Case Report

Pure Cortical Stroke Causing Hemichorea-Hemiballismus
Sara Strauss, DO, Daniel Rafie, MD, Anitha Nimma, MD,
Raquel Romero, MD, and Philip A. Hanna, MD

Background: Movement disorders including hemichorea-hemiballism as the initial
presentation of an acute ischemic stroke are uncommon. Structures outside of the
deep subcortical areas such as the subthalamic nucleus or basal ganglia are rarely
involved. Case Report: We report a case of a 72-year-old man with vascular risk factors who presented with acute onset right-sided hemichorea-hemiballism. Metabolic-, infectious-, and toxic-related conditions were ruled out, his EEG was
without epileptiform changes. An MRI confirmed an acute ischemic stroke in the
parieto-occipital region without any subcortical structures involved. Atrial Fibrillation was later discovered during his hospitalization and was treated appropriately.
Conclusions: Although rare, strokes outside of the subthalamic nucleus can result in
hemichorea-hemiballism.
Key Words: Stroke—movement disorder—hemichorea—hemiballism
Published by Elsevier Inc.

Introduction
Movement disorders including hemichorea-hemiballism as the initial presentation of an acute ischemic stroke
are uncommon. In a large hospital-based registry of 5009
acute stroke patients, the incidence was reported to be
0.54%.1 The etiologic lesion is classically subcortical, with
or without involvement of the subthalamic nucleus. Alarcon et al. showed that the probability of developing a
poststroke involuntary movement disorder was 3 times
higher when the vascular lesion was deep in location visa-vis surface infarcts.2 We report a case of a 72-year-old
male clinically presenting with acute right-sided hemichorea-hemiballism resultant of an acute parieto-occipital
lobe infarct, without involvement of the deeper structures.

From the Hackensack Meridian Health JFK Medical Center, Neurology Department, Edison, New Jersey.
Received April 25, 2019; revision received July 1, 2019; accepted
July 6, 2019.
There were no sponsorships or financial support for the study.
Address correspondence to Sara Strauss, DO, 65 James Street, Edison, NJ, 08820. E-mails: sara.strauss@hackensackmeridian.org,
straussy07@gmail.com.
1052-3057/$ - see front matter
Published by Elsevier Inc.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2019.07.003

Case Report
A 72-year-old male with a past medical history of
hypertension, diabetes, and COPD, was transferred from
an outside hospital for evaluation of abnormal movements of the right upper extremity. He was noted to have
involuntary, nonrhythmic, flailing, uncontrollable movements of the right upper extremity. Noncontrast CT scan
of the head was without acute findings. Metabolic, infectious, and toxic encephalopathy was ruled out. He was
treated with Keppra 1 g BID for possible seizures without
improvement of his symptoms. The patient was subsequently transferred to our hospital for further care.
Upon evaluation he had persistent right-sided hemichorea-hemiballistic movements as described above. The
movements were absent during sleep. An EEG was negative for epileptiform changes. An MRI of the brain without contrast demonstrated patchy areas of restricted
diffusion consistent with acute infarcts in the left parietooccipital region (Fig 1). MRA of the head and neck ruled
out stenosis or occlusions. Aspirin 81 mg daily and a high
dose statin were initiated for secondary stroke prevention.
Laboratory investigations including HIV, ANA, lupus
anticoagulants, ASO antibodies, RPR, and ceruloplasmin
levels were within normal limits. The patient’s hemiballismus improved with initiation of Clonazepam. Keppra
was subsequently discontinued. His hospital course was

Journal of Stroke and Cerebrovascular Diseases, Vol. 28, No. 10 (October), 2019: 104287

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Figure 1. Diffusion-weighted MRI brain.

complicated by pneumonia and MRSA bacteremia with
septic shock, which correlated with an acute worsening of
his hemiballismus associated with increased amplitude
and frequency. A repeat EEG returned negative for seizure activity. Paroxysmal atrial fibrillation was noted during his ICU stay which was treated appropriately. Mild
improvement with residual hemiballismus was noted. He
was discharged on clonazepam with planned outpatient
follow-up.

Discussion
Subcortical ischemic strokes are most commonly
reported to cause hemichorea-hemiballismus.1-3 Infarcts
classically involve the contralateral subthalamic nucleus.
Pure cortical strokes causing hemichorea-hemiballism are
rare and infrequently reported. The prognosis is however
better in patients with cortical strokes, as the rate of disappearance of hemichorea is significantly higher than in those
with subthalamic lesions.1 The proposed pathophysiologic
mechanism of our patient’s movement disorder is suspected to be from interruptions of the intercortical and/or
cortical-ganglionic connections. A study using lesion

network mapping techniques showed that although lesions
identified in cases of hemichorea-hemiballismus were heterogeneous in location, a shared network was present.4 The
patient’s hospitalization was complicated by sepsis with
multiple metabolic derangements which likely exacerbated
his involuntary movements. Our case highlights that
lesions outside of the subthalamic nucleus can result in
hemichorea-hemiballismus.

References
1. Chung SJ, Joo-Hyuk Im, Lee Myoung C, et al. Hemichorea
after stroke: clinical-radiological correlation. J Neurol
2004;251:725-729.
2. Alarcon F, Zijlmans JCM, Duenas G, et al. Post-stroke
movement disorders: reports of 56 patients. J Neurol Neurosurg Psychiatry 2004;75:1568-1574.
3. Ghika-Schmid F, Ghika J, Regli F, et al. Hyperkinetic
movement disorders during and after acute stroke:
the Lausanne Stroke Registry. J Neurol Sci 1997;146:
109-116.
4. Laganiere Simon, Boes Aaron D, Fox Michael D. Network
localization of hemichorea-hemiballismus. Neurology
2016;86(23):2187-2195.