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Basilar-type migraine

Clinical, epidemiologic, and genetic features

From the Danish Headache Center, Department of Neurology, Glostrup Hospital, University of Copenhagen, Denmark.

Address correspondence and reprint requests to Dr. Malene Kirchmann, Danish Headache Center, University of Copenhagen, Department of Neurology, Glostrup Hospital, Nordre Ringvej 57, DK-2600 Glostrup, Denmark; e-mail: kirchmann{at}dadlnet.dk

Background: It remains uncertain whether basilar-type migraine (BM) is a subtype of migraine with typical aura (MTA) or a distinct phenotype or genotype.

Objective: To analyze the symptomatology, familial distribution, and genotype of BM.

Methods: The authors recruited 105 families comprising 362 patients with MTA or BM (International Classification of Headache Disorders–1 criteria). Among these patients, 38 patients from 29 families had BM. In 12 of the families with BM with an apparently dominant inheritance the authors sequenced all exons of the CACNA1A (chromosome 19) and ATP1A2 (chromosome 1) genes responsible for most cases of the autosomal dominantly inherited familial hemiplegic migraine and performed a linkage analysis of chromosome 1 and 19 with a nonparametric or autosomal dominant parametric model using an affected only analysis.

Results: BM occurred in 10% (38/362) of patients with MTA. The basilar-type aura had a median duration of 60 minutes and comprised vertigo 61%, dysarthria 53%, tinnitus 45%, diplopia 45%, bilateral visual symptoms 40%, bilateral paresthesias 24%, decreased level of consciousness 21%, hypacusia 21%, and ataxia 5%. The relative frequency of the individual basilar-type symptoms was not different from patients with hemiplegic migraine from a previous study. The patients with BM were equally distributed among the 105 families with MTA (p = 0.37). The attacks of MTA were identical in families with or without BM. No causative mutations and no linkage was identified.

Conclusions: Basilar-type aura seemingly may occur at times in any patient with migraine with typical aura. There is no firm clinical, epidemiologic, or genetic evidence that BM is an independent disease entity different from MTA.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 28 issue to find the title link for this article.

Supported by grants from the University of Copenhagen, the Lundbeck Foundation, the Jeppe Juhl Foundation, the A.P. Møller Foundation for Advancement of Medical Science, the Foundation for Research in Neurology, the Codan Foundation, The Cool Sorption Foundation, the King Christian X Foundation, the International Headache Society, and the GSK Foundation for Headache Research.

Disclosure: The authors report no conflicts of interest.

Received September 14, 2005. Accepted in final form November 21, 2005.

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March 28 Highlights

Neurology 2006 66: 790-791. [Full Text]