Functional Anatomy of Trigeminovascular Pain

Meßlinger, Karl; Dux, Mária

doi:10.1002/9781118967225.ch1

Cited by 1 publication

(2 citation statements)

References 187 publications

(213 reference statements)

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“…Like all other nociceptors, the trigeminal nociceptors consist of small primary sensory neurons with unmyelinated Cand thinly myelinated Aδ-fibers, the central terminals of which run through the trigeminal nerve, enter the pontine brainstem and synapse on neurons in the spinal trigeminal nucleus (STN). The STN is also called trigemino-cervical brainstem complex, because it passes into the upper cervical segments without clear structural and functional boundary [3,4].…”

Section: Anatomical Basis Of Headache Generationmentioning

confidence: 99%

“…All three trigeminal partitions (V1-V3) participate in innervating the meninges, in the occipital region complemented by cervical afferents from segments C1-C3. In addition, the meninges are densely innervated also by postganglionic sympathetic fibers and sparsely by parasympathetic fibers originating in the cranial ganglia [4].…”

Section: Anatomical Basis Of Headache Generationmentioning

confidence: 99%

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TRP Channels in the Focus of Trigeminal Nociceptor Sensitization Contributing to Primary Headaches

Dux

Rosta

Meßlinger

2020

IJMS

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Pain in trigeminal areas is driven by nociceptive trigeminal afferents. Transduction molecules, among them the nonspecific cation channels transient receptor potential vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1), which are activated by endogenous and exogenous ligands, are expressed by a significant population of trigeminal nociceptors innervating meningeal tissues. Many of these nociceptors also contain vasoactive neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P. Release of neuropeptides and other functional properties are frequently examined using the cell bodies of trigeminal neurons as models of their sensory endings. Pathophysiological conditions cause phosphorylation, increased expression and trafficking of transient receptor potential (TRP) channels, neuropeptides and other mediators, which accelerate activation of nociceptive pathways. Since nociceptor activation may be a significant pathophysiological mechanism involved in both peripheral and central sensitization of the trigeminal nociceptive pathway, its contribution to the pathophysiology of primary headaches is more than likely. Metabolic disorders and medication-induced painful states are frequently associated with TRP receptor activation and may increase the risk for primary headaches.

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Section: Anatomical Basis Of Headache Generationmentioning

confidence: 99%

Section: Anatomical Basis Of Headache Generationmentioning

confidence: 99%