The Platelet and Migraine: A Nonspecific Association

Joseph, Rajiv; Welch, K. M. A.

doi:10.1111/j.1526-4610.1987.hed2707375.x

Cited by 27 publications

(23 citation statements)

References 59 publications

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“…In this respect, review of the literature suggests that platelet membrane disturbance may be attributed to systemic and metabolic effects. Serotonin release appears to be the consequence and not the cause of the migraine attack [12].…”

Section: Pathophysiologymentioning

confidence: 99%

Migraine headache

Carmen-Wilson

1998

Current Review of Pain

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A lthough there is a significant amount of data derived from multiple epidemiologic studies, it is difficult to establish the epidemiology of migraine headache with accuracy. The lack of a universally accepted definition, the absence of objective signs and diagnostic testing, the heterogeneity of the study population, and variability in the methodology accruing the data, make it difficult to study [1]. However, analysis of available epidemiologic data suggests that the prevalence of migraine is 3% to 5.7% in men and 7.4% to 17.6% in women. In a study of 10,169 individuals 12 to 19 years of age whom suffered with headache including migraine, the latter occurred more frequently in adolescents and young adults with a prevalence of 3% in men and 7.4% in women [2]. Genetics of MigraineThe familial inheritance of migraine has long been recognized. The recent literature supports this clinical impression [3]. However, as twin studies reveal a higher concordance rate among monozygotic than dizygotic twin pairs, the exact mode of inheritance is not clear [4,5]. Although several have been proposed, it is possible that the mechanism of migraine inheritance may differ from traditional patterns [6]. The discovery of a genetic locus on chromosome 19 for familial hemiplegic migraine has led to further interest in the genetic basis of more common forms of migraine [7]. Several genetic markers and their possible pathophysiologic relation to migraine are currently being studied [8].Family history of migraine predicts a decrease in the average age of onset of migraine headache [9]. The approximate risk of the offspring of parents affected with migraine is 70% if both parents are affected. The risk falls to 45% if one parent is affected and 30% in case of a close relative [10].Pathophysiology Sicuteri et al. [11] first considered migraine to be a systemic, metabolic derangement; he observed elevated levels of 5-hydroxyindoleacetic acid (5-HIAA) in the urine of patients following migraine attacks. Later, the discovery of platelet serotonin release during the attack resulted in exhaustive study of platelet function on migraineur. In this respect, review of the literature suggests that platelet membrane disturbance may be attributed to systemic and metabolic effects. Serotonin release appears to be the consequence and not the cause of the migraine attack [12]. Migraine MechanismA complete migraine attack has five phases: prodrome, aura, headache phase, termination of headache, and the postdrome. ProdromeAltered mood, libido, cognitive state, motor activity, response to sensory stimuli, thirst, and appetite characterize the prodromal phase. AuraMigraine with aura is characterized by increased neuronal central excitability and susceptibility to spontaneous neuronal depolarization. A wave of intense excitation followed by a spreading inhibition that originates in the occipital cortex and progresses anteriorly throughout the cerebral cortex at a rate of approximately 3 mm/min following the pattern of gyri and sulci and not vascular territo...

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Section: Pathophysiologymentioning

confidence: 99%

Migraine headache

Carmen-Wilson

1998

Current Review of Pain

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“…However, these changes seem to be largely secondary phenomena, rather than primary causative factors [6][7][8]. More than twenty years ago, several groups [9][10][11] noted the presence of a serotonin-releasing factor in plasma drawn during a migraine attack.…”

Section: Introductionmentioning

confidence: 99%

Desialylated transferrin in plasma of patients with migraine without aura

Launay

Tabuteau

Pradalier³

2000

J Headache Pain

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oxidants, CTAP III and NAP2 have already been described [17,18].Transferrin (TF) not only transports iron in all extracellular fluids but also exerts many additional properties, including cell growth stimulation, bacteriostatic action and inhibition of histamine release from mast cells and basophils [19][20][21][22][23]. TF is a 75 kDa glycoprotein containing 679 amino acids and two glycan chains. For each, the last residue is a sialic (N-acetyl neuraminic) acid which can be hydrolyzed by neuraminidase. Circulating TF mainly originates from hepatocytes, its intracellular precursor being asialoapotransferrin. Transferrin receptors, which are present throughout the body, are abundant (10 6 /cell) on the basophil plasma membrane [24]. They are also involved in the development of the nervous system [25].Because of the known relationships between TF and histamine release, we decided to investigate the histamine-releasing ability of this glycoprotein in the plasma of MO patients. Jean-Marie Launay François Tabuteau André PradalierAbstract Patients with migraine without aura (MO), either during or between attacks, present elevated histamine levels in platelet-poor plasma but normal whole blood histamine levels, compared with controls. This finding is usually interpreted as an increased histamine release from basophils due to unidentified histamine-releasing factors. Compared with 10 control plasma samples, each sample from 12 MO patients (5 during and 7 between in attacks) contained normal amounts of iron and immunologically reactive transferrin but decreased transferrin iron-binding capacity. As transferrin inhibits histamine release in vitro, such a functional abnormality, probably due to modifications of the transferrin glycan moiety (desialylated transferrin), may well account for the increased histamine release observed in MO patients. We suggest that glycanmodified transferrin may be related to migraine histamine-releasing factors.

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“…Platelet hyperactivity in migraine has been well documented and seems to be generally accepted (1- 16). At the present time, one of the most important problems concerning the platelet function is whether the platelet abnormality is an essential one or only an epiphenomenon in the pathophysiology of the migraine attack.…”

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confidence: 99%

“…At the present time, one of the most important problems concerning the platelet function is whether the platelet abnormality is an essential one or only an epiphenomenon in the pathophysiology of the migraine attack. On the contrary, several investigators have obtained some evidence to the effect that the platelet abnormality in migraine is an epiphenomenon (12)(13)(14)(15)(16)(17). It is noteworthy that some of these observations were obtained during headache-free periods (4,6-8,lO).…”

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confidence: 99%

“…A platelet hypothesis of migraine pathogenesis has been submitted by Hanington et al (3,4), and some recent investigations have supported this hypothesis (5-9). Some researchers who are opposed to the platelet hypothesis believe that platelet activation in migraine patients is caused by the stress of pain or sympathetic hyperactivity (16,17). On the contrary, several investigators have obtained some evidence to the effect that the platelet abnormality in migraine is an epiphenomenon (12)(13)(14)(15)(16)(17).…”

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Muscle Contraction Headache and Migraine: Platelet Activation and Plasma Norepinephrine during the Cold Pressor Test

Takeshima¹,

Takao²,

Urakami³

et al. 1989

Cephalalgia

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For clarification of possible platelet activation in migraine and chronic muscle contraction headache (MCH) under stress, plasma platelet factor 4 (PF4), norepinephrine (NE), and free fatty acids (FFA) were investigated during the cold pressor test. Both PF4 and NE increased significantly, whereas FFA showed no remarkable changes. The increases of PF4 in MCH and migraine during this test were significantly greater than in healthy controls. The increase of PF4, however, was independent of NE increase and FFA changes. On the other hand, we observed decreased NE levels in both MCH and migraine, which might suggest peripheral sympathetic hypofunction. The platelets of MCH or migraine patients seem to be impaired, and the impairment may be caused by continuous sympathetic hypofunction. The behaviour of the above three substances in MCH was similar to that in migraine throughout the present study.

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The Platelet and Migraine: A Nonspecific Association

Cited by 27 publications

References 59 publications

Migraine headache

Migraine headache

Desialylated transferrin in plasma of patients with migraine without aura

Muscle Contraction Headache and Migraine: Platelet Activation and Plasma Norepinephrine during the Cold Pressor Test

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