Post-stroke hemiballismus and Contralateral
Report of two cases
Dr. Fernando Alarcón1, Dr. Michael
Andrade1, Dr. José Rivera1, MD
Involuntary abnormal movements may occur as part of the
symptomatology of acute stroke or may be delayed or progressive.
We report two cases of post-stroke hemiballismus and
contralateral tremor. Both patients presented acute
hemiballismus. In one of the patients, the tremor started with
acute symptomatology and the other was delayed. We discuss the
possible pathogenic mechanisms for their movement disorders. To
our knowledge, this is the first report of two cases with the
unusual presentation of post-stroke hemiballismus and
Key words: Hemiballismus,
Contralateral tremor, Pathophysiology, Stroke.
Movimientos involuntarios anormales pueden presentarse como
parte de la sintomatología de la enfermedad cerebrovascular
aguda o pueden ser de inicio tardío o progresivo. Reportamos dos
casos de hemibalismo y temblor contralateral después de
enfermedad cerebrovascular aguda. Ambos pacientes presentaron
hemibalismo agudo. En un paciente el temblor se inició en forma
aguda y en otro fue tardía. Discutimos los posibles mecanismos
patogénicos para sus desórdenes del movimiento. A nuestro
conocimiento, éste es el primer reporte de dos casos con la
presentación inusual de hemibalismo y temblor contralateral
después de una enfermedad vascular cerebral.
Palabras clave: Hemibalismo,
Temblor contralateral, Patofisiología, Enfermedad vascular
Rev. Ecuat. Neurol. Vol. 15, No 2-3, 2007
Chorea and ballismus often coexist and usually involve
hemibody.1 Chorea is reported as the most frequent post-stroke
involuntary movement.2, 3 It is often thought that
hemiballismus is caused most commonly by a lesion in the
contralateral subthalamic nucleus (STN),1 but the
localization is usually elsewhere.1-5 The pathogenesis of
hemiballismus has not as yet been sufficiently elucidated.1
Lesions in the thalamus, basal ganglia, brainstem,
cerebellum, white subcortical matter and cortex have been
associated with post-stroke tremor.6-8 Action tremor occurs
with lesions in the cerebellum or in their outflow tracts.9
Vascular Parkinsonian tremor may share a pathogenic basis
identical to those associated with idiopathic Parkinsonism.10
In February 2003, while watching TV, an 80-year-old
hypertensive, right-handed male developed sudden, mild left
hemiparesis. In 1998, he had sudden ataxia of right limbs
and gait, from which he recovered in three months. Since
1998, the patient had been taking antihypertensive drugs and
aspirin on a regular basis. The patient and his wife
indicated that, one month after the stroke of 1998, he
presented with occasional mild right-hand tremor when he
At the Emergency Room, the patient’s initial blood pressure
was 200/110 mmHg. On neurological examination, the patient
was alert and oriented and had mild left hemiparesis. In the
hours following admission, the patient developed ballistic
movements on the left side. He did not have any anosognosia
or abnormal cortical sensations (two-point discrimination
and stereognosis). Over the next weeks, his hemiballismus
gradually worsened. He was treated with Haloperidol, up to
10 mg per day, with minimal improvement in abnormal movement.
Three weeks after admission, the patient was
able to walk with difficulty and was then discharged. MRI
scan was obtained four days after admission and showed in
T2- Flair a right cerebellar hemisphere atrophy, secondary
to an old infarct (figure 1), and infarcts at the gray-white
matter junction in the frontal and parietal regions (figure
Figure 1: Axial T1W MR scan shows right
cerebellar hemisphere atrophy secondary to an
Figure 2: Axial FLAIR contiguous MR images show
hyperintense ischemic lesions in the
supratentorial white matter and right infarcts
at the gray-white matter junction in the frontal
and parietal regions.
Echocardiogram showed hypertrophy of the left
ventricle and did not show evidence of thrombus formation. A
carotid echo-doppler scan and complete blood test results
were unremarkable. The patient had no history of treatment
with neuroleptic drugs or exposure to toxins. There was no
family history of movement disorders.
During the next months, the patient took
Haloperidol, Olanzapine, Risperidone, Quetiapine, Clozapine,
Mirtazapine and Clonazepan until he reached the maximum dose.
In February 2004, the patient presented with a progressive
form of postural and kinetic tremor in his upper right limb.
Four weeks later, the tremor became disabling. There was no
rest hand tremor or cogwheel rigidity in his right hand. The
tremor was from 3 to 5 Hz and was shown as an irregular
oscillation in an intended direction and was more prominent
toward the end. A new MRI did not show new vascular lesions
compared to that of February 2003. The patient had a partial
improvement of the tremor and the hemiballismus, until the
last follow-up in May 2005.
A 78-year-old right-handed woman, who developed dysarthria
and left hemiparesis-hemihypoesthesia while taking a nap. In
the Emergency Room, the patient had a blood pressure of
190/105 mg Hg. Twelve hours later, she suddenly and
progressively presented with ballistic movements in the left
hemibody, with greater proximal severity in the upper limb.
In the following three weeks, the hemiballismus disappeared
spontaneously. On the third day after admission to the
hospital, she progressively presented with intermittent rest
and postural tremor of the right hand, which in less than 48
hours tended to become permanent. The rest tremor that
appeared only during the day at a frequency of 4-7 Hz was
characterized by flexion-extension movements of all the
right fingers, mainly at the metacarpophalangeal joints.
Occasional mild adduction-abduction movements
of the fingers were also noticed. The tremor had a tendency
to be more prominent when the patient remained at rest with
the arm and especially the hand on her bed or body. The
postural tremor was intermittent, at a frequency of 4-6 Hz,
and was more intense when the patient used the right hand
and diminished when she moved her left arm, talked or
focused attention on other activities. There was no cogwheel
rigidity. At the last follow-up a year after the stroke, the
patient was walking and her tremor did not show any
Magnetic Resonance Imaging (MRI) was obtained
three days after admission and showed in T2-Flair ischemic
foci in the pontine tegmentum, and bilateral globus pallidus
(figure 3). The angioresonance showed segmentary narrowing
in the proximal segment of the left posterior cerebral
artery, suggesting atheromatosis. The echocardiagram showed
myocardiosclerosis. Complete blood test results were
unremarkable. The patient did not have any history of
movement disorders, nor had she been administered any
neuroleptic drugs or been exposed to toxins.
Lesions affecting the afferent or efferent pathways of the
STN may result in hemiballismus.1-5 In our patient 1, the
infarcts in the frontal and parietal lobes may have induced
changes in the firing patterns of the neural fibers being
projected to the basal ganglia, reducing the excitatory
inputs from the STN to the pars intern of the globus
pallidus, which in turn disinhibits the thalamus and cortex
resulting in hyperkinetic movement.1 In patient 2, the
bilateral lesion in the globus pallidus could explain the
pathophysiology of hemiballismus.1-3
Figure 3: Axial FLAIR MR scan demonstrates small
bilateral high signal intensities in the globus
pallidus, in relation with ischemic foci.
Action tremor in the ipsilateral upper
extremities occurs with lesions in the nucleus dentate and
interposittus or brachium conjunctivum.9 Patient 1 showed
action tremor, which has characteristics similar to those of
cerebellar tremor.9 These tremors occur, as a result of the
loss of cerebellar influence in motor control,9 and appears
to be a result of an excessive reliance on feedback control,
which results in abnormal mechanical reflex oscillation.9
The increase in severity of tremor until it is disabling,
after the second stroke, may be related to neuroleptic drugs
used to treat hemiballismus, to certain changes in brain
plasticity,3 or the development of post-synaptic denervation
supersensitivity and release of the inferior olive.11 Our
patient 2 had a Parkinsonian rest tremor, characterized by a
rhythmic “pill-rolling”- ype finger tremor. Her tremor,
however, was less monotonous than Parkinsonian tremor and
occurred more intermittently.
Our patient did not have rigidity or
bradykinesia and therefore could not be classified as having
a vascular Parkinsonism. 3 In spite of this, her rest tremor
may share a pathogenic basis similar to the tremor of
idiopathic Parkinsonism. In this patient, the genesis of the
rest tremor could be the result of a thalamic dysfunction,10,
11 secondary to pallidal or midbrain damage.7
The coexistence of two movement disorders in
the same patient suggests an imbalanced bilateral
integration of the ganglia-sensorimotor cortex circuits.
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