Objective: Describing 3 unique post-stroke dystonia cases.

Background: Dystonia, the 2^nd most common post-stroke movement disorder, presents commonly contralateral to the lesion, focally, and 9.5 months post-stroke [1-5]. The basal ganglia (44%) and thalamus (37%) are the most common sites of infarction [3], and botulinum toxin (BoNT-A) is effective treatment [6]. We present 3 diverse post-stroke dystonia cases treated successfully with BoNT-A.

Method: Patient presentations and clinical course were retrospectively collected from 2018 to 2021.

Results: Case 1, a 78-year-old man, initially presented with mild dysarthria, left arm numbness, and dexterity loss of left hand; he had a left pontine infarct. 14 months later, he developed segmental oromandibular and lingual protrusion dystonia causing dysarthria, orolingual ulcers, difficulty chewing, and weight loss. BoNT-A into the bilateral masseters, temporalis, and pterygoids improved symptoms. Case 2, a 77-year-old man, was diagnosed with a punctate right cerebellar infarction after presenting with acute onset dizziness, nausea, and vomiting. He developed a right arm irregular tremor 1 month later, with null point with palm up and posturing of fingers and radial deviation of the wrist while writing. BoNT-A into right pronator teres, supinator, and flexor carpi radialis markedly improved functionality. Case 3, a 48-year-old woman, had a left thalamic hemorrhage with right- hemiparesis and severe dysarthria. 6 months later, she developed an irregular head tremor with left turn and right tilt of neck. Her focal cervical dystonia improved with BoNT-A into bilateral sternocleidomastoids and left splenius.

Conclusion: Similar to previous reports, 2 cases (1,2) had ischemic strokes, all had delayed onset, 2 were focal (Case 2, 3), and all responded to BoNT-A [5]. MRI demonstrated thalamic lesion in only Case 3; functional imaging may have suggested more expansive basal ganglia-thalamo-cortical circuitry involvement. Cerebellar ischemia causing dystonic tremor (Case 2) and oromandibular and lingual dystonia developing after pontine infarct (Case 1) are rare [7]. The various infarct locations and diverse dystonia presentation in our series suggest less of a role of classically defined discrete lesions and support the need for further research into the development of post-stroke dystonia [4, 5, 8, 9].

References: 1. Bansil, S., et al., Movement disorders after stroke in adults: a review. Tremor Other Hyperkinet Mov (N Y), 2012. 2. 2. Handley, A., et al., Movement disorders after stroke. Age and Ageing, 2009. 38(3): p. 260-266. 3. Park, J., Movement Disorders Following Cerebrovascular Lesion in the Basal Ganglia Circuit. J Mov Disord, 2016. 9(2): p. 71-9. 4. Suri, R., et al., Post-stroke Movement Disorders: The Clinical, Neuroanatomic, and Demographic Portrait of 284 Published Cases. J Stroke Cerebrovasc Dis, 2018. 27(9): p. 2388-2397. 5. Gupta, N. and S. Pandey, Post-Thalamic Stroke Movement Disorders: A Systematic Review. Eur Neurol, 2018. 79(5-6): p. 303-314. 6. Siniscalchi, A., et al., Post-stroke Movement Disorders: Clinical Manifestations and Pharmacological Management. Curr Neuropharmacol, 2012. 10(3): p. 254-62. 7. Pandey, S. and P. Tater, Post-Stroke Lingual Dystonia: Clinical Description and Neuroimaging Findings. Tremor Other Hyperkinet Mov (N Y), 2018. 8: p. 610. 8. Lehéricy, S., et al., The anatomical basis of dystonia: current view using neuroimaging. Mov Disord, 2013. 28(7): p. 944-57. 9. Mehanna, R. and J. Jankovic, Movement disorders in cerebrovascular disease. Lancet Neurol, 2013. 12(6): p. 597-608.

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