Mitochondrial dysfunction and migraine: evidence and hypotheses

  1. M Sparaco1,*,
  2. M Feleppa1,
  3. RB Lipton2,3,4,
  4. AM Rapoport5,6,
  5. ME Bigal2,4,5

Article first published online: 6 DEC 2005

DOI: 10.1111/j.1468-2982.2005.01059.x

Issue

Cephalalgia

Cephalalgia

Volume 26, Issue 4, pages 361–372, April 2006

Additional Information

How to Cite

Sparaco, M., Feleppa, M., Lipton, R., Rapoport, A. and Bigal, M. (2006), Mitochondrial dysfunction and migraine: evidence and hypotheses. Cephalalgia, 26: 361–372. doi: 10.1111/j.1468-2982.2005.01059.x

Author Information

  1. 1

    Department of Neurology and Headache Centre, Hospital ‘G. Rummo’ Benevento, Benevento, Italy, Departments of

  2. 2

    Neurology and

  3. 3

    Epidemiology and Population Health, Albert Einstein College of Medicine and

  4. 4

    Montefiore Headache Unit, Bronx, NY,

  5. 5

    The New England Center for Headache, Stamford, CT, and

  6. 6

    Department of Neurology, Columbia University College of Physicians & Surgeons, New York, NY, USA

*M. Sparaco, Department of Neurology and Headache Center, Hospital ‘G. Rummo’ Benevento, Italy. E-mail marcosparaco@aliceposta.it

Publication History

  1. Issue published online: 14 FEB 2006
  2. Article first published online: 6 DEC 2005
  3. Received 8 December 2004, accepted 12 May 2005

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Keywords:

  • Brain oxidative metabolism;
  • magnetic resonance spectroscopy;
  • migraine;
  • mitochondrial dysfunction;
  • mutation

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.

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