Neurogenic Model of Migraine

  title={Neurogenic Model of Migraine},
  author={M. Gabriella Buzzi and Michela Bonamini and MA Moskowitz},
  pages={277 - 280}
Activation of peripheral trigeminal fibers induces neurogenic inflammation in rat dura mater, as well as vascular and mast cell changes. These changes parallel an increase of vasodilating and permeability promoting peptides in venous effluent of the cephalic circulation. The experimental model of electrical trigeminal ganglion stimulation or systemic capsaicin administration has proven effective in detecting cellular activation in brainstem trigeminal nuclei. Animal experimental models of… 

Neurogenic inflammation in primary headaches

The evidence in support of the hypothesis that a sterile neurogenic inflammation in the meninges may be involved in generating or sustaining, via occurrence of a vicious cycle, the pain accompanying the migraine attacks is reviewed.

Dural inflammation model of migraine pain.

This theory proposes that, during a migraine, there is an idiopathic activation of trigeminal sensory afferents, resulting in nociceptive transmission to the CNS as well as the release of pro-inflammatory substances in the periphery, particularly the dura.

Depletion of calcitonin gene-related peptide from the caudal trigeminal nucleus of the rat after electrical stimulation of the Gasserian ganglion

Electrical stimulation of the Gasserian ganglion resulted in partial depletion of calcitonin gene-related peptide (CGRP) from ipsilateral central terminals of pseudounipolar primary sensory ganglions cells, which might be of importance in the pathogenesis of migraine headache.

TRPV1 in migraine pathophysiology.

Role of pituitary adenylate cyclase-activating polypeptide in nociception and migraine.

It is clear that PACAP plays an excitatory role in migraine, but its target and signalling pathways have not yet been elucidated due to the lack of non-peptide, selective agonists and antagonists.

New insights into the molecular actions of serotonergic antimigraine drugs.

Spontaneous Trigeminal Allodynia in Rats: A Model of Primary Headache

This model can be used as a predictive model for drug development and for studies of putative biomarkers for headache diagnosis and treatment, and to validate this as a model for migraine.

The pathophysiology of migraine: year 2005

It is possible that visual, motor or sensory aura might be responsible for the generation of the pain through the above mechanisms of cortical spreading depression underlies migraine.



The neurobiology of vascular head pain

The relationship of trigeminovascular fibers to the pathogenesis of vascular head pain sheds light on possible mechanisms of migraine and other central nervous system conditions associated with headache and inflammation.

The trigeminovascular system and migraine: Studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats

These data characterize some aspects of the cerebrovascular physiology of the trigeminovascular system and demonstrate important interactions between this system and the effective antimigraine agents sumatriptan and dihydroergotamine and that such interactions can be represented in animal models.

Ergot alkaloids block neurogenic extravasation in dura mater: Proposed action in vascular headaches

It is proposed that the therapeutic effects of ergots in vascular headaches may result from peripheral blockade of small fiber (C or A‐delta)‐dependent neurogenic inflammation within the dura mater.

Enrichment of a vasoactive neuropeptide (calcitonin gene related peptide) in the trigeminal sensory projection to the intracranial arteries

The population of trigeminal ganglion cells projecting to the cerebral vasculature is enriched in C GRP-containing neurons, and especially in the population of neurons containing CGRP and not Sub P.

Cluster Headache: Ultrastructural Evidence for Mast Cell Degranulation and Interaction with Nerve Fibres in the Human Temporal Artery

Observations of human temporal arteries from cluster headache patients and their comparison to those from a control group strongly suggest that mast cells may be this link to the pathophysiology of cluster headache.

Controlled thermocoagulation of trigeminal ganglion and rootlets for differential destruction of pain fibers: facial pain other than trigeminal neuralgia.

  • W. Sweet
  • Medicine
    Clinical neurosurgery
  • 1976
I describe the results of retrogasserian differential lidocaine block to aid in the selection of patients for a differential thermal lesion in the trigeminal ganglion and rootlets. This procedure