Biobehavioral Analysis of Self-Injury & Pain

自伤的生物行为分析

• 批准号: 7417617
• 负责人: FRANK J SYMONS
• 金额: $ 31.05万
• 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 2010-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7417617
• 关键词: Animals; Area; Autistic Disorder; Behavior; Behavioral; Behavioral Mechanisms; Behavioral Model; Biological; Biological Markers; Bite; Blindness; Body Surface Area; Brain Injuries; Chronic; Classification; Clinical; Condition; Data; Denervation; Developmental Disabilities; Exhibits; Eye; Facial Expression; Facial Pain; Frequencies; Functional disorder; Goals; Hand; Head Banging; Health; Hormones; Human; Hydrocortisone; Individual; Injury; Lead; Learning; Link; Literature; Localized; Location; Measures; Mediating; Mediation; Mental Retardation; Modeling; Morphology; Negative Reinforcements; Nerve Fibers; Neurobiology; Neuropeptides; Nociception; Nociceptors; Numbers; Pain; Pathway interactions; Pattern; Peptides; Peripheral; Peripheral Nerves; Persons; Purpose; Rate; Refractory; Relative (related person); Research; Research Personnel; Role; Sampling; Sampling Studies; Self-Injurious Behavior; Sensory; Sensory Process; Signal Transduction; Site; Social Reinforcement; Stress; Substance P; Testing; Time; Tissues; afferent nerve; base; behavior measurement; biobehavior; chronic pain; deafness; density; developmental disease; indexing; millimeter; neurochemistry; reinforcer; response; sensory mechanism; social; treatment effect

DESCRIPTION (provided by applicant): 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.

描述（由申请人提供）：关于非社会介导的自我伤害行为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。既定的文献和研究者的初步数据为慢性非社会SIB的感觉功能障碍和疼痛假设提供了初始支持，并指出了慢性非社会SIB表达表达疼痛的周围和中心机制的重要作用。拟议的研究的目的是在与感觉功能和疼痛行为有关的一系列行为和生物学测量中对社会和非社会介导的SIB病例进行比较。总体目标是完善对慢性非社交SIB背后的行为和生物学机制的综合分析。为此，我们开发了一系列的损伤和疼痛的行为和生物学标记，可以在发育障碍和SIB的人中可靠地测量。遵循垂直研究策略，慢性SIB病例（n = 80）将通过行为机制（即社交与非社会中介）来尺寸。每个受试者的SIB的代表性样本将以其形式，频率，强度和身体位置的形式精确测量。每个受试者将使用疼痛的行为表达（面部作用单位），形态（表皮神经纤维的密度）和神经化学（物质P，Cortisol）的行为表达的量度进一步表征。这项研究将提供第一个机会，以系统地研究针对慢性非社会介导的SIB的疼痛特异性机制。