Objective: To report a case of acute hemichorea after infarction over globus pallidus interna

Background: Movement disorders occurred after stroke have been recognized in previous reports, and chorea is one of the commonest movement disorders following stroke occurrence. Chorea may be induced by unilateral or bilateral lesions, including thalamus, cortical surface or lentiform nucleus. [1]. Most patients with hemichorea-hemiballismus are often caused by contralateral sub-thalamic nucleus.[2][3] Globus pallidus lesions have been rarely reported to be associated with chorea. Herein, we reported a case of hemichorea induced by isolated infarction over globus pallidus interna.

Method: This 26 year-old young man suffered from acute onset of involuntary movement over right side limbs. Initial presentation was writing difficulty and gait disturbance. Heichorea was diagnosed due to semi-rhythmic, irregular pattern without repetition. His right foot movement persisted all day and his sleep was affected.

Results: Diffuse weighted imaging (DWI) of brain magnetic resonance imaging (MRI) revealed hyper intensity  left globus pallidus interna suggestive of acute infarction. We also checked possible  risk factors of young stroke including metabolic syndrome profiles, thyroid function, coagulation factors, autoimmune profiles, syphilis, vitamin B12, homocysteine ,and folic acid. Uncontrolled hypertension and elevated cholesterol level were found. Elevated rheumatoid factors (75.3 IU/ml ) and borderline positive lupus anticoagulants were also detected.Carotid doppler and cardiac echo showed no abnormalities. Brain MRA revealed no evidence of focal stenosis or occlusion of intracranial vessels. Chorea improved gradually 2 weeks later and subsided  1 month after stroke without other sequelae.

Conclusion: Globus pallidus interna is rarely reported to be associated with hemichorea. The possible mechanism remained unknown. Lesions of the subthalamic nucleus presumably decreased the normal excitatory drive to the internal segment of the globus pallidus and reduce the inhibitory output of the globus pallidus on the thalamus. Thalamus disinhibition may contribute to overactivity of cerebral cortex. We presumed that lesions of globus pallidus interna may also decrease inhibition on thalamus with excessive excitatory drive to cerebral cortex, which is represented as contralateral hyperkinetive movement.

References: 1.Alarcón F, Zijlmans JC, Dueñas G, Cevallos N.Post-stroke movement disorders: report of 56 patients.J Neurol Neurosurg Psychiatry. 2004 Nov;75(11):1568-74. 2.Dewey RB Jr, Jankovic J. Hemiballism-hemichorea. Clinical and pharmacologic findings in 21 patientsArch Neurol. 1989 Aug;46(8):862-7. 3.Chung SJ, Im JH, Lee MC, Kim JS. Hemichorea after stroke: clinical-radiological correlation. J Neurol. 2004 Jun;251(6):725-9.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/acute-hemichorea-caused-by-infarction-over-globus-pallidus-interna/