Little is known about the sensory and neurobiological basis of nonsocially-mediated self-injurious behavior. In behavioral models of SIB, sensory mechanisms function as putative positive or negative automatic reinforcers but there is little evidence directly linking behavioral and biological mechanisms. Evidence from both clinical and animal studies of chronic pain and its behavioral sequelae supports the hypothesis that some forms of SIB may be regulated by altered pain mechanisms. An established body of literature and the investigator's preliminary data provide initial support for the sensory dysfunction and pain hypothesis of chronic nonsocial SIB and point to an important role for the peripheral and central mechanisms of pain in the expression of chronic nonsocial SIB. The purpose of the proposed study is to compare socially and nonsocially-mediated SIB cases on a set of behavioral and biological measures related to sensory function and pain behavior. The overall goal is to refine an integrative analysis of the behavioral and biological mechanisms underlying chronic nonsocial SIB. Towards this end, we have developed a set of behavioral and biological markers of injury and pain that can be reliably measured in persons with developmental disorders and SIB. Following a vertical research strategy, chronic SIB cases (N = 80) will be functionally subtyped by behavioral mechanism (i.e., social versus nonsocial mediation). Representative samples of each subject's SIB will be precisely measured for its form, frequency, intensity, and body location. Each subject will be further characterized using measures of behavioral expression of pain (facial action units), morphology (density of epidermal nerve fibers), and neurochemistry (substance P, cortisol). This study will provide the first opportunity to systematically investigate mechanisms specific to pain underlying chronic nonsocially-mediated SIB.
NIH ExPorter
NIH ExPorter