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Case Reports

Ataxic Hemiparesis FollowingThalamic InfarctionJelis Boiten, MD, and Jan Lodder, MD

We describe a 73-year-old man with ataxic hemiparesis following infarction of the ventrolateralnucleus of the thalamus demonstrated by computed tomography and magnetic resonanceimaging. Cerebellar ataxia was most likely due to interruption of the dentatorubrothalamocor-tical fibers at the level of the injured ventrolateral nucleus. Hemiparesis was probably causedby local edema compressing the corticospinal tract in the adjacent posterior limb of the internalcapsule. We believe this to be the first reported case of classic ataxic hemiparesis followingthalamic infarction. {Stroke 1990^21^39-340)

Ataxic hemiparesis, first described by Fisher andCole1 in 1965, consists of hemiparesis and

^ cerebellar ataxia on the same side of thebody.2 Ataxic hemiparesis is usually caused by lacu-nar infarction in the contralateral posterior limb ofthe internal capsule, in the pons, or in the coronaradiata1-4 but may also be caused by a hemorrhage ora tumor.5-7 We report a case of ataxic hemiparesis inwhich computed tomography (CT) and magneticresonance imaging (MRI) showed an infarct in thecontralateral ventrolateral nucleus of the thalamus.

Case ReportA 73-year-old man suddenly developed dysarthria

and weakness of his right arm and leg with unsteadi-ness of gait. There was no history of hypertension,diabetes, cardiac disease, or peripheral vascular dis-ease. On examination the next day, he had a regularpulse of 76/min. Blood pressure was 150/80 mm Hg.There were no carotid bruits, and cardiac examina-tion was normal. He was alert and fully oriented.

Neurologic examination showed a slight right-sided hemiparesis with an extensor plantar response.Finger-to-nose and heel-to-shin tests showedcerebellar-type right-sided dysmetria, hypermetria,and intention tremor out of proportion to the degreeof weakness. Sensation was normal. His hemiparesisdisappeared after 4-5 days, while his ataxia persisted.After 4 weeks there was only clumsiness of his righthand, with slight ataxia on the finger-to-nose test.Results of electrocardiography, 24-hour electrocar-

From the Department of Neurology, University Hospital Maas-tricht, Maastricht, The Netherlands.

Address for reprints: J. Boiten, Department of Neurology,University Hospital Maastricht, PO Box 1918, 6201 BX Maas-tricht, The Netherlands.

Received March 17, 1989; accepted September 28, 1989.

FIGURE 1. Computed tomogram showing recent hypo-dense lesion in ventrolateral part of thalamus, with involve-ment of ventrolateral nucleus. Right side of body appears onleft side of figure.

diographic (Holter) monitoring, echocardiography,and duplex carotid sonography were normal. Serumcholesterol concentration was slightly elevated.

CT scan on day 4 revealed a hypodense lesion inthe ventrolateral nucleus of the contralateral thala-mus, compatible with a recent infarction (Figure 1).MRI 1 year later showed the same infarct in the leftthalamus (Figure 2). There were no other lesionsvisible in the internal capsule, corona radiata, brain-stem, or cerebellum.

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340 Stroke Vol 21, No 2, February 1990

FIGURE 2. Magnetic resonance image 1 year later showingsame lesion in left thalamus.

Discussion"Painful ataxic hemiparesis" following thalamic

infarction and "hypesthetic ataxic hemiparesis" inthalamic hemorrhage and infarction have beenreported.8-10 Sole unilateral cerebellar ataxia hasbeen described following contralateral thalamicinfarction.1112 Murthy13 described a case of ataxichemiparesis following thalamic infarction, but thelesion appeared to be located in the head of thecaudate nucleus instead of in the thalamus.14 CT andMRI in our patient showed an infarct in the contra-lateral thalamus. To our knowledge, this is the firstreported case of classic ataxic hemiparesis followinginfarction strictly confined to the thalamus.

The lesion was located in the ventrolateral part ofthe thalamus, with involvement of the ventrolateralnucleus. From experimental evidence it was con-cluded that the ventrolateral nucleus receives fibers

from the contralateral cerebellar dentate nucleus(the dentatorubrothalamic projection).15 From theventrolateral nucleus, fibers run to the sensorimotorcortex.15 Cerebellar ataxia in our patient was mostlikely caused by interruption of the dentatorubro-thalamocortical fibers at the level of the injuredventrolateral nucleus. Hemiparesis was probablycaused by initial local edema compressing the adja-cent corticospinal tract in the posterior limb of theinternal capsule because MRI did not reveal involve-ment of the internal capsule. The hemiparesis clear-ing much more rapidly than the hemiataxia supportsthis assumption.

Our case illustrates that the ventrolateral part ofthe thalamus takes part in the cerebellar projectionto the sensorimotor cortex, disruption of which atdifferent levels can induce the classic lacunar syn-drome of ataxic hemiparesis.

References1. Fisher CM, Cole M: Homolateral ataxia and crural paresis: A

vascular syndrome. / Neurol Neurosurg Psychiatry 1965;28:48-55

2. Fisher CM: Ataxic hemiparesis. A pathologic study. ArchNeurol 1978;35:126-128

3. Sage JI, Lepore FE: Ataxic hemiparesis from lesions of thecorona radiata. Arch Neurol 1983;40:449-450

4. Huang CY, Lui FS: Ataxic-hemiparesis, localization and clin-ical features. Stroke 1984;15:363-366

5. Bendheim PE, Berg BO: Ataxic hemiparesis from a midbrainmass. Ann Neurol 1981;9:405-407

6. Helweg-Larsen S, Larsson H, Henriksen O, Sorensen PS:Ataxic hemiparesis: Three different locations of lesions stud-ied by MRI. Neurology 1988;38:1322-1324

7. Mori E, Tabuchi M, Yamadori A: Lacunar syndrome due tointracerebral hemorrhage. Stroke 1985;16:454-459

8. Bogousslavsky J, Regli F, Ghika J, Feldmeyer JJ: Painfulataxic hemiparesis. Arch Neurol 1984;41:892-893

9. Verma AK, Maheshwari MC: Hypesthetic-ataxic-hemiparesisin thalamic hemorrhage. Stroke 1986;17:49-51

10. Lee N, Roh JK, Myung H: Hypesthetic ataxic hemiparesis in athalamic lacune. Stroke 1989;20:819-821

11. Garcin R: Syndrome ce're'bello-thalamique par lesion localiseddu thalamus: Avec une disgression sur le "signe de la maincreuse" et son intdrfit semiologique. Rev Neurol (Paris) 1955;93:143-149

12. Garcin R, Lapresele J: Incoordination c6r6belleuse du mem-bre inferieur par lesion localised de la region interne duthalamus contralateral. Rev Neurol (Paris) 1969;120:5-13

13. Murthy JMK: Ataxic hemiparesis —Ventrolateral nucleus ofthe thalamus: Yet another site of lesion (letter). Stroke 1988;19:122

14. Gomez CR, Gomez SM: Thalamic lesion producing ataxichemiparesis (letter). Stroke 1988;19:1181

15. Brodal A: Neurological Anatomy. Oxford, Oxford UniversityPress, 1981, pp 359-370

KEY WORDS • hemiplegia • lacunar infarction • thalamus

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J Boiten and J LodderAtaxic hemiparesis following thalamic infarction.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1990 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.21.2.339

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