Sensory Mechanisms and Self-Injury

二十多年前，美国国立卫生研究院估计了与自残行为(SIB)相关的成本 智力和发育障碍(IDD)超过30亿美元(美国)。几乎没有理由认为 流行率估计值发生了变化，但可以肯定的是，护理费用也发生了变化。尽管在行为方面取得了进展 对个别SIB病例的评估和治疗，我们对这种疾病风险的科学认识仍然存在 严重受限。“等到它发展”的方法的一个后果是，个别SIB病例往往是 在疾病发作后很长一段时间内接受治疗，使其成为临床上困难和昂贵的(而且通常是难以治愈的) 有问题。与我们自己的预测相反，很明显，在发育迟缓的非常年幼的儿童中 延迟，通常被认为是SIB‘风险因素’的变量(例如，表达能力差的语言)可能会有预后 重视这一点，但在区分儿童最初的风险方面做得很少。同样清楚的是，可能有不同的个体标记 应该在SIB风险的综合生物行为模型中考虑哪些因素来对易感儿童进行分层 更精确地进入“高/低”风险组。根据我们迄今的工作，出现了以下框架： (1)有一组患有IDD的幼儿周围神经和免疫细胞改变。 活性；(2)这可能是形成表型的生物底物的一部分，其特征是 感觉反应的异常模式。我们假设在以下情况下更有可能出现SIB 有这种早期的表型。 我们已经证实外周神经支配、免疫细胞活性和 异常感觉反应可以在早期被客观可靠地检测到 发育迟缓，在SIB开始之前。 此应用程序的总体目标是将 建立SIB风险模型的前瞻性发展方法。因此，我们假设儿童的子组 (I)周围感觉神经支配改变，(Ii)炎症和免疫活动增加，以及(Iii) 感觉反应性增强将是SIB的最高病因风险。其结果将产生临床影响。 因为(A)目前对SIB的评估和处理方法依赖于SIB的出现，因此很可能 错过更大生物和行为可塑性的早期机会，以及(B)假定的风险标志是 调查提供了可信的和新的目标，以转向早期预防这种毁灭性和 昂贵的临床条件。

Over two decades ago, NIH estimated costs associated with self-injurious behavior (SIB) associated with intellectual and developmental disabilities (IDD) exceeded $3 billion (US). There is little reason to think the prevalence estimates have changed but assuredly the costs of care have. Despite progress in the behavioral assessment and treatment of individual SIB cases, our scientific understanding of risk for the disorder remains severely limited. One consequence of the `wait till it develops' approach is that individual SIB cases tend to be treated long after the onset of the disorder making it a clinically difficult and expensive (and often intractable) problem. Contrary to our own predictions, it has become clear that in very young children with developmental delay, variables typically considered as SIB `risk factors' (e.g., poor expressive language) may have prognostic value but do little to separate children on initial risk. Equally clear is there may be individual difference markers which should be considered in an integrated bio-behavioral model of SIB risk to stratify vulnerable children with more precision into `high/low' risk groups. Based on our work to date, the following framework has emerged: (1) there is a subgroup of very young children with IDD with altered peripheral innervation and immune cell activity; (2) this may be part of the biological substrate for the development of a phenotype characterized by abnormal patterns of sensory responsiveness. We hypothesize that SIB is more likely to emerge in cases that have this early phenotype. We have already established that peripheral innervation, immune cell activity, and abnormal sensory responsiveness can be objectively and reliably measured very early in children with developmental delays, prior to the onset of SIB. The overall objective of this application is to apply a prospective developmental approach to model SIB risk. Accordingly, we hypothesize the subgroup of children with (i) altered peripheral sensory innervation, (ii) increased inflammatory and immune activity, and (iii) increased sensory reactivity will be at the highest etiological risk for SIB. The outcomes will have clinical impact because (a) current methods of assessment and treatment of SIB rely on the emergence of SIB and thus likely miss early opportunities for greater biological and behavioral plasticity, and (b) the putative risk markers being investigated provide plausible and novel targets in a shift towards early prevention of this devastating and costly clinical condition.