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. 1994 Oct;51(10):999-1007.
doi: 10.1001/archneur.1994.00540220045013.

Cognitive dysfunction following subcortical infarction

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Cognitive dysfunction following subcortical infarction

A Corbett et al. Arch Neurol. 1994 Oct.

Abstract

Objective: To determine the association between computed tomographic scan findings of subcortical infarction, periventricular lucency, and ventricular enlargement and a patient's performance on a range of neuropsychological tests.

Design: Prospective study of patients in whom computed tomographic scanning identified discrete areas of subcortical lucency that were consistent with multiple subcortical infarcts and in whom there was no evidence for additional cerebral computer tomographic pathology.

Setting: Hospital practice that included both inpatients and ambulatory patients.

Patients: One hundred forty-seven consecutive appropriate computed tomographic scans were identified. Sixty-two patients were excluded because of concomitant medical disorders, and eight refused participation. We describe 77 patients.

Main outcome measures: Performance on a battery of neuropsychological tests.

Results: The number of infarcts but not the volume of infarction, periventricular lucency, and cerebral ventricular enlargement but not cortical atrophy were significantly associated with impaired performance on neuropsychological tests. The number of infarcts correlated with impaired performance on tests, and this impaired performance was thought to be dependent on the function of frontal systems, while periventricular lucency and ventricular enlargement correlated with impaired performance on a wider range of tests, including tests that depended on memory and language.

Conclusions: The number of infarcts, periventricular lucency, and ventricular enlargement are the computed tomographic head scan parameters that correlated with severity of impaired performance on neuropsychological tests in patients with subcortical infarction. Cognitive impairment is presumed to be the result of cortical disconnection following disruption of the connections between the subcortical regions and the frontal cortex.

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