丘脑出血性中风后的福尔摩斯震颤

Abhishek Dixit
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摘要

福尔摩斯震颤(HT)是一种罕见的运动障碍,其特征是影响上肢的低频(<4.5 Hz)震颤,随着姿势和自主运动而加剧。它通常由脑干、小脑或丘脑的病变引起,中风是常见的病因。由于神经通路重组异常,震颤通常在最初的损伤发生数周至数月后出现。一例67岁男性高血压患者,左丘脑出血性卒中伴脑室内扩张,表现为右侧麻木和构音障碍。出院后10天,患者出现低频(3-4 Hz)左臂震颤,伴有休息、体位和动力成分。神经学检查显示轻度运动障碍,无运动迟缓或僵硬。使用三己苯基和加巴喷丁治疗效果极小,而左旋多巴100mg,每日三次可显著改善肢体控制。延迟发作、震颤特征和丘脑定位支持福尔摩斯震颤的诊断。本病例强调了HT的复杂病理生理,涉及小脑-丘脑-皮质和牙状-红宝石-橄榄通路的破坏。HT的罕见性(占所有震颤病例的2-4 %)及其对药物治疗的不同反应强调了多学科管理的必要性。目前的文献支持左旋多巴作为主要的治疗选择,在一些研究中反应率超过50% %。该患者对左旋多巴的阳性反应进一步证实了多巴胺能通路参与病理生理。对于难治性病例,可以考虑针对丘脑腹侧中间核的深部脑刺激(DBS),最近的证据表明,与单独药物治疗相比,深部脑刺激能更好地抑制震颤。本病例强调了认识HT及其表现对正确诊断和治疗的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Holmes tremor following thalamic hemorrhagic stroke

Background

Holmes tremor (HT) is a rare movement disorder characterized by low-frequency (<4.5 Hz) tremors affecting the upper limbs, exacerbated by posture and voluntary movements. It typically arises from lesions to the brainstem, cerebellum, or thalamus, with stroke being a common etiology. The tremor usually emerges weeks to months after the initial insult due to aberrant neural pathway reorganization.

Case presentation

A 67-year-old man with hypertension presented with Right-sided numbness and dysarthria from a left thalamic hemorrhagic stroke with intraventricular extension. Ten days post-discharge, he developed a low-frequency (3–4 Hz) left arm tremor with rest, postural, and kinetic components. Neurological examination revealed mild dysmetria without bradykinesia or rigidity. Treatment with trihexyphenidyl and gabapentin provided minimal benefit, while levodopa 100 mg three times daily yielded substantial improvement in limb control. The delayed onset, tremor characteristics, and localization to the thalamus supported the diagnosis of Holmes tremor.

Discussion

This case highlights the complex pathophysiology of HT involving disruption of cerebello-thalamo-cortical and dentato-rubro-olivary pathways. The rarity of HT (2–4 % of all tremor cases) and its variable response to pharmacotherapy underscore the need for multidisciplinary management. Current literature supports levodopa as a primary treatment option, with response rates exceeding 50 % in some studies. This patient's positive response to levodopa further confirms dopaminergic pathway involvement in the pathophysiology. For refractory cases, deep brain stimulation (DBS) targeting the ventral intermediate nucleus of the thalamus can be considered, with recent evidence suggesting superior tremor suppression compared to pharmacotherapy alone. This case emphasizes the importance of recognizing HT and its manifestations for proper diagnosis and management.
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