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Neurology 2002;59:724-728
© 2002 American Academy of Neurology

Association of µ-opioid receptor subunit gene and idiopathic generalized epilepsy

H. Wilkie, BSc, A. Osei–Lah, MRCP, B. Chioza, MSc, L. Nashef, FRCP, D. McCormick, FRACP, P. Asherson, PhD and A. J. Makoff, PhD

From the Department of Psychological Medicine (Dr. Makoff, H. Wilkie, and B. Chioza) and Social Genetic and Developmental Psychiatry Research Centre (Dr. Asherson), Institute of Psychiatry; Department of Neuroscience (Drs. Osei–Lah and Nashef), King’s College Hospital, London; and Department of Neurology (Dr. Nashef) and Paediatric Department (Dr. McCormick), Kent and Canterbury Hospital, Canterbury, United Kingdom.

Address correspondence and reprint requests to Dr. A.J. Makoff, Department of Psychological Medicine, Institute of Psychiatry, Denmark Hill, London, SE5 8AF, UK; e-mail: a.makoff{at}iop.kcl.ac.uk

Objective: To replicate and extend the previously reported association between the opioid receptor µ subunit gene (OPRM1) and idiopathic absence epilepsy (IAE), using a sample of 230 probands with idiopathic generalized epilepsy (IGE).

Background: In humans and in animal models, several lines of evidence implicate opioid receptors with seizures. The G118 allele of OPRM1 was associated with IAE (p = 0.019).

Methods: Three single nucleotide polymorphisms (SNP) of OPRM1 were investigated by association studies with IGE using a case/control design, one of which also used a within-family design.

Results: Association was found for G118 with IGE (p = 0.00027, odds ratio [OR] = 1.86), replicating the previous association. Within-family tests of linkage and association (haplotype-based haplotype relative risk and transmission disequilibrium test) confirmed this result. Further evidence for involvement of OPRM1 in IGE was provided by an association with G-172T, located in the 5' untranslated region (p = 0.0015, OR = 2.36). Haplotypes of the two SNPs were associated with IGE with a greater level of significance (p = 0.000087) suggesting that both SNPs might be in linkage disequilibrium with a single functional variant. Analysis of the results by subgroups of IGE showed association with all subgroups tested.

Conclusions: These results confirm the previous association and support the hypothesis of a role for OPRM1 in IGE, including absence syndromes. However, the authors found no evidence for a specific association between OPRM1 and idiopathic absence epilepsy. The data suggest that the functional variant predisposing to IGE is located within 60kb of exon 1.






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