Department of Neurology University Hospital 12 de Octubre Madrid Spain.
Center of Biomedical Network Research on Neurodegenerative Diseases (CIBERNED) Madrid Spain.
Ann Clin Transl Neurol. 2018 Nov 8;6(1):83-97. doi: 10.1002/acn3.681. eCollection 2019 Jan.
Although the cerebello-thalamo-cortical network has often been suggested to be of importance in the pathogenesis of essential tremor (ET), the origins of tremorgenic activity in this disease are not fully understood. We used a combination of cortical thickness imaging and neurophysiological studies to analyze whether the severity of tremor was associated with anatomical changes in the brain in ET patients
Magnetic resonance imaging (MRI) and a neurophysiological assessment were performed in 13 nondemented ET patients. High field structural brain MRI images acquired in a 3T scanner and analyses of cortical thickness and surface were carried out. Cortical reconstruction and volumetric segmentation was performed with the FreeSurfer image analysis software. We used high-density surface electromyography (hdEMG) and inertial measurement units (IMUs) to quantify the tremor severity in upper extrimities of patients. In particular, advanced computer tool was used to reliably identify discharge patterns of individual motor units from surface hdEMG and quantify motor unit synchronization.
We found significant association between increased motor unit synchronization (i.e., more severe tremor) and cortical changes (i.e., atrophy) in widespread cerebral cortical areas, including the left medial orbitofrontal cortex, left isthmus of the cingulate gyrus, right paracentral lobule, right lingual gyrus, as well as reduced left supramarginal gyrus (inferior parietal cortex), right isthmus of the cingulate gyrus, left thalamus, and left amygdala volumes.
Given that most of these brain areas are involved in controlling movement sequencing, ET tremor could be the result of an involuntary activation of a program of motor behavior used in the genesis of voluntary repetitive movements.
尽管小脑-丘脑-皮质网络常被认为在特发性震颤(ET)的发病机制中具有重要意义,但该病震颤原的起源尚不完全清楚。我们使用皮质厚度成像和神经生理学研究的组合来分析 ET 患者的震颤严重程度是否与大脑的解剖结构变化有关。
对 13 名非痴呆 ET 患者进行了磁共振成像(MRI)和神经生理学评估。在 3T 扫描仪上采集高磁场结构脑 MRI 图像,并进行皮质厚度和表面分析。使用 FreeSurfer 图像分析软件进行皮质重建和体积分割。我们使用高密度表面肌电图(hdEMG)和惯性测量单元(IMU)来定量患者上肢的震颤严重程度。特别是,使用先进的计算机工具来从表面 hdEMG 中可靠地识别单个运动单位的放电模式,并量化运动单位同步。
我们发现,运动单位同步增加(即震颤更严重)与广泛的大脑皮质区域的皮质变化(即萎缩)之间存在显著关联,包括左侧内侧眶额皮质、左侧扣带回峡部、右侧旁中央小叶、右侧舌回,以及左侧缘上回(顶下小叶)、右侧扣带回峡部、左侧丘脑和左侧杏仁核体积减少。
鉴于这些大脑区域中的大多数都参与了运动序列的控制,ET 震颤可能是用于产生自愿重复运动的运动行为程序的无意识激活的结果。