Effects of subcortical cerebral infarction on cortical glucose metabolism and cognitive function

Lawrence T. Kwan, Bruce R Reed, Jamie L. Ebcrling, Norbert Schliff, Jody Tanabc, David Norman, Michael W. Vcincr, William J. Jagust

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)809-814
Number of pages6
JournalArchives of Neurology
Volume56
Issue number7
DOIs
StatePublished - Jul 1999
Externally publishedYes

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Cerebral Infarction
Cognition
Stroke
Glucose
Positron-Emission Tomography
Dementia
Cognitive Function
Metabolism
Fluorodeoxyglucose F18
Brain
Frontal Lobe
Atrophy
Magnetic Resonance Imaging
Control Groups
Cognitive Dysfunction
Cognitive Impairment

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Effects of subcortical cerebral infarction on cortical glucose metabolism and cognitive function. / Kwan, Lawrence T.; Reed, Bruce R; Ebcrling, Jamie L.; Schliff, Norbert; Tanabc, Jody; Norman, David; Vcincr, Michael W.; Jagust, William J.

In: Archives of Neurology, Vol. 56, No. 7, 07.1999, p. 809-814.

Research output: Contribution to journalArticle

Kwan, LT, Reed, BR, Ebcrling, JL, Schliff, N, Tanabc, J, Norman, D, Vcincr, MW & Jagust, WJ 1999, 'Effects of subcortical cerebral infarction on cortical glucose metabolism and cognitive function', Archives of Neurology, vol. 56, no. 7, pp. 809-814. https://doi.org/10.1001/archneur.56.7.809
Kwan, Lawrence T. ; Reed, Bruce R ; Ebcrling, Jamie L. ; Schliff, Norbert ; Tanabc, Jody ; Norman, David ; Vcincr, Michael W. ; Jagust, William J. / Effects of subcortical cerebral infarction on cortical glucose metabolism and cognitive function. In: Archives of Neurology. 1999 ; Vol. 56, No. 7. pp. 809-814.
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AU - Norman, David

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AB - 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.

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