Saudi Journal for Health Sciences

: 2014  |  Volume : 3  |  Issue : 3  |  Page : 179--181

Hemiballism following putaminal hemorrhage

Ishrat Hussain Dar, Faiz Ahmed Kuchaai, Samia Rashid Mir, Showkat H Dar 
 Department of Medicine, Goverment of Medical College, Srinagar, Jammu and Kashmir, India

Correspondence Address:
Ishrat Hussain Dar
Department of Medicine, Government Medical College, Srinagar - 190 010, Jammu and Kashmir


Movement disorders occur uncommonly after stroke and include both hyperkinetic and parkinsonian conditions. They can occur at the time of stroke or appear as later manifestations. Post-stroke hemiballism is an uncommon involuntary hyperkinetic disorder involving unilateral body parts. The incidence and precise lesion location of post-stroke hemiballism remain unclear. Cerebrovascular disease, particularly hemorrhage, due to the involvement of middle or posterior cerebral artery or vessels supplying the basal ganglia are commonly implicated in the causation of movement disorders. Deep vascular lesions are more frequent in patients with movement disorders. Chorea or hemiballism is a rare presentation of putaminal hemorrhage and is the most common movement disorder to appear in older patients. Involuntary movements tend to persist despite good functional recovery of the motor deficit. Presented here is a case of hemiballism in a 74-year-old man, who had a hemorrhagic stroke.

How to cite this article:
Dar IH, Kuchaai FA, Mir SR, Dar SH. Hemiballism following putaminal hemorrhage.Saudi J Health Sci 2014;3:179-181

How to cite this URL:
Dar IH, Kuchaai FA, Mir SR, Dar SH. Hemiballism following putaminal hemorrhage. Saudi J Health Sci [serial online] 2014 [cited 2021 Jun 13 ];3:179-181
Available from:

Full Text


Hemiballism is a relatively rare hyperkinetic disorder characterized by irregular wide amplitude, vigorous movements of the limbs primarily due to involuntary activity of the proximal limb and associated axial muscles. [1] Hemiballism has an incidence of 1 in 500000 in the general population and only 0.7% of patients with movement disorders have this type of dyskinesia. [2] The most consistent neuropathological finding in hemiballism is a lesion of the contralateral sub thalamic nucleus usually of vascular origin but high resolution neuro- radiological imaging has provided evidence of lesions elsewhere like globus pallidus, striatum, thalamus, cerebral cortex and internal capsule. [3] Chorea is defined as an arrhythmic involuntary movement, which intrudes in a sudden, brief and non-repetitive fashion and appear to move from one muscle to another typically worsened by volitional movements.


A 74-year-old elderly hypertensive male was admitted to our hospital with 1 day history of weakness of the right upper and lower limb associated with dysarthria and mild headache without history of loss of consciousness, alteration of sensorium, convulsions or incontinence of urine and feces. General physical examination was unremarkable and vitals revealed a pulse of 74/minute with a blood pressure of 180/110 mm Hg. Examination revealed a normal chest, cardiovascular and abdominal systems. Central nervous system examination revealed a conscious, co-operative well-oriented male without any cranial nerve palsy. Fundus examination showed grade II arteriosclerotic changes and motor examination revealed mild weakness on the right side (power grade 3+) with an up going plantar on the right side. Routine blood investigations (complete blood count [Table 1], blood sugar, kidney function tests, liver function tests, electrolytes and lipid profile) were normal. Urine examination, electrocardiogram (ECG), [Table 2]. X-ray chest and ultrasound abdomen were all normal. A non-contrast computed tomography (CT) scan [Figure 1] taken showed a small left putaminal bleed. Patient was started on conservative management in form of antihypertensive drugs, oral glycerol and physiotherapy in view of the small bleed. On the 4 th day of hospitalization, patient developed wide flinging movements of the right upper and lower limb, which were hemiballistic in nature (Video). A diagnosis of hypertension, left putaminal bleed, right hemiparesis and hemiballism was made and the patient was started on dopamine receptor blockers in form of haloperidol. Marginal improvement in symptoms was noted at the end of two weeks on follow-up and risperidone was subsequently added, which provided better control of hemiballism. The patient continues to be on regular follow-up till date.{Figure 1}{Table 1}{Table 2}



Involuntary abnormal movements (IAM) caused by strokes are relatively uncommon and chorea, tremor (Holme's, tremor, Palatal tremor), dystonia, parkinsonism, tics, asterixis and myoclonus have all been described and associated with both infarcts and cerebral hemorrhage and may occur acutely or as a delayed manifestation. [4] Hemorrhagic strokes appear to cause more movement disorders than ischemic ones. Hemiballism/hemichorea is the most common movement disorder reported to occur after stroke present in 40% of cases in a case series. [5] Hemiballism is characterized by vigorous, irregular, poorly patterned, high- amplitude movements of the limbs on one side of the body and is often viewed as a severe type of chorea. Besides hemiballism, ballism can involve one limb (monoballism) or all the limbs (biballism or paraballism). The majority of patients with hemiballism have both choreic and ballistic movements. [2],[6] It has been reported that 72% cases of hemiballism are caused by stroke, with an average age at onset for stroke induced hemiballism of 66 years. [3] Among patients with post- stroke hyperkinetic movement disorders, one of the most common is the lower amplitude hemichorea with a prevalence of one in every 200 stroke patients. After stroke, hemichorea correlates with motor weakness and mild sensory symptoms and is often accompanied by athetosis. Individuals with post stroke chorea tend to be older than those with other post stroke movement disorders. [7] About 80% of patients with hemiballism experience immediate onset after stroke, whereas in the others it is delayed by days, weeks or months the longest reported delay being 5 months. [3] Our patient presented with hemiballism/hemichorea within 4 days of stroke occurrence. Jones et al. first described a patient with hypertensive putaminal hemorrhage presenting with hemichorea. [8] A close association between hemiballism and lesions of the contralateral subthalamic nucleus was recognized by the turn of the century. A pathophysiological explanation for hemiballism due to subthalamic nucleus lesion proposed the loss of an excitatory subthalamic influence on the internal segment of the globus pallidus. [1] Cases with hemiballism are more often associated with a lesion that affected the afferent and efferent pathways of the subthalamic nucleus or its projection areas as well as the striatum, thalamus and the cerebral cortex. Most lesions that induce hemiballism are of vascular origin. Ischemic and hemorrhagic strokes were identified as a cause of involuntary movements in 72% of patients and virtually any structural lesion if properly situated could induce hemiballism, was confirmed by its association with metastatic tumors, multiple sclerosis, head trauma, tuberculoma, systemic lupus erythromatosus, scleroderma, transient ischemic attacks, subarachnoid hemorrhage, thalamotomy, syphilis, acquired immune deficiency syndrome, hyperglycemia, arteriovenous malformations, cerebral toxoplasmosis, neurodegenerative diseases, cystic glioma of the midbrain, basal ganglia calcifications and administration of oral contraceptives, levodopa, phenytoin and neuroleptics. [3] Altafullah and Nagakawa first reported two patients with non-ketotic hyperglycemic chorea, whose neuroimages had faintly increased densities over the contralateral basal ganglion suggesting petechial hemorrhage and they proposed that non-ketotic hyperglycemia complicated by multiple putaminal petechial hemorrhage was the cause of hemichorea and since then it has been generally accepted that non-ketotic hyperglycemia is the cause of putaminal hemorrhage manifesting with chorea. [9],[10] Cava et al. described two cases of acute hemiballism-hemichorea associated with basal ganglion hemorrhage in two females, with uncontrolled diabetes mellitus and non-ketotic hyperglycemia. [11] Smoking has been seen to worsen the hemiballism-hemichorea symptoms as has been reported by Mochizuki from Japan in a case of putaminal bleed with hemiballism-hemichorea. [12] Polycythemia vera has been reported to cause hemichorea in one reported case from India by Bhagava et al. [13] Size of the putaminal hemorrhage has no bearing on the development of hemiballism-hemichorea and the small hematoma syndrome with chorea as the cardinal manifestation has been described lately. The small hematoma is very dense and homogenous and is not restricted to the putamen and the head of the caudate nucleus. Our patient too had a similar presentation with a very small hematoma but profound hemiballism/hemichoric symptoms. A CT brain of a similar elderly female patient with a larger sized hemorrhage in the same area on the same date who did not develop hemiballism - hemichorea is provided for comparison [Figure 2]. Patients with post stroke hemichorea tend to have magnetic resonance imaging (MRI) hyperintensities in the basal ganglia, particularly the putamen. A clinical and radiological correlation study showed that the subthalamic nucleus, caudate, putamen and cortical lesions contralateral to the affected side were the sites most commonly associated with hemichorea, a localization that is similar to hemiballism. [7] Ballism and chorea typically respond to the same therapies and the commonly reported pharmacological therapies have been the dopamine receptor blocker agents particularly haloperidol. Resolution of symptoms with this drug usually takes 3-15 days. Other reported treatment options include diazepam, clonazepam, topiramate, tetrabenzine, valproic acid and in severe and persistent cases local intramuscular injections of botulinum toxin or ventrolateral thalamotomy. Risperidone is used in place of haloperidol in some cases to minimize the side effects of the latter drug. 56% of patients have complete resolution within 40 days, but some patients have chorea as long as 41 months, despite multiple treatment options. [3],[6]{Figure 2}


1Shannon KM. Hemiballismus. Clin Neuropharmacol 1990;13:413-25.
2Dewey RB Jr, Jankovic J. Hemiballism-hemichorea: Clinical and pharmacological findings in 21 patients. Arch Neurol 1989;46:862-7.
3Vidakovic A, Dragasevic N, Kostic VS. Hemiballism: Report of 25 cases.J Neurol Neurosurg Psychiatry 1994;57:945-9.
4Alarcon F, Zijlmans JC, Duenas G, Cevallos N. Post stroke movement disorders: Report of 56 patients. J Neurol Neurosurg Psychiatry 2004;75:1568-74.
5Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry. J Neurol Sci 1997;152:109-16.
6Bansil S, Prakash N, Kaye J, Wrigley S, Manata C, Stevens-Haas C, et al. Movement Disorders after Stroke in Adults: A Review. Tremor Other Hyperkinet Mov (N Y) 2012;2.
7Chung SJ, Im JH, Lee MC, Kim JS. Hemichorea after stroke: Clinical-radiological correlation. J Neurol 2004;251:724-9.
8Jones HR JR, Baker RA, Kott HS. Hypertensive putaminal hemorrhage presenting with hemichorea. Stroke 1985;16:130-1.
9Altafullah I, Pascual-Leone A, Duvali K, Anderson DC, Taylor S. Putaminal hemorrhage accompanied by hemichorea-hemiballism. Stroke 1990;21:1093-4.
10Nagakawa T, Mitani K, Nagura H, Bando M, Yamanouchi H. Chorea- ballism associated with non ketotic hyperglycemia and presenting with bilateral hyperintensity of the putamen on MR T1 weighted images: A case report. Rinsho Shinkeigaku 1994;34:52-5.
11Cava PA, Kowacs PA, Werneck LC. Hemichorea-hemiballism associated to basal ganglia hemorrhage in uncontrolled diabetes mellitus: Report of two cases. Arq Neuropsiquiatr 1996;54:461-5.
12Mochizuki H, Miwa H, Imai H, Muzuno Y. Hemiballism-hemichorea caused by a putaminal hemorrhage with worsening after smoking- A case report. Rinsho Shinkeigaku 1993;33:562-4.
13Bhargava R, Dass J, Singh S, Vaid A. Hemichorea, a rare presenting feature of polycythemia vera. Neurol India 2013;61:86-7.