NEUROGENIC INFLAMMATION - WITH ADDITIONAL DISCUSSION OF CENTRAL AND PERCEPTUAL INTEGRATION OF NONNEUROGENIC INFLAMMATION

The Working Group on Neurogenic inflammation proposed 11 testable hypo theses in the three domains of neurogenic inflammation, perceptual and central integration, and nonneurogenic inflammation. The working grou p selected the term people reporting chemical sensitivity (PRCS) to id entify the primary subject group. in the domain of neurogenic inflamma tion, testable hypotheses included. PRCS have an increased density of c-fiber neurons in symptomatic tissues; PRCS produce greater quantitie s of neuropeptides and prostanoids than nonsensitive subjects in respo nse to exposure to low-level capsaicin or irritant chemicals; PRCS hav e an increased and prolonged response to exogenously administered c-fi ber activators such as capsaicin; PRCS demonstrate augmentation of cen tral autonomic reflexes following exposure to agents that produce c-fi ber stimulation; PRCS have decreased quantities of neutral endopeptida se in their mucosa; exogenous neuropeptide challenge reproduces sympto ms of PRCS. In the domain of perceptual and central integration, testa ble hypotheses included: PRCS have alterations in adaptation, habituat ion, cortical representation, perception, cognition, and hedonics comp ared to controls; the qualitative and quantitative interactions betwee n trigeminal and olfactory systems are altered in PRCS; higher integra tion of sensory inputs is altered in PRCS. In the domain of nonneuroge nic inflammation testable hypotheses included: increased inflammation is present in PRCS in symptomatic tissues and is associated with a hei ghtened neurosensory response; PRCS show an augmented inflammatory res ponse to chemical exposure. The working group recommended that studies be initiated in these areas.