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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 4  |  Page : 1138-1139

Upper Limb Monochorea Due to Cerebral Venous Sinus Thrombosis: Rare Occurrence

Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru, Karnataka, India

Date of Web Publication10-Sep-2019

Correspondence Address:
Dr. Rohan Mahale
Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru - 560 054, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.266255

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How to cite this article:
Mahale R, Mehta A, Konnur A, Acharya P, Srinivasa R. Upper Limb Monochorea Due to Cerebral Venous Sinus Thrombosis: Rare Occurrence. Neurol India 2019;67:1138-9

How to cite this URL:
Mahale R, Mehta A, Konnur A, Acharya P, Srinivasa R. Upper Limb Monochorea Due to Cerebral Venous Sinus Thrombosis: Rare Occurrence. Neurol India [serial online] 2019 [cited 2021 Jan 19];67:1138-9. Available from:


Movement disorders can be the presenting manifestation of stroke. They have been associated with both infarct and cerebral hemorrhage of arterial origin.[1] It can be hyperkinetic or hypokinetic movement disorders. The most common hyperkinetic movement disorder in stroke is hemichorea (HC) and hemiballism (HB). HC is a unilateral continuous, random, and distally predominant jerking movement that may involve proximal muscles.[1] Rarely a patient may have chorea in only one limb, known as monochorea or focal chorea. Cerebral venous thrombosis (CVT) is an uncommon cause of stroke with different clinical presentations.[2] Hyperkinetic movement disorder in the form of HC or monochorea has not been described in CVT. Hereby, we report a middle-aged man who presented with headache and right upper limb monochorea and found to have bilateral fronto-parietal hematoma due to superior sagittal sinus and right transverse sinus thrombosis.

A 46-year-old man presented with a history of the headache of 1 week duration and involuntary movements involving right upper limb of 2 days duration. Headache was new onset and acute, right hemicranial becoming holocranial, throbbing type, lasting for hours, aggravating on coughing and straining, exposure to sounds, relieving with analgesics associated with episodes of vomiting. Headache increased in severity 2 days before admission. Patient also developed abnormal involuntary, random, irregular, continuous, more prominent on action than rest, hyperkinetic movements involving right upper limb of 2 days duration. There were no seizures, weakness of limbs, sensory disturbances, or fever. He used to consume alcohol thrice a week and cigarette smoker. There were no other comorbidities. The systemic examination was unremarkable. He was conscious, disoriented to time and place, used to follow simple verbal commands. Fundus examination showed papilledema. Cranial nerves examination was normal. Motor examination revealed hypotonia of right limbs and hyporeflexia of right limbs. There were irregular, coarse, continuous, rapid, large-amplitude, nonsuppressible, involuntary movements, which were more prominent on action than rest involving right upper limb suggestive of right monochorea [Video 1]. Computed tomography (CT) of brain showed multiple bilateral fronto-parietal hematomas. Magnetic resonance venogram of brain showed multiple bilateral fronto-parietal hematomas and nonvisualization of superior sagittal sinus and right transverse sinus [Figure 1] and [Figure 2]. Complete hemogram, renal, liver, and thyroid function tests were normal. Serological testing for human immunodeficiency virus, hepatitis B surface antigen, and venereal disease research laboratory was negative. Serum antinuclear antibodies and antiphospholipid were negative. Serum homocysteine levels were high. He was started on low-molecular weight heparin bridged with oral anticoagulant and carbamazepine (400 mg daily) for chorea. At the time of discharge, his headache got subsided and there was mild choreiform movement involving right upper limb.
Figure 1: Brain MRI fluid attenuated inversion recovery (FLAIR) axial images (a-c) show multiple bilateral fronto-parietal hypointense lesions with surrounding hyperintensity and subarachnoid hemorrhages (red arrows); T1 sagittal view (d) shows isodense lesion in parietal region (red arrow); T2* gradient-echo axial images (e) and (f) show multiple bilateral fronto-parietal hematomas (red arrows)

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Figure 2: MR venogram brain (i) and (ii) show nonvisualization of superior sagittal sinus and right transverse sinus (red arrows)

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Ischemic or hemorrhagic lesions of the basal ganglia can cause vascular HC. The prevalence of HC in acute arterial stroke is 1% and incidence ranges between 0.4% and 0.54%.[3] The more common site of lesion causing HC is corpus striatum. Other sites causing HC are cortical, thalamic, and subthalamic regions.[4] Infarcts in following arterial territories cause HC: lateral lenticulostriate branches of middle cerebral artery; thalamoperforators, thalamogeniculate, and choroidal arteries of posterior cerebral artery; and recurrent artery of Huebner of anterior cerebral artery.[1] The usual location for monochorea due to arterial stroke has been reported in the subthalamic nucleus, putamen, caudate nucleus, and thalamus. Cerebral venous sinus thrombosis (CVST) has varied clinical presentation and is difficult to diagnose on clinical grounds only unlike arterial infarct. Headache is the most common symptom. Other manifestations include altered level of consciousness, seizure, and focal deficits in the form of hemiparesis.[2] CVST causing monochorea has not been reported. Lesions involving contralateral striatum interrupt inhibitory gamma-aminobutyric acid pathways to the globus pallidus externa (GPe) resulting in increased GPe neuronal activity. The increased inhibitory GPe neuronal activity causes greater inhibition of neurons within the STN. Increased inhibition of the STN leads to a loss of excitatory control over the globus pallidus interna (GPi) causing disinhibition of the motor thalamus. The deficient GPi inhibitory input to the motor component of the thalamus results in excessive thalamocortical motor movement causing hyperkinetic movements.[5]

Arterial infarct or hemorrhage is known to cause HC and monochorea. Venous thrombosis causing monochorea has not been reported. The present case reports the rare occurrence of monochorea due to CVST. The pathophysiology of chorea and location of the lesion producing it are not fully understood.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Handley A, Medcalf P, Hellier K, Dutta D. Movement disorders after stroke. Age Ageing 2009;38:260-6.  Back to cited text no. 1
Dash D, Prasad K, Joseph L. Cerebral venous sinus thrombosis: An Indian perspective. Neurol India 2015;63:318-28.  Back to cited text no. 2
[PUBMED]  [Full text]  
Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry. J Neurol Sci 1997;146:109-16.  Back to cited text no. 3
Pareés I, Hernández-Vara J, Álvarez-Sabín J. Post-stroke hemichorea: Observation-based study of 15 cases. Rev Neurol2010;51:460-4.  Back to cited text no. 4
Chung SJ, Im JH, Lee MC, Kim JS. Hemichorea after stroke: Clinical-radiological correlation. J Neurol2004;251:725-9.  Back to cited text no. 5


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