Holmes tremor is recognized as an irregular, usually slow (2-5 Hz), variable amplitude, action, postural and resting tremor which can present secondary to lesions located in the midbrain peduncles including red nucleus, cerebellothalamic, and nigrostriatal pathways.

A 44-year-old man presented with subacute progressive vision loss, more pronounced in the right visual field. Imaging revealed a large enhancing skull base lesion extending into the frontal and ethmoid sinuses, compressing the optic apparatus. He underwent bifrontal craniotomy and skull base reconstruction, with pathology confirming meningioma, CNS/WHO grade 1. On post-operative day 5, he developed right arm tremors, affecting the elbow and wrist, present at rest and accentuated by posture and intention. The tremors were involuntary, low frequency (3-4 Hz), large in amplitude, and associated with head bobbing. There were no Parkinsonian symptoms, and tremors were triggered by fatigue and somnolence.

Concerns for focal seizures led to continuous EEG monitoring and initiation of antiepileptics, but the movements had no EEG correlates. MRI showed T2 FLAIR changes in the midbrain, dura enhancement, pituitary enhancement, and brain sagging, suggestive of intracranial hypotension. Despite treatment with levetiracetam, benzodiazepines, and primidone, symptoms persisted. Conservative management with hydration resulted in gradual improvement. At the 3 month follow-up visit, the tremors had resolved, and repeat MRI showed resolution of intracranial hypotension findings.

Distortion of midbrain anatomy secondary to intracranial hypotension (IH) explains the development of Holmes tremor. Focal seizures although are a reasonable differential however repeat MRI Brain can be a reasonable and diagnostic step. It is therefore essential to include differential diagnosis of movement disorders in patients presenting with symptoms of IH.