Elsevier

The Lancet

Volume 338, Issue 8758, 6 July 1991, Pages 13-17
The Lancet

Migraine pain associated with middle cerebral artery dilatation: reversal by sumatriptan

https://doi.org/10.1016/0140-6736(91)90005-AGet rights and content

Abstract

The combination of measurements of regional cerebral blood flow (rCBF) and blood velocity in the middle cerebral arteries (MCA) by transcranial doppler sonography was used to investigate cerebrovascular involvement in migraine. Ten migraine patients with unilateral headache were studied during an attack and when they had been free of attacks for 5 days (non-attack). On both occasions they were given an intravenous infusion of sumatriptan (2 mg), a 5-HT1-like receptor agonist, which relieved the symptoms within 30 min without affecting rCBF. The MCA velocity was normal on both sides on the non-attack day and on the unaffected side during the attack. However, during the attack the MCA velocity on the headache side was significantly lower than that on the non-headache side (45 vs 61 cm/s:mean difference 16·3 [95% confidence interval 10·3-22·3]; p=0·02). The MCA velocity on the headache side returned to normal after treatment with sumatriptan and recovery. Since rCBF in the MCA supply territory was unaffected, the lower velocity can be explained only by dilatation of the MCA. The mean MCA diameter increase was estimated to be 20%. Thus, headache was associated with intracranial large arterial dilatation on the headache side. Sumatriptan predominantly had effects on the distended artery, which suggests that the 5-HT receptor system has a role in the pathogenesis of migraine.

References (31)

  • J. Olesen et al.

    The common migraine attack may not be initiated by cerebral ischaemia

    Lancet

    (1981)
  • A. Doenicke

    HT1-like receptor agonist, for the treatment of severe migraine

    Lancet

    (1988)
  • Hk Iversen et al.

    Arterial responses during migraine headache

    Lancet

    (1990)
  • E. Skinho̸j

    Hemodynamic studies within the brain during migraine

    Arch Neurol

    (1973)
  • J. Olesen et al.

    Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine

    Ann Neurol

    (1981)
  • M. Lauritzen et al.

    The changes of regional cerebral blood flow during the course of classical migraine attacks

    Ann Neurol

    (1983)
  • T. Skyho̸j Olsen et al.

    Ischemia may be the primary cause of the neurological deficits in classic migraine

    Arch Neurol

    (1987)
  • M. Lauritzen et al.

    Regional cerebral blood flow during migraine attacks by xenon-133 inhalation and emission tomography

    Brain

    (1984)
  • J. Olesen et al.

    Timing and topography of cerebral blood flow, aura and headache during migraine attacks

    Ann Neurol

    (1990)
  • L. Friberg et al.

    Focal ischaemia caused by instability of cerebrovascular tone during attacks of hemiplegic migraine: a regional cerebral blood flow study

    Brain

    (1987)
  • Ar Andersen et al.

    Delayed hyperemia following hypoperfusion in classic migraine: single photon emission computed tomographic demonstration

    Arch Neurol

    (1988)
  • L. Friberg et al.

    Regional cerebral blood flow during attacks and when free of symptoms in a large group of migraine patients

    Cephalalgia

    (1989)
  • R. Aaslid (Eds), Transcranial doppler sonography. 19, Springer-Verlag, New...
  • Doenicke A, Brand J, Perrin VL. Possible benefit of GR 43175, a...
  • P. Tfelt-Hansen et al.

    Early clinical experience with subcutaneous GR43175 in acute migraine: an overview

    Cephalalgia

    (1989)
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