Transient Cerebral Ischemia and Brain Serotonin: Relevance to Migraine

Welch, K. M. A.; Gaudet, Robert; Wang, T.P.F.; Chabi, E

doi:10.1111/j.1526-4610.1977.hed1704145.x

Cited by 7 publications

(4 citation statements)

References 11 publications

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“…As discussed above, it seems quite probable that serotonin is released by the brain tissue during hypoxia. Such a release leads to a temporary reduction of the brain serotonin levels (116,140,208). Brain hypoxia could also hamper the synthesis of serotonin, again facilitating brain serotonin depletion (209).…”

Section: The Hypoxia Hypothesis Confronted With Other Theoriesmentioning

confidence: 99%

“…Whether or not intermittent episodes of brain hypoxia may produce a more chronic type of CNS serotonin depletion is not clear, however. According to some authors, post-ischemia serotonin levels may be enhanced above control levels (140), though others have reported that the ischemia-induced depletion of serotonin may be maintained for at least one hour despite cerebral reperfusion (208). 4.…”

Section: The Hypoxia Hypothesis Confronted With Other Theoriesmentioning

confidence: 99%

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Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

Amery

1982

Cephalalgia

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The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack of migraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be provoked by different mechanisms in different patients; the potential role of decreased oxygen supply and of increased oxygen need are reviewed and excess sympathetic drive is considered a potential key mechanism in a majority of patients. Whether or not focal hypoxia leads to a genuine migraine attack, depends largely upon the quality of the whirlpool of biochemical, vascular and hematological changes that follow the hypoxic episode. These changes are discussed and it is concluded that those which have been reported to occur during migraine attacks could be due to a preceding hypoxic event. Finally, the hypoxia viewpoint is confronted with some popular theories about the pathogenesis of migraine. It is found that the other points of view are compatible with the hypoxia hypothesis.

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Section: The Hypoxia Hypothesis Confronted With Other Theoriesmentioning

confidence: 99%

Section: The Hypoxia Hypothesis Confronted With Other Theoriesmentioning

confidence: 99%

Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

Amery

1982

Cephalalgia

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“…Besides exhibiting effects directly on vascular smooth muscle (10), it has been postulated that serotonin modifies vascular reactivity via brainstem mechanisms (11). For these and other reasons, serotonin has frequently been implicated in the pathogenesis of a number of vascular disorders, including migraine and ischemia (12). The development of methods for isolating an enriched preparation of brain microvessels (13) has made possible the biochemical and pharmacological studies we now report.…”

mentioning

confidence: 92%

Serotonin Neurons Project to Small Blood Vessels in the Brain

Reinhard

Liebmann

Schlosberg

et al. 1979

Science

196

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Electrolytic lesions of the nucleus raphe dorsalis and medianus reduce the concentration of serotonin (5-hydroxytryptamine) within rat brain intraparenchymal blood vessels. The concentration of serotonin within these vessels increases or decreases after the administration of drugs that modify the biosynthesis and degradation of serotonin or destroy nerve terminals by an uptake-dependent mechanism. These studies provide evidence for the existence of a serotonin-containing pathway seemingly analogous to the neuronal projection that terminates on small parenchymal blood vessels from noradrenergic neurons of the locus coeruleus.

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“…The theory suggesting that IH may be due to an imbalance of the homeostasis between pain transmission and pain control has received attention and scientific support in the course of recent years. [18][19][20] The purpose of the present investigation was to determine whether PTP occurred predominantly or exclusively, in subjects with a history of IH; and was absent or rare in subjects with a negative personal and family history of IH.…”

Section: Introductionmentioning

confidence: 99%

Idiopathic Headache as a Possible Risk Factor for Phantom Tooth Pain

Sicuteri¹,

Nicolodi²,

Fusco³

et al. 1991

Headache

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Following tooth pulp extirpation, some subjects suffer from persistent pain which affects edentate sites in absence of any local pathology. As regards this peculiar pain, called phantom tooth pain (PTP), what is puzzling is the fact there is a low prevalence of PTP in a very large population showing identical conditions of tooth pulp extirpation. The present investigation indicates that PTP mainly affects migraine (M) and cluster headache (CH) sufferers, whereas it does not affect subjects who have a negative personal and family history for idiopathic headache (IH). These results circumscribe the presence of PTP to a specific section of the population. The present results, besides indicating that PTP may be the result of a peculiar neuronal predisposition relating to IH pathogenesis, suggests some practical therapeutic hints. In fact, successful anti- M and anti-CH prophylactic treatment greatly improve PTP syndrome.

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Transient Cerebral Ischemia and Brain Serotonin: Relevance to Migraine

Cited by 7 publications

References 11 publications

Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

Serotonin Neurons Project to Small Blood Vessels in the Brain

Idiopathic Headache as a Possible Risk Factor for Phantom Tooth Pain

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