OBSERVATION

Neurogenic Pain and Abnormal Movements
Contralateral to an Anterior Parietal Artery Stroke
Andrea O. Rossetti, MD; Joseph A. Ghika, MD; François Vingerhoets, MD; Jan Novy, MD; Julien Bogousslavsky, MD

Background: Unlike delayed pain syndrome, acute central pain is a very rare symptom in acute stroke. In addition, the incidence of hemiballismus in acute cerebrovascular diseases is less than 1%. To our knowledge, the
association of these 2 clinical conditions has not been previously described.

hemichorea, the observed patient was the only one to have
acute pain at the onset of stroke. Magnetic resonance imaging showed acute infarction in the territory of the right
anterior parietal artery, whereas the basal ganglia, thalamus, and subthalamic region were intact.

hemiballismus accompanied by ipsilateral acute limb pain
at stroke onset, we retrospectively examined more than
4000 patients in the Lausanne Stroke Registry for hemiballismus-hemichorea occurring together with acute ipsilateral pain.

Conclusions: The syndrome of acute limb pain associated with hemiballismus may result from disconnection
of the parietal lobe from deeper structures. In contrast
with isolated hemiballismus, we suggest that the simultaneous occurrence of this movement disorder with ipsilateral pain is specific for an anterior parietal artery
stroke.

Results: Of the 29 subjects with hemiballismus-

Arch Neurol. 2003;60:1004-1006

Patient and Methods: After observing one patient with

I

N CONTRAST with the delayed pain

syndrome, acute central pain is an
infrequent symptom in acute
stroke1 and is mainly found in association with parietal, thalamic, or brainstem lesions. On the other
hand, hemiballismus, which is also relatively rare, classically results from a stroke
in the contralateral subthalamic nucleus
or the caudate, lenticular, and thalamic nuclei.2 As far as we are aware, the simultaneous occurrence of both clinical conditions has not been previously described.
We describe a patient with a right anterior parietal artery stroke who had contralateral hyperkinetic movement disorders accompanied by acute limb pain on
initial examination.
METHODS
REPORT OF A CASE

From the Service de Neurologie,
Centre Hospitalier
Universitaire Vaudois,
Lausanne, Switzerland.

A 74-year-old man with untreated nonvalvular atrial fibrillation was referred to our hospital because of “uncontrollable agitation” of
sudden onset. On admission, he was well oriented but complained of an unbearable burning pain deep in the distal left arm. He had in-

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voluntary, brisk, high-amplitude, very fast,
unpredictable movements of the proximal segment of the left upper extremity with elements of flexion or rotation, and similar movements of the ipsilateral leg, although of smaller
amplitude. Any attempt to move the left arm
or contralateral posturing increased the abnormal movements, leading to several arm contusions. In addition, neurologic examination
disclosed left inferior quadrantanopia, discrete sensory deficits on the left hemibody (tactile hemiextinction without position sense impairment), and a slight ataxic hemiparesis,
mainly in the upper limb. Plantar responses
were bilaterally flexor. The abnormal movements subsided during sleep and could be partially inhibited for a short time on demand. The
painful symptoms disappeared spontaneously after 48 hours, while the involuntary
movements were favorably managed with haloperidol (2 mg, 2 times per day), and subsided
after 3 weeks. Magnetic resonance imaging performed 5 days after admission showed an acute
infarction of the right anterior parietal cortex,
extending to the upper posterior temporal lobe
and the adjacent white matter and involving
mainly the territory of the anterior parietal artery, and a hygroma surrounding the left hemisphere (Figure, A-C). The basal ganglia, thalamus, and subthalamic region were intact
(Figure, B-D). We considered the infarction to
be cardioembolic and treated the patient with

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anticoagulants, not regarding the chronic subdural hematoma
as a contraindication. He was then referred to another hospital for rehabilitation.

A

STROKE REGISTRY REVIEW
After observing the patient, we retrospectively reviewed the history of more than 4000 patients in the Lausanne Stroke Registry,3 looking for hemiballismus-hemichorea associated with
acute pain symptoms. The registry considers this movement
disorder when abnormal movements are involuntary, brisk, fast,
and unpredictable, with some element of rotation, occurring
mainly in the proximal segment of the limbs, and when these
movements are increased by attempts to move a limb.2 It is differentiated from other movement disorders that occur during
acute stroke, such as pseudochoreoathetois, dystonia, tremor,
asterixis, and myoclonus.2,4 The radiologic investigations consisted of computed tomographic scans and/or magnetic resonance imaging (after 1989) of the brain.

B

RESULTS

Only 29 patients with hemiballismus-hemichorea were identified and, of these, only 2 showed an association of abnormal movements with pain. A female patient described
delayed painful paresthesias in her affected hand; unfortunately, the computed tomographic scan performed during the acute phase (1981) failed to show any lesion. The
patient whom we described in the “Methods” section was
the only patient with a hemispheric lesion and contralateral acute pain associated with hemiballismus.

C

COMMENT

Our patient had the unusual association of acute pain and
hemiballismus secondary to an anterior parietal infarction. Since, to the best of our knowledge, movement disorders have not been described following ipsilateral subdural hematoma, it is unlikely that the latter accounted for
the clinical signs and symptoms in our patient. Furthermore, the possibility of embolic involvement of the basal
ganglia was ruled out by magnetic resonance imaging.
Acute limb pain in stroke is a rare phenomenon1 and
has been described in subjects with hemispheric,5-8 thalamic,5,9-11 and, less frequently, brainstem1,5 lesions. It must
be differentiated from the more common acute paresthesias, which are not accompanied by definite and intense pain,12 from delayed central pain occurring weeks
or months after a thalamic or parietal lesion,10,13,14 which
is often seen after improvement of the sensory deficits,
and from “acute hemiconcern,”15 a right anterior parietotemporal syndrome without painful symptoms. The
interruption of spinothalamoparietal projections is supposed to lead to spontaneous pain.5,14 Pathophysiologically, a disinhibition of the phylogenetically old pain pathway that passes through the intralaminar thalamic nuclei
and projects to the anterior cingulate cortex and an imbalance of the putative modulatory action of the lemniscal system on the pain pathways have been postulated.11
Another theory points to the hyperactivity of the deafferentiated parietal neurons, especially in the secondary
somatosensory area, leading to a spontaneous painful sensation as a result of their disconnection.7,14 A functional
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D

Magnetic resonance images (diffusion-weighted [left] and T2-weighted
[right]. A, Right anterior parietal acute ischemia, barely visible, and a chronic
subdural hematoma surrounding the left hemisphere. B, Right
superior-posterior temporal ischemia (anterior parietal artery territory),
without acute or chronic lesion in the cranial part of the thalamus and the
caudate nucleus. C, Punctiform acute ischemia in the thalamic-parietal
radiation with no lesion in the thalamus and basal ganglia. D, No lesion in the
subthalamic region.

study16 underscored the importance of the ipsilateral insular and parietal areas, although this work focused on
delayed allodynic pain. In a review study,7 all 6 patients
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with spontaneous pain following a hemispheric stroke
had right lesions, mainly in the parietal lobe, suggesting
a role of the “minor” hemisphere. Our patient showed
ischemia involving the right thalamoparietal fibers as well
as the primary somatosensory cortex. The secondary somatosensory cortex was left intact, and thus disconnected from deeper structures. The pain was described
as burning, as in previous reported instances of acute
pain,5,7,9,10 and lasted for only a short time (2 days), which
was in agreement with some of the reports.5,9
Hemiballismus or, since the clinical signs and symptoms may overlap in some instances, hemiballismushemichorea, is an extremely rare manifestation in acute
stroke (Lausanne Stroke Registry4 prevalence, 0.4%). Its
differential diagnosis primarily involves the more common pseudochoreoathetosis, which results from severe impairment of proprioceptive sensation and appears as slow,
snake-like, involuntary movements principally confined
to the distal extremity.10,17 Our present understanding of
basal ganglia function considers a balance between the direct pathway (cortex-caudate-internal pallidum, accounting for dyskinesias) and the indirect pathway (cortexcaudate-external pallidum-subthalamic nucleus-internal
pallidum, accounting for akinesia), which modulate the
glutamatergic activator thalamocortical retroactive pathway.18 Lesions that disrupt this balance, which are classically located in the subthalamic nucleus2 but have also been
described in the subthalamic-pallidal fibers, striatopallidal connections, basal ganglia, thalamus,19-21 corona radiata,4,22 and the frontal19 or parietal23,24 lobe, may induce
hemiballismus. More recently, a report stressed the occurrence of this movement disorder after lesions of the parietal cortex or adjacent white matter pointed to the role
of the interruption of the parietostriatal pathways,22 and
this was corroborated by the finding of reduced perfusion of the radiologically unaffected striatum in some of
these cases.23,24 Under normal physiologic conditions, the
cerebral cortex provides excitatory stimuli to the basal ganglia25; thus, lesions involving corticostriatal fibers may disrupt the balance of basal ganglia circuits. Compared with
conditions that result from destruction of the subthalamic nucleus,4,22 our patient’s hemiballismus was milder
and easier to treat with neuroleptics. This feature may reflect a slightly different pathophysiologic mechanism.
In conclusion, our patient showed acute limb pain
associated with ipsilateral hemiballismus following a contralateral hemispheric infarction. This syndrome may result from a diaschisis: the lesion (Figure 1C) interrupting the pathways between the hemisphere and thalamus/
basal ganglia caused disconnection of the parietal cortex
from the thalamus, leading to acute central pain, and the
striatum, generating the movement disorder. We suggest that, in contrast to isolated hemiballismus (which
is not painful), the simultaneous occurrence of acute limb
pain is specific to a lesion in the territory of the anterior
parietal artery.
Accepted for publication October 25, 2002.
Author contributions: Study concept and design
(Drs Rossetti, Ghika, and Bogousslavsky); acquisition of
data (Drs Rossetti, Ghika, Vingerhoets, and Novy); analy-

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sis and interpretation of data (Drs Rossetti, Ghika, and
Vingerhoets); drafting of the manuscript (Drs Rossetti and
Novy); critical revision of the manuscript for important intellectual content (Drs Ghika, Vingerhoets, and Bogousslavsky); administrative, technical, and material support
(Dr Novy); study supervision (Drs Ghika, Vingerhoets,
and Bogousslavsky).
This research was presented in part at the 12th meeting of the European Neurological Society, June 25, 2002,
Berlin, Germany.
We thank Alexandre Croquelois, MD, for helpful discussion of the clinical case.
Corresponding author: Andrea O. Rossetti, MD, Service de Neurologie, BH 07, Centre Hospitalier Universitaire Vaudois, 1011-Lausanne, Switzerland (e-mail:
andrea.rossetti@chuv.hospvd.ch).
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