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From the Schools of Psychiatry (Drs. Sachdev, Brodaty, and Wen, and M.J. Valenzuela and L. Lorentz) and Medicine (Dr. Zagami), University of New South Wales; Neuropsychiatric Institute (Drs. Sachdev, Looi, and Wen, and M.J. Valenzuela), Department for Old Age Psychiatry (Dr. Brodaty and L. Lorentz), Institute of Neurological Sciences (Dr. Zagami), the Prince of Wales Hospital, Sydney; Centre for Mental Health Research and Medical School (Dr. Looi), Australian National University, Canberra ACT 0200; and Research Centre for the Neurosciences of Ageing (RESCENA) (Dr. Looi), Calvary Hospital, Bruce ACT 2615, Australia.
Address correspondence and reprint requests to Professor P. Sachdev, NPI, Prince of Wales Hospital, Barker Street, Randwick NSW 2031, Australia; e-mail: p.sachdev{at}unsw.edu.au
Objective: To characterize the neuropsychological profile of vascular cognitive impairment (VCI) and vascular dementia (VaD).
Methods: The authors examined 170 patients with stroke or TIA at 3 to 6 months after the vascular event, and 96 age-matched healthy controls, with detailed neuropsychological and medical-psychiatric assessments, with a majority (66.7%) undergoing MRI brain scans. The subjects were diagnosed as having VaD, VCI, or no cognitive impairment by consensus. The neuropsychological tests were classified into cognitive domains, and composite z-scores adjusted for age and education.
Results: VaD subjects had disturbance in all cognitive domains, with verbal memory, especially retention, being less affected. VCI subjects had similar but less severe disturbance. The domains that best discriminated cognitively impaired from unimpaired patients were abstraction, mental flexibility, information processing speed, and working memory. Cognitive impairment had a significant correlation with deep white matter hyperintensities, but not with volume and number of infarctions, even though the VaD subjects had larger infarct volumes than VCI subjects. The MRI variables did not provide additional discrimination between subgroups.
Conclusions: The cognitive deficits in VaD and VCI are characterized by disturbance of frontal functions, with less verbal memory impairment. VaD and VCI differ in severity but not pattern of disturbance. The brain lesions that best account for these deficits are noninfarct subcortical white matter and gray matter changes due to ischemia. The picture of VaD/VCI presented shows subcortical deficits embellished by cognitive deficits from cortical infarctions.
Received September 2, 2003. Accepted in final form November 26, 2003.
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