Migraine: theories of pathogenesis

Blau, J.N.

doi:10.1016/0140-6736(92)91140-4

Cited by 164 publications

(118 citation statements)

References 25 publications

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“…Our finding highlights the importance of taking the time to the next attack into account when investigating migraine patients. Just as the migraine cycle spans several days and contains up to five phases (prodromi, aura, headache, resolution, and recovery) (Blau, 1992), the trigeminal activity in migraine patients is not constant but strongly variable (Ambrosini et al, 2003;. Averaged imaging data point to hyporeactive trigeminal neurons during trigemino-nociceptive stimulation in migraine patients compared with controls.…”

Section: Discussionmentioning

confidence: 99%

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Stankewitz¹,

Aderjan²,

Eippert³

et al. 2011

J. Neurosci.

245

221

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Several lines of evidence suggest a major role of the trigeminovascular system in the pathogenesis of migraine. Using functional magnetic resonance imaging (fMRI), we compared brain responses during trigeminal pain processing in migraine patients with those of healthy control subjects. The main finding is that the activity of the spinal trigeminal nuclei in response to nociceptive stimulation showed a cycling behavior over the migraine interval. Although interictal (i.e., outside of attack) migraine patients revealed lower activations in the spinal trigeminal nuclei compared with controls, preictal (i.e., shortly before attack) patients showed activity similar to controls, which demonstrates that the trigeminal activation level increases over the pain-free migraine interval. Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event.

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Section: Discussionmentioning

confidence: 99%

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Stankewitz¹,

Aderjan²,

Eippert³

et al. 2011

J. Neurosci.

245

221

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“…Role of cortical spreading depression in the pathophysiology of migraine 813 by unilateral, intense, and pulsatile headaches lasting 4-72 h [18] , and is often associated with symptoms including nausea, vomiting, and sensitivity to light, sound, or smell [19] .…”

Section: Migraine Pathophysiologymentioning

confidence: 99%

Role of cortical spreading depression in the pathophysiology of migraine

2014

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A migraine is a recurring neurological disorder characterized by unilateral, intense, and pulsatile headaches. In one-third of migraine patients, the attacks are preceded by a visual aura, such as a slowly-propagating scintillating scotoma. Migraine aura is thought to be a result of the neurovascular phenomenon of cortical spreading depression (SD), a self-propagating wave of depolarization that spreads across the cerebral cortex. Several animal experiments have demonstrated that cortical SD causes intracranial neurogenic infl ammation around the meningeal blood vessels, such as plasma protein extravasation and pro-inflammatory peptide release. Cortical SD has also been reported to activate both peripheral and central trigeminal nociceptive pathways. Although several issues remain to be resolved, recent evidence suggests that cortical SD could be the initial trigger of intracranial neurogenic inflammation, which then contributes to migraine headaches via subsequent activation of trigeminal afferents.Keywords: cortical spreading depression; migraine; neurogenic inflammation; PET; trigeminal nociceptive pathway ·Review· IntroductionCortical spreading depression (SD), described first by Leao [1] , is a self-propagating wave of transient neuronal/ glial membrane depolarization that is accompanied by a transient negative shift of the direct current (DC) potential [2] and temporal elevation of cerebral blood flow (CBF) [3,4] throughout the cerebral hemisphere at a rate of 2-5 mm/ min [1, 5,6] . The rate of spreading correlates with the observed spread of the aura of a classical migraine [7] , which is characterized by a spot of fl ickering light that appears near the center of the visual field and then gradually expands outward [8][9][10] . Recently, cortical SD has been hypothesized to be the initial event involved in migraine headaches.Moskowitz et al. [11,12] proposed that pro-inflammatory peptides, such as substance P and calcitonin generelated peptide (CGRP), released from trigeminocervical nerve terminals in response to some unknown stimulation, probably cortical SD, induces vasodilation and plasma protein extravasation. Such neurogenic inflammation is thought to trigger a headache via stimulation of trigeminal afferents. Consistent with this hypothesis, cortical SD induced intracranial neurogenic inflammation around the meningeal blood vessels [13][14][15] , and subsequent activation of both peripheral [16] and central [17] trigeminal nociceptive pathways has been described. Here, we review the experimental evidence mainly from neurophysiological studies that has advanced the understanding of whether and how the neurovascular phenomenon of cortical SD causes intracranial neurogenic inflammation, and subsequently participates in triggering a migraine headache. Migraine PathophysiologyA migraine is a recurring neurological disorder characterized Yilong Cui, et al . Role of cortical spreading depression in the pathophysiology of migraine 813 by unilateral, intense, and pulsatile headaches lasting 4-72 h [18] , a...

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“…Several hypotheses have been considered in order to explain its pathogenetic background. Since all of them are supported by notable scientific evidence, the vascular involvement represents the conditio sine qua non for migraine attack [4].…”

Section: Introductionmentioning

confidence: 98%

Beneficial effects of Helicobacter pylori eradication on migraine: a 12-month follow-up study

Gabrielli¹,

Franceschi²,

Fiore

et al. 2001

J Headache Pain

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Helicobacter pylori (H. pylori) has been recently associated with some organic and functional vascular disorders. In particular, our group found a high prevalence of H. pylori in patients affected by migraine and a significant improvement of migraine symptoms after eradication of the bacterium, during a follow-up period of 6 months. However, seasonal variations may affect clinical manifestations of migraine, thus influencing our previous results. The present study evaluated the effect of H. pylori eradication during a 1-year follow-up period in a population of 148 consecutively enrolled migraine patients. H. pylori infection was assessed by 13 C-urea breath test. Infected subjects underwent specific antibiotic treatment in order to eradicate the bacterium. Frequency, intensity and duration of attacks of migraine were assessed during a 1-year follow-up period. 42% of the patients showed H. pylori infection. 82% resulted eradicated. Interestingly, 28% of the patients reported a disappearance of migraine during the follow-up period. Moreover, a significant decrease of intensity, frequency and duration of the migraine attacks evaluated 2, 4, 6 and 12 months from H. pylori eradication was observed in the remaining patients. The beneficial effects of H. pylori eradication on migraine seem to be confirmed by this prolonged 1-year follow-up study.

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Migraine: theories of pathogenesis

Cited by 164 publications

References 25 publications

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Trigeminal Nociceptive Transmission in Migraineurs Predicts Migraine Attacks

Role of cortical spreading depression in the pathophysiology of migraine

Beneficial effects of Helicobacter pylori eradication on migraine: a 12-month follow-up study

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