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Familial hemiplegic migraine.

Maria Dolores Villar-Martinez1, David Moreno-Ajona1, Peter J Goadsby1

  • 1Wolfson Sensory, Pain and Regeneration Research Centre (SPaRRC), Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.

Handbook of Clinical Neurology
|August 22, 2024
PubMed
Summary
This summary is machine-generated.

Familial hemiplegic migraine is a subtype of migraine with aura, characterized by reversible motor weakness. Genetic mutations in CACNA1A, ATP1A2, or SCN1A are linked to this condition, affecting ion channels.

Keywords:
ATP1A2CACNA1AEtiopathogenesisFamilial hemiplegic migraine type 3 (FHM3)Hemiplegic migrainePRRT2SCN1A

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Area of Science:

  • Neurology
  • Genetics
  • Molecular Biology

Background:

  • Hemiplegic migraine involves migraine with aura and reversible motor weakness.
  • It is classified as familial or sporadic, with familial forms linked to specific genetic mutations.
  • Familial hemiplegic migraine subtypes (FHM1, FHM2, FHM3) involve mutations in CACNA1A, ATP1A2, and SCN1A genes.

Purpose of the Study:

  • To review the genetic basis and clinical manifestations of hemiplegic migraine.
  • To discuss the implications of genetic mutations on disease penetrance and phenotype.
  • To outline current treatment strategies for hemiplegic migraine.

Main Methods:

  • Literature review of familial hemiplegic migraine.
  • Analysis of genetic mutations (CACNA1A, ATP1A2, SCN1A) and their encoded ion channels.
  • Compilation of clinical features and treatment options.

Main Results:

  • Mutations in CACNA1A, ATP1A2, and SCN1A are associated with FHM1, FHM2, and FHM3, respectively.
  • These mutations affect neuronal and glial cell ion channels (P/Q-type calcium, Na/K pump, Na channel).
  • Patients with known mutations may exhibit variable genetic penetrance and complex phenotypes, including epilepsy and ataxia.

Conclusions:

  • Genetic mutations significantly contribute to hemiplegic migraine pathogenesis.
  • Understanding these mutations aids in diagnosing and managing complex neurological comorbidities.
  • Treatment involves antiepileptics, calcium channel blockers, and acetazolamide.