Selected Confirmed, Probable, and Exploratory Migraine Biomarkers

Loder, Elizabeth; Harrington, Michael G.; Cutrer, Michael F.; Sándor, Péter; Vries, Boukje de

doi:10.1111/j.1526-4610.2006.00525.x

Cited by 15 publications

(10 citation statements)

References 182 publications

(245 reference statements)

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“…The pendulum has swung from neural to vascular and back again and the rationale and search for migraine prevention has swung with it. Extensive summaries of possible pathophysiological mechanisms can be found in “Biomarkers for Migraine” 3‐9 and in Sanchez‐del‐Rio et al 10 and Goadsby 11 …”

Section: Hypothesesmentioning

confidence: 99%

“…2 The pendulum has swung from neural to vascular and back again and the rationale and search for migraine prevention has swung with it. Extensive summaries of possible pathophysiological mechanisms can be found in "Biomarkers for Migraine" [3][4][5][6][7][8][9] and in Sanchez-del-Rio et al 10 and Goadsby. 11 Vascular Factors.-Pain originating inside the head must necessarily arise from its large blood vessels or the tissue which surrounds the blood vessels of the dura mater, because these are the only structures to receive substantial sensory innervations.…”

Section: Hypothesesmentioning

confidence: 99%

“…What might be termed "sub-pathological" small differences exist between chronic migraineurs and the normal population. These differences include differences in relevant biochemical markers such as 5-HT and its metabolites, [3][4][5][6][7][8]228 neurophysiological measures which are seen in tests of contingent negative variation, 229 and a few minor CNS abnormalities. 230 But all of these markers are subtle and it is not even clear whether they are the cause or the consequence of migraine.…”

Section: How Are Migraineurs Different From Non-migraineurs?mentioning

confidence: 99%

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The Mode of Action of Migraine Triggers: A Hypothesis

Lambert

Zagami

2009

Headache

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Objectives.-To review conjectured modes of action of migraine triggers and to present a new hypothesis about them. Background.-Migraine attacks are initiated in many migraineurs by a variety of "triggers," although in some patients no external trigger can be identified. Many triggers provoke attacks with such a short latency that only some kind of neural mechanism can explain the triggering.Results.-We present here a hypothesis that the pain of migraine has its ultimate origin in the cortex, but that the immediate generator is in the brainstem. Our hypothesis is that most migraines have triggers that produce excitation of cortical neurons and that this directly causes withdrawal of descending sensory inhibition originating in the brainstem. A wide range of evidence from the literature that cortical activation induced by a number of different mechanisms often produces headache is presented to support this notion. Several nuclei in the brainstem appear to participate in the selective control of trigeminovascular sensation through descending inhibitory mechanisms that arise in the cortex. In this review we focus on 2 of them, the periaqueductal gray matter and nucleus raphe magnus. Our own past results and those of others show that this inhibition is specific for craniovascular sensation and involves the neurotransmitter 5-hydroxytryptamine. Finally, we summarize our own recent experiments, which show that cortical activation by migraine triggers (including cortical spreading depression) inhibits neuronal discharge in the brainstem and facilitates trigeminovascular sensation. Conclusion.-If the hypothesis can be proven and the neurotransmitters involved in the hypothetical trigger pathway can be identified, it may be possible to develop novel migraine preventative therapies.Key words: migraine, migraine trigger, cerebral cortex, brainstem, trigeminovascular sensory system Abbreviations: 5-HT 5-hydroxytryptamine, CGRP calcitonin gene-related peptide, CSD cortical spreading depression, DC direct current, ECT electroconvulsive therapy, LC locus coeruleus, NO nitric oxide, NRM nucleus raphe magnus, NTS nucleus tractus solitarius, PAG periaqueductal gray matter, PET positron emission tomography, SP substance P, TMS transcranial magnetic stimulation (Headache 2009;49:253-275) In this review, we present the hypothesis that most migraines have triggers that produce excitation of cortical neurons and that this excitation directly inhibits neurons in 2 brainstem nuclei: the periaqueductal gray matter (PAG) and the nucleus raphe magnus (NRM). These nuclei then release their ongoing descending control of dura mater sensation in the trigeminal nucleus and cause normal sensory traffic from the dura to be perceived as migraine pain.Migraine is one of our most common and debilitating organic diseases, yet bafflingly has no apparent pathology. It is a condition involving the "trigeminovascular system," in which the cranial vasculature, the trigeminal sensory system, and the central nervous system all play a part. Its cardinal fe...

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Section: Hypothesesmentioning

confidence: 99%

Section: Hypothesesmentioning

confidence: 99%

Section: How Are Migraineurs Different From Non-migraineurs?mentioning

confidence: 99%

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The Mode of Action of Migraine Triggers: A Hypothesis

Lambert

Zagami

2009

Headache

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“…Migraine has no reliable biomarker and is diagnosed by medical history (1). The International Classification of Headache Disorders (2) proposes diagnostic criteria that define episodic migraine as recurrent attacks lasting 4 to 72 hours, where the headache has at least two out of four characteristics (unilateral, pulsating, medium or severe intensity, increased by routine physical activity) and is accompanied by photophobia and phonophobia, and/or nausea/vomiting.…”

Section: Introductionmentioning

confidence: 99%

Visual and auditory cortical evoked potentials in interictal episodic migraine: An audit on 624 patients from three centres

et al. 2016

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Background Many studies report a habituation deficit of visual evoked potentials (VEP) and/or increased intensity dependence of auditory evoked cortical potentials (IDAP) in episodic migraine patients between attacks. These findings have a pathophysiological interest, but their diagnostic utility is not known. Aims To perform an audit on a large database of interictal VEP and IDAP recordings in episodic migraine patients and evaluate their diagnostic accuracy. Methods We pooled data for VEP habituation and IDAP measured in 624 episodic migraineurs (EM) and 360 healthy volunteers (HV) from three centers. Thresholds were calculated by Receiver Operating Curve analysis and used to calculate sensitivity, specificity, positive and negative likelihood ratios (LR+ and LR-) and the accuracy of each test, using ICHD diagnostic criteria as the gold standard. Results In EM, VEP habituation was significantly lower than in HV, and IDAP slopes were significantly steeper. VEP (five blocks of 50 responses), VEP (six blocks of 100 responses) and IDAP had respectively 61.0%, 61.4% and 45.7% sensitivity, and 77.9%, 77.9% and 87.2% specificity. Their positive (LR+) and negative (LR-) likelihood ratios were respectively 2.760, 2.778, 3.570 and 0.500, 0.495, 0.623, with diagnostic accuracies of 65.3%, 69.0% and 54.3%. In combined VEP + IDAP recordings, an abnormality of at least one test had 83.4% sensitivity, 66.7% specificity, 2.504 LR+, 0.249 LR- and 81.1% accuracy. Conclusions In this large database, VEP habituation is significantly reduced and IDAP increased in episodic migraine patients between attacks. Taken alone, neither VEP nor IDAP has sufficient diagnostic accuracy. However, when both tests are performed in the same patient, an abnormality of at least one of them is highly predictive of interictal episodic migraine.

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“…Multiple studies have considered the relationship of migraine to systemic abnormalities. 1 Clinically, migraine patients are more likely than controls to have ischemic stroke, patent foramen ovale, livedo reticularis, 2 essential tremor, 3 and preeclampsia. 4 Susceptibility to stroke in migraine may be related to abnormal arterial function, oxidative stress, inflammatory factors, endothelial dysfunction, or hypercoagulability.…”

mentioning

confidence: 99%