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Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model.

Abstract

Although the trigeminal nerve innervates the meninges and participates in the genesis of migraine headaches, triggering mechanisms remain controversial and poorly understood. Here we establish a link between migraine aura and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache. Cortical spreading depression caused long-lasting blood-flow enhancement selectively within the middle meningeal artery dependent upon trigeminal and parasympathetic activation, and plasma protein leakage within the dura mater in part by a neurokinin-1-receptor mechanism. Our findings provide a neural mechanism by which extracerebral cephalic blood flow couples to brain events; this mechanism explains vasodilation during headache and links intense neurometabolic brain activity with the transmission of headache pain by the trigeminal nerve.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Stroke and Neurovascular Regulation Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

    , , , ,

    Source

    Nature medicine 8:2 2002 Feb pg 136-42

    MeSH

    Brain
    Caudate Nucleus
    Cerebrovascular Circulation
    Cortical Spreading Depression
    Functional Laterality
    Humans
    Meninges
    Migraine Disorders
    Models, Neurological
    Regional Blood Flow
    Sumatriptan
    Trigeminal Nerve

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Research Support, U.S. Gov't, P.H.S.

    Language

    eng

    PubMed ID

    11821897

    Citation

    Bolay, Hayrunnisa, et al. "Intrinsic Brain Activity Triggers Trigeminal Meningeal Afferents in a Migraine Model." Nature Medicine, vol. 8, no. 2, 2002, pp. 136-42.
    Bolay H, Reuter U, Dunn AK, et al. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med. 2002;8(2):136-42.
    Bolay, H., Reuter, U., Dunn, A. K., Huang, Z., Boas, D. A., & Moskowitz, M. A. (2002). Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nature Medicine, 8(2), pp. 136-42.
    Bolay H, et al. Intrinsic Brain Activity Triggers Trigeminal Meningeal Afferents in a Migraine Model. Nat Med. 2002;8(2):136-42. PubMed PMID: 11821897.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. AU - Bolay,Hayrunnisa, AU - Reuter,Uwe, AU - Dunn,Andrew K, AU - Huang,Zhihong, AU - Boas,David A, AU - Moskowitz,Michael A, PY - 2002/2/1/pubmed PY - 2002/5/4/medline PY - 2002/2/1/entrez SP - 136 EP - 42 JF - Nature medicine JO - Nat. Med. VL - 8 IS - 2 N2 - Although the trigeminal nerve innervates the meninges and participates in the genesis of migraine headaches, triggering mechanisms remain controversial and poorly understood. Here we establish a link between migraine aura and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache. Cortical spreading depression caused long-lasting blood-flow enhancement selectively within the middle meningeal artery dependent upon trigeminal and parasympathetic activation, and plasma protein leakage within the dura mater in part by a neurokinin-1-receptor mechanism. Our findings provide a neural mechanism by which extracerebral cephalic blood flow couples to brain events; this mechanism explains vasodilation during headache and links intense neurometabolic brain activity with the transmission of headache pain by the trigeminal nerve. SN - 1078-8956 UR - https://www.unboundmedicine.com/medline/citation/11821897/full_citation L2 - http://dx.doi.org/10.1038/nm0202-136 DB - PRIME DP - Unbound Medicine ER -