Buse Judith, Kirschbaum Clemens, Leckman James F, Münchau Alexander, Roessner Veit
Department of Child and Adolescent Psychiatry, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Germany.
Institute of Biopsychology, Department of Psychology, Technische Universität Dresden.
Behav Modif. 2014 Mar;38(2):184-216. doi: 10.1177/0145445514522056. Epub 2014 Feb 10.
Accumulating data indicate a common occurrence of tic exacerbations and periods of psychosocial stress. Patients with Tourette's syndrome (TS) also exhibit aberrant markers of hypothalamic-pituitary-adrenal (HPA) axis activation. Based on these findings, a functional relationship between stress and tic disorders has been suggested, but the underlying mechanism of how stress may affect tic pathology remains to be elucidated. We suggest that dopaminergic and noradrenergic neurotransmission as well as immunology play a crucial role in mediating this relationship. Two possibilities of causal direction might be assumed: (a) psychosocial stress might lead to an exacerbation of tics via activation of HPA axis and subsequent changes in neurotransmission or immunology and (b) TS-related abnormalities in neurotransmission or immunology result in a higher vulnerability of affected patients to respond to psychosocial stress with a strong activation of the HPA axis. It may also be the case that both assumptions hold true and interact with each other.
越来越多的数据表明,抽动加剧和心理社会压力时期很常见。患有妥瑞氏症(TS)的患者还表现出下丘脑-垂体-肾上腺(HPA)轴激活的异常标志物。基于这些发现,有人提出压力与抽动障碍之间存在功能关系,但压力如何影响抽动病理的潜在机制仍有待阐明。我们认为多巴胺能和去甲肾上腺素能神经传递以及免疫学在介导这种关系中起着关键作用。可能存在两种因果关系方向:(a)心理社会压力可能通过激活HPA轴以及随后神经传递或免疫学的变化导致抽动加剧;(b)与TS相关的神经传递或免疫学异常导致受影响患者对心理社会压力做出反应时HPA轴强烈激活的易感性更高。也有可能两种假设都成立且相互作用。