Frontal lobe hypometabolism predicts cognitive decline in patients with lacunar infarcts

Background: A proportion of patients with subcortical lacunes will suffer p rogressive cognitive dysfunction, but the basis for this decline is controv ersial and little is known about predicting cognitive decline in these pati ents. Studies of Alzheimer disease have shown that imaging measures of temp oral and parietal metabolism and blood flow predict disease course. Objective: To determine whether regional cerebral glucose metabolism predic ts cognitive decline by testing 2 opposing hypotheses: (1) temporoparietal activity predicts decline (based on the idea that concomitant Alzheimer dis ease 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 l acunes and baseline cognitive function ranging from normal to moderately de mented. 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 Mi ni-Mental State Examination score. Results: Bilateral and right hemisphere dorsolateral frontal metabolism sig nificantly predicted cognitive decline, with right dorsolateral frontal met abolism explaining 19% of the variance. No other positron emission tomograp hic region was a significant predictor, nor were demographic variables or b aseline Mini-Mental State Examination scores significant predictors. Conclusion: Cognitive decline in patients with lacunes may result in part f rom progressive vascular compromise in subcortical frontal circuits.