Transient Acute-onset Holmes-like Tremor After Cortical Stroke

Holmes tremor is a low-frequency movement disorder combining rest, postural and intention tremor, developing weeks to months after lesions involving the brainstem, thalamus, or cerebellothalamic pathways. We report an acute-onset Holmes-like tremor following an isolated precentral cortical ischemic stroke.

A 68-year-old man presented with acute right-sided facial and upper limb weakness and aphasia, with rapid clinical improvement. Within 24 hours, he developed rhythmic low-frequency pronation-supination movements of the right hand and forearm, present at rest and enhanced during posture and voluntary movement. EEG showed no epileptiform discharges or cortical correlates, and lacosamide produced no clinical benefit. Multichannel surface polygraphy and accelerometry demonstrated relatively regular oscillations at approximately 3 Hz at rest and 3.5-4 Hz during action, supporting a Holmes-like tremor phenotype. Brain MRI revealed acute ischemic lesions confined to the left precentral cortex, without involvement of the thalamus, brainstem, basal ganglia, or cerebellum. The tremor resolved within days and did not recur at 1-month follow-up.

This case is unusual because of the acute onset, isolated precentral cortical lesions, distal predominance of tremor, and spontaneous remission. The absence of prior tremor, the close temporal relationship with the new infarct, and complete recovery suggest that the acute cortical lesion was the most likely trigger. The cortical localization is consistent with network-based models suggesting that Holmes tremor may arise from disruption of a distributed motor circuit rather than a single anatomical structure. The rapid resolution supports the hypothesis of a transient functional network disturbance rather than a stable oscillatory circuit dysfunction.