Ellis Elizabeth G, Meyer Garance M, Kaasinen Valtteri, Corp Daniel T, Pavese Nicola, Reich Martin M, Joutsa Juho
Turku Brain and Mind Center, University of Turku, Turku, Finland.
Cognitive Neuroscience Unit, School of Psychology, Deakin University, Geelong, VIC, Australia.
NPJ Parkinsons Dis. 2024 Aug 14;10(1):154. doi: 10.1038/s41531-024-00774-3.
Movement disorders, such as Parkinson's disease, essential tremor, and dystonia, are characterized by their predominant motor symptoms, yet diseases causing abnormal movement also encompass several other symptoms, including non-motor symptoms. Here we review recent advances from studies of brain lesions, neuroimaging, and neuromodulation that provide converging evidence on symptom-specific brain networks in movement disorders. Although movement disorders have traditionally been conceptualized as disorders of the basal ganglia, cumulative data from brain lesions causing parkinsonism, tremor and dystonia have now demonstrated that this view is incomplete. Several recent studies have shown that lesions causing a given movement disorder occur in heterogeneous brain locations, but disrupt common brain networks, which appear to be specific to each motor phenotype. In addition, findings from structural and functional neuroimaging in movement disorders have demonstrated that brain abnormalities extend far beyond the brain networks associated with the motor symptoms. In fact, neuroimaging findings in each movement disorder are strongly influenced by the constellation of patients' symptoms that also seem to map to specific networks rather than individual anatomical structures or single neurotransmitters. Finally, observations from deep brain stimulation have demonstrated that clinical changes, including both symptom improvement and side effects, are dependent on the modulation of large-scale networks instead of purely local effects of the neuromodulation. Combined, this multimodal evidence suggests that symptoms in movement disorders arise from distinct brain networks, encouraging multimodal imaging studies to better characterize the underlying symptom-specific mechanisms and individually tailor treatment approaches.
运动障碍,如帕金森病、特发性震颤和肌张力障碍,以其主要的运动症状为特征,但导致异常运动的疾病还包括其他几种症状,包括非运动症状。在此,我们回顾了来自脑损伤、神经影像学和神经调节研究的最新进展,这些研究为运动障碍中症状特异性脑网络提供了一致的证据。尽管传统上运动障碍被认为是基底神经节的疾病,但导致帕金森症、震颤和肌张力障碍的脑损伤累积数据现已表明,这种观点是不完整的。最近的几项研究表明,导致特定运动障碍的损伤发生在不同的脑区,但会破坏共同的脑网络,这些网络似乎特定于每种运动表型。此外,运动障碍的结构和功能神经影像学研究结果表明,脑异常远远超出了与运动症状相关的脑网络。事实上,每种运动障碍的神经影像学结果都受到患者症状组合的强烈影响,这些症状似乎也映射到特定的网络,而不是单个解剖结构或单一神经递质。最后,深部脑刺激的观察结果表明,临床变化,包括症状改善和副作用,取决于对大规模网络的调节,而不是神经调节的纯粹局部效应。综合起来,这些多模态证据表明,运动障碍的症状源于不同的脑网络,这鼓励进行多模态成像研究,以更好地描述潜在的症状特异性机制,并个性化定制治疗方法。