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Common Mechanisms in Migraine and Epilepsy: A Comment

Common Mechanisms in Migraine and Epilepsy: A Comment With great interest I read Dr Rogawski's review titled “Common Pathophysiologic Mechanisms in Migraine and Epilepsy.”1 I would like to comment on 3 aspects. First, the article suggests that the vascular theory of migraine has been replaced by the neural theory. Most researchers agree that vascular and neural mechanisms are involved in migraine pathophysiology.2 While the neural mechanisms have been examined in detail, many studies also suggest that vascular aspects are involved.3 Although the significance of these vascular phenomena and the interrelationship between neural and vascular mechanisms is unclear, I suggest using the term neurovascular with regard to migraine pathophysiology.2 Second, the term hyperexcitability may unequivocally apply to epilepsy pathophysiology, but it is controversial with regard to migraine.4 Electrophysiological studies have shown an altered response to repetitive stimuli characterized by a dyshabituation or hyperresponsiveness. While this may be considered a semantic issue, I believe that hyperresponsiveness more adequately describes the mechanisms in the migraine-prone brain. Third, familial hemiplegic migraine has been attributed to variants in genes coding for ion channels and may thus, together with certain forms of epilepsy, be categorized as channelopathies. However, available studies failed to show that ion channels also play a key role in common forms of migraine. This is most likely due to the heterogeneous nature of migraine with a broad clinical spectrum.5 Migraine and hemiplegic aura may be distinct entities, occurring together in individuals with familial hemiplegic migraine. Genetic variants in ion channels may be characteristic for the monomorphic aura; thus, they may only be markers for some forms but not causative of migraine. Likewise, certain physiological pathways, eg, involving glutamate, may only be associated with certain forms of migraine. These migraine forms may be responsive only to certain medications inhibiting glutamate actions, eg, topiramate. This may be part of the reason for the large number of migraine preventive medication nonresponders. Correspondence: Dr Schürks, Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave E, Third Floor, Boston, MA 02215-1204 (mschuerks@rics.bwh.harvard.edu). Financial Disclosure: Dr Schürks has received within the last 5 years investigator-initiated research funds from the Deutsche Forschungsgemeinschaft and an unrestricted research grant from Merck, Sharp, and Dohme. References 1. Rogawski MA Common pathophysiologic mechanisms in migraine and epilepsy. Arch Neurol 2008;65 (6) 709- 714PubMedGoogle ScholarCrossref 2. Goadsby PJLipton RBFerrari MD Migraine: current understanding and treatment. N Engl J Med 2002;346 (4) 257- 270PubMedGoogle ScholarCrossref 3. Dodick DW Examining the essence of migraine: is it the blood vessel or the brain? a debate. Headache 2008;48 (4) 661- 667PubMedGoogle ScholarCrossref 4. Coppola GPierelli FSchoenen J Is the cerebral cortex hyperexcitable or hyperresponsive in migraine? Cephalalgia 2007;27 (12) 1427- 1439PubMedGoogle ScholarCrossref 5. Wessman MTerwindt GMKaunisto MAPalotie AOphoff RA Migraine: a complex genetic disorder. Lancet Neurol 2007;6 (6) 521- 532PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Neurology American Medical Association

Common Mechanisms in Migraine and Epilepsy: A Comment

Archives of Neurology , Volume 65 (11) – Nov 10, 2008

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Publisher
American Medical Association
Copyright
Copyright © 2008 American Medical Association. All Rights Reserved.
ISSN
0003-9942
eISSN
1538-3687
DOI
10.1001/archneur.65.11.1546-b
Publisher site
See Article on Publisher Site

Abstract

With great interest I read Dr Rogawski's review titled “Common Pathophysiologic Mechanisms in Migraine and Epilepsy.”1 I would like to comment on 3 aspects. First, the article suggests that the vascular theory of migraine has been replaced by the neural theory. Most researchers agree that vascular and neural mechanisms are involved in migraine pathophysiology.2 While the neural mechanisms have been examined in detail, many studies also suggest that vascular aspects are involved.3 Although the significance of these vascular phenomena and the interrelationship between neural and vascular mechanisms is unclear, I suggest using the term neurovascular with regard to migraine pathophysiology.2 Second, the term hyperexcitability may unequivocally apply to epilepsy pathophysiology, but it is controversial with regard to migraine.4 Electrophysiological studies have shown an altered response to repetitive stimuli characterized by a dyshabituation or hyperresponsiveness. While this may be considered a semantic issue, I believe that hyperresponsiveness more adequately describes the mechanisms in the migraine-prone brain. Third, familial hemiplegic migraine has been attributed to variants in genes coding for ion channels and may thus, together with certain forms of epilepsy, be categorized as channelopathies. However, available studies failed to show that ion channels also play a key role in common forms of migraine. This is most likely due to the heterogeneous nature of migraine with a broad clinical spectrum.5 Migraine and hemiplegic aura may be distinct entities, occurring together in individuals with familial hemiplegic migraine. Genetic variants in ion channels may be characteristic for the monomorphic aura; thus, they may only be markers for some forms but not causative of migraine. Likewise, certain physiological pathways, eg, involving glutamate, may only be associated with certain forms of migraine. These migraine forms may be responsive only to certain medications inhibiting glutamate actions, eg, topiramate. This may be part of the reason for the large number of migraine preventive medication nonresponders. Correspondence: Dr Schürks, Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave E, Third Floor, Boston, MA 02215-1204 (mschuerks@rics.bwh.harvard.edu). Financial Disclosure: Dr Schürks has received within the last 5 years investigator-initiated research funds from the Deutsche Forschungsgemeinschaft and an unrestricted research grant from Merck, Sharp, and Dohme. References 1. Rogawski MA Common pathophysiologic mechanisms in migraine and epilepsy. Arch Neurol 2008;65 (6) 709- 714PubMedGoogle ScholarCrossref 2. Goadsby PJLipton RBFerrari MD Migraine: current understanding and treatment. N Engl J Med 2002;346 (4) 257- 270PubMedGoogle ScholarCrossref 3. Dodick DW Examining the essence of migraine: is it the blood vessel or the brain? a debate. Headache 2008;48 (4) 661- 667PubMedGoogle ScholarCrossref 4. Coppola GPierelli FSchoenen J Is the cerebral cortex hyperexcitable or hyperresponsive in migraine? Cephalalgia 2007;27 (12) 1427- 1439PubMedGoogle ScholarCrossref 5. Wessman MTerwindt GMKaunisto MAPalotie AOphoff RA Migraine: a complex genetic disorder. Lancet Neurol 2007;6 (6) 521- 532PubMedGoogle ScholarCrossref

Journal

Archives of NeurologyAmerican Medical Association

Published: Nov 10, 2008

Keywords: epilepsy,migraine disorders

References