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It belongs to a group of four diseases characterized under the name Neuroacanthocytosis.
Onset of Neuroacanthocytosis usually occurs during adolescence or early adulthood.
It is consistent with many of the general symptoms of neuroacanthocytosis.
The symptoms are mostly consistent with the general symptoms for neuroacanthocytosis disorders.
Seizures may also be a symptom of neuroacanthocytosis.
Currently, no treatment slows the neurodegeneration in neuroacanthocytosis disorders.
Sometimes, physicians will prescribe antidepressants for the psychological problems that accompany neuroacanthocytosis.
The hallmark feature of a neuroacanthocytosis disease is the presence of Acanthocytes.
Chorea, involuntary dance-like movement, is another very common symptom of neuroacanthocytosis.
Four syndromes are classified as neuroacanthocytosis.
Neuroacanthocytosis information and research.
The onset of a neuroacanthocytosis disease is usually between ages 20 and 40 with an average onset of symptoms occurring at age 32.
The Advocacy for neuroacanthocytosis patients and leading medical schools co-sponsor international symposia annually to also aid in furthering the research that is being done.
Institute for Neuroacanthocytosis.
Alteration in membrane structural proteins are seen in neuroacanthocytosis and McLeod syndrome.
Signs and symptoms of a neuroacanthocytosis diseases may vary slightly from case to case but usually include several predominant symptoms.
Advocacy for Neuroacanthocytosis Patients.
"Neuroacanthocytosis."
These syndromes are caused by different genetic mutations, but the signs and symptoms are usually similar, leading to the unified classification as forms of neuroacanthocytosis.
"Neuroacanthocytosis Information Page."
Individuals with neuroacanthocytosis also usually suffer from parkinsonism, the uncontrolled slowness of movements, and dystonia, abnormal body postures.
"Neuroacanthocytosis: New Developments in a Neglected Group of Dementing Disorders."
"McLeod Neuroacanthocytosis Syndrome."
A second form of neuroacanthocytosis, Levine-Critchley syndrome, was discovered by the American internist Irvine M. Levine in 1960.
The first symposium was held in 2002 and organized by a specialist in neuroacanthocytosis, Professor Adrian Danek in Seeon, Bavaria.
Irvine M. Levine first discovered Levine-Critchley syndrome in 1960.
A second form of neuroacanthocytosis, Levine-Critchley syndrome, was discovered by the American internist Irvine M. Levine in 1960.
Levine-Critchley syndrome: Acanthocytosis Neuroacanthocytosis with neurologic disorders detailed by Edmund Critchley not Macdonald Critchley).
Acanthocytosis-Neurologic Disorder Amyotrophic Chorea with Acanthocytosis, Familial Choreoacanthocytosis Levine-Critchley Syndrome None Neuroacanthocytosis is a very rare disorder inherited as an autosomal recessive or possibly an autosomal dominant genetic trait.
"Choreoacanthocytosis NCBI Bookshelf."
Chorea-acanthocytosis (ChAc, also called Choreoacanthocytosis), is a rare hereditary disease caused by a mutation of the gene that directs structural proteins in red blood cells.
Acanthocytosis-Neurologic Disorder Amyotrophic Chorea with Acanthocytosis, Familial Choreoacanthocytosis Levine-Critchley Syndrome None Neuroacanthocytosis is a very rare disorder inherited as an autosomal recessive or possibly an autosomal dominant genetic trait.
It may occur after injuries to the brain such as stroke and encephalitis; in other neurological conditions such as choreoacanthocytosis, seizures, and Lesch-Nyhan syndrome; and rarely in persons with dementia or obsessive-compulsive disorder in the absence of tics.
However, self-injurious behaviors occur in other conditions, including nonspecific mental retardation, autism, Rett syndrome, Cornelia de Lange syndrome, Tourette syndrome, familial dysautonomia, choreoacanthocytosis, sensory neuropathy including hereditary sensory neuropathy type 1, and several psychiatric conditions.