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Diagnostic and therapeutic aspects of hemiplegic migraine
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  • Published on:
    Hemiplegic migraine, genetic mutations, and cortical spreading depression: a presumed pathophysiologic nexus that defies scientific logic
    • Vinod K. Gupta, Physician (Internist) Migraine-Headache Institute, GUPTA MEDICAL CENTRE, New Delhi, India

    I read the article by Stefano et al with interest.1 Genetic predisposition per se cannot explain discrete self-limited recurrent attacks of headache and aura manifestations of hemiplegic migraine, with the state/clinical predisposition appearing and disappearing seemingly inexplicably over several decades or the life-time of a sufferer.2

    More than two decades ago, I elucidated a fundamental clinico-theoretical principle for the understanding of migraine-linked physiologic mechanisms that has well-stood the test of time, technology and biologic commonsense: “No systemic influence can explain the characteristic lateralizing headache of migraine, unilateral, bilateral, side-shifting or side-locked”.3 Over the last fifty years, some of the "systemic" influences believed to play key pathogenetic roles in migraine include serotonin, platelets, catecholamines, calcitonin-gene related peptide, magnesium depletion, stress, post-stress state, and recurrent micro thrombo-embolisms across the patent foramen ovale at the level of the cardiac inter-atrial septum. 4,5,6 Little vertical and biologically-plausible robust generalizable progress, however, has been made in gestalt understanding of the disorder well into the 21st century.7 Trait-linked genetic association is also a “systemic” influence. Ion transporters – as well as the three main causative genes—CACNA1A, ATP1A2 and SCN1A—which encode for ion transporters1 do not offer clues to the mechanistic physiological b...

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    Conflict of Interest:
    None declared.