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Logo of jnnpsycJournal of Neurology, Neurosurgery and PsychiatryCurrent TOCInstructions for authors
J Neurol Neurosurg Psychiatry. Apr 1995; 58(4): 422–427.
PMCID: PMC1073426

Vascular ataxic hemiparesis: a re-evaluation.

Abstract

Ataxic hemiparesis is commonly considered as one of the "typical" lacunar syndromes. Using the prospective stroke registries from Lausanne and Besançon, 100 patients were selected consecutively (73% men, 27% women; age 64.7 (SD 13.6) years) with a first stroke and ataxic hemiparesis (hemiparesis or pyramidal signs and ipsilateral incoordination without sensory loss). Brain CT or MRI was performed on all patients. A primary haemorrhage was present in 5%, an infarct in 72%, isolated leukoaraiosis in 9%, and no apparent abnormality in 14%. The locations of lesions were the internal capsule (39%), pons (19%), thalamus (13%), corona radiata (13%), lentiform nucleus (8%), cerebellum (superior cerebellar artery territory) (4%), and frontal cortex (anterior cerebral artery territory) (4%). The clinical features of ataxic hemiparesis with different locations were almost identical. Only minor associated signs allowed the localisation of the lesions (paraesthesiae with a lesion in the thalamus; nystagmus or dysarthria with a cerebellar or pontine location). Crural paresis with homolateral ataxia was seen only with cortical paramedian frontal lesions. Presumed hypertensive small artery disease was not always found, but was still the leading cause of stroke, being present in 59% of the patients and in 62% of those with small deep infarcts. A potential source of embolism (arterial or cardiac) was found in one fourth of the patients. Therefore no definite association can be made between ataxic hemiparesis and lacunar infarction. In particular, so called uncommon lesion locations may not be rare. After extensive investigations a diagnosis of lacunar infarct can be retained in only slightly more than half of the cases.

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