Neurogenic inflammatory reaction

As a result of vascular or neurogenic alteration, amyotrophies and osteopathies have been observed in diabetes. The muscle atrophy involves the individual fibers and is usually not associated with an inflammatory reaction. The electron microscope may reveal a marked increase in the granular osmiophilic material between myofibrils. Frequently, the basement membrane of the capillaries nourishing the muscle is greatly thickened. Abnormalities of motor end plates resulting in a soap bubble appearance have been described in diabetes. 

Mediator-induced inflammatory processes can lead to increased vascular permeability, neurogenic inflammation of airways and blood vessels, chemotaxis, and bronchospasm (Smith and Topford, 1999). Furthermore, capsaicin activates the vanilloid receptor family TRPVl (transient receptor potential cation channel subfamily V) within sensory neurons. Activation of these receptors leads to prolonged refractory periods and to a nonconducting desensitization. One study suggests that TRPV pathways may not be enhrely responsible for all of the adverse reactions caused by capsaicin (Holzer, 1991). 

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