Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27293326
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Ann+Indian+Acad+Neurol
2016 ; 19
(2
): 175-82
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Understanding migraine: Potential role of neurogenic inflammation
#MMPMID27293326
Malhotra R
Ann Indian Acad Neurol
2016[Apr]; 19
(2
): 175-82
PMID27293326
show ga
Neurogenic inflammation, a well-defined pathophysiologial process is
characterized by the release of potent vasoactive neuropeptides, predominantly
calcitonin gene-related peptide (CGRP), substance P (SP), and neurokinin A from
activated peripheral nociceptive sensory nerve terminals (usually C and A
delta-fibers). These peptides lead to a cascade of inflammatory tissue responses
including arteriolar vasodilation, plasma protein extravasation, and
degranulation of mast cells in their peripheral target tissue. Neurogenic
inflammatory processes have long been implicated as a possible mechanism involved
in the pathophysiology of various human diseases of the nervous system,
respiratory system, gastrointestinal tract, urogenital tract, and skin. The
recent development of several innovative experimental migraine models has
provided evidence suggestive of the involvement of neuropeptides (SP, neurokinin
A, and CGRP) in migraine headache. Antidromic stimulation of nociceptive fibers
of the trigeminal nerve resulted in a neurogenic inflammatory response with
marked increase in plasma protein extravasation from dural blood vessels by the
release of various sensory neuropeptides. Several clinically effective abortive
antimigraine medications, such as ergots and triptans, have been shown to
attenuate the release of neuropeptide and neurogenic plasma protein
extravasation. These findings provide support for the validity of using animal
models to investigate mechanisms of neurogenic inflammation in migraine. These
also further strengthen the notion of migraine being a neuroinflammatory disease.
In the clinical context, there is a paucity of knowledge and awareness among
physicians regarding the role of neurogenic inflammation in migraine. Improved
understanding of the molecular biology, pharmacology, and pathophysiology of
neurogenic inflammation may provide the practitioner the context-specific
feedback to identify the novel and most effective therapeutic approach to
treatment. With this objective, the present review summarizes the evidence
supporting the involvement of neurogenic inflammation and neuropeptides in the
pathophysiology and pharmacology of migraine headache as well as its potential
significance in better tailoring therapeutic interventions in migraine or other
neurological disorders. In addition, we have briefly highlighted the
pathophysiological role of neurogenic inflammation in various other neurological
disorders.