Neural mechanisms of motor dysfunction in individuals at clinical high-risk for psychosis: Evidence for impairments in motor activation.
Neural mechanisms of motor dysfunction in individuals at clinical high-risk for psychosis: Evidence for impairments in motor activation.
复制标题
DOI：
10.1037/abn0000754
复制
发表时间：
2022-05
期刊：
影响因子：
--
通讯作者：
Mittal, Vijay A
中科院分区：
文献类型：
--
作者：
Osborne, K Juston;Zhang, Wendy;Farrens, Jaclyn;Geiger, McKena;Kraus, Brian;Glazer, James;Nusslock, Robin;Kappenman, Emily S;Mittal, Vijay A
运动异常是从发病前到慢性疾病所观察到的精神障碍的核心特征，提示运动功能障碍可能反映了精神病的病理生理学。精神分裂症的电生理学研究表明，运动激活和准备受损可能是这些运动异常的原因。尽管行为研究表明，精神疾病的临床高危人群存在类似的运动障碍，但还没有研究探讨临床高危精神病患者运动功能障碍的神经机制，研究可以为病理生理学和风险模型提供信息。本研究使用偏侧就绪电位(LRP)，一种反映运动激活和准备的事件相关电位指数，对42名CHR和41名对照组(N=83，女性56%)的运动功能障碍机制进行了研究。反应竞争被操纵，以确定缺陷是次要于认知控制障碍还是反映了初级运动障碍。在行为上，CHR参与者的反应总体上比对照组慢。此外，与对照组相比，CHR参与者对正确反应而不是错误反应的激活减少，反映在弱反应竞争下钝化的LRP幅度，而在强反应竞争下与不正确反应相关的幅度没有差异。这一结果模式表明，精神病患者在激活和准备行为反应方面表现出初级运动缺陷，与认知控制缺陷相反。此外，LRP波幅迟钝与12个月随访时阴性症状的恶化有关。总之，这些发现与LRP在精神病中的研究是一致的，并暗示运动激活缺陷是高危时期运动功能障碍的潜在机制。运动行为缺陷在有发展成精神病风险的个体中很普遍。这项研究支持这样的观点，即对于有精神病风险的人来说，激活和准备运动反应的障碍可能是这些缺陷的基础，并预测症状的进展。这些发现表明，运动激活和准备的缺陷可能在疾病发生之前就已经存在，并反映了疾病的核心特征。
Motor abnormalities are a core feature of psychotic disorders observed from the premorbid period through chronic illness, suggesting motor dysfunction may reflect the pathophysiology of psychosis. Electrophysiology research in schizophrenia suggests impaired motor activation and preparation may underlie these motor abnormalities. Despite behavioral studies suggesting similar motor dysfunction in those at clinical high-risk (CHR) for psychosis, there have been no studies examining neural mechanisms of motor dysfunction in the CHR period, where research can inform pathophysiological and risk models. The present study used the lateralized readiness potential (LRP), an event-related potential index of motor activation and preparation, to examine mechanisms of motor dysfunction in 42 CHR and 41 control participants (N=83, 56% female). Response competition was manipulated to determine if deficits are secondary to cognitive control impairments or reflect primary motor deficits. Behaviorally, CHR participants exhibited overall slower responses than controls. Further, relative to controls, CHR participants showed reduced activation of correct but not incorrect responses, reflected in blunted LRP amplitude under weak response competition, and no difference in amplitude associated with the incorrect response under strong response competition. This pattern of results suggests individuals at CHR for psychosis exhibit primary motor deficits in activating and preparing behavioral responses and are contrary to a deficit in cognitive control. Further, blunted LRP amplitude was associated with worsening of negative symptoms at 12-month follow-up. Together, these findings are consistent with LRP studies in psychosis and implicate motor activation deficits as potential mechanisms of motor dysfunction in the high-risk period. Deficits in motor behavior are prevalent in individuals at risk for developing psychosis. This study supports the notion that for individuals at risk for psychosis, impairments in activating and preparing motor responses may underlie these deficits and predict the progression of symptoms. These findings suggest that deficits in motor activation and preparation may be present before illness onset and reflect a core feature of the illness.