Acanthocytes are seen less frequently in other conditions including Huntington's disease-like syndrome 2 (HDL2) and pantothenate kinase-associated neurodegeneration (PKAN).

[3] Individuals with neuroacanthocytosis also often have parkinsonism, the uncontrolled slowness of movements, and dystonia, abnormal body postures.

Many affected individuals also have cognitive (intellectual) impairment and psychiatric symptoms such as anxiety, paranoia, depression, obsessive behavior, and pronounced emotional instability.

[7] Chorea acanthocytosis is an autosomal recessive disorder caused by mutations in the VPS13A, also called CHAC, on chromosome 9q21.

Antipsychotics are used to block dopamine, anticonvulsants treat seizures and botulinum toxin injections may control dystonia.

It was first noted by the North American physician Frank Bassen, who later partnered with the ophthalmologist Abraham Kornzweig to identify and describe causes and symptoms of the disease.

[13][14] A second form of neuroacanthocytosis, Levine-Critchley syndrome, was discovered by the American internist Irvine M. Levine in 1960 and reported in Neurology in 1964, and again in 1968.

[16] In both cases, the physicians described a hereditary syndrome that combined acanthocytosis with neurological peculiarities but normal serum lipoprotein.

Specific symptoms included tics, grimacing, movement disorders, difficulty swallowing, poor coordination, hyporeflexia, chorea, and seizures.

[17] Research is underway worldwide to increase scientific understanding of these disorders as well to identify prevention and treatment methods.