Sensory Mechanisms and Self-Injury

感觉机制和自残

• 批准号: 7784611
• 负责人: FRANK J SYMONS
• 金额: $ 38.32万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-04-01 至 2015-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7784611
• 关键词: Adaptive Behaviors; Age; Animals; Autistic Disorder; Behavior; Behavioral; Behavioral Model; Biochemistry; Biological; Biological Markers; Biological Response Modifiers; Brain; Brain Injuries; Cells; Cerebral Palsy; Child; Childhood; Chronic; Clinical; Data; Desire for food; Developmental Disabilities; Disease; Eating; Environmental Risk Factor; Etiology; Fiber; Frequencies; Functional disorder; Funding; Gender; Hyperalgesia; Hypersensitivity; Immune; Immune system; Individual; Individual Differences; Inflammatory; Lead; Lesion; Link; Literature; Maintenance; Malignant Neoplasms; Measures; Mediating; Modeling; Morphology; Nerve; Neurobiology; Neuropathy; Nociception; Pain; Peptides; Peripheral; Physiological; Population; Public Health; Research Personnel; Respondent; Role; Sampling; Self-Injurious Behavior; Sensory; Series; Signs and Symptoms; Sleep; Social Behavior; Social Interaction; Structure; Subgroup; Substance P; System; Testing; Tissues; Work; afferent nerve; base; case control; chemokine; chronic pain; comparison group; conditioning; cytokine; density; design; inflammatory pain; mast cell; nerve supply; novel; painful neuropathy; pre-clinical; public health relevance; reinforcer; response; sensory depression; sensory mechanism; social; tumor

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.

描述（由申请人提供）：关于智力和发育障碍的人（IDD），慢性自我伤害行为（SIB）的感觉和神经生物学基础知之甚少。在SIB的行为模型中，感觉机制是推定的阳性或负自动增强剂，但几乎没有任何直接联系行为和生物学机制的证据。来自慢性疼痛及其行为后遗症的临床和动物研究的证据支持了以下假设：某些形式的SIB可能会受到改变的疼痛机制的调节。从我们的工作和其他人的工作中，我们知道疼痛会导致该人群中的痛苦，但我们几乎对慢性同胞是否导致疼痛和由此产生的神经免疫级联效应一无所知。建立的临床前和临床文献的机构以及研究者的初步数据为工作感觉功能障碍和神经性疗法提供了初始支持，例如慢性SIB的假设，并指出了疼痛和炎症/免疫活性的外围和中心机制的重要作用。该项目的目的是开始测试由于炎症和免疫系统激活而导致的慢性神经性疼痛的新型SIB模型。我们假设将有一个慢性SIB的个体子组显着（a）周围的感觉创新改变，（b）炎症和免疫活性的增加，以及（c）类似免疫介导的“疾病”行为。病例对照设计将用于比较患有IDD的儿童（n = 40）和没有SIB的匹配（年龄，性别，IQ）组（n = 40）。将根据（a）外围神经支配（AIM 1），（b）炎症/免疫细胞因子和相关肽（AIM 2）和（c）类似疾病/社交行为，睡眠/睡眠/饮食，感觉反应性和疼痛迹象/疼痛迹象/症状以及在Sib sib sibs contional contimistional and suptiantional and（c），将两组进行比较。我们的初步结果表明，至少在周围，持续的神经免疫相互作用中可能部分与尚未了解的慢性自我伤害的病理生理学有关。这项研究将为IDD儿童中与SIB相关的Syro-rmmune变量系统地研究第一个机会。