Migraine: A Platelet Disorder

Hanington, Edda; Jones, Richard J.; Amess, J. A. L.; Wachowicz, Barbara

doi:10.1016/s0140-6736(81)91049-7

Cited by 159 publications

(79 citation statements)

References 21 publications

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“…The hypothesis of migraine being primarily a platelet dysfunction has been put forward nearly 30 years ago. In a period without headaches, spontaneous platelet aggregation and platelet adhesion of the migraine patients were found to be more than the healthy controls, thus it was argues that the different platelet behavior in migraine patients may play a role in the recurrence of the attacks (19). The limitation of our study was that, since it was retrospectively conducted, we were not able to record whether the sample collection was done at a period of attacks or no attacks and therefore we could not make the comparison between the two in terms of platelet and MPV values.…”

Section: Discussionmentioning

confidence: 99%

“…For this reason, a relationship on the cellular level between migraine and stroke has been suggested. Serotonin plays an important role in the pathogenesis of migraine, 90% of which is contained within platelets and it is released from the platelets depending on the demand (19). Zeller et al evaluated the P-selectin expression on platelets in patients with migraine and found an increase in platelet activation and leucocyte-platelet aggregation formation as compared to healthy controls, especially in migraine patients without auras (20).…”

Section: Discussionmentioning

confidence: 99%

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Migrenli Hastaların Kanında Ortalama Trombosit Hacmi ve Trombosit Sayısının Araştırılması

Varol¹,

Akıl²,

Çevik³

et al. 2013

Tnd

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Sum maryObjective: Mean platelet volume (MPV) is an indicator for platelet function and activation. Studies researching MPV and platelet level on the patients with migraine are insufficient. In this study, we aimed to find a difference in MPV and platelet count in individuals with migraine compared to healthy controls, which are indicators for platelet activation. We compared MPV and platelet counts between the patients with migraine and healthy controls. Both groups were similar in terms of age and gender. Re sults: A statistically insignificant increase was found in MPV in patients with migraine (7.98±1.34 fL) when compared to the control group (7.85±0.96 fL) (p=0.34). Platelet levels were significantly lower in patients with migraine (367.6±74.2) than the platelet levels of the control group (286.9±68.3) (p=0.02). Dis cus si on: We found lower platelet levels in the patients with migraine compared to the control group. There was also statistically insignificant increase in MPV in patients with migraine, suggesting that these findings may indicate an insignificant platelet activation in patients with migraine. New prospective studies are needed on this subject. Benzer yaş ve cinsiyette migren tanısı konmuş hastalar ile sağlıklı olan kontrol grubu arasında OTH ve trombosit sayıları karşılaştırıldı. Bulgular: Migren hastalarında OTH (7,98±1,34 fL) kontrol grubuna göre (7,85±0,96 fL) istatistiksel olarak anlamlı olmayan artış bulundu (p=0,34). Trombosit düzeyi migrenli hastalarda (267,6±74,2) kontrollere (286,9±68,3) göre anlamlı düzeyde düşüktü (p=0,02). Sonuç: Çalışmamızda trombosit sayısını migrenli hastalarda sağlıklı kontrol grubuna göre düşük bulurken OTH ise migrenli hastalarda kontrol grubuna göre istatistiksel olarak anlamlı olmayan artış bulduk. Bu bulgular migren hastalarında istatistiksel olarak belirgin olmayan trombosit aktivasyonunu gösterebilir. Bu konuda prospektif yeni çalışmalara ihtiyaç vardır. (

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Migrenli Hastaların Kanında Ortalama Trombosit Hacmi ve Trombosit Sayısının Araştırılması

Varol¹,

Akıl²,

Çevik³

et al. 2013

Tnd

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“…In 1981, Jones et al [17] demonstrated that 5-hydroxytryptamine (5-HT, serotonin) release after platelet stimulation after a migraine attack was significantly less than that during a migraine-free interval in combination with decreased platelet aggregation and increased platelet adhesion when compared to controls. They suggested that increased circulating platelet aggregates could play a primary role in producing prodromal symptoms of migraine.…”

Section: Discussionmentioning

confidence: 99%

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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“…It is of interest however to note that as early as in 1976 it was observed that the platelets from classical migraine patients showed a higher tendency for spontaneous aggregation and adhesion during the headache-free period when compared with the platelets from controls [8]. Similarly, serotonin release from the platelets within three days of a migraine attack was found to be significantly less than that measured during a migraine-free interval [9]. Though serotonin is still considered to be a key molecule in the neurobiology of migraine, the exact role of brain serotonergic mechanisms still remains a matter of controversy [10].…”

Section: Serotonin Platelets and Migrainementioning

confidence: 99%

Platelet Alloantigen Polymorphism and Migraine Headache - An Observation in the Malaysian Population at Kelantan

Bhaskar¹

2017

Int J Neurorehabilitation Eng

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Migraine: A Platelet Disorder

Cited by 159 publications

References 21 publications

Migrenli Hastaların Kanında Ortalama Trombosit Hacmi ve Trombosit Sayısının Araştırılması

Migrenli Hastaların Kanında Ortalama Trombosit Hacmi ve Trombosit Sayısının Araştırılması

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

Platelet Alloantigen Polymorphism and Migraine Headache - An Observation in the Malaysian Population at Kelantan

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