Further studies of neurohumoral agents in patients with vascular headaches

Kimball, Robert W.; Friedman, Arnold P.

doi:10.1212/wnl.11.2.116

Cited by 15 publications

(8 citation statements)

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“…injection of 5‐HT was reported elsewhere to relieve spontaneous migraine attacks 49 . Kimball and Friedman 50 also showed that reserpine, a 5‐HT depleter, can induce migraine which was relieved by 5‐HT infusion. During a migraine attack, 5‐HT turnover increases significantly in the plasma 51,52 and saliva 53 .…”

Section: ‐Ht and Migrainementioning

confidence: 83%

Chemical Mediators of Migraine: Preclinical and Clinical Observations

2011

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Migraine is a neurovascular disorder, and although the pathophysiology of migraine has not been fully delineated, much has been learned in the past 50 years. This knowledge has been accompanied by significant advancements in the way migraine is viewed as a disease process and in the development therapeutic options. In this review, we will focus on 4 mediators (nitric oxide, histamine, serotonin, and calcitonin gene-related peptide) which have significantly advanced our understanding of migraine as a disease entity. For each mediator we begin by reviewing the preclinical data linking it to migraine pathophysiology, first focusing on the vascular mechanisms, then the neuronal mechanisms. The preclinical data are then followed by a review of the clinical data which support each mediator’s role in migraine and highlights the pharmacological agents which target these mediators for migraine therapy.

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Section: ‐Ht and Migrainementioning

confidence: 83%

Chemical Mediators of Migraine: Preclinical and Clinical Observations

2011

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“…These investigators experienced difficulty in explaining their results in terms of 5HT depletion, as neither this amine nor its precursor, 5-hydroxytryptophan, induced migraine when given intravenously to thirty-five patients. Kimball and Friedman (1961) noted the paradox that although 5HT could not induce migraine attacks in migraine patients, the 5HT antagonist methysergide appeared to be an effective prophylactic. This is highly suggestive that 5HT plays no significant role in the genesis of the migraine attack, despite the findings of an increased excretion of 5HIAA following reserpine injection, or during some spontaneous attacks of migraine (Sicuteri, Testi and Anselmi, 1961).…”

Section: Reserpinementioning

confidence: 99%

“…Firstly, the intravenous infusion of 5HT or its metabolic precursor, 5-hydroxytryptophan, does not induce migraine in migraine sufferers (Kimball et al, 1960;Kimball and Friedman, 1961). Secondly, in those patients depleted of the monoamine by treatment with reserpine, intravenous infusion of 5HT alleviated the headache (Anthony et al, 1967).…”

Section: Antagonism Of 5-hydroxytryptaminementioning

confidence: 99%

A basis for migraine therapy — the autonomic theory reappraised

Johnson

1978

Postgraduate Medical Journal

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Summary The concept that migraine results from an initial vasoconstriction due to increased release of noradrenaline from the sympathetic nerves to cranial blood vessels has been reappraised in the light of recently acquired knowledge of the mechanisms of action of drugs used in the treatment of migraine, physiological and pharmacological evidence implicating noradrenaline, and the observations by others that several migraine variants may be associated with some degree of sympathetic overactivity. If the theory is correct, it suggests that both prophylaxis and management of the acute condition should be possible by means of selective alpha-adrenoceptor antagonism. The use of drugs with potentially dangerous vasoconstrictor properties appears to be unnecessary. The suggestion is made that the increased adrenergic activity might result from changes within the hypothalamus.

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“…Classical migraine is associated with two distinct cerebrovascular phases: an initial vasoconstriction (not associated with pain) followed by vasodilatation (reactive hyperemia) associated with pain, with early hints of the involvement of ATP (Kimball and Friedman 1961;Hardebo and Edvinsson 1979;Rydzewski and Wachowicz 1987). The 'purinergic' hypothesis for migraine was formally put forward in 1981 as a basis for the reactive hyperaemia and pain during the headache phase (Burnstock 1981).…”

Section: Migrainementioning

confidence: 99%