1226

ORIGINAL ARTICLE

Ballism After Stroke Responds to Standard Physical
Therapeutic Interventions
Victor W. Mark, MD, Anne Marie Oberheu, MD, Cathy Henderson, PT, MS, Adam J. Woods, BS
ABSTRACT. Mark VW, Oberheu AM, Henderson C,
Woods AJ. Ballism after stroke responds to standard physical
therapeutic interventions. Arch Phys Med Rehabil 2005;86:
1226-33.
Objective: To report the effects of noninvasive standard
physical therapy (PT) interventions on an involuntary movement disorder after stroke.
Design: Single case with clinical follow-up over 2 years.
Setting: Inpatient stroke and rehabilitation services and outpatient clinic.
Participant: A man with acute bilateral ballism after unilateral subthalamic infarction.
Interventions: Rhythmic coordinated bilateral limb movements and firm tactile stimulation to the hand.
Main Outcome Measures: We had not anticipated that
dyskinesia itself would specifically improve during treatment.
Consequently, we used qualitative clinical observations, including review of videotaped performance, and self-reported
limb control. Hypotheses concerning treatment effects were
developed after data collection.
Results: Involuntary movements recurrently improved
within treatment sessions.
Conclusions: PT may improve dyskinesia after stroke. The
benefit may be adjunctive or alternative to current invasive
treatments of movement disorders after brain injury and merits
confirmation. The improvements are consistent with current
research indicating that (1) intact cortical, subcortical, cerebellar, and spinal areas interact to generate bilateral rhythmic limb
movements that can overcome dyskinesia and (2) tactile stimulation can improve motor deficits associated with basal ganglia disorders. Finally, because functional activities assessments improved our evaluation of ballism, these should be
routinely used along with conventional neurologic examination
to assess involuntary movement disorders.
Key Words: Activities of daily living; Ballismus; Cerebrovascular accident; Rehabilitation; Subthalamic nucleus.
© 2005 by American Congress of Rehabilitation Medicine
and the American Academy of Physical Medicine and
Rehabilitation

From the Departments of Physical Medicine and Rehabilitation (Mark, Oberheu,
Woods) and Rehabilitation Services (Henderson), University of Alabama,
Birmingham, AL. Henderson is currently affiliated with Methodist Rehabilitation
Center, Spinal Injury Program, Jackson, MS; Woods is currently affiliated with the
Department of Neurobiology and Developmental Sciences, University of Arkansas
for Medical Sciences, Little Rock, AR.
Supported in part by the National Institutes of Health (grant nos. R03 AG21256-01,
R03 HD042519-01 A1, R01 HD34273-04-05, R01 NS39348-01A2) and the John
Hartford Foundation/Southeast Center of Excellence in Geriatric Medicine.
No commercial party having a direct financial interest in the results of the research
supporting this article has or will confer a benefit on the author(s) or on any
organization with which the author(s) is/are associated.
Reprint requests to Victor W. Mark, MD, Dept of Physical Medicine and Rehabilitation, University of Alabama, 619 19th St S, SRC 190, Birmingham, AL 252497330, e-mail: vwmark@uab.edu.
0003-9993/05/8606-9308$30.00/0
doi:10.1016/j.apmr.2004.08.013

Arch Phys Med Rehabil Vol 86, June 2005

EMIBALLISM IS AMONG the most impressive of the
rarely encountered “hyperkinetic” movement disorders
H
that can follow cerebral infarction, consisting of the involun1

tary, erratic flinging of the proximal limbs on 1 side. It is most
commonly associated with a lesion in or near the contralateral
subthalamic nucleus,2 although other solitary lesion sites have
also been implicated.3 The bilateral presentation of this movement disorder, which may be simply termed ballism, is less
often described.4,5 Clinical reports3,4,6,7 of ballism with neuroanatomic findings have generally indicated bilateral focal structural lesions or diffuse injury. However, a few case reports4,8
have associated ballism with strictly a unilateral lesion.
Case studies seldom describe the functional effects of ballism. Self-inflicted soft-tissue or skeletal injuries have been
reported.4,7,9-12 Some studies9,13 have indicated interference
with eating, writing, speaking, buttoning, and walking, but
functional assessment tools were not indicated. Published treatments of persisting ballism have been limited to pharmacologic
or surgical interventions14,15 and have not evaluated responses
to physical therapy (PT). Although specific medications are
often effective, side effects frequently occur.14 Stereotactic
neurosurgery (eg, pallidotomy) is reserved for refractory cases
and is highly successful for ameliorating symptoms yet is
associated with residual functional impairment in 30% of patients.15 Ballism of vascular etiology resolves within several
months in most cases, with or without invasive treatment.14
However, patients with ballism after stroke have an increased
risk of stroke recurrence and mortality, as is consistent with
stroke in general. One study16 found a survival rate after
vascular ballism of 51% at 36 months and 32% at 150 months.
We recently observed acute bilateral ballism after unilateral
subthalamic nucleus infarction in a patient. We followed the
movement disorder’s interference with his functional activities
over 2 years and report the favorable response to noninvasive
therapeutic interventions, which we had not anticipated. Because we did not have access to physiologic instruments that
could have objectively assisted this evaluation (eg, movement
analysis kinematics), our report relies on clinical observation
and self-report. Nonetheless, our observations suggest that
noninvasive rehabilitation techniques may at least temporarily
ameliorate the symptoms, which could improve treatment participation and outcomes. These findings merit verification in
other patients with ballism.
METHODS
Acute Patient Presentation
A 66-year-old right-handed retired salesman, previously
functionally independent, awoke one morning with right-sided
involuntary limb jerks that were precipitated by intentional
movement, affecting the arm more than the leg. He also noted
impaired speech fluency and word retrieval. He was admitted
to our institution’s acute stroke service on the same day.
The patient’s medical history included multiple vascular
disease risk factors (diabetes, hypertension, hyperlipidemia,
recurrent myocardial infarction, smoking) and several episodes
of left facial weakness during the preceding 20 years that had

BILATERAL BALLISM, Mark

Fig 1. MRI sequences from the patient. (A–C) Consecutive FLAIR
sequences. Arrow indicates abnormal signal. (D) FLAIR sequence
above the lateral ventricles. (E) Diffusion-weighted sequence at the
same level as B. (F) Adjusted diffusion coefficient map at the same
level. Division marks equal 1cm.

lasted up to a few days each. The most recent cerebral magnetic
resonance imaging (MRI) study from 2 years before the present
admission (when the patient had last experienced facial weakness) had shown microangiopathic changes but no infarction.
The patient’s admission medical examination indicated bilateral involuntary limb movements (detailed below), modest
right hemiparesis (diffusely 4/5 power by Medical Research
Council criteria17), and a 50% reduction in light touch appreciation on the right hand and face when compared with the left
side. Joint position sense and pin appreciation were preserved
in all limbs. No other cranial nerve deficits were present.
Confrontational visual fields to finger counting were full without extinction. Myotatic reflexes18 were brisk on the right,
normal on the left. Plantar responses were flexor. Admission
blood test results were unremarkable apart from moderately
elevated serum glucose (182mg/dL). The chest radiograph examination result was normal.
MRI on the day of admission showed a bright signal in the
left subthalamic nucleus on the fluid-attenuated inversion recovery (FLAIR) sequence (figs 1A–C), as well as extensive
bilateral supraventricular white matter disease (fig 1D). The
diffusion-weighted imaging (DWI) sequence and apparent diffusion coefficient maps indicated signal changes only in the left
subthalamic nucleus (figs 1E, 1F). These findings were compatible with acute ischemia.19
Transesophageal echocardiography showed a dilated left
atrium (43mm); thickened, nonstenotic mitral and aortic
valves; and normal ejection fractions. Four-vessel angiography
indicated a normal right carotid system, with persistent fetal
origin of the right posterior cerebral artery and mild stenosis at
the origin of the left internal carotid. The transcranial Doppler
examination result was completely normal, with no evidence of
hemodynamic abnormalities.
Rehabilitation Course
The patient’s neurologists decided against further intervention other than to add aspirin and clopidogrel to his medications. The patient was then transferred to our acute inpatient

1227

stroke rehabilitation service on day 6 of his illness. His impairments included mild word-finding deficits, impaired short-term
verbal memory, mild dysarthria, profound ambulatory deficits,
and inability to perform self-care tasks safely. The patient’s
wife thought the cognitive impairments originated with this
illness and have continued to the present. Formal neuropsychologic assessment yielded a normal score of 27 out of 30 on the
Mini-Mental State Examination,20 with deficits restricted to
delayed verbal recall. On the Boston Naming Test,21 the patient
named 54 out of 60 items, normal for his age.22 Tests of limb
praxis that were conducted after hospital discharge, while he
was still symptomatic from his movement disorder, showed
normal performance on the Florida Apraxia Screening Test
pantomimes to command,23 the imitating of meaningless hand
postures,24 and the reproduction of meaningless limb movement sequences.25 At no time were complex involuntary movements observed, such as mirror movements, disinhibited grasping, compulsive tool use, or intermanual conflict.
The patient consented to videotaping and investigational
evaluation of his motor progress during inpatient and outpatient
rehabilitation, as approved by our institution’s human subjects
research board. Involuntary movements seldom occurred at
rest, but attempts to actively move the right arm invariably
caused wide, erratic, and rapid gyrations of the proximal limb,
such that he once struck his face and repeatedly bruised his
right arm. The nondominant left arm displayed no such movements while the patient was supine at rest. However, simulated
shaving by his left hand with an unplugged shaver produced
jerky but noninjurious movements about the face. Rapid alternating movements (supination and pronation) and finger-tonose touching were bilaterally clumsy, right much more so than
left. The left hand also showed past-pointing that resolved with
a few reattempts. Occasional isolated jerks of the trunk appeared during limb movements. Although stuttering and wordfinding delays disrupted speech, there were no involuntary
movements of the eyes, face, oropharynx, or neck.
The bilateral reciprocal forearm rolling test26 was used to
evaluate motor control. The test simply requires rapid, antiphase cycling of both forearms in the same direction in the
midsagittal plane about a common focal point without synchronization to an external stimulus. Initially he showed wild,
dangerous excursions by the right arm and smaller movement
amplitude with the left. However, after continuing the maneuver for half a minute, the arm movements unexpectedly equalized, so that the right arm moved with reduced amplitude and
jerkiness, while the left arm amplitude increased. The movement disorder immediately worsened with reversed arm rotation, but again subsided with continuation.
Initially, the patient required moderate to maximal assistance
to come from sitting to standing and maximal assistance to use
a hemi-walker, because of interference from the concurrent
irregular movements. When he walked with 2 therapists as they
gripped his hands for support, all limbs showed proximal
ballistic movements at various times, more so on the right.
When he walked with a single-point cane in the right hand,
bilateral contact guard assistance of 2 therapists was required,
because the right hand and leg and his trunk shook severely.
Unexpectedly, however, when he supported himself with the
cane in his left hand, he required contact guard assistance from
only 1 individual, because the ballism had diminished. These
findings were reproducible.
The patient’s ambulatory training involved wearing a 5-lb
(2.3-kg) weight on his right leg and manually restraining the
right upper limb as he walked with a rolling walker. Nonetheless, flailing movements occurred repeatedly, requiring maximal assistance to maintain his safety. By day 8 after stroke
Arch Phys Med Rehabil Vol 86, June 2005

1228

BILATERAL BALLISM, Mark

Fig 2. Signatures from the patient according to day of illness and
hand. Only the top halves of the signatures are shown to conceal
the patient’s identity. All samples are to the same scale. Measurement bar equals 5cm.

onset, the movement disorder had reduced in weight-bearing
positions, such as when grasping a hemi-walker. Having the
patient walk in an intentionally rhythmic manner markedly
reduced the hyperkinesia within the therapy sessions. The
ballism gradually subsided during the hospital course.
Self-care activities were minimally impaired, but the patient
consistently relied on his nondominant left upper limb. Reaching was practiced with a 5-lb weight on the right wrist; however, the right upper limb would flail when he used an openchain movement sequence (absence of fixed distal limb contact
with a surface for weight bearing).27
Serial evaluation of our patient’s handwriting with both
hands (fig 2) showed that early in his illness he was completely
unable to put pen to paper with his right hand. His left hand
could sign his name legibly but with an irregular speed and
large strokes. The irregular motion of the right hand during
signing could not be ameliorated by having his left hand
simultaneously grip an object (a different pen). We did not
assess signing with the right hand while the left hand was
engaged in a closed-chain activity. During subsequent days
both hands improved in control and amplitude.
The patient’s initial FIM instrument28 score was 57, and by
discharge on the eighth inpatient rehabilitation day it had
improved to 82 (maximum score, 126). By this time he still
primarily used his nondominant hand for self-care, because fine
motor function in the right hand remained impaired. He required only minimal assistance from his wife to walk with a
standard rolling walker or to climb stairs, but he had to be
cautious, because ambulation without assistance provoked
right-sided ballism, especially in the lower limb. Similar to
earlier observations, the ballism abated when he gripped the
examiner’s hand with his left hand or gripped a walker with
both hands but not when he gripped the examiner’s hand with
his right hand. Coming from sitting to standing without assistance provoked truncal jerking, which required minimal to
moderate assistance for stability, but once up, he could safely
commence walking.
We treated the patient with 50mg/d of sertraline because of
its reported rapid and well-tolerated benefit for hemiballism.29
However, the severity of the movement disorder failed to
improve over a few months after hospital discharge while on
this medication.
Outpatient Course
The patient had outpatient therapy 3 hours a week for 1
month. Initially, self-care activities were performed primarily
Arch Phys Med Rehabil Vol 86, June 2005

with the left hand. He was noted to have a pronounced startle
affecting the trunk and proximal limb muscles when he was
surprised by visual or auditory stimuli. By this time he could
walk unassisted without tremor and did not need an assistive
device. The forearm rolling test was performed flawlessly.
Writing had improved such that his right-hand signature was
better controlled than that of the left hand (see fig 2). Although
he could feed himself independently, irregular proximal arm
tremors persisted on tasks that involved repetitious fine distal
movement of the right hand, particularly when he felt fatigued.
The facial and right-hand sensory impairments did not improve. By the end of outpatient therapy he had resumed his
pastime of fishing, and in the clinic he competently demonstrated casting with a rod and reel without losing standing
balance. He also resumed driving without difficulty. The patient was satisfied with his progress and terminated therapy.
The movement disorder and hemisensory deficit were
acutely exacerbated 5 months after illness onset, but he declined hospitalization. Conventional MRI studies at 6 and 10
months were unchanged. In our outpatient clinic at 6 months,
his speech was more dysfluent, and ballism was present in his
right upper extremity at rest. Because the patient had concurrent depression that had not responded to sertraline, the sertraline was changed to 75mg/d of venlafaxine (which, like sertraline, inhibits serotonin reuptake, but additionally inhibits
norepinephrine reuptake). The depression subsequently improved, but the movement disorder did not. On the 30-item
Motor Activity Log (MAL)30 amount of use scale, he rated his
right arm function at a mean of 3.6 and 3.1 (maximum score,
5.0) at 7 and 8 months into his illness, respectively, which
indicates moderate nonuse. At 10 months after illness onset his
stroke neurologist started him on 1mg of haloperidol twice
daily. Consistent with earlier reports,16,31 ballism severity was
reduced but not abolished. His MAL score improved to 4.3. At
11 months, a neurologist substituted 1mg of clonazepam 3
times a day for the haloperidol to avoid tardive dyskinesia, and
the patient noted further reduction of symptom severity. When
evaluated at 17 months, he indicated that he could control
right-sided involuntary movements by clenching a pocketknife
in his right pocket, and rhythmic walking continued to benefit
his gait. Postural stability during walking was better controlled
with a single-point cane in his left hand than in his right.
Speech remained hesitant. The patient terminated physiatric
follow-up at this time because he felt his recovery had plateaued.
On informal follow-up at 24 months after illness onset, he
indicated that the movement disorder was overall unchanged
but often fluctuated, in particular becoming aggravated when
he was in crowded settings such as church. He had experienced
3 falls from sudden dyskinesia-associated imbalance in the
preceding 3 months, fracturing his right shoulder at one point.
He reported no further improvement from the clonazepam and
continued to ameliorate his involuntary movements by grasping a pocketknife with his right hand. He continued to be
followed up by his stroke neurologist twice yearly, but without
further medication changes.
DISCUSSION
Our case has several notable findings. One, detailed neuroimaging suggested an acute unilateral infarction that apparently
precipitated bilateral ballism. Two, the functional impact of the
ballism is described in considerably more detail than in previous reports. Three, the ballism was ameliorated by noninvasive
therapeutic techniques, which has not been reported.

BILATERAL BALLISM, Mark

Neuroimaging Findings and Anatomic Relationships
DWI is more sensitive than conventional MRI to cerebral
infarction.32 Our patient apparently had acute infarction confined to the left subthalamic nucleus, despite bilateral motor
signs. Previous studies of bilateral ballism did not use this
imaging technique, although patients with unilateral ballism
that follows marked hyperglycemia have shown DWI findings
similar to ours.33 The symptom exacerbation that occurred at
the fifth month of the illness was most likely caused by recurrent subthalamic infarction that was not visible on standard
MRI.
Most contemporary reviews of the subthalamic nucleus’s
contribution to purposive movement indicate only its ipsilateral
connections with other basal ganglia.34-37 Hemiballism that
follows subthalamic nucleus lesions is thought to result from
loss of excitatory drive to the ipsilateral medial globus pallidus.
This, in turn, disinhibits the ipsilateral ventrolateral thalamus
and thus unleashes excessive cortical motor activation of the
contralateral limbs. However, this model does not explain how
a unilateral cerebral infarction would precipitate a bilateral
hyperkinetic disorder.
In contrast, other investigators have indicated that the subthalamic nuclei are also interconnected across the body midline
via an interhemispheric commissure.6,8,38,39 The excitatory
subthalamic nucleus efferents are glutamatergic.40 Thus, injury
to 1 nucleus could reduce excitation to the opposite nucleus,
resulting in bilateral but asymmetric ballism, as shown by our
patient. In the marmoset, unilateral subthalamic ablation results
in bilateral neurochemical changes in the basal ganglia that are
thought to be mediated by commissural relays.41 Unilateral
subthalamic stimulation to relieve Parkinsonism primarily has
contralateral benefits, but nonetheless mild improvement of
ipsilateral motor deficits also results.42 It has been suggested
that the bilateral supplementary motor area activation that
occurs with unilateral subthalamic stimulation for Parkinsonism43 reflects relays between either the globus pallidus internus
or the substantia nigra and the contralateral thalamus.44 Regardless of the specific pathways involved with bilateral ballism, these studies support our impression that acute unilateral
subthalamic injury in humans can have bilateral motor effects.
It is also conceivable that the extensive bilateral white matter
ischemic changes suggested by our patient’s MRI scan may
have contributed to the bilateral presentation of ballism after
unilateral infarction.
In contrast to many other cases of ballism,3 the disorder was
rarely present at rest and did not involve the face. Consequently, our patient manifested relatively mild ballism, the
self-injuries notwithstanding. At times the upper limbs (particularly the left) also presented classic cerebellar disturbances
(past-pointing, clumsy alternating movements). These disturbances may have resulted in part from the infarction’s involving the dentatorubrothalamic tract,45 which courses close to the
subthalamic nucleus.46 Frequently, ballism is not “pure” but is
instead associated with other involuntary movements.3,47 Thus,
the co-occurrence of diverse movement disorders in our patient
is consistent with other reports of ballism.
Results of Functional Assessments
Unlike previous reports of ballism, we extensively assessed
functional activities. Bilateral ballism was more evident during
functional activities (walking and writing in particular) than on
standard bedside neurologic evaluation. Consequently, the
omission of functional activities assessments from movement
disorder studies may preclude identifying bilateral ballism. The
additional sensitivity of functional assessment beyond labora-

1229

tory or simple clinical evaluations has been noted for unilateral
spatial neglect48,49 and Parkinson’s disease.50 Therefore, the
infrequency of reports of bilateral ballism, relative to hemiballism, may be because conventional neurologic examination is
insensitive to its bilateral but asymmetric presentation. Similarly, bilateral motor deficits are well known to follow unilateral cerebral infarction associated with clinical contralateral
hemiparesis, but special testing or functional evaluation are
usually required to uncover the ipsilesional deficits.51
Our patient showed moderate nonuse of the more-affected
upper extremity—that is, reduced spontaneous use of the limb
on functional tasks, despite intact movement to command—
based on a validated self-report instrument (ie, the MAL).30
Previous reports of nonuse after stroke have assessed hemiparesis but did not indicate limb hyperkinesia. Our report thus
shows that moderate nonuse of the more-affected upper extremity after stroke may include asymmetric hyperkinesia. As
has been hypothesized for other cases of nonuse after neurologic injury, the nonuse of our patient’s more-affected arm was
probably learned,52 secondary to adverse conditioning from
attempted movement.
Responses to Noninvasive Interventions
As was seen in our patient, vascular ballism commonly
subsides within weeks of cerebral infarction. The various medications that were used to treat his movement disorder at best
only partially ameliorated the symptoms. We cannot exclude
the possibility that higher doses might have been more beneficial. However, after our initial medication attempt to treat the
movement disorder, we favored treating the patient’s depression because (1) we were concerned about possible side effects
from increasing doses of existing medication, (2) the patient
had behaviorally adapted to his movement disorder (as has
been reported for ballism15), and (3) we did not want to neglect
his depression. The depression responded quickly and impressively to venlafaxine,53 which was thereafter chronically continued without discernible effect on the ballism.
Because our patient’s ballism incompletely responded to
medication, it is important to consider whether the favorable
results that apparently followed the standard stroke rehabilitation techniques we used suggest that these approaches may
benefit ballism in general. These interventions— continuous
repetitive movement (rhythmic walking, forearm rolling) and
partial weight bearing (closed-chain activity) or gripping an
object with either hand— generally improved control of the
movement disorder except when the patient was fatigued. As a
result, locomotion stabilized and could be more easily treated.
These improvements may have facilitated PT for functional
motor recovery.
The physiologic bases for these improvements are unclear.
However, several lines of evidence from related disorders and
studies in healthy subjects suggest contributing mechanisms.
Rhythmic, synchronized bilateral limb movement. Patients with neurodegenerative movement disorders (Parkinson’s disease, Huntington’s disease) improve ambulation when
they synchronize their walking to environmental rhythmic
stimuli.54,55 Similarly, patients with diverse cerebellar disorders can overcome action tremor of the upper extremity with
continuous, self-developed rhythmic limb movements.56 Physiologic neuroimaging studies suggest that an extensive network
of neural structures collaborates in the motor learning of repetitive limb movements, including the cerebellum, sensorimotor cortex, premotor and supplementary motor areas, and striatum (caudate and putamen).57 Central pattern generators in the
spinal cord are also postulated to mediate bilaterally coordinated rhythmic behavior.58,59 The premotor, dorsolateral preArch Phys Med Rehabil Vol 86, June 2005

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BILATERAL BALLISM, Mark

frontal, and parietal areas may be particularly involved when
coupling the limbs during self-developed repetitive movements, unlike when synchronizing the limbs to rhythmic environmental stimuli.60 This suggests that attentional and executive mechanisms are recruited for self-paced rhythmic
movements. As learning a self-paced, reciprocal bimanual task
proceeds, the activation of dorsolateral prefrontal and parietal
areas diminishes,61 which suggests reduced attentive monitoring during procedural learning.
Within-session improvement when learning tasks,62,63 as
was shown by our patient, is consistent with a 2-phase model
of skill acquisition: first, a rapid within-session improvement,
followed by a slower, continued improvement with practice
over several days.64 Neuroimaging studies64 in humans suggest
that corticocerebellar loops are recruited early during motor
learning, whereas corticostriate loops may be preferentially
activated later as the individual becomes proficient at a particular skill. However, when humans must adapt to perturbations
from external forces on the limbs, the opposite order of anatomic activations has been described.65 Thus, the specific sequence of regional brain activation may be task dependent, in
part affected by whether the person must adapt to instability in
limb movements.64 The dyskinetic movements of ballism are
similar to external forces on the limbs, because they challenge
the individual to rapidly adapt to uncontrollable and abrupt
perturbations, as indeed our patient did.
In addition, the corpus callosum and the supplementary
motor area appear necessary for interhemispheric inhibition as
a person learns reciprocal bilateral limb movements,66-68 as
well as to facilitate bilateral coordination.69 Lesions to these
areas result in synkineses (mirror movements) or intermanual
conflict. These abnormal movements did not appear in our
patient, which along with our apraxia assessments suggested
functional integrity of these structures.
The contribution of the subthalamic nucleus to procedural
learning is unknown, probably because (1) its small size might
be difficult to resolve during functional imaging studies, (2)
ballism is uncommonly reported, and (3) motor learning in
ballism has not previously been addressed. Nonetheless, the
foregoing studies suggest that patients with ballism that follows
subthalamic nucleus lesions may improve bilateral rhythmic
limb movements with practice, because of the functional integrity of cortical, striatal, and cerebellar areas. The white
matter abnormalities seen in our patient were apparently not
sufficient to prevent these improvements. Because we evaluated only a single patient, we cannot indicate whether the
reduction in dyskinesia in the weeks after the initial stroke’s
onset had been directly due to motor training effects rather than
spontaneous recovery.
Somatosensory stimulation. The movement disorder also
improved with partial weight bearing by the upper extremities
or gripping an object within a physically restricting space (a
pocket). In contrast, initiating limb movements without weight
bearing, grasping an object without constraining movement
(eg, using a pen), or even simply imagining the right arm
moving induced ballism. Hence, improved control apparently
was related to substantial somatosensory stimulation, at least to
the hands.
Converging evidence implicates the basal ganglia in gating
somatosensory information, particularly proprioception, which
may be fundamental to the pathophysiology of diverse involuntary movement disorders70-72 as well as their responses to
peripheral stimuli. Substantial cortical somatosensory projections reach the basal ganglia via the ipsilateral subthalamic
nucleus and putamen.73,74 The basal ganglia are active primarily during closed-loop limb movements (ie, those that are
Arch Phys Med Rehabil Vol 86, June 2005

modified by afferent feedback75), whereas the cerebellum and
motor cortex are active during both closed-loop as well as
open-loop ballistic movements that rely less on feedback.76,77
Consequently, basal ganglial injury may preferentially impair
proprioception and hence the monitoring of slow limb movements, whereas ballistic movements may be spared. Subtle
proprioceptive disturbance has been found in Parkinson’s disease,78-80 which is considered primarily a basal ganglia disorder. Compensation for Parkinsonian akinesia or bradykinesia
by environmental (visual or auditory) cuing81 may recruit relatively spared sensory channels to improve motor control.82
Choreoathetosis has been shown to follow proprioceptive loss
from lesion anywhere in the nervous system, which may reflect
aberrant sensorimotor integration in the basal ganglia.83 The
subthalamic nucleus is especially responsive to proprioceptive
input relative to other somatosensory (eg, cutaneous) stimuli.84-86 It is therefore not surprising that experimentally induced ballism in monkeys can be aggravated by dorsal rhizotomy, which abolishes peripheral somatosensory input.87 In a
case report of human hemiballism, microelectrode recording
showed reduced activation of the globus pallidus by proprioceptive stimulation, relative to healthy monkeys and patients
with other involuntary movement disorders.88
The foregoing suggests that our patient’s acute right facial
and upper-extremity somatosensory loss resulted from his contralateral subthalamic infarction. Our failure to find proprioceptive disturbance may have been due to the crude manner by
which standard neurologic examination assesses joint position
sense in the fingers and toes.
Dystonias are similar to ballism in that they involve disinhibited muscular contraction,88 although the contraction in
dystonia is prolonged, whereas in ballism it is brief. Dystonias
often improve with a “sensory trick” (geste antagonistique),
which usually involves firm contact between the affected body
part and another object, such as a bed or the patient’s own
finger.38,89-92 Thus, dystonias resemble Parkinson’s disease in
their benefit from external stimulation. The basis for improvement after sensory tricks is not completely understood. However, several basal ganglia disorders (cervical dystonia, Parkinson’s disease, Huntington’s disease) show ipsilateral sensory
cortex activation rather than the usual contralateral activation
when patients are touched on the more-affected side of the
body.70,91 This shift may reflect compensation for contralateral
basal ganglial somatosensory dysfunction, such as by reduced
transcallosal inhibition of the ipsilateral hemisphere. In cervical dystonia this shift may help to counteract torticollis.
The effect of external stimulation on ballism, in contrast, has
not been systematically evaluated. One case study93 noted
temporary amelioration of ballism after applying cutaneous
electromyographic electrodes. Early in his illness our patient
benefited from left-hand weight bearing, but right-hand weight
bearing aggravated his symptoms. Later in his illness, when
ballism was less severe, clutching an object with the right hand
in his pocket improved motor control further. These observations suggest that increased tactile contact reduced involuntary
movements, but only when such movements were not already
severe in the limb that attempted tactile contact. Consequently,
when the less-involved left hand adopted weight bearing early
in the illness, the right hemisphere may have been preferentially activated, which in turn may have helped to suppress the
left hemisphere’s disinhibited motor cortical activity through
transcallosal inhibition. Later in the illness, when ballism was
less severe, right-hand tactile stimulation may have benefited
the movement disorder, because partial recovery of the subthalamic nucleus may have allowed improved proprioceptive processing from the right hand and hence reduced contralateral

BILATERAL BALLISM, Mark

motor cortical excitation. Alternatively, as shown in cervical
dystonia and Parkinson’s disease, tactile stimulation to the
more-affected side of the body may have preferentially activated the ipsilateral sensory cortex, which may have secondarily inhibited the contralateral motor cortex through transcallosal inhibition. This would not have been possible earlier in
the illness because of the severity of the ballism in the right
upper extremity.
Our patient had excessive startle to unexpected abrupt visual
or auditory stimuli. This phenomenon has not been reported in
ballism. Experimental ablation of the subthalamic nucleus in
animal models induces impulsivity and hyperactive complex
behaviors such as feeding and locomotion.41,94-97 These findings suggest that the subthalamic nucleus has a general inhibitory function. The basal ganglia are hypothesized to participate in a general frontothalamic loop of functionally segregated
circuits that mediate motor, cognitive, and affective processes.98 Disruption of the “limbic” loop would result in impaired response inhibition or general hyperexcitability,99 as
was seen in our patient. Cognitive or affective interactions with
our patient’s movements were reflected in the aggravation of
his ballism when he simply imagined purposive limb use or had
to mingle with crowds. These activities may have stressed
attentional resources that were important for suppressing unwanted movements. Many case reports of ballism have indicated its aggravation during emotional arousal or concurrent
cognitive activities (eg, speaking),4,7,8,10,12,93,100,101 whereas, in
contrast, considerable attentional effort or, paradoxically, relaxation can suppress the involuntary movements.9,102
CONCLUSIONS
Although hyperkinetic movement disorders after stroke are
apparently much less common than hemiparesis, they may be
similarly disabling. Unfortunately, rehabilitation approaches
for movement disorders in stroke are less well developed than
for hemiparesis. Furthermore, rehabilitation approaches to involuntary movement disorders in general have seen little
progress50,103 compared with invasive pharmacologic and surgical treatments, despite some promising indications. Our patient with bilateral involuntary hyperkinesia responded favorably to standard stroke therapy, at least within treatment
sessions. Our interventions were initiated before our literature
review and thus were not informed by diverse research findings
in motor physiology. The improvements that were seen are
consistent with different lines of experimental and clinical
evidence. We hope that our findings will encourage other
rehabilitation programs that may treat patients with acquired
involuntary movement disorders to evaluate the benefit of our
approaches.
Our clinical, neuroimaging, and therapeutic observations
invite new questions about such disorders. In particular, it is
important to know whether ballism consistently responds to the
noninvasive rehabilitation interventions we have identified and
whether the severity of the disorder affects outcomes. Because
of the infrequency of ballism, it would be impractical to conduct extensive controlled clinical trials. However, further detailed case studies that would systematically control noninvasive interventions would contribute invaluable expertise. A
national stroke registry to identify involuntary motor disorders
would help to acquaint clinicians with their existence and foster
information exchange that could expedite developing specific
treatments. These findings would help to determine whether
medications or neurosurgery are essential to control such disorders.
In addition, ballism may be underappreciated during conventional neurologic examination. Anatomic-functional studies

1231

of ballism should include standard assessments of daily living
activities. Such investigations would help to clarify the contributions of the subthalamic nucleus and related structures to the
control of voluntary movement and cognition and their associated disorders.
Acknowledgment: We are grateful for the critical comments of
an anonymous reviewer.
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