Neurogenic inflammation

Neurogenic inflammation is inflammation arising from the local release from afferent neurons of inflammatory mediators such as Substance P and Calcitonin Gene-Related Peptide (CGRP).

This process appears to play an important role in the pathogenesis of numerous diseases including psoriasis,  asthma,  fibromyalgia, eczema, rosacea, dystonia, multiple chemical sensitivity,  and migraine.

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP. leading to a "sterile neurogenic inflammation."

Treatment
Anticipating later botox therapy for migraine, early work by Jancsó et al. found some success in treatment using denervation or pretreatment with capsaicin to prevent uncomfortable symptoms of neurogenic inflammation.

Current study of the treatment of migraine with CGRP blockers show promise. In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks, but elevated liver enzymes in two participants were found. Other therapies and other links in the neurogenic inflammatory pathway for interruption of disease are under study, including migraine therapies.

Given the pathogenesis of neurogenic inflammation the anti-inflammatory and analgesic compound palmitoylethanolamide seems a logical inroad into the treatment of a number of neurogenic inflammation-states and neuropathic pain.

Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis, the University of Minnesota has begun a clinical trial to follow up on the observation that patients treated with botulinum toxin for dystonia had dramatic improvement in psoriasis.

Astelin (Azelastine) "is indicated for symptomatic treatment of vasomotor rhinitis including rhinorrhea, nasal congestion, and post nasal drip in adults and children 12 years of age and older."

Statins may be useful for treating diseases presenting with predominant neurogenic inflammation

Prevention
Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, IL-6, and TNF-alpha, which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation. In a later study, researchers observed bone loss in rats that received reduced levels of dietary magnesium, but within the range of dietary intake found in the human population. Even that marginal magnesium deficiency was found to result in an increase in substance P, TNFalpha, and IL1beta. These and other data support the notion that deficient dietary magnesium intake, even at levels not uncommon in humans, not only triggers neurogenic inflammation but may also be a risk factor for osteoporosis.