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Episodic ataxias.

Joanna C Jen1, Jijun Wan2

  • 1Departments of Neurology, Otolaryngology, and Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY, United States.

Handbook of Clinical Neurology
|June 13, 2018
PubMed
Summary
This summary is machine-generated.

Primary episodic ataxias (EAs) are inherited neurological disorders causing recurrent incoordination. Genetic mutations in ion channels and transporters are identified, aiding diagnosis and management of these channelopathies.

Keywords:
calcium channelchannelopathiesepisodic ataxiasglial excitatory amino acid transporterpotassium channel

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Area of Science:

  • Neurology
  • Genetics
  • Channelopathies

Background:

  • Primary episodic ataxias (EAs) are dominantly inherited neurological disorders.
  • Characterized by transient incoordination and truncal instability, often triggered by exertion or stress.
  • Eight subtypes are recognized, primarily based on genetic loci.

Purpose of the Study:

  • To review the clinical assessment, genetic diagnosis, and management of well-characterized episodic ataxia syndromes.
  • To discuss newly identified allelic disorders expanding the clinical spectrum of EA2.
  • To highlight diagnostic and therapeutic challenges in sporadic congenital cases.

Main Methods:

  • Review of genetic loci and identified mutations for EA1, EA2, and EA6.
  • Focus on KCNA1 (EA1), CACNA1A (EA2), and SLC1A3 (EA6) gene mutations.
  • Discussion of clinical presentations, including allelic disorders and sporadic congenital cases.

Main Results:

  • Mutations in KCNA1 (EA1), CACNA1A (EA2), and SLC1A3 (EA6) are identified, primarily with childhood onset.
  • EA1 and EA2 represent prototypical neurologic channelopathies.
  • Allelic disorders associated with EA2 have broadened the clinical spectrum.

Conclusions:

  • Genetic identification is crucial for diagnosing and managing episodic ataxias.
  • Understanding channelopathies like EA1 and EA2 informs therapeutic strategies.
  • Further research is needed for rare and sporadic EA presentations.