Post-stroke hyperkinetic movement disorders: a brain network issue
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LETTER TO THE EDITOR
Post-stroke hyperkinetic movement disorders: a brain network issue Francesco Motolese 1
&
Francesca Romana Pezzella 2 & Massimo Marano 1 & Vincenzo Di Lazzaro 1 & Sabrina Anticoli 2
Received: 20 March 2020 / Accepted: 13 October 2020 # Fondazione Società Italiana di Neurologia 2020
Dear Editor, Stroke-related hyperkinesias are reported in 1–4% of all cerebrovascular accidents [1]. Given that the evaluation of involuntary movements is not included in the routine stroke evaluation (i.e., not considered in the NIHSS), they could be overlooked and undertreated. Even if epidemiological data are controverted, chorea and dystonia are the most frequent poststroke movement disorders (PSMD), being often present in the acute phase [1]. Traditionally, the mechanism underlying the development of post-stroke chorea or dystonia includes a lesion in basal ganglia or subthalamic nucleus (STN) [1]. However, our knowledge about the pathophysiology of movement disorders is evolving—they are now considered the result of dysfunctions in large networks including structures outside basal ganglia, such as sensorimotor cortices and cerebellum. Herein, we present an emblematic case of hemiballismus and choreic movements due to ischemic lesions located in areas not traditionally associated with the development of PSMD.
non-fluent expressive aphasia. The cranial nerves were normal and there was no papilledema. Motor examination revealed a slight right pronator drift and ballismus of the right upper and lower limbs associated with choreic movements of the right foot (Video 1). Sensation was normal, while plantar response was equivocal on the right. Her medical history was remarkable for the surgical replacement of the aortic valve 20 years before and she was on treatment with vitamin K antagonist. Laboratory tests results—including blood glucose and electrolytes—were normal except for an elevated international normalized ratio (INR). Brain magnetic resonance imaging (MRI) showed multiple high-signal lesions on diffusionweighted imaging (DWI) with decreased apparent diffusion coefficient values scattered in the left frontal lobe cortex, insula, and parietal and temporal lobe, indicating the presence of multiple acute infarcts (Fig. 1). MR angiography of intracranial vessels was unremarkable. Because of an INR value > 1.7—outside the therapeutic range for a mechanical valve carrier—and because of timing, she was not eligible for intravenous thrombolysis. After 48 h, the involuntary movements disappeared and she fully recovered from aphasia.
Case report An 81-year-old woman with a history of atrial fibrillation presented to the emergency department because of the acute onset of aphasia and abnormal involuntary movements of her right limbs. On physical examination, she was alert and had Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10072-020-04832-5) contains supplementary material, which is available to authorized users. * Francesco Motolese [email protected] 1
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