Platelet Activity in Migraine

Andrea, Giovanni D'; Toldo, Moreno; Cortelazzo, Sergio; Milone, Francesco

doi:10.1111/j.1526-4610.1982.hed2205207.x

Cited by 93 publications

(40 citation statements)

References 13 publications

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“…On the contrary, whilst levels decreased during attacks, platelet serotonin remained unmodified in headache-free periods. 15 A more extensive study of the possible occurrence of platelet activation in vivo in headache-free periods in subjects suffering from either common or classic migraine may perhaps yield some further information about: a) the incidence of platelet activation in common and/or classic migraine, b) the relevance of this to migraine pathogenesis or to accompanying side-effects. 16 Possible predisposition of migraine sufferers to cerebrovascular and cardiac diseases is known.…”

mentioning

confidence: 99%

Study of platelet activation in migraine: control by low doses of aspirin.

D’Andrea¹,

Toldo²,

Cananzi³

et al. 1984

Stroke

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SUMMARY 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 03-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 IS patients affected by classic migraine, basal plasma levels of /3-TG and PF4 were significantly higher than control subjects. On the other hand, only /3-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 (>90%) in comparison with common migraine patients (-33%). This suggests that platelet activation occurs in vivo in migrainous patients also during headachefree periods.Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma /3-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.

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mentioning

confidence: 99%

Study of platelet activation in migraine: control by low doses of aspirin.

D’Andrea¹,

Toldo²,

Cananzi³

et al. 1984

Stroke

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“…Within a few days of the migraine attack, levels of B-TG and PF-4 decreased to that of migraine-free periods (fig. 1, 2) [18]. We could extend these observations by the demonstration of shortened platelet survival, increased platelet activation markers B-TG and PF-4 (fig.…”

Section: Discussionmentioning

confidence: 98%

“…They showed a significant increase of B-TG and PF-4 and a decrease of platelet 5-HT content during a documented migraine attack (grey area). This demonstrates that, in these patients, migraine is a platelet disorder with documented in vivo platelet activation during the attacks [18]. …”

Section: Discussionmentioning

confidence: 99%

“…1 D'Andrea et al [18] identified a group of migraine patients with increased basal levels of B-TG and PF-4 in their migraine-free periods. They showed a significant increase of B-TG and PF-4 during attacks of migraine (open circles).…”

Section: Discussionmentioning

confidence: 99%

“…They suggested that increased circulating platelet aggregates could play a primary role in producing prodromal symptoms of migraine. D'Andrea et al [18 ]studied ‘in vivo' platelet activation by measuring levels of platelet 5-HT and plasma β-thromboglobulin (B-TG) and platelet factor 4 (PF-4), during migraine attacks and migraine-free periods. In migraine-free periods, there were no differences in platelet 5-HT values between the migraine patients and the controls, but 2 groups of migraine patients were identified in the migraine-free periods: one with normal B-TG and PF-4 plasma levels and the other with high B-TG and PF-4 plasma levels (fig.…”

Section: Discussionmentioning

confidence: 99%

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Aspirin-Responsive, Migraine-Like Transient Cerebral and Ocular Ischemic Attacks and Erythromelalgia in JAK2<sup>V617F</sup>-Positive Essential Thrombocythemia and Polycythemia Vera

et al. 2014

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Migraine-like cerebral transient ischemic attacks (MIAs) and ocular ischemic manifestations were the main presenting features in 10 JAK2^V617F-positive patients studied, with essential thrombocythemia (ET) in 6 and polycythemia vera (PV) in 4. Symptoms varied and included cerebral ischemic attacks, mental concentration disturbances followed by throbbing headaches, nausea, vomiting, syncope or even seizures. MIAs were frequently preceded or followed by ocular ischemic events of blurred vision, scotomas, transient flashing of the eyes, and sudden transient partial blindness preceded or followed erythromelalgia in the toes or fingers. The time lapse between the first symptoms of aspirin-responsive MIAs and the diagnosis of ET in 5 patients ranged from 4 to 12 years. At the time of erythromelalgia and MIAs, shortened platelet survival, an increase in the levels of the platelet activation markers β-thromboglobulin and platelet factor 4 and also in urinary thromboxane B2 were clearly indicative of the spontaneous in vivo platelet activation of constitutively JAK2^V617F-activated thrombocythemic platelets. Aspirin relieves the peripheral, cerebral and ocular ischemic disturbances by irreversible inhibition of platelet cyclo-oxygenase (COX-1) activity and aggregation ex vivo. Vitamin K antagonist, dipyridamole, ticlopidine, sulfinpyrazone and sodium salicylate have no effect on platelet COX-1 activity and are ineffective in the treatment of thrombocythemia-specific manifestations of erythromelalgia and atypical MIAs. If not treated with aspirin, ET and PV patients are at a high risk of major arterial thrombosis including stroke, myocardial infarction and digital gangrene.

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Naproxen in Prophylaxis of Migraine

Ziegler¹,

Ellis²

1985

Archives of Neurology

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Platelet Activity in Migraine

Cited by 93 publications

References 13 publications

Study of platelet activation in migraine: control by low doses of aspirin.

Study of platelet activation in migraine: control by low doses of aspirin.

Aspirin-Responsive, Migraine-Like Transient Cerebral and Ocular Ischemic Attacks and Erythromelalgia in JAK2<sup>V617F</sup>-Positive Essential Thrombocythemia and Polycythemia Vera

Naproxen in Prophylaxis of Migraine

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