Neurogenic Inflammation

Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury.
Also Known As:
Inflammation, Neurogenic; Inflammations, Neurogenic; Neurogenic Inflammations
Networked: 986 relevant articles (20 outcomes, 102 trials/studies)

Relationship Network

Disease Context: Research Results

Related Diseases

1. Pain (Aches)
2. Inflammation
3. Migraine Disorders (Migraine)
4. Hyperalgesia
5. Asthma (Bronchial Asthma)


1. Geppetti, Pierangelo: 14 articles (07/2014 - 04/2004)
2. Vink, Robert: 14 articles (01/2014 - 10/2004)
3. Bunnett, Nigel W: 13 articles (11/2015 - 06/2004)
4. Bhatia, Madhav: 10 articles (11/2011 - 05/2003)
5. Nassini, Romina: 9 articles (07/2014 - 08/2007)
6. Materazzi, Serena: 9 articles (07/2014 - 03/2006)
7. Szolcsányi, János: 8 articles (05/2015 - 08/2002)
8. Birklein, Frank: 8 articles (05/2014 - 07/2006)
9. Lin, Qing: 8 articles (09/2010 - 02/2003)
10. Szolcsányi, J: 8 articles (12/2008 - 12/2001)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Neurogenic Inflammation:
1. Substance PIBA
2. Capsaicin (Zostrix)FDA Link
3. NeuropeptidesIBA
4. Calcitonin Gene-Related PeptideIBA
5. TachykininsIBA
6. Serotonin (5 Hydroxytryptamine)IBA
7. Histamine (Histamine Dihydrochloride)FDA Link
8. Sumatriptan (Imigran)FDA LinkGeneric
9. SmokeIBA
10. Complement System Proteins (Complement)IBA
01/01/2012 - "A new treatment for neurogenic inflammation caused by EV71 with CR2-targeted complement inhibitor."
01/01/1994 - "Peptidergic activation of mast cells may also be a pathophysiological process having an important role in neurogenic inflammation and in diseases involving extensive activation of the blood complement cascade."
11/01/1996 - "These studies complement prior experiments showing that valproic acid and allopregnanolone block neurogenic inflammation within the meninges via GABAA receptor-mediated mechanisms. "
03/01/2002 - "The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-alpha and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. "

Therapies and Procedures

1. Intradermal Injections
2. Intravenous Injections
3. Nerve Block (Nerve Blocks)
4. Subcutaneous Injections
5. Lasers (Laser)