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Phenotype – lesion correlation in post-stroke movement disorders: Lessons learnt from two cases

A. Mukherjee, S. Pandey (Kolkata, India)

Meeting: 2026 International Congress

Keywords: Holmes tremor, Palatal tremor(see Tremors), Tremors: Etiology and Pathogenesis

Category: Tremor

Objective: To understand the phenotype-lesion correlation in post-stroke movement disorders (PSMD) from insights gained from two cases.

Background: PSMD is an important complication after stroke, and the phenotype-lesion correlation may be quite intriguing.

Method: Two patients who developed movement disorders following stroke were followed up, and their clinical phenotype and neuroimaging changes were documented.

Results: Case 1- A 71-year-old male patient, known hypertensive, non-diabetic, non-smoker developed acute onset right hemiparesis and numbness 2.5 years ago, associated with mild swaying and dysarthria due to a left thalamic infarct. He showed good improvement by 1 month. After about 3 months, he presented with clumsiness and some tremulous movements in the right upper limb (mostly while reaching for an object). After 6 months, he developed choreodystonic movements of the right hand, but he was lost to follow-up. After 1.5 years, the patient returned with increased difficulty in using his right hand due to dystonic tremor. About 24 months after the stroke, he returned with significant increase in the tremor in the form of Holmes tremor (∽ 4 Hz) which became disabling. The tremor was refractory to levodopa.

Case 2- A 59-year-old male patient known hypertensive and diabetic, developed an acute onset left hemiparesis 2 years ago (right basal ganglia region hemorrhage), and one year later he had an acute onset of diplopia, dysarthria, ataxia, and increased left sided weakness (due to a pontine hemorrhage). There was partial improvement. After 1 month, he noted stiffness of the left upper and lower limbs with posturing. He presented after 3 months, with dystonic tremor of the left upper limb and head tremor. The tremulousness increased over the next 6 months, then became static. At that time, he had left upper limb, head, and palatal tremor. The repeat MRI showed hypertrophic olivary degeneration.

Conclusion: The first case – in PSMD, a single lesion (such as a thalamic infarct) can lead to multiple hyperkinetic movement disorders in various combinations, and the movements can evolve over time with one component becoming more prominent. The second case- in a PSMD phenotype, neuroimaging may reveal multiple discrete lesions, and it is useful if a temporal association can be established with a specific lesion.

To cite this abstract in AMA style:

A. Mukherjee, S. Pandey. Phenotype – lesion correlation in post-stroke movement disorders: Lessons learnt from two cases [abstract]. Mov Disord. 2026; 41 (suppl 1). https://www.mdsabstracts.org/abstract/phenotype-lesion-correlation-in-post-stroke-movement-disorders-lessons-learnt-from-two-cases/. Accessed October 1, 2026.
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