A Functional Imaging Study of Self-Regulatory Capacities in Persons Who Stutter

Developmental stuttering is a disorder of speech fluency with an unknown pathogenesis. The similarity of its phenotype and natural history with other childhood neuropsychiatric disorders of frontostriatal pathology suggests that stuttering may have a closely related pathogenesis. We investigated in this study the potential involvement of frontostriatal circuits in developmental stuttering. We collected functional magnetic resonance imaging data from 46 persons with stuttering and 52 fluent controls during performance of the Simon Spatial Incompatibility Task. We examined differences between the two groups of blood-oxygen-level-dependent activation associated with two neural processes, the resolution of cognitive conflict and the context-dependent adaptation to changes in conflict. Stuttering speakers and controls did not differ on behavioral performance on the task. In the presence of conflict-laden stimuli, however, stuttering speakers activated more strongly the cingulate cortex, left anterior prefrontal cortex, right medial frontal cortex, left supplementary motor area, right caudate nucleus, and left parietal cortex. The magnitude of activation in the anterior cingulate cortex correlated inversely in stuttering speakers with symptom severity. Stuttering speakers also showed blunted activation during context-dependent adaptation in the left dorsolateral prefrontal cortex, a brain region that mediates cross-temporal contingencies. Frontostriatal hyper-responsivity to conflict resembles prior findings in other disorders of frontostriatal pathology, and therefore likely represents a general mechanism supporting functional compensation for an underlying inefficiency of neural processing in these circuits. The reduced activation of dorsolateral prefrontal cortex likely represents the inadequate readiness of stuttering speakers to execute a sequence of motor responses.发育性口吃（Developmental Stuttering）是一种发病机制尚未明确的言语流畅性障碍。其表型与自然病程与其他累及额纹状体通路的儿童期神经精神疾病存在相似性，这提示发育性口吃的发病机制可能与之密切相关。本研究旨在探讨额纹状体环路在发育性口吃发病中的潜在作用。 本研究收集了46名口吃患者与52名言语流畅对照组在完成西蒙空间不相容任务（Simon Spatial Incompatibility Task）时的功能磁共振成像（functional magnetic resonance imaging, fMRI）数据，并对比分析了两组受试者在两种神经认知过程中相关的血氧水平依赖（blood-oxygen-level-dependent, BOLD）激活差异，这两种过程分别为认知冲突解决以及针对冲突变化的情境适应性调节。 两组受试者在该任务的行为表现上无显著差异。但在呈现冲突性刺激时，口吃患者的扣带回皮层（cingulate cortex）、左前额叶前部、右内侧前额叶皮层、左辅助运动区、右尾状核以及左顶叶皮层的激活程度显著高于对照组。口吃患者的前扣带回皮层（anterior cingulate cortex）激活强度与症状严重程度呈负相关。 此外，在进行情境适应性调节过程中，口吃患者的左背外侧前额叶皮层（left dorsolateral prefrontal cortex, DLPFC）激活出现钝化；该脑区负责介导跨时间偶联过程。 口吃患者面对冲突时额纹状体通路的过度激活，与其他额纹状体通路病变相关疾病的既往研究结果一致，因此这可能代表了一种通用代偿机制，用于弥补此类环路神经加工过程本身存在的低效性。而背外侧前额叶皮层激活不足，则可能提示口吃患者在执行一系列运动性言语反应时的准备状态欠佳。