Non-invasive Brain Stimulation Unit, Santa Lucia Foundation IRCCS, Via Ardeatina 306, 00179 Rome, Italy; University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy.
Unidad de Trastornos del Movimiento, Servicio de Neurología y Neurofisiología Clínica, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, Spain.
Brain Stimul. 2014 Jul-Aug;7(4):564-72. doi: 10.1016/j.brs.2014.05.002. Epub 2014 May 9.
Dystonia is generally regarded as a disorder of the basal ganglia and their efferent connections to the thalamus and brainstem, but an important role of cerebellar-thalamo-cortical (CTC) circuits in the pathophysiology of dystonia has been invoked. Here in a sham controlled trial, we tested the effects of two-weeks of cerebellar continuous theta burst stimulation (cTBS) in a sample of cervical dystonia (CD) patients. Clinical evaluations were performed by administering the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) and the Burke-Fahn-Marsden Dystonia Rating Scale (BFMDRS). We used TMS to measure the inhibitory connectivity between the cerebellum and the contralateral motor cortex (cerebellar brain inhibition [CBI]), and the excitability of the contralateral primary motor cortex assessing intracortical inhibition (SICI), intracortical facilitation (ICF) and cortical silent period (CSP). Paired associative stimulation (PAS) was tested to evaluate the level and the topographical specificity of cortical plasticity, which is abnormally enhanced and non-focal in CD patients. Two weeks of cerebellar stimulation resulted in a small but significant clinical improvement as measured by the TWSTRS of approximately 15%. Cerebellar stimulation modified the CBI circuits and reduced the heterotopic PAS potentiation, leading to a normal pattern of topographic specific induced plasticity. These data provide novel evidence CTC circuits could be a potential target to partially control some dystonic symptoms in patients with cervical dystonia.
特发性肌张力障碍通常被认为是基底节及其与丘脑和脑干的传出连接的障碍,但小脑-丘脑-皮质(CTC)回路在肌张力障碍的病理生理学中起着重要作用。在这里,我们在一项假对照试验中,测试了连续两周小脑 theta 爆发刺激(cTBS)对颈肌张力障碍(CD)患者样本的影响。临床评估通过多伦多西部痉挛性斜颈评定量表(TWSTRS)和 Burke-Fahn-Marsden 肌张力障碍评定量表(BFMDRS)进行。我们使用 TMS 测量小脑与对侧运动皮质之间的抑制性连接(小脑脑抑制[CBI]),以及评估对侧初级运动皮质兴奋性的抑制性内皮质抑制(SICI)、内皮质易化(ICF)和皮质静息期(CSP)。我们测试了配对关联刺激(PAS),以评估皮质可塑性的水平和拓扑特异性,在 CD 患者中,皮质可塑性异常增强且非局部化。两周的小脑刺激导致 TWSTRS 约 15%的临床改善,尽管改善幅度较小,但具有统计学意义。小脑刺激改变了 CBI 回路,减少了异位 PAS 增强,导致了具有正常拓扑特异性的诱导可塑性。这些数据提供了新的证据,表明 CTC 回路可能是部分控制 CD 患者某些肌张力障碍症状的潜在靶点。