Heinen Theresa V, Schmidgen Julia, Paul Theresa, Hensel Lukas, Fink Gereon R, Volz Lukas J, Grefkes Christian, Bender Stephan, Konrad Kerstin
Child Neuropsychology Section, Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Medical Faculty, RWTH Aachen University, Aachen 52074, Germany.
JARA-BRAIN Institute II, Molecular Neuroscience and Neuroimaging (INM-11), Forschungszentrum Jülich GmbH and RWTH Aachen University, Juelich 52428, Germany.
Brain Commun. 2025 Jun 30;7(4):fcaf260. doi: 10.1093/braincomms/fcaf260. eCollection 2025.
Tic disorders (TD) are childhood-onset neurodevelopmental disorders characterized by sudden, repetitive motor and vocal tics, often with partial or complete remission by the time young adulthood is reached. We here investigated motor control and compensatory neural processes in drug-naïve children and adolescents with chronic Motor Tic Disorder or Tourette Syndrome (TD) by examining motor network activity and connectivity compared to healthy controls. Using a reaction time (RT) task under varying cueing conditions, combined with functional magnetic resonance imaging (fMRI) and dynamic causal modelling (DCM), we explored how TD-related motor networks adapt to support volitional movement control. Participants with TD demonstrated enhanced task accuracy across internally and externally cued conditions despite deficits in sustained motor inhibition (blink suppression). Relative to controls, individuals with TD exhibited increased task-related activation in ipsilateral motor regions, particularly in the primary motor cortex, and somatosensory cortex, and enhanced interhemispheric connectivity between parietal sensory-motor hubs. Notably, while in typically developing participants, age-related increases in parietal lobe activation and modulatory connectivity between primary motor and premotor regions were linked to improved task accuracy, working memory and visuomotor coordination, TD patients deviated from this normative developmental trajectory with distinct, atypical but neither delayed nor accelerated neural activation and connectivity patterns. Our data suggest that TD involves compensatory neuroplastic adaptations that leverage additional sensorimotor resources to improve motor control but do not extend to motor inhibition processes. Moreover, the findings emphasize the intricate interplay between motor control and neural plasticity in TD, highlighting how compensatory mechanisms may serve as adaptive responses to motor challenges. These findings open avenues for therapeutic strategies that harness the brain's compensatory capacities to enhance motor control and facilitate TD management.
抽动障碍（TD）是一种起病于儿童期的神经发育障碍，其特征为突然出现的重复性运动和发声抽动，通常在青年期时部分或完全缓解。我们在此通过检查运动网络活动和连接性，并与健康对照进行比较，研究了患有慢性运动性抽动障碍或图雷特综合征（TD）的未用药儿童和青少年的运动控制及代偿性神经过程。使用在不同提示条件下的反应时间（RT）任务，结合功能磁共振成像（fMRI）和动态因果模型（DCM），我们探究了与TD相关的运动网络如何适应以支持意志性运动控制。尽管在持续运动抑制（眨眼抑制）方面存在缺陷，但TD患者在内部和外部提示条件下均表现出更高的任务准确性。相对于对照组，TD患者在同侧运动区域，特别是在初级运动皮层和体感皮层，表现出与任务相关的激活增加，并且顶叶感觉运动枢纽之间的半球间连接增强。值得注意的是，在典型发育的参与者中，顶叶激活以及初级运动和运动前区之间的调节性连接随年龄增长而增加与任务准确性、工作记忆和视觉运动协调的改善相关联，而TD患者偏离了这一正常发育轨迹，具有独特的、非典型的但既未延迟也未加速神经激活和连接模式。我们的数据表明，TD涉及代偿性神经可塑性适应，利用额外的感觉运动资源来改善运动控制，但并不扩展到运动抑制过程。此外，这些发现强调了TD中运动控制与神经可塑性之间复杂的相互作用，突出了代偿机制如何作为对运动挑战的适应性反应。这些发现为治疗策略开辟了途径，利用大脑的代偿能力来增强运动控制并促进TD的管理。
