Download PDFPDF

Migraine and stroke
Compose Response

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g.
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests


  • A rapid response is a moderated but not peer reviewed online response to a published article in a BMJ journal; it will not receive a DOI and will not be indexed unless it is also republished as a Letter, Correspondence or as other content. Find out more about rapid responses.
  • We intend to post all responses which are approved by the Editor, within 14 days (BMJ Journals) or 24 hours (The BMJ), however timeframes cannot be guaranteed. Responses must comply with our requirements and should contribute substantially to the topic, but it is at our absolute discretion whether we publish a response, and we reserve the right to edit or remove responses before and after publication and also republish some or all in other BMJ publications, including third party local editions in other countries and languages
  • Our requirements are stated in our rapid response terms and conditions and must be read. These include ensuring that: i) you do not include any illustrative content including tables and graphs, ii) you do not include any information that includes specifics about any patients,iii) you do not include any original data, unless it has already been published in a peer reviewed journal and you have included a reference, iv) your response is lawful, not defamatory, original and accurate, v) you declare any competing interests, vi) you understand that your name and other personal details set out in our rapid response terms and conditions will be published with any responses we publish and vii) you understand that once a response is published, we may continue to publish your response and/or edit or remove it in the future.
  • By submitting this rapid response you are agreeing to our terms and conditions for rapid responses and understand that your personal data will be processed in accordance with those terms and our privacy notice.
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

Other responses

Jump to comment:

  • Published on:
    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:
    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...

    Show More
    Conflict of Interest:
    None declared.