MITOCHONDRIAL-DNA IN MIGRAINE WITH AURA

Citation
T. Klopstock et al., MITOCHONDRIAL-DNA IN MIGRAINE WITH AURA, Neurology, 46(6), 1996, pp. 1735-1738
Citations number
28
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
46
Issue
6
Year of publication
1996
Pages
1735 - 1738
Database
ISI
SICI code
0028-3878(1996)46:6<1735:MIMWA>2.0.ZU;2-U
Abstract
Migraine and the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome have some clinical featu res in common. First, cerebral infarctions, most often in the posterio r cerebral regions, which are a main symptom of MELAS, may complicate migraine. Second, migrainous headache with vomiting is also a characte ristic feature of the MELAS syndrome. Less frequently, hemicranial hea dache is present in another mitochondrial disease, myoclonic epilepsy with ragged-red fibers (MERRF). Moreover, there is a mild bias toward maternal transmission in migraine. Apart from clinical resemblance, th ere is some experimental evidence for mitochondrial dysfunction in mig raine. There may be depression of respiratory chain enzyme activity in muscle and platelets, and magnetic resonance spectroscopy has reveale d a defective energy metabolism in brain and muscle of migraine patien ts. There has not been a systematic study of mitochondrial DNA in migr aine, however. We therefore analyzed the mitochondrial DNA in lymphocy tes of 23 migraine patients with aura. Southern blot and polymerase ch ain reaction analysis of mitochondrial DNA failed to detect any large- scale deletions or point mutations at base pair 3243 (MELAS) and base pair 8344 (MERRF). Our data show that deletions of mitochondrial DNA a nd the most frequent point mutations of MELAS and MERRF syndromes are not common in migraine with aura. In particular, these data do not sup port the hypothesis that some cases of migraine may be monosymptomatic forms of a MELAS syndrome. We cannot exclude, however, that migraine may be associated with different point mutations of mitochondrial DNA or with mutations of autosomally coded respiratory chain subunit genes .