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Migraine and stroke
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  • Published on: 15 December 2017
    RE: RE: Migraine and stroke
    • Yonghua Zhang, Doctor Edward Neurosciences Institute in affiliation with Northwestern Medicine, Naperville, Illinois

    The role of CSD in migraine is actually generally accepted as one of the pathophysiological process. In fact several novel CGRP targeted migraine medications are showing that CGRP-mAb can prevent the activation and sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depression. Some of them are currently under review by FDA and expect to be on the market in late 2018. The research in rodents may not always be applicable to human with migraine and this theory has been in existence for over a decade. On your view of posterior cerebral circulation vulnerability to stroke, that was not quite relevant to the theme of current paper, which was about the association of migraine and stroke, not why stroke occurs more in posterior circulation. One fact of interest is that migraine sequelae related white matter changes would involve the entire brain, not limited to posterior circulation.

    Conflict of Interest:
    None declared.
  • Published on: 15 December 2017
    RE: Migraine and stroke
    • Vinod K. Gupta, Physician, New Delhi, New Delhi-110048, INDIA - 110048 Migraine-Headache Institute, New Delhi, India

    I read with interest the article by Zhang et al., (SVN, 2017, 2: e000077) [1] about "Migraine and stroke". At a time when the pathophysiology of migraine is poorly understood and the pathogenetic role of cortical spreading depression (CSD) is far from being generally accepted (Gupta, 2009) [2], Zhang et al. underscore the link between migraine with aura and ischemic stroke. With nosological splitting having been taken to the extreme end of the spectrum, Zhang et al., believe that migraine with aura (MwA) and migraine without aura (MwoA) are distinct entities.1 With the same epidemiology, the same clinical features (except the aura), and the same migraine preventive agents like propranolol, we have split wide the classification of the primary headache disorders, and maintain the belief-in-belief strategy at the cost of remaining confused at several levels, including the pathophysiology of primary headache disorders.

    The concept of CSD is maintained by key omissions and assumptions (see Box 1, p. 1601, reference No. 2). The fact that atenolol, a hydrophilic pharmacologic agent, that does not cross the blood-brain barrier and does not influence any brain neuronal function including the CSD in unconscious experimental animals and prevents both MwA and MwoA equally efficiently is a pharmacologic absolute known since 1980, [3,4,] that is by itself sufficient to eliminate the concept of CSD from migraine pathophysiology.

    The rodent model of...

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    Conflict of Interest:
    None declared.