Self-injury: Pain and Stress Mechanisms

自残：疼痛和压力机制

基本信息

批准号：
7931945
负责人：
FRANK J SYMONS
金额：
$ 11.29万
依托单位：
UNIVERSITY OF MINNESOTA
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-09-22 至 2012-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7931945
关键词：
Absence of pain sensation Accounting Acute Adult Afferent Neurons Area Autonomic nervous system Award Behavior Behavior Disorders Behavioral Behavioral Genetics Behavioral Mechanisms Biological Biology Bite Child Childhood Chronic Clinical Commit Complex Consensus Detection Development Development Plans Developmental Disabilities Educational Psychology Environment Event Fiber Frequencies Functional disorder Funding Genes Goals Hand Head Hormones Hydrocortisone Hyperalgesia Hypothalamic structure Impairment Individual Injury Institution Learning Leg Measures Mediating Medical Minnesota Modeling Nature Nerve Fibers Nervous system structure Neurobiology Neurologic Neurosciences Nociception Nociceptors Opioid Outcome Study Pain Pain Threshold Pattern Peripheral Persons Physiological Physiology Pituitary Gland Pituitary-Adrenal System Play Population Process Psychopathology Recording of previous events Regulation Relative (related person)Research Research Design Research Training Resistance Resources Risk Role Self-Injurious Behavior Sensory Sensory Process Sensory Thresholds Severities Site Spottings Stimulus Stress Substance P System Testing Time Tissues Training Translational Research Treatment outcome Universities Validity and Reliability Work allodynia base biobehavior biological adaptation to stress career career development chronic neuropathic pain desensitization developmental disease early experience experience high risk hypothalamic-pituitary-adrenal axis improved neurochemistry novel pain behavior programs prospective psychobiologic psychobiology response skills somatosensory stressor transmission process

项目摘要

DESCRIPTION (provided by applicant): Goals: My research has dealt primarily with the behavioral mechanisms underlying chronic SIB among individuals with developmental disorders. A more complete understanding of the pathophysiology of SIB will require integrating our rich understanding of pain neurobiology and stress psychobiology with our emerging understanding of the role of early experience on multiple pain and stress-sensitive physiological systems. Research: During my R29 funding period, I extended the opioid model of SIB in line with clinical features suggestive of altered pain processing, formed collaborative relations, and began developing the necessary expertise allowing me to seek funding to test an integrative pain and stress model of SIB in adults. The purpose of the funded R01 is to compare socially and nonsocially-mediated SIB adult cases on a set of behavioral and biological measures related to sensory function, stress physiology, and pain behavior. Career Plan: The career development plan uses a translational research training framework as an organizing set of principles to guide research and training goals specific to new developments in neuroscience and behavioral genetics, integrating the wider research program of developmental psychopathology, and expanding the self- injury research agenda to embrace gene-environmental interplay and improve our understanding of individual vulnerability. Preliminary work and collaborative relations are described to support the need for release time to enhance my training and research into these related areas. The plan emphasizes the need to extend self- injury research to issues germane to pediatric and neurological research (i.e., pain regulation, high risk populations), and to include other systems important in the regulation of pain (i.e., peripheral and central transmission mechanisms), stress (i.e., the HPA axis), and the autonomic nervous system (i.e., fronto-limbic and autonomic circuitry). Specifically, I want to gain the expertise to test the following three preliminary hypotheses. First, there will be differences in hypothalamic-pituitary-adrenal (HPA) axis activity (cortisol) and sensory function (detection thresholds) in children with severe neurological impairment and self-injury compared with matched controls without self-injury (between group analyses). Second: the frequency and temporal sequencing of self-injury will be correlated with HPA axis activity and sensory function (within group analyses). Third, the relation between HPA axis activity, sensory function, and SIB will change over time such that the degree of dysregulation in the former predicts increasing severity in the latter (prospective analysis). Institution and Environment Commitment: The Department of Educational Psychology and the University of Minnesota are committed to this award and provide rich resources for my career development.

描述（由申请人提供）：目标：我的研究主要涉及发育障碍患者中慢性 SIB 的行为机制。要更全面地了解 SIB 的病理生理学，需要将我们对疼痛神经生物学和压力心理生物学的丰富理解与我们对早期经历对多种疼痛和压力敏感的生理系统的作用的新理解结合起来。研究：在我的 R29 资助期间，我根据表明疼痛处理改变的临床特征扩展了 SIB 的阿片类药物模型，形成了合作关系，并开始发展必要的专业知识，使我能够寻求资金来测试综合疼痛和压力模型成人 SIB。资助的 R01 的目的是通过一系列与感觉功能、应激生理学和疼痛行为相关的行为和生物测量来比较社会和非社会介导的 SIB 成人病例。职业发展计划：职业发展计划使用转化研究培训框架作为一套组织原则，指导针对神经科学和行为遗传学新发展的研究和培训目标，整合更广泛的发展精神病理学研究计划，并扩大自我伤害范围。研究议程涵盖基因与环境的相互作用并提高我们对个体脆弱性的理解。描述了初步工作和协作关系，以支持释放时间的需要，以加强我对这些相关领域的培训和研究。该计划强调需要将自伤研究扩展到与儿科和神经学研究密切相关的问题（即疼痛调节、高危人群），并包括在疼痛调节中重要的其他系统（即外周和中枢传递机制）、压力（即 HPA 轴）和自主神经系统（即额叶边缘和自主神经回路）。具体来说，我想获得检验以下三个初步假设的专业知识。首先，与没有自伤的匹配对照相比，患有严重神经损伤和自伤的儿童的下丘脑-垂体-肾上腺（HPA）轴活动（皮质醇）和感觉功能（检测阈值）存在差异（组间分析）。第二：自伤的频率和时间顺序将与 HPA 轴活动和感觉功能相关（在组分析内）。第三，HPA 轴活动、感觉功能和 SIB 之间的关系会随着时间的推移而变化，因此前者的失调程度预示着后者的严重程度会增加（前瞻性分析）。机构和环境承诺：教育心理学系和明尼苏达大学致力于这个奖项，并为我的职业发展提供丰富的资源。

项目成果

期刊论文数量（9）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Self-injurious behavior in neurodevelopmental disorders: relevance of nociceptive and immune mechanisms.

神经发育障碍中的自残行为：伤害感受和免疫机制的相关性。

DOI：
10.1016/j.neubiorev.2011.01.002
发表时间：
2011
期刊：
Neuroscience and biobehavioral reviews
影响因子：
8.2
作者：
Symons,FrankJ
通讯作者：
Symons,FrankJ

Peripheral Innervation in Children With Global Developmental Delay: Biomarker for Risk for Self-Injurious Behavior?

整体发育迟缓儿童的周围神经支配：自伤行为风险的生物标志物？

DOI：
10.1177/0883073815579704
发表时间：
2015
期刊：
Journal of child neurology
影响因子：
1.9
作者：
Symons,FrankJ;Tervo,RaymondC;Barney,ChantelC;Damerow,John;Selim,Mona;McAdams,Brian;Foster,Shawn;WendelschaferCrabb,Gwen;Kennedy,William
通讯作者：
Kennedy,William

Proopiomelanocortin (POMC) sequencing and developmental delay: Preliminary evidence for a SNP in the 3' UTR region of the POMC gene-Possible relevance for biological risk and self-injurious behavior.

阿黑皮质素原 (POMC) 测序和发育迟缓：POMC 基因 3 UTR 区域中 SNP 的初步证据 - 可能与生物风险和自残行为相关。

DOI：
10.1017/s0954579418000718
发表时间：
2019
期刊：
Development and psychopathology
影响因子：
3.3
作者：
Damerow,JohnA;Tervo,RaymondC;Ehrhardt,Michael;Panoskaltsis-Mortari,Angela;Symons,FrankJ
通讯作者：
Symons,FrankJ

Biomarkers, behavior, and intellectual and developmental disabilities.

生物标志物、行为以及智力和发育障碍。