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Biomedical subjects

R Peatfield

Publications and source records attributed to R Peatfield.

At least 19 recordsLinked to original sources
PubMed2001

Migrainous features in cluster headache.

Migraine and cluster headache have been considered entirely separate clinical syndromes, both in routine clinical practice and in the 1988 International Headache Society classification. Neurologists seeing large numbers of patients soon realize, however, that there is a considerable overlap between the two conditions. Some patients have attacks with the cardinal features of cluster headache, but also have a few symptoms (especially a visual aura) usually attributed to migraine. In addition, it is not uncommon for a patient with a lifetime's history of migraine to experience a typical bout of cluster headache, although the reverse is less common. This article reviews the published series of such patients.

Autonomic Pathways↗
PubMed1997

Red wine is less stress reducing than vodka; no differences in neuroendocrine challenge test.

Red wine, like the drugs reserpine and fenfluramine, causes the release of 5-hydroxytryptamine (5-HT) from storage sites in vitro. This study used a neuroendocrine challenge test design to determine whether the parallel between red wine and these drugs can be extended to central actions in healthy volunteers. Vodka diluted to an equal alcohol content was used as a control. No significant differences were observed between the groups in plasma cortisol, plasma prolactin or in temperature levels. Thus no evidence was obtained for a central 5-HT releasing action by red wine. Self-rating stress and arousal questionnaires were also given. No differences were found in arousal. However whereas vodka had a clear effect in reducing stress, red wine did not. This suggests that red wine does have psychoactive properties independent of its alcohol effects.

Adult↗
PubMed1993

Orofacial neuralgia. Diagnosis and treatment guidelines.

Patients with facial pain, without overt dental disease, are often seen in both medical and dental practice. The differential diagnosis includes (a) cluster headache, in which patients have severe unilateral pains lasting 30 to 120 minutes that respond to verapamil, corticosteroids or lithium; (b) migraine, in which attacks are longer and are often accompanied by nausea and visual disturbance, and can be managed using anti-inflammatory analgesics, with or without metoclopramide, or sumatriptan, although frequent attacks are best suppressed by continuous propranolol or pizotifen; (c) trigeminal neuralgia, knifelike unilateral pains usually responsive to carbamazepine; and (d) temporal arteritis, a steadier pain very responsive to corticosteroids. There is no evidence that continuous 'idiopathic facial pain' is a result of malocclusion (i.e. the way in which the teeth fit together), and its aetiology remains obscure, although there is some biochemical evidence linking it to depression. Many patients respond to simple analgesia and firm reassurance from the physician, although antidepressant therapy (e.g. nortriptyline or dothiepin) is often of great value.

Anti-Inflammatory Agents↗
PubMed1984

Low platelet monoamine oxidase activity in headache: no correlation with phenolsulphotransferase, succinate dehydrogenase, platelet preparation method or smoking.

Platelet monoamine oxidase activity in male migrainous and cluster headache patients was significantly lower than in male controls, confirming our previous study. The activity range showed a normal distribution and low mean values could not be attributed to a subgroup with particularly low activity. When Corash 's platelet preparation method was used, with its high platelet yield, specific enzyme activities of a similar order were obtained. Thus, the low values encountered were not due to abnormal recovery within the platelet population. Two other enzyme activities, phenolsulphotransferase M and succinate dehydrogenase, were also measured in the same platelet samples. Although low succinate dehydrogenase activity was identified in the headache groups, it appeared to represent a separate phenomenon and there was no significant correlation between activity of either enzyme and that of monoamine oxidase. This shows that the low activity of platelet monoamine oxidase in headache is not related to a generalised platelet enzyme deficit. It was also shown that the low monoamine oxidase activity in the headache patients could not be attributed to smoking.

Arylsulfotransferase↗
PubMed1983

Pressor sensitivity to tyramine in patients with headache: relationship to platelet monoamine oxidase and to dietary provocation.

The pressor responses to oral and intravenous tyramine were not different from controls in migrainous patients with or without a history of attacks triggered by foods. However, patients who reported a dietary trigger were more likely to develop headache after tyramine administration than those without such a dietary history. Pressor responses to intravenous tyramine in patients with cluster headache were indistinguishable from controls. A group of five males with platelet monoamine oxidase activity one standard deviation or more below that of male controls required less intravenous tyramine to raise blood pressure by 30 mm Hg than males with monoamine oxidase levels within one standard deviation of the controls. This finding suggests that platelet monoamine oxidase activity to some extent reflects that of total body monoamine oxidase A plus B.

Administration, Oral↗
PubMed1982

Platelet monoamine oxidase: specific activity and turnover number in headache.

Monoamine oxidase turnover numbers (molecules of substrate converted to product per minute per active site) have been calculated for the human platelet enzyme using [3H]pargyline. Headache patients with high and low monoamine oxidase specific activities relative to controls were found to have turnover numbers very close to those for controls. This finding suggests that their specific activities vary because of differences in the concentration of active monoamine oxidase molecules, rather than differences in the ability of those enzyme molecules to catalyse the deamination reaction.

Binding Sites↗
PubMed1982

Platelet phenolsulphotransferase deficiency in dietary migraine.

Patients with dietary migraine were found to have significantly lower levels of platelet phenolsulphotransferase activity than either migrainous patients without a history of dietary provocation or normal controls. Of the two known human variants of this enzyme, the phenol-inactivating P form, for which no endogenous substrate has so far been identified, was more severely involved than the M enzyme, which inactivates monoamines (including tyramine). Such commonly implicated dietary triggering agents as chocolate and cheese may contain as-yet-unidentified phenolic substrates of phenolsulphotransferase P; if the platelet enzyme deficiency were mirrored by low gut activity, abnormally large amounts of potentially toxic substances might gain access to the circulation in consequence.

Adult↗
PubMed1981

Platelet monoamine oxidase activity and headache.

Mean platelet monoamine oxidase activity was reduced compared with control values in groups of headache-free male (but not female) patients suffering from classical migraine and from tension headache. Mean activity in male cluster patients, headache free, both during acute and quiescent phases of their illness, was also notably reduced. Retesting some migraine subjects after up to four years, showed that low activity may be a persistent feature: the correlation coefficient for repeated assays was 0.91 (p less than 0.01). There was no relationship between platelet monoamine oxidase activity and history of dietary migraine. A subgroup of headache patients with permanently low monoamine oxidase activity values may have been defined.

Blood Platelets↗