Sensory Mechanisms and Self-Injury

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DESCRIPTION (provided by applicant): Little is known about the sensory and neurobiological basis of chronic self-injurious behavior (SIB) among individuals with intellectual and developmental disabilities (IDD). 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. From our work and that of others, we know that pain can lead to SIB in this population but we know almost nothing about whether chronic SIB leads to pain and the resulting neuro-immune cascade of effects. An established body of preclinical and clinical literature and the investigator's preliminary data provide initial support for a working sensory dysfunction and neuropathic-pain like hypothesis of chronic SIB and point to an important role for the peripheral and central mechanisms of pain and inflammatory/immune activity. The purpose of this project is to begin testing a novel model of SIB in relation to chronic neuropathic-like pain due to inflammatory and immune system activation. We hypothesize that there will be a subgroup of individuals with chronic SIB that have significantly (a) altered peripheral sensory innveration, (b) increased inflammatory and immune activity, and (c) increased immune-mediated 'sickness' like behavior. A case-control design will be used to compare matched (age, gender, IQ) groups of children with IDD with (n = 40) and without SIB (n = 40). The groups will be compared on measures of (a) peripheral innervation (Aim 1), (b) inflammatory/immune cytokines and related peptides (Aim 2), and (c) functional indicators of 'sickness'-like behavior including adaptive/social behavior, sleeping/eating, and sensory reactivity and pain signs/symptoms as well as within SIB group comparisons of functional and structural variables (Aim 3). Our preliminary results suggest that, at least in the periphery, ongoing neuro-immune interactions may, in part, be related to the as of yet poorly understood pathophysiology of chronic self-injury. This study will provide the first opportunity to systematically investigate neuro-immune variables in relation to SIB among children with IDD.