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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).[1]

This process appears to play an important role in the pathogenesis of numerous diseases including psoriasis,[2][3] asthma,[4] fibromyalgia, eczema, rosacea, dystonia, multiple chemical sensitivity,[5][6] and migraine.[7][8][9]

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.[10][11] leading to a "sterile neurogenic inflammation."[12]


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.[13]

Current study of the treatment of migraine with CGRP blockers show promise.[14] In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks,[15] 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.[16]

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,[17] 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.[18]

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."[19]

Statins may be useful for treating diseases presenting with predominant neurogenic inflammation [20]


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.[21] 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.[22]


  1. (March 2008). The concept of neurogenic inflammation. BJU Int. 101 Suppl 3: 2–6.
  2. Schön and Boehncke, Psoriasis: Neurogenic inflammation and other mechanisms NEJM 352:1899-1912, Number 18, 2005
  3. (2006). The role of neuropeptides in psoriasis. The British journal of dermatology 155 (5): 876–82.
  4. (December 2001). Neurogenic inflammation and particulate matter (PM) air pollutants. Neurotoxicology 22 (6): 795–810.
  5. (December 2009). Brain dysfunction in multiple chemical sensitivity. J. Neurol. Sci. 287 (1–2): 72–8.
  6. (1997). Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation. Environmental health perspectives 105 Suppl 2: 531–7.
  7. (2008). Peripheral mechanism of action of antimigraine prophylactic drugs. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 29 Suppl 1: S127–30.
  8. (2005). Neurogenic inflammation and migraine: implications for the therapeutics. Molecular interventions 5 (5): 304–11.
  9. (2005). CGRP and migraine: neurogenic inflammation revisited. The journal of headache and pain 6 (2): 61–70.
  10. (June 2007). Acute migraine: Current treatment and emerging therapies. Ther Clin Risk Manag 3 (3): 449–459.
  11. (23 January 2008). Treatment of migraine attacks based on the interaction with the trigemino-cerebrovascular system. J Headache Pain 9 (1): 5–12.
  12. Werner Grossmann, MD, and Hanns Schmidramsl, MD An Extract of Petasites hybridus is Effective in the Prophylaxis of Migraine Alternative Medicine Review, Volume 6, Number3 2001, Page303
  13. (September 1967). Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin. Br J Pharmacol Chemother 31 (1): 138–51.
  14. (2010). Calcitonin gene-related peptide (CGRP) receptor antagonists in the treatment of migraine. CNS Drugs 24 (7): 539–48.
  15. (2008). Proinflammatory mediators and migraine pathogenesis: moving towards CGRP as a target for a novel therapeutic class. Expert Review of Neurotherapeutics 8 (9): 1347–54.
  16. (2009). Future drugs for migraine. Internal and emergency medicine 4 (5): 367–73.
  17. (2006). The role of neuropeptides in psoriasis. The British Journal of Dermatology 155 (5): 876–82.
  18. NCT00816517
  19. Product Information: Astelin, azelastine. Wallace Laboratories, Cranbury, NJ. (PI Revised 08/2000) PI Reviewed 01/2001
  20. (2008). Statins decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons. The Journal of Pharmacology and Experimental Therapeutics 324 (3): 1172–80.
  21. Weglicki WB, Phillips TM. Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis PMID 1384353 Am J Physiol. 1992 Sep;263(3 Pt 2):R734-7
  22. (April 2009). Skeletal and hormonal effects of magnesium deficiency. J Am Coll Nutr 28 (2): 131–41.

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