© 1991 S. Karger AG, Basel
0014-3022/91/0314-0257S2.75/0

Eur Neurol 1991;31:257-258

Monochorea Caused by a Striatal Lesion
Masayuki Ikeda3, Hiroshi Tsukagoshib
3 Division of Neurology, Department of Medicine, Asahi General Hospital, Chiba, Japan, and
b Department of Neurology, School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan

Key Words. Chorea • Striata • Somatotopic organization
Abstract. A 76-year-old man developed choreic movement restricted to the arm. Computed tomography sug­
gested an old infarction mainly involving the head of the right caudate nucleus. Monochorea may indicate a striatal
lesion and suggests the somatotopic localization.

Introduction
Involuntary movement of sudden onset is usually
attributed to a vascular lesion in the contralateral deep
hemispheric structures [1]. In the majority of recorded
cases, the limbs on one side were both affected (hemiballism or hemichorea). The question of somatotopic orga­
nization within the basal ganglia has long been debated.
However, monoballism and monochorea, suggesting a
correlation between the specific body parts and the basal
ganglia, are relatively uncommon [2-5]. The purpose of
this case report is to elucidate the somatotopic organiza­
tion of the basal ganglia and the diagnostic significance
of monochorea.

A 76-year-old right-handed man was admitted to our hospital to
be evaluated for choreic movement of his arm. He suddenly devel­
oped left hemiparesis 10 years before. An equivocal low-density
lesion in the right caudate head was indicated on computed tomog­
raphy (CT). There was no hemorrhage. The result of cerebral angi­
ography was negative and aspirin was prescribed. Within 2 months,
motor weakness was alleviated, but choreic movement appeared in
his left arm and hand. His symptoms remained unchanged through­
out the next 10 years. Neurologic examination on admission re­
vealed mild dysarthria and left hyperreflexia without overt weak-

Fig. 1. CT scan reveals dilation of the anterior horn of the right
lateral ventricle, indicating old infarction around the head of the
caudate nucleus.

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Case Report

258

Ikeda/Tsukagoshi

Discussion
Monochorea involves the relationship between the
specific body parts and the basal ganglia, but there are
few reports on it. Davison and Goodhart (2) reported a
monochorea of the arm. Pathological examination iden­
tified a lesion in the putamen and caudate nucleus. Some
of symptomatic dystonia is limited to one arm or leg. In
most cases the principal lesion lay in the striata [3, 4].
Saris [5] described a monochorea in a patient whose
hand movement is almost identical with that of the
present case, namely flexion and extension of metacar­
pophalangeal and interphalangeal joints. A CT scan re­
vealed an infarction of the anterior body caudate nucleus
and the corona radiata. In the present case, the caudate
head is the main lesion with less involvement of the
putamen and internal capsule. This clinico-pathological
relationship suggests topographic localization in the
striata. Recent basic studies also show somatotopic orga­
nization [6], Concerning the subdivisions of the basal
ganglionic region, lesions of the gray matter alone do not
always cause involuntary movements [7]. Development
of chorea or ballism may need disruption of the tracts
connecting the nuclei such as striatopallidal or striatonigral fibers.
In the present case, chorea appeared after the hemiparesis had been resolved. Why there should be a delay
in the development of chorea following a stroke is not
certain. Motor weakness itself may prevent the appear­

ance of the involuntary movement but this cannot al­
ways be true [4], Delayed onset may be the result of
slowly evolving aberrant neuronal sprouting [4],
Although it is difficult on the basis of only 1 case to
draw a firm conclusion, monochorea in the hand may be
symptomatic of a lesion of the striata and somatotopic
localization may exist. We need to investigate it further
both clinically and basically.

Acknowledgements
We are grateful to Dr. Kaichirou Tanba who referred the patient
to us for evaluation.

References
1 Martin JP: Choreatic syndromes; in Vinken PJ, Bruyn GW
(eds): Diseases of the Basal Ganglia. Handbook of Clinical Neu­
rology. Amsterdam, North-Holland, 1968, vol 6, pp 435-439.
2 Davison C, Goodhart SP: Monochorea and somatotopic local­
ization. Arch Neurol 1940;43:792-803.
3 Dooling EC, Adams RD: The pathological anatomy of post­
hemiplegic athetosis. Brain 1975;98:29-48.
4 Marsden CD, Obeso JA. Zarranz JJ. Lang AE: The anatomical
basis of symptomatic hemidystonia. Brain 1985;108:463-483.
5 Saris S: Chorea caused by caudate infarction. Arch Neurol 1983;
40:590-591.
6 Alexander GE, Delong MR: Microstimulation of the primate
neostriatum. II. Somatotopic organization of striatal microexcitable zones and their relation to neuronal response properties. J
Neurophysiol 1985;53:1417-1430.
7 Richfield EK, Twyman R, Berent S: Neurological syndrome fol­
lowing bilateral damage to the head of the caudate nuclei. Ann
Neurol 1987;22:768-771.

Received: August 27, 1990
Accepted: November 5, 1990
Masayuki Ikeda, MD
Wellcome Surgical Institute and Hugh Fraser Neurosciences
Laboratories University of Glasgow
Garscube Estate
Bearsden Road
Glasgow G61 1QH(UK)

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ness. Coordination and sensorium were unaffected. There was
choreic movement with some dystonic component in the arm. The
movement was composed of a shrug of the shoulder, flexion of the
elbow and involuntary shaking hand, namely flexion and extension
of metacarpophalangeal and interphalangeal joints, at 1-1.5 Hz.
Concentration and volitional movement could suppress this move­
ment, but not eliminate it. It ceased during sleep. Other extremities
showed no involuntary movement. CT demonstrated an enlarged
anterior horn of the lateral ventricle indicating an old infarction
around the caudate head (fig. 1). There was no other lesion. EEG
and somatosensory evoked potentials of short and long latency were
normal. Clonazepam diminished the chorea but haloperidol, carbamazepine, diphenylhydantoin and propranolol did not affect it.