Geissler Julia, Romanos Marcel, Hegerl Ulrich, Hensch Tilman
Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital of Würzburg, University of Würzburg, Füchsleinstr. 15, 97080, Würzburg, Germany,
Atten Defic Hyperact Disord. 2014 Sep;6(3):159-73. doi: 10.1007/s12402-014-0144-z. Epub 2014 Jul 6.
Hypoarousal as indicated by skin conductance and electroencephalography (EEG) has been discussed as a pathogenetic factor in attention-deficit/hyperactivity disorder (ADHD). The aim of this paper was to review these arousal-related pathogenetic concepts and to present the more recently proposed vigilance regulation model of affective disorders and ADHD. The latter builds on methodological advances in classifying short EEG segments into vigilance stages (Vigilance Algorithm Leipzig, VIGALL), indicating different states of global brain function ("brain arousal"). VIGALL allows the objective assessment of vigilance regulation under defined conditions, e.g. how fast vigilance declines to lower vigilance stages associated with drowsiness during 15-20-min EEG recordings under resting conditions with eyes closed. According to the vigilance regulation model, the hyperactivity and sensation seeking observed in overtired children, ADHD and mania may be interpreted as an autoregulatory attempt to create a stimulating environment in order to stabilize vigilance. The unstable regulation of vigilance observed in both mania and ADHD may thus explain the attention deficits, which become especially prominent in monotonous sustained attention tasks. Among the arguments supporting the vigilance regulation model are the facts that destabilizing vigilance (e.g., via sleep deprivation) can trigger or exacerbate symptoms of ADHD or mania, whereas stabilizing vigilance (e.g., via psychostimulants, reducing sleep deficits) alleviates these symptoms. The potential antimanic effects of methylphenidate are presently being studied in an international randomized controlled trial. We propose vigilance regulation as a converging biomarker, which could be useful for identifying treatment responders to psychostimulants and forming pathophysiologically more homogeneous ADHD subgroups for research purposes.
皮肤电导和脑电图（EEG）所显示的低唤醒被认为是注意力缺陷多动障碍（ADHD）的一个致病因素。本文的目的是回顾这些与唤醒相关的致病概念，并介绍最近提出的情感障碍和ADHD的警觉调节模型。后者建立在将短EEG片段分类为警觉阶段（莱比锡警觉算法，VIGALL）的方法学进展基础上，该算法可指示整体脑功能的不同状态（“脑唤醒”）。VIGALL允许在规定条件下对警觉调节进行客观评估，例如在闭眼静息状态下15 - 20分钟的EEG记录中，警觉下降到与困倦相关的较低警觉阶段的速度有多快。根据警觉调节模型，在过度疲劳的儿童、ADHD和躁狂症中观察到的多动和寻求刺激行为，可被解释为一种自动调节尝试，即创造一个刺激环境以稳定警觉。因此，在躁狂症和ADHD中观察到的不稳定警觉调节可能解释了注意力缺陷，这在单调的持续注意力任务中尤为突出。支持警觉调节模型的论据包括：破坏警觉（如通过睡眠剥夺）可引发或加重ADHD或躁狂症的症状，而稳定警觉（如通过精神兴奋剂、减少睡眠不足）可缓解这些症状。目前正在一项国际随机对照试验中研究哌甲酯的潜在抗躁狂作用。我们提出将警觉调节作为一个聚合生物标志物，它可用于识别对精神兴奋剂有反应的治疗对象，并为研究目的形成病理生理学上更同质的ADHD亚组。
