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  Vol. 56 No. 7, July 1999 TABLE OF CONTENTS
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Effects of Subcortical Cerebral Infarction on Cortical Glucose Metabolism and Cognitive Function

Lawrence T. Kwan, BS; Bruce R. Reed, PhD; Jamie L. Eberling, PhD; Norbert Schuff, PhD; Jody Tanabe, MD; David Norman, MD; Michael W. Weiner, MD; William J. Jagust, MD

Arch Neurol. 1999;56:809-814.

Background  The mechanism of dementia in subcortical cerebral infarction is incompletely understood.

Objective  To determine how cognitive function is related to cortical metabolism in patients with subcortical infarction and a continuum of cognitive impairment.

Methods  We used positron emission tomography (PET) and the glucose metabolic tracer fludeoxyglucose F 18 to study 8 patients with subcortical stroke and normal cognitive function (S-CN), 5 patients with subcortical stroke and cognitive impairment (S-CI) who did not have dementia, 8 patients with subcortical stroke and dementia (S-D), and 11 controls with no cognitive impairment or stroke. A subset of patients had absolute regional cerebral metabolic rate of glucose (CMRglc) determined, while in all subjects regional tracer uptake normalized to whole brain tracer uptake was calculated. PET data were analyzed by constructing volumes of interest using coregistered magnetic resonance imaging data and correcting the PET data for atrophy.

Results  Global CMRglc was significantly lower in the patients with S-D than in the control and S-CN groups, with S-CI rates intermediate to those of the S-D and S-CN groups. Absolute regional CMRs of glucose were similar in the S-D and S-CI groups and in the control and S-CN groups. The regional pattern, however, showed lower right frontal regional CMRglc ratios in all stroke groups compared with the controls. There were modest correlations between performance on the Mini-Mental State Examination and whole brain CMRglc when all 4 groups were included.

Conclusions  These results demonstrate that subcortical infarction produces global cerebral hypometabolism, which is related to the clinical status of the patients. In addition, specific frontal lobe hypometabolism also appears to be a feature of subcortical infarction. Taken together, both global and regional effects on cortical function mediate the production of clinical symptoms in patients with subcortical strokes.


From the Center for Functional Imaging, Lawrence Berkeley National Laboratory, Berkeley, Calif (Mr Kwan and Drs Reed, Eberling, and Jagust); Department of Veterans Affairs, Martinez, Calif (Drs Reed and Jagust); Department of Neurology, University of California, Davis (Mr Kwan and Drs Reed and Jagust); Departments of Veterans Affairs Medical Center, Magnetic Resonance Unit (Drs Schuff, Tanabe, and Weiner), Radiology (Drs Schuff, Tanabe, Norman, and Weiner), Psychiatry (Dr Weiner), and Neurology (Dr Weiner), University of California, San Francisco.



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