Effect of cortical spreading depression on basal and evoked traffic in the trigeminovascular sensory system

Lambert, Geoffrey; Truong, Linda; Zagami, Alessandro S

doi:10.1177/0333102411422383

Cited by 69 publications

(68 citation statements)

References 73 publications

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“…Studies performed with human neocortical sections showed that even a single CSD event could facilitate excitatory post-synaptic potentials and elicit long-term potentiation, thus contributing to cortical hyperexcitability (53). CSD may also generate headache by activating central trigeminovascular neurons through subcortical pathways that result in disinhibition of sensory neurons within the TNC (54). Meningeal plasma extravasation has been detected by photon-emission tomography during migraine (55).…”

Section: Discussionmentioning

confidence: 99%

Increased susceptibility to cortical spreading depression in an animal model of medication-overuse headache

Green

Felice

et al. 2013

Cephalalgia

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Objective The objective of this article is to evaluate electrically evoked thresholds for cortical spreading depression (CSD) and stress-induced activation of trigeminal afferents in a rat model of medication-overuse headache (MOH). Methods Sumatriptan or saline was delivered subcutaneously by osmotic minipump for six days to Sprague-Dawley rats. Two weeks after pump removal, animals were anesthetized and recording/stimulating electrodes implanted. The animals were pretreated with vehicle or topiramate followed by graded electrical stimulation within the visual cortex. CSD events were identified by decreased EEG amplitude and DC potential shift. Additional unanesthetized sumatriptan or saline-pretreated rats were exposed to bright light environmental stress and periorbital and hindpaw withdrawal thresholds were measured. Following CSD stimulation or environmental stress, immunohistochemical staining for Fos in the trigeminal nucleus caudalis (TNC) was performed. Results Sumatriptan pre-exposure significantly decreased electrical stimulation threshold to generate a CSD event. Topiramate normalized the decreased CSD threshold as well as stress-induced behavioral withdrawal thresholds in sumatriptan-treated rats compared to saline-treated animals. Moreover, CSD and environmental stress increased Fos expression in the TNC of sumatriptan-treated rats, and these effects were blocked by topiramate. Environmental stress did not elicit cutaneous allodynia or elevate TNC Fos expression in saline-treated rats. Conclusions A previous period of sumatriptan exposure produced long-lasting increased susceptibility to evoked CSD and environmental stress-induced activation of the TNC that was prevented by topiramate. Lowered CSD threshold, and enhanced consequences of CSD events (increased activation of TNC), may represent an underlying biological mechanism of MOH related to triptans.

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Section: Discussionmentioning

confidence: 99%

Increased susceptibility to cortical spreading depression in an animal model of medication-overuse headache

Green

Felice

et al. 2013

Cephalalgia

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“…Based on these new data, that could also explain the reasons for the previous study negative findings, the crucial role of CSD as a sufficient migraine pain trigger, at least in MA, has been fully rehabilitated [31]. However, the assumption that CSD-dependent peripheral trigeminovascular activation is the main pathway involved in the second-order trigeminal neurons activation has been challenged by a very interesting work by Lambert et al [32]. The direct recording of trigeminal nuclei neurons involved in meningeal pain processing following CSD induction showed only minor differences in firing pattern before versus after the peripheral exclusion of trigeminal input by lignocaine injection in Gasser ganglion, confirming that CSD could directly modulate the trigeminal nuclei activity.…”

Section: New Evidences On the Cortical Spreading Depression Role In Mmentioning

confidence: 89%

Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective

et al. 2013

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The role of the cortical spreading depression (CSD)-dependent trigeminovascular activation in migraine etiopathogenesis, long considered paradigmatic, has remained substantially unproven in humans. The parallel advancement of functional neuroimaging techniques promoted the extensive exploration of the brain networks involved in pain processing in search of a possible central migraine generator. However, despite initial enthusiasms, it has not been possible to clarify whether the functional central ''markers'' of pain observed in primary headaches could be considered as causative or just the neural correlates of the ongoing pain. Nonetheless, our knowledge on the complex interactions between CSD, neurogenic inflammation, peripheral trigeminovascular input, central cortico-trigeminal nuclei direct modulation and pain processing and limbic system networks has enormously grown, allowing the reconceptualisation of migraine from a neurovascular to a pure neurolimbic pain disorder, therefore relocating it in the much broader frame of the brain and whole organism homeostatic control. In this work, the available evidences currently supporting the relevance of CSD, of peripheral trigeminovascular input and of direct cortico-trigeminal nuclei modulation in migraine pathogenesis are reviewed in the light of a possible integrated migraine etiopathogenetic perspective.

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“…A dense network of dural nerve fibres that react with substance P and calcitonin gene-related peptide (CGRP) has been found [12], the role of the latter in the development of new treatments is discussed further in this review. CSD has also been reported to cause changes in brainstem nociceptive neuronal activity even when the trigeminal pathway has been inhibited [13]. In humans, functional imaging has shown changes in cortical function and blood flow and the patterns of spread are suggestive of CSD [10].…”

Section: Pathophysiology Of Migrainementioning

confidence: 99%

New and Emerging Treatments for Migraine

Ahmed¹

2015

J Pain Relief

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Migraine can be extremely disabling with a considerable impact on the life of an individual in their ability to work or perform activities of daily living. The arrival of 'triptans' in the early 1990s saw a major change in the way migraines were treated, and 'triptans' remain the gold standard in treating an acute attack. For a long time there was very little progress in identifying new targets for acute treatment and there was virtually nothing new in migraine prevention. However, in recent times, considerable research has been made in understanding the pathophysiology of migraine and the coming decade should see a drastic change in treating and preventing migraines with potential neuro-pharmacological agents and non-invasive neuro-stimulation. This article briefly discusses the pathophysiology of migraine and reviews new therapeutic options as well as some promising treatments undergoing clinical trials.

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Effect of cortical spreading depression on basal and evoked traffic in the trigeminovascular sensory system

Cited by 69 publications

References 73 publications

Increased susceptibility to cortical spreading depression in an animal model of medication-overuse headache

Increased susceptibility to cortical spreading depression in an animal model of medication-overuse headache

Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective

New and Emerging Treatments for Migraine

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