[Peripheral neuropathy induced with methylguanidine. (Experimental study in the dog)].
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Biomedical subjects
Publications and source records attributed to F Ferro-Milone.
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Although platelet activation is known to occur during migraine attacks, the cause-effect relationship remains to be determined. This problem was approached by studying the possible occurrence of platelet activation in vivo in headache-free periods of subjects affected by common or classic migraine and, subsequently, by verifying the possibility of its pharmacological control through administration of a classic anti-aggregation drug such as aspirin (ASA). The plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), indices of the occurrence of platelet activation in vivo, were therefore first assayed in both groups of migraine sufferers in the absence of therapy and then during the administration of aspirin (50 mg/daily). In the group of 15 patients affected by classic migraine, basal plasma levels of beta-TG and PF4 were significantly higher than control subjects. On the other hand, only beta-TG plasma levels were significantly higher in the group of 18 patients affected by common migraine. Patients suffering from classic migraine showed a high incidence of platelet activation (greater than 90%) in comparison with common migraine patients (approximately 33%). This suggests that platelet activation occurs in vivo in migrainous patients also during headache-free periods. Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma beta-TG and PF4 concentration. Consequently, pharmacological treatment with aspirin in adequate dose may prove to be helpful in diminishing the vascular side-effects known to occur in migraine sufferers.
The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.
In order to evaluate the role of the sympathetic autonomic nervous system (SANS) in common migraine we measured platelet catecholamine levels in a group of patients and in control subjects after 1 and 30 min of supine rest. Common migraine patients showed, at 1 min of supine rest, higher platelet norepinephrine (NE) content in comparison with the controls. This result may reflect a decreased release of platelet dense bodies in migraineurs. The same patients showed after 30' of supine rest a hardly significant increase of platelet NE levels in contrast to the clearly significant increase found in controls. These findings support the hypothesis of sympathetic hypofunction in migraine.
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