DOPS has been described as being "very effective for restoring noradrenergic tone and correcting postural hypotension, response to treatment is variable and the long-term and functional outcome is unknown."

Researchers have put together retrospective data collections in order to better under the progression of this orphan disease. Most studies show a perinatal period marked by inadequacy of the ANS to control blood pressure, blood sugar, and body temperature. The experiences of orthostatic hypotension, exercise intolerance, and "traumatic morbidity related to falls and syncope" have been documented later in lives of people with this condition. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation, outcome of these diseases, their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies, a patient registry was established by the non-commercial International Working Group on Neurotransmitter Related Disorders (iNTD).

5 had positive response to immunotherapy and tumor therapy, 10 partial response, and 6 no response. Eventually 5 patients died; all had a tumor or additional paraneoplastic symptoms related to onconeuronal antibodies. Coexistence of onconeuronal antibodies predicted a poor outcome.

Five different clinical entities have been described under hereditary sensory and autonomic neuropathies – all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves. Their incidence has been estimated to be about 1 in 25,000.

Sydenham's chorea is the foremost classic autoimmune basal ganglia disorder. Possible autoimmune mechanism for encephalitis lethargica with Parkinsonian syndrome has been suggested. The evidence for an autoimmune disorder is less clear for paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). An autoimmune subgroup may exist in Tourette's syndrome, although results remain controversial. Autoimmune movement disorder with basal ganglia encephalitis associated with D2RA have found recently.

Psychoorganic syndrome is a combination of various symptoms that are caused by organic changes in the brain. The exact component of the solvents that causes the neurological disorder is difficult to isolate due to worker generally being exposed to mixtures of various grades, compositions, and purity of solvents.

At the initial stage, asthenia is prevalent and the progress of the disorder is slow. Acute onset can be diagnosed when a large amount of psychological symptoms surface. The final stage of the disorder is made up of numerous disorders, including demntia, Korsakov's syndrome, and includes severe personality change such as depression, anxiety, memory loss, and drastic change in intellect. Level of kindness, happiness, and insight are greatly affect in the final stage.

The disorder stems from a defect in brain tissue, usually atrophy from another neurological disorder." In pathological findings, focal or diffuse signs of atrophy without inflammation or severe vascular insufficiency are present. Basic clinical picture depends on the localization of atrophy in brain."Although the exact mechanism that solvents have on the nervous system are not fully understood, the metabolism of the solvents in the body that turn them into toxic intermediates are important. Some evidence shows that genetic polymorphisms affect the activity of metabolic enzymes that metabolize foreign chemicals.

While only a few adults have been reported with 2q37 microdeletion syndrome, it is predicted that this number will rise as various research studies continue to demonstrate that most with the disorder do not have a shortened life span.

Autonomic neuropathy (also AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

The number of events that can lead to the development of PSH symptoms is many. The exact pathways or causes for the development of the syndrome are not known. Traumatic brain injury, hypoxia, stroke, anti-NMDA receptor encephalitis (although further associations are being explored), injury of the spinal cord, and many other forms of brain injury can cause onset of PSH. Even more obscure diseases such as intracranial tuberculoma have been seen to cause onset of paroxysmal sympathetic hyperactivity. It is observed that these injuries lead to the development of PSH or are seen in conjunction with PSH, but the pathophysiology behind these diseases and the syndrome is not well understood.

Avolition, as a symptom of various forms of psychopathology, is the decrease in the motivation to initiate and perform self-directed purposeful activities. Such activities that appear to be neglected usually include routine activities, including hobbies, going to work and/or school, and most notably, engaging in social activities. A person experiencing avolition may stay at home for long periods of time, rather than seeking out work or peer relations.