Pearls & Oy-sters: Resolution of hemichorea following endarterectomy for severe carotid stenosis

ArticleinNeurology 71(24):e80-2 · January 2009
Impact Factor: 8.29 · DOI: 10.1212/01.wnl.0000336975.80810.74 · Source: PubMed
    • "At that point, the tiapride hydrochloride was discontinued without a relapse of HC–HB. extracranial carotid artery stenosis, [8,22,27] and cerebral hemorrhage. [2,18] Traditionally, the mechanism underlying poststroke HC–HB is believed to be ischemia of the basal ganglia, particularly the lentiform nucleus and the thalamus. "
    [Show abstract] [Hide abstract] ABSTRACT: Movement disorders after the clipping for an unruptured giant aneurysm are rare. The information on the pathogenesis and treatment options for this condition is largely unknown. An 82-year-old female with no neurological deficits underwent a clipping for a giant middle cerebral artery (MCA) aneurysm. Immediately after surgery, she presented with hemichorea-hemiballismus (HC-HB) on the left side. Postoperative angiograms and single-photon emission computed tomography demonstrated the hyperperfusion in the right frontal cortex and the decreased perfusion in the basal ganglia, indicating that the abrupt hemodynamic changes due to the obliteration of the giant aneurysm caused the dysfunction of the frontal cortical and subcortical pathway and the basal ganglia. Administration of tiapride hydrochloride was dramatically effective in controlling the HC-HB until the hyperperfusion resolved. Single-photon emission computed tomography obtained 8 weeks after surgery revealed that the cerebral blood flow had been normalized in the right frontal cortex. The relative hypoperfusion of the right basal ganglia was also resolved. Then tiapride hydrochloride was discontinued without a relapse of HC-HB. This case appears consistent with the theory that the connecting fibers responsible for the development of HC-HB are also located in the frontal lobe. The treatment of giant aneurysms involving the M1 portion can cause abrupt hemodynamic changes in both frontal cortex and the basal ganglia, which can potentially induce postoperative movement disorders.
    Full-text · Article · May 2015 · Surgical Neurology International
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    • "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.4–9 However, these hyperkinetic movement disorders seem to be related to ischemic lesions in the basal ganglia or subthalamic nucleus in the majority of patients. "
    [Show abstract] [Hide abstract] ABSTRACT: Involuntary movement associated with deep watershed ischemic lesions has been rarely reported. A 67-year-old woman presented with acute hemichorea on the left side. Magnetic resonance imaging showed acute infarcts in the anterior border zone. On perfusion studies, impaired cerebral blood flow was observed on the subcortical region sparing the basal ganglia. Cerebral angiogram confirmed severe stenosis in the right internal carotid artery. Her hemichorea gradually improved along with normalization of perfusion after carotid artery stenting with angioplasty. We suggest that impaired cerebral blood flow in critical watershed territories may be an important contributing factor in hemichorea associated with carotid occlusive disease.
    Full-text · Article · May 2013
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    • "Chorea has a wide differential diagnosis including infections, autoimmune diseases, genetic and neurodegenerative disorders, drug-exposure, metabolic diseases, neoplasm and stroke [1]. So far, only a recent report has suggested that carotid artery stenosis should be considered in the differential diagnosis of chorea, even in the absence of a preceding stroke or transient ischemic attack [2]. Interestingly, few reports have suggested that impaired cerebral blood flow in basal ganglia is a key contributing factor. "
    [Show abstract] [Hide abstract] ABSTRACT: Hemichorea associated with carotid artery occlusive disease is extremely rare. It has been recently suggested that carotid artery stenosis should be considered in the differential diagnosis of chorea, even in the absence of a preceding stroke or transient ischemic attack. Although the pathophysiology of this condition is still under discussion, some reports suggest that impaired cerebral blood flow in the basal ganglia is a key contributing factor. We herein report a case of hemichorea related to severe stenosis of the left internal carotid artery with no basal ganglia lesions on brain MRI. After carotid revascularization, hemichorea gradually subsided and reversible left thalamic and putaminal hypoperfusion were demonstrated by functional neuroimaging. This case report supports the hypothesis about the central role of hemodynamic ischemia in the pathophysiology of hemichorea associated with carotid artery stenosis, and highlights the importance of vascular imaging studies for the early identification of carotid disease in patients with chorea, even in the absence of other clinical signs.
    Full-text · Article · Sep 2010 · Journal of the neurological sciences
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