Capsular ataxic tetraparesis U. Utku”, H.Z. Kars* *, and 0. Mengii* Introduction Ataxic hemiparesis was first described by Fisher and Cole’ in 1965. These authors believed that a contralateral lesion in the posterior part of the internal capsule was responsible for this clinical syndrome though multiple cerebral lacunar infarcts were demonstrated at postmortem examination. Pontine lacunar infarcts were also observed at autopsies of three patients with ataxic hemiparesis2. In recent years, this syndrome was described in conjunction with contralateral internal capsule infarcts”*4*“,pontine hemorrhage’, and a mesencephalic tumor’. A case with cerebellar ataxia and tetraparesis “ataxic tetraparesis” was reported by Van Gijn and Vermeulen8 in 1983. In this patient computerized tomography (CT) revealed a Iacunar infarct involving the basis pontis. We report another patient with ataxic tetraparesis. Bilateral infarcts at the junctions of the posterior limb of the internal capsule and the corona radiata were detected at CT. A 42-year-old man with ataxic tetraparesis is reported. Computerized tomography showed bilateral and symmetrical lacunar infarcts at the junctions of the posterior limb of the internal capsule and the corona radiata. Previously this clinical syndrome had been reported only with a lesion in the pons. Key words: ataxia, paresis, quadriparesis. A 42-year-old man with hypertension and diabetes was admitted for left hemiparesis of sudden onset two days before. A year before admis- and dysarthria. Physical examination showed moderate arterial hypertension (160/100 mm Hg). The patient was alert and mentally normal. Speech was dysarthric. Fundoscopy showed retinal exudates and hemorrhages. A left facial palsy of the upper motor neuron type was evident. All four extremities were minimally paretic, though more marked in the legs. The tendon jerks were hyperactive at both sides. He had bilateral Babinski signs and ankle clonus. Left hemihypesthesia, bilateral dysmetria and dysdiadochokinesia were observed. The patient was unable to stand or walk alone. CT scans showed bilateral and symmetrical lacunar infarcts at the junctions of the posterior limb of the internal capsule and the corona radiata (Fig. sion he had had an attack 1). Report of a case of right hemiparesis * Department of Neurology, Trakya University Medical School, Universi~ Medical School, Sivas, Turkey Address for correspondence Edirne, and * * Department of Neurosurgery’, Cumhuriyet and reprint requests: H. Zafer Kars, CGTF Hastanesi. Ntirosiriirji ABD, 58040 Sims, Turkey Accepted 27.5.91 Clin Neural Neurosurg 1991. Vol. 93-4 327 Figure I. CT scan of the patient shows infarcts located at both internal capsuIe posterior limbs and corona radiata. Discussion Homolateral ataxia with crural paresis was first described by Fisher and Cole’ in 1965. In this syndrome weakness is minimal, more prominent in the lower limbs, and the degree of weakness does not explain the severity of ataxia. Although Fisher and Cole demonstrated a lesion in the posterior internal capsule-corona radiata region at postmortem examination they added that lesions found in other parts of the brain could also cause this syndrome. In 1978, Fisher demonstrated contralateral upper basis pontis infarcts at autopsies of three patients with this syndrome’. He pointed that this pathologic study has furnished a definite solution to an old neurologic problem-the site of the lesion for this syndrome and coined the term ‘ataxic hemiparesis”. In 1980, Perman and Racy observed fresh infarcts in the posterior limb of internal capsule and thalamus with ipsdilaterai ataxia and crural hemiparesis”. They concluded that the lesion in posterior internal capsule-corona radiata may suffice to cause this syndrome. In recent years, it is stressed that ataxic hemiparesis may exist more frequently with capsular lesions than with pontine lesions3s4. In these reports, posterior limb of internal capsule which involves corticospinal and frontopontine fibers was held responsible for this syndrome. The temporopon328 tine, parietopontine, and occipitopontine fibers which together form the Turck bundle course in the retrolenticular and sublenticular portions of the internal capsule. The frontopontine tract named the “Arnold bundle” arises from the prefrontal cortex and the precentral gyrus. Prcfrontal fibers occupy the anterior limb of the interal capsule, but frontopontine fibers from the precentral cortex descend in the posterior limb of the internal capsule adjacent to the corticospinal tract’.“. Ataxic tetraparesis was first described by Van Gijn and Vermeulen’. These authors suggested that occlusion of a perforating branch of the basilar artery with subsequent bilateral pontine ischemia was the cause of this syndrome. It is obvious that this explanation does not hold true in our case. The hypodense lesion at the juction of the posterior limb of the left internal capsule and the corona radiata which was demonstrated by CT may be responsible for the ataxic hemiparesis on the right which had occured one year before. The left ataxic hemiparesis that had developed two days before admission was obviously caused by a new right capsular lesion. Therefore we suggest that recurrent capsular infarctions may cause ataxic tetraparesis. Symmetrical appearance of posteriorly situated internal capsule infarcts, and absence of any pontine lesion on CT scanning support this suggestion. It seems that ataxic tetraparesis, like ataxic hemiparesis, may be a consequence of different central nervous system lesions. References FISHER CM, COLE M. 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