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Delayed post-stroke parkinsonism: description of two cases and possible mechanism

T. Friedeman- Korn, M. Bauer, M. Abu Snineh, C. Weill, D. Arkadir (Jerusalem, Israel)

Meeting: 2022 International Congress

Abstract Number: 1518

Keywords: Basal ganglia, Ischemia, Parkinsonism

Category: Parkinson's Disease: Pathophysiology

Objective: To present two patients who developed delayed parkinsonism years after experiencing midbrain strokes and to suggest a possible mechanism for this delayed phenomenon.

Background: Both parkinsonism, and hyperkinetic movement disorders, have been reported after ischemic and hemorrhagic midbrain strokes. While hyperkinetic movement disorders may appear as either acute or delayed stroke sequela, delayed post-stroke parkinsonism is rarely described.

Method: Describing two young patients who developed levodopa-responsive parkinsonism decades after experiencing a single stroke involving the upper part of the midbrain.

Results: The first patient had a basilar artery occlusion, successfully opened by a thrombectomy, at the age of 56 years. He rapidly recovered but was left with mild to moderate spastic weakness of his left limbs. A decade later he developed hypomimia, slowed gait and bradykinesia of his right (previously intact) limbs. Fluorodopa pet scan demonstrated reduced intake in his left putamen. These parkinsonian signs clearly responded to a low-dose levodopa therapy.
The second patient experienced a large subcortical hemorrhagic stroke involving his right midbrain, at 30 years of age. Sequela included left spastic-dystonia, which remained stable for two decades. After a long period of clinical stability, the patient developed a rapidly progressive impaired gait, eventually leading to the diagnosis of parkinsonism. His gait dramatically improved with a low dose of levodopa therapy.

Conclusion: Although idiopathic Parkinson’s disease cannot be ruled out in these patients, we believe that the cases described above may represent delayed levodopa responsive post-stroke parkinsonism. We suggest here, that the subpopulation of midbrain dopamine neurons that innervate the dorsal striatum may have suffered during the vascular event. We further suggest that post-stoke subclinical parkinsonism was noticed only decades later following age-dependent shrinking of this neuronal population.

References: 1. Antonio Siniscalchi, Luca Gallelli, Angelo Labate, Giovanni Malferrari, Caterina Palleria and Giovambattista De Sarro. Post-stroke Movement Disorders: Clinical Manifestations and Pharmacological Management.Curr Neuropharmacol. 2012 Sep; 10(3): 254–262
2. Thomas H.McNeill,, Sally A. Brown , Jose A. Rafols , IraShoulson1. Atrophy of medium spiny I striatal dendrites in advanced Parkinson’s diseaseBrain Research Volume 455, Issue 1, 5 July 1988, Pages 148-152

To cite this abstract in AMA style:

T. Friedeman- Korn, M. Bauer, M. Abu Snineh, C. Weill, D. Arkadir. Delayed post-stroke parkinsonism: description of two cases and possible mechanism [abstract]. Mov Disord. 2022; 37 (suppl 2). https://www.mdsabstracts.org/abstract/delayed-post-stroke-parkinsonism-description-of-two-cases-and-possible-mechanism/. Accessed May 24, 2025.
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