Regional Cerebral Blood Flow in the Diagnosis of Vascular Headache

Mathew, Ninan T.; F, Hrastnik; Meyer, John Stirling

doi:10.1111/j.1526-4610.1976.hed1504252.x

Cited by 73 publications

(53 citation statements)

References 16 publications

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“…A transient hyperaemia occurs, as had been shown already byLeão in 1944 (19), but the new finding was the persistent oligaemia in the wake of CSD(29).…”

mentioning

confidence: 68%

History of migraine with aura and cortical spreading depression from 1941 and onwards

Tfelt-Hansen

2009

Cephalalgia

109

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Several personal descriptions of migraine with aura from 1870 onwards reported a slow, gradual progression of symptoms. Lashley in 1941 meticulously chartered his own auras and concluded that the symptomatology reflected a cortical process progressing with a speed of 3 mm/min across the primary visual cortex. Leão described cortical spreading depression (CSD) in rabbits in 1944 and noticed its similarity to the migraine aura. Despite these scattered pieces of evidence, the prevailing theory was that the migraine aura was caused by a vasospasm and cortical ischaemia. The advent of a technique for measurements of regional cerebral blood flow (rCBF) in 1974 made it possible to detect spreading oligaemia during migraine aura. Between 1981 and 1990 a series of studies of rCBF during migraine attacks showed reduced brain blood flow posteriorly spreading slowly and contiguously anteriorly and crossing borders of supply of major cerebral arteries. These observations refuted the ischaemic hypothesis. The human studies showed initial hyperaemia followed by prolonged hypoperfusion. The relation between aura and CSD was known to cause short-lasting, and therefore not obvious vasodilation and it was considerably strengthened by the demonstration of a long-lasting oligaemia in rats in the wake of CSD. In the primates CSD is not easily elicited, but it has in recent years been clearly demonstrated in patients with brain trauma and stroke. Finally, mutations for familial hemiplegic migraine have been expressed in mice and lower the threshold for CSD. The seminal papers on rCBF and CSD published in the 1980s caused a dramatic shift in our concepts of migraine aura. They moved attention from ischaemia to CSD and thereby to the brain itself, and paved the way for subsequent discoveries of brainstem mechanisms.

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“…A transient hyperaemia occurs, as had been shown already byLeão in 1944 (19), but the new finding was the persistent oligaemia in the wake of CSD(29).…”

mentioning

confidence: 68%

History of migraine with aura and cortical spreading depression from 1941 and onwards

Tfelt-Hansen

2009

Cephalalgia

109

View full text Add to dashboard Cite

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“…It has been claimed that the oligemia in migraine was localized to, or most marked in areas corresponding to, the neurological deficit [4,10,22,231. But in most cases the spatial resolution has been too poor or the material too small to allow a detailed description of the development of oligemia.…”

Section: Intensity Localization and Spread Of Oligemiamentioning

confidence: 99%

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

Olesen¹,

Larsen

Lauritzen³

1981

Annals of Neurology

846

544

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Regional cerebral blood flow (rCBF) was measured in 254 areas of a hemisphere with the xenon 133 intraarterial injection method. Six cases of classic migraine were followed from the normal state into the prodromal phase, and in 3 cases further into the headache phase. One patient with common migraine was similarly followed during his only classic attack. The attacks were initiated by focal hyperemia in 3 patients. During prodromes all patients displayed occipitoparietal rCBF reduction (oligemia), but in only 1 case did the reduction approach critical values. Oligemia gradually spread anteriorly in the course of 15 to 45 minutes. In 4 patients a global oligemia was observed. In 4 patients severe headache was present concomitantly with oligemia and with no sign of hyperemia or nonhomogeneous brain perfusion. The normal rCBF increase during cortical activity (hand movement, speech, and similar activities) was impaired in 6 patients. The results indicate that the vasospastic model of the migraine attack is too simplistic.

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“…Although abnormal platelet function has been found in patients with migraine, the real cause of migraine is not yet clearly known. The decrease in regional blood flow during an attack of migraine is most probably due to a vasoconstriction [42][43][44][45]. It has been suggested that blood viscosity might play a role in the functional vascular diseases [46][47][48][49].…”

Section: Etiology and Pathogenesis Of Vascular Spasmmentioning

confidence: 99%

Influence of vasospasm on visual function

Gasser¹,

Flammer²

1987

Doc Ophthalmol

113

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In a number of patients with etiologically unexplained visual field loss, a vasospastic syndrome could be found with the help of a capillaroscopic local cooling test on the fingers. In the patients with proven vasospastic syndrome, the visual field defects were increased after a cold water test and decreased after a therapy with calcium entry blockers. General aspects of the physiology and pathophysiology of the circulation and especially of the circulation in the eye are presented.

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Regional Cerebral Blood Flow in the Diagnosis of Vascular Headache

Cited by 73 publications

References 16 publications

History of migraine with aura and cortical spreading depression from 1941 and onwards

History of migraine with aura and cortical spreading depression from 1941 and onwards

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

Influence of vasospasm on visual function

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