Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry

Ghika-Schmid, Florence; Ghika, Joseph; Régli, F; Bogousslavsky, Julien

doi:10.1016/s0022-510x(96)00290-0

Cited by 249 publications

(253 citation statements)

References 44 publications

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“…A canonical example is stroke-induced hemichorea-hemiballismus, a syndrome consisting of 2 movement disorders that typically coexist 2 and together comprise the most frequently reported poststroke movement disorder. [3][4][5] Classic teaching in neurology 6 and landmark studies in humans 7 and nonhuman primates 8 highlight the role of lesions to the contralateral subthalamic nuclei (STN) in producing hemichorea-hemiballismus. However, causative lesions have been reported in the cortex, caudate, putamen, thalamus, and brainstem [9][10][11] and strokes directly affecting the STN constitute a minority (10%-30%) of cases.…”

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confidence: 99%

Network localization of hemichorea-hemiballismus

2016

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Objective: To determine whether neuroanatomically heterogeneous strokes causing hemichoreahemiballismus localize to a common functional network. Methods:We identified 29 cases of lesion-induced hemichorea-hemiballismus from the literature and mapped each lesion volume onto a reference brain. Using a recently validated technique termed lesion network mapping, we tested whether these lesions belonged to the same functional network. To accomplish this, the network of brain regions functionally connected to each lesion was identified using a connectome dataset from healthy participants. Network maps were overlapped to identify any region functionally connected to our set of lesions. Specificity was evaluated using a case-control design; control cohorts included a group of similar lesions randomized to different brain locations and a second group of lesions causing a separate movement disorder, asterixis. Reproducibility was evaluated using an independent cohort of 10 additional hemichorea-hemiballismus cases.Results: Lesions showed heterogeneity in anatomical location, consistent with prior reports. However, at least 90% of these lesions showed network overlap in the posterolateral putamen. This result was specific to lesions causing hemichorea-hemiballismus and reproducible in an independent cohort. The putaminal overlap site was itself connected to a broader motor network that predicted the distribution of lesions causing hemichorea-hemiballismus.Conclusions: Strokes causing hemichorea-hemiballismus, while anatomically heterogeneous, localize to a common functional network. Specifically, lesions occur in regions functionally connected to the posterolateral putamen, a region previously implicated in hyperkinetic movement disorders. Lesion network mapping may be useful in identifying the neuroanatomical substrates of heterogeneous lesion-based disorders. Neurology ® 2016;86:2187-2195 GLOSSARY rs-fcMRI 5 resting-state functional connectivity MRI; STN 5 subthalamic nuclei.

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confidence: 99%

Network localization of hemichorea-hemiballismus

2016

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“…3 Hemichorea is a very rare presentation of carotid occlusive disease to cause hemodynamic compromise in watershed territories. In searching the literature, we have found several reports of acute hemichorea or hemiballism associated with carotid artery occlusive disease.…”

Section: Discussionmentioning

confidence: 99%

Hemichorea Resulting from Ischemic Stroke in the Ipsilateral Caudate Nucleus

Lee¹,

Kim²,

Lee³

et al. 2015

J Neurocrit Care

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“…7 Lesions to the basal ganglia are most frequently implicated in post-stroke movement disorders. [1][2][3] Focal lesions interrupting either the direct or the indirect pathways could result in a variety of movement disorders.…”

Section: Discussionmentioning

confidence: 99%

Generalized Myoclonus

Inoa

McCullough

2013

The Neurohospitalist

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Movement disorders have been reported as rare complications of stroke. The basal ganglia have been implicated in the pathophysiology of most post-stroke dyskinesias. We outline different types of post-stroke myoclonus and their possible pathophysiology. A middle-aged man developed generalized myoclonus after an ischemic stroke in the superior midbrain and subthalamic nuclei. Spontaneous resolution was seen by 72 hours. A lesion to the subthalamic nuclei disrupted the normal thalamic inhibition, which likely led to the involuntary movements seen in our patient. In this case, myoclonus was generalized, which, to the best of our knowledge, has not been reported in the literature as a direct consequence of focal stroke.Keywords stroke, cerebrovascular disorders, movement disorders, clinical specialty, stroke and cerebrovascular disease, clinical specialty Movement disorders are rare complications of stroke. These can manifest as either long-term sequelae (usually after motor function has been partially or totally regained) or, less commonly, an immediate consequence of brain ischemia or hemorrhage. We report a case of a 61-year-old man with controlled hypertension on metroprolol who was found unresponsive in his home. He was initially transferred by ambulance to an outside hospital, where a nonenhanced head computed tomography (CT) was negative. He was given phenytoin 1000 mg intravenously (IV) and decadron 20 mg IV prior to arrival at our center. On our initial neurologic examination performed 3.5 hours after he was found unresponsive, he was stuporous and not responding to commands. He was withdrawing to pain in all 4 extremities and an extensor plantar reflex was noted on the right. Cranial nerves showed fixed and unequal pupils (right 5 mm and left 2 mm), left eye hypertropia, and right eye exotropia. Corneal and gag reflexes were present. No involuntary movements were appreciated. His National Institutes of Health Stroke Scale score was 22. General examination revealed an irregular heart rate and a blood pressure of 131/76 mm Hg. His electrocardiography showed atrial fibrillation. He was intubated immediately for airway protection after apneic breathing episodes were noted. Rocuronium was used for intubation, and he was premedicated with lidocaine and etomidate. After intubation, a single propofol bolus was given for transient hypertension and agitation. His oxygen saturation remained over 95% at all times. Urine toxicology and serum biochemistry that included a basic metabolic panel, cardiac, and liver enzymes were normal, except for the serum creatine kinase level that was found to be elevated (ie, 748 IU/L). A repeat nonenhanced head CT showed areas of hypoattenuation in the brain stem. Subsequent CT angiography was normal, with no evidence of large-vessel stenosis or embolus. Brain magnetic resonance imaging (MRI) showed clear evidence of restricted diffusion in the right and superior aspects of the midbrain, extending bilaterally upward into the subthalamic nuclei, which was also seen on fluidatten...

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Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry

Cited by 249 publications

References 44 publications

Network localization of hemichorea-hemiballismus

Network localization of hemichorea-hemiballismus

Hemichorea Resulting from Ischemic Stroke in the Ipsilateral Caudate Nucleus

Generalized Myoclonus

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