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Frontal Lobe Hypometabolism Predicts Cognitive Decline in Patients With Lacunar Infarcts
Bruce R. Reed, PhD;
Jamie L. Eberling, PhD;
Dan Mungas, PhD;
Michael Weiner, MD;
William J. Jagust, MD
Arch Neurol. 2001;58:493-497.
Background A proportion of patients with subcortical lacunes will suffer progressive
cognitive dysfunction, but the basis for this decline is controversial and
little is known about predicting cognitive decline in these patients. Studies
of Alzheimer disease have shown that imaging measures of temporal and parietal
metabolism and blood flow predict disease course.
Objective To determine whether regional cerebral glucose metabolism predicts cognitive
decline by testing 2 opposing hypotheses: (1) temporoparietal activity predicts
decline (based on the idea that concomitant Alzheimer disease causes decline)
vs (2) frontal hypometabolism predicts decline (based on evidence that subcortical
frontal circuits are especially vulnerable to small vessel ischemia).
Design Prospective cohort study.
Setting University outpatient dementia center.
Patients A convenience sample of 26 patients with radiologically defined lacunes
and baseline cognitive function ranging from normal to moderately demented.
Main Outcome Measures Regional cerebral metabolism was quantitated in the form of atrophy-corrected
positron emission tomographic activity ratios in cortical regions that were
defined a priori. Patients were followed up at a mean of 1.8 years, and the
dependent variable was rate of change in the Mini-Mental State Examination
score.
Results Bilateral and right hemisphere dorsolateral frontal metabolism significantly
predicted cognitive decline, with right dorsolateral frontal metabolism explaining
19% of the variance. No other positron emission tomographic region was a significant
predictor, nor were demographic variables or baseline Mini-Mental State Examination
scores significant predictors.
Conclusion Cognitive decline in patients with lacunes may result in part from progressive
vascular compromise in subcortical frontal circuits.
From the Department of Neurology, University of California, Davis (Drs
Reed, Eberling, Mungas, and Jagust); Department of Veterans Affairs, Northern
California Health Care System, Martinez (Drs Reed, Mungas, and Jagust); Center
for Functional Imaging, Lawrence Berkeley Laboratory, Berkeley, Calif (Dr
Eberling); and Departments of Medicine, Radiology, Psychiatry, and Neurology,
University of California, San Francisco, and Department of Veterans Affairs
Medical Center, San Francisco (Dr Weiner).
Corresponding author and reprints: Bruce R. Reed, PhD, UCD-Alzheimer's
Disease Center, 150 Muir Rd (127A), Martinez, CA 94553 (e-mail: BRReed{at}ucdavis.edu).
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