Hemichorea after stroke: Clinical-radiological correlation

Abstract

Post-stroke hemichorea is an uncommon involuntary hyperkinetic disorder involving unilateral body parts. The incidence and precise lesion location of post-stroke hemichorea remain unclear. The authors describe 27 consecutive patients with hemichorea after stroke. The incidence of post-stroke hemichorea was 0.54 % (27 out of 5,009 patients). The lesions were located in the caudate and putamen (n = 6), cortex (n = 6), thalamus and subthalamic area (n = 4), subthalamus (n = 4), putamen (n = 3), caudate (n = 2), and the globus pallidus (n = 2). Over the mean follow-up period of 22 months, the hemichorea disappeared in 56% of the patients, while it persisted in others. The rate of disappearance of hemichorea was significantly higher in patients with cortical strokes than in those with subthalamic lesions (P < 0.05). We conclude that hemichorea is a rare manifestation of stroke and most often produced by lenticular lesions followed by subthalamic and cortical lesions. The functional prognosis is better in patients with cortical lesions than those with subthalamic strokes.

Hemichorea Resulting from Ischemic Stroke in the Ipsilateral Caudate Nucleus

“…15 The involuntary movements in our patient disappeared along with an improvement in perfusion in subcortical region after carotid artery stenting. Impaired cerebral blood flow in critical watershed territories may be an important contributing factor in hemichorea associated with carotid stenosis.…”

Network localization of hemichorea-hemiballismus

“…J Neurol 2004;251:725-729). 9 Lesion 13 was composed of 2 separate lesions. When run independently, 1 lesion showed significant connectivity to the posterolateral putamen (figure e-2B).…”

“…[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. 5,9,12 Such findings have led to the hypothesis that the locus of pathology in hemichorea-hemiballismus resides in the disruption of a common distributed motor network rather than a single anatomical site.…”

“…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. 5,9,12 Such findings have led to the hypothesis that the locus of pathology in hemichorea-hemiballismus resides in the disruption of a common distributed motor network rather than a single anatomical site. 5,[12][13][14] However, evidence linking these heterogeneous lesion locations to a specific network is lacking.…”

İskemik inme sonrası gelişen hemikore

“…Hemikore-hemiballismusta sıklıkla orta serebral arter, posterior serebral arter ve nadiren de anterior serebral arter etkilenir 5,6 . Hemikore lentiform nükleus veya talamusu etkileyen vasküler olaylar sonrası sıklıkla bildirilmiştir 2,3,6,7 . İskemik inme, hemoraji gibi vasküler olayların yanında otoimmün-genetik hastalıklar, metabolik endokrin bozukluklar, enfeksiyonlar gibi çok sayıda hastalık hemikore ve hemiballismusa neden olabilmektedir 6,8 .…”