Neuro.-- Neuroradiology (1992) 34:345-346 radiology 9 Springer-Vedag 1992 Ataxic quadriparesis due to bilateral capsular infarcts P. Ambrosetto Neurological Institute, Medical School, University of Bologna, Italy Received: 21 February 1990 Summary. A most unusual case of ataxic quadriparesis due to bilateral infarcts involving the posterior capsulecorona radiata region is reported. The literature concerning ataxic hemiparesis is briefly discussed. K e y words: Ataxic hemiparesis - Lacunar infarct - Computed t o m o g r a p h y Ataxic hemiparesis is a syndrome characterized by cerebellar-type ataxia, weakness and pyramidal signs involving the limbs of the same side, the leg m o r e than the a r m [1]. Although other lesions have been reported, a lacunar infarct in the contralateral pons is the most frequent cause. A lacunar infarct in the posterior capsular-corona radiata region has b e e n reported, if not pathologically documented [2, 3]. I report a most unusual case of ataxic quadriparesis due to bilateral infarcts involving the junction of the internal capsule with the corona radiata. Case report A 69-year-old hypertensive women was admitted after having suffered acute episodes of left and right hemiparesis, 8 and 6 months respectively prior to admission. On admission she was alert and cooperative. General physical examination revealed evidence of generalized atheroma; the blood pressure was 170/110 mm Hg. Cranial nerve function was intact, the face moved symmetrically and the speech was clear. Mild quadriparesis was present, more marked in the legs and on the right. Deep tendon reflexes were brisk, more so on the right and the Babinski sign was positive bilaterally. Sensation was normal. The finger-nose and heel-shin tests revealed bilateral intention tremor and a slow irregular dysmetria out of proportion with the limb weakness. The intensity of the tremor and dysmetria was not influenced by eye opening or closure. Fundoscopy was normal. CI" showed almost symmetrical lacunar infarcts involving the junction of the internal capsules with the corona radiata (Fig. 1). Discussion The unusual combination of ipsilateral hemiparesis and ataxia was first described by Fisher and Cole [1]. Pathological examination in one of their cases showed a large in- farct in the posterior limb of the internal capsule extending upward to the corona radiata, but clinicopathological correlation was not definitive, because of the presence of m a n y other infarcts elsewhere in the brain. Nevertheless the authors postulated tentatively that the causative lesion was in the posterior capsular-corona radiata region on the side opposite the neurological deficit. In 1978, on the basis of clinicopathological study Fisher [2] concluded that the lesion was in the contralateral basis pontis. Subsequent cases reported by P e r m a n and Racy [3] and Ichikawa et al. [4] seem to confirm the first hypothesis of Fisher and Cole [1]. Of course, in the absence of pathological confirmation it is possible that in these two cases a small lesion in some other location, especially within the basis pontis, not visualized by CT, could also be responsible for the clinical findings, but this seems unlikely in the case of Ichikawa et al. [4], in which CT disclosed sequential changes characteristic of a lacunar infarct in the posterior capsule-corona radiata region, which correlated well chronologically with the stroke suffered by the patient [3]. P e r m a n and Racy [4] argued that in their case the possibility of a different location of the causative lesion could be excluded on the basis of the history and angiography. Fig.1. Unenhanced CT shows almost symmetrical lacunar infarcts at the junction of the internal capsules with the corona radiata 346 In cases of ataxic hemiparesis due to contralateral posterior capsule-corona radiata infarct, it has been suggested that the lesion could interrupt the reciprocal fibre connections between the ventrolateral nucleus of the thalamus and the precentral cortex, which pass through the superior portion of the posterior limb of the internal capsule, or could destroy the corticopontine fibres passing from the precentral cortex through the posterior limb. In the present case appropriately located bilateral, symmetrical lacunar infarcts, monstrated by CT, produced bilateral ataxic hemiparesis. This would appear to be the first report of ataxic quadriparesis due to bilateral infarcts at the junction of the posterior limb of the internal capsule with the corona radiata. References 1. Fischer CM, Cole M (1965) Homolateral ataxia and crural paresis: a vascular syndrome. J Neurol Neurosurg Psychiatry 28:48-55 2. Fischer CM (1798) Ataxic hemiparesis: a pathologic study. Arch Neuro135:126-128 3. Perman GR Racy A (1980) Homolateral ataxia and crural paresis: case report. Neurology 30:1013-1015 4. Ichikawa K, Tsutsumishita AS, Fujioka A (1982) Capsular ataxic hemiparesis. Arch Neuro139:585-586 R Ambrosetto M.D. Casa di Cura "Villa Maria" Via Corriera 1 Cotignola (Ravenna) Italy