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Volume 16 Supplement 1

1st Joint ANIRCEF-SISC Congress

  • Invited speaker presentation
  • Open Access

Migraine and epilepsy: what value today?

  • 1Email author,
  • 2,
  • 1,
  • 3,
  • 1 and
  • 1, 4
The Journal of Headache and Pain201516 (Suppl 1) :A44

  • Published:


  • Migraine
  • NMDA
  • Epileptic Patient
  • Asymptomatic Carrier
  • Underlying Pathophysiology

More than 100 years of investigation have found that seizures and migraine co-occur in some affected individuals and families, and there is much evidence that these diseases share genetic susceptibility. In particular, in a recent review, the prevalence of migraine in epileptic patients was about 12%[1]. On the other hand, epilepsy exhibits a prevalence of about 6% in migraineurs[2]. Moreover, epilepsy has also been reported in patients with familial hemiplegic migraine (FHM). Although few studies showed a prevalence of epilepsy of about 7% in FHM, currently no conclusive data are available.

Certainly, epilepsy and migraine share common characteristics that the underlying pathophysiology relates to alterations in ion channels or ion transporters. In these episodic functional diseases, in which susceptible brain regions are hyperexcitable, the attacks begin with hypersynchronous neuronal firing[3]. In epilepsy, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors play a predominant role in mediating the generation and spread of seizure activity whereas in migraine mainly N-methyl-D-aspartate (NMDA) receptors are involved in triggering CSD. However, the nature of the ionic conductance changes leading to the massive but transitory neuronal depolarization underlying CSD has not yet been define[4].

Genetically determined dysfunction of ion transporters seems to point at a common underlying mechanism for both paroxysmal disorders. In the last two decades the mutations in the ion transportation genes CACNA1A, ATP1A2 and SCN1A have been identified for FHM. Conversely, only a few CACNA1A and ATP1A2 mutations have been reported in patients with sporadic hemiplegic migraine (SHM). These cases can be caused by a de novo mutation or by inheritance of a gene mutation from asymptomatic carrier and are usually characterized by early-onset, severe and complex disorders.

Certainly, genetic analysis can provide greater insight into the potential causes of both disorders and it could contribute to better treatment choices.

Authors’ Affiliations

Clinica Neurologica, Università di Perugia, Ospedale S. Maria della Misericordia, Perugia, Italy
Sezione di Genetica Medica, Dipartimento di Medicina Clinica e Sperimentale, Azienda Ospedaliera e Università di Perugia, Perugia, Italy
Centro Cefalee, UOC Neurologia, Ospedale S. Eugenio, Rome, Italy
Fondazione Santa Lucia, IRCCS, Rome, Italy


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  4. Rogawski MA: Migraine and epilepsy-shared mechanisms within the family of episodic disorders. Jasper's Basic Mechanisms of the Epilepsies. Edited by: Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado-Escueta AV. 2012, Bethesda (MD): National Center for Biotechnology Information (US), 4Google Scholar


© Costa et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.


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