Mitochondrial dysfunction and migraine: Evidence and hypotheses

M. Sparaco, M. Feleppa, R. B. Lipton, A. M. Rapoport, M. E. Bigal

Research output: Contribution to journalReview articlepeer-review

131 Scopus citations


The molecular basis of migraine is still not completely understood. An impairment of mitochondrial oxidative metabolism might play a role in the pathophysiology of this disease, by influencing neuronal information processing. Biochemical assays of platelets and muscle biopsies performed in migraine sufferers have shown a decreased activity of the respiratory chain enzymes. Studies with phosphorus magnetic resonance spectroscopy (31P-MRS) have demonstrated an impairment of the brain oxidative energy metabolism both during and between migraine attacks. However, molecular genetic studies have not detected specific mitochondrial DNA (mtDNA) mutations in patients with migraine, although other studies suggest that particular genetic markers (i.e. neutral polymorphisms or secondary mtDNA mutations) might be present in some migraine sufferers. Further studies are still needed to clarify if migraine is associated with unidentified mutations on the mtDNA or on nuclear genes that code mitochondrial proteins. In this paper, we review morphological, biochemical, imaging and genetic studies which bear on the hypothesis that migraine may be related to mitochondrial dysfunction at least in some individuals.

Original languageEnglish (US)
Pages (from-to)361-372
Number of pages12
Issue number4
StatePublished - Apr 2006


  • Brain oxidative metabolism
  • Magnetic resonance spectroscopy
  • Migraine
  • Mitochondrial dysfunction
  • Mutation

ASJC Scopus subject areas

  • Clinical Neurology


Dive into the research topics of 'Mitochondrial dysfunction and migraine: Evidence and hypotheses'. Together they form a unique fingerprint.

Cite this