Positron emission tomography in evaluation of dementia: Regional brain metabolism and long-term outcome.

CONTEXT: Deficits in cerebral glucose utilization have been identified in patients with cognitive dysfunction attributed to various disease processes, but their prognostic and diagnostic value remains to be defined. OBJECTIVE: To assess the sensitivity and specificity with which cerebral metabolic patterns at a single point in time forecast subsequent documentation of progressive dementia. DESIGN, SETTING, AND PATIENTS: Positron emission tomography (PET) studies of [(18)F]fluorodeoxyglucose in 146 patients undergoing evaluation for dementia with at least 2 years' follow-up for disease progression at the University of California, Los Angeles, from 1991 to 2000, and PET studies in 138 patients undergoing evaluation for dementia at an international consortium of facilities, with histopathological diagnoses an average of 2.9 years later, conducted from 1984 to 2000. MAIN OUTCOME MEASURES: Regional distribution of [(18)F]fluorodeoxyglucose in each patient, classified by criteria established a priori as positive or negative for presence of a progressive neurodegenerative disease in general and of Alzheimer disease (AD) specifically, compared with results of longitudinal or neuropathologic analyses. RESULTS: Progressive dementia was detected by PET with a sensitivity of 93% (191/206) and a specificity of 76% (59/78). Among patients with neuropathologically based diagnoses, PET identified patients with AD and patients with any neurodegenerative disease with a sensitivity of 94% and specificities of 73% and 78%, respectively. The negative likelihood ratio of experiencing a progressive vs nonprogressive course over the several years following a single negative brain PET scan was 0.10 (95% confidence interval, 0.06-0.16), and the initial pattern of cerebral metabolism was significantly associated with the subsequent course of progression overall (P<.001). CONCLUSION: In patients presenting with cognitive symptoms of dementia, regional brain metabolism was a sensitive indicator of AD and of neurodegenerative disease in general. A negative PET scan indicated that pathologic progression of cognitive impairment during the mean 3-year follow-up was unlikely to occur.

Effects of stroke on local cerebral metabolism and perfusion: mapping by emission computed tomography of 18FDG and 13NH3.

By means of emission computed tomography (ECT), we used 18F-fluorodeoxyglucose (18FDG) and 13N-ammonia (13NH3) as indicators of abnormalities in local cerebral glucose utilization (LCMRglc) and relative perfusion, respectively. The ECAT positron tomograph was used to scan normal control subject and 10 stroke patients at various times during recovery. In normal subjects, mean CMRglc was 5.28 +/- 0.76 mg per 100 gm tissue per minute (mean +/- SD; N = 8). In patients with stroke, mean CMRglc in the contralateral hemisphere was moderately decreased during the first week, profoundly depressed in irreversible coma, and normal after clinical recovery. Quantification was restricted by incomplete understanding of tracer behavior in diseased brain, but relative local distributions of 18FDG and 13NH3 trapping qualitatively reflected the increases and decreases as well as coupling and uncoupling expected for local alterations in glucose utilization and perfusion in stroke. Early after cerebrovascular occlusion there was a greater decrease in local trapping of 13NH3, than 18FDG within the infarct, probably because of increased anaerobic glycolysis. Otherwise, 18FDG was a more sensitive indicator of cerebral dysfunction than was 13NH3. Hypometabolism, due to deactivation or minimal damage, was demonstrated with the 18FDG scan in deep structures and broad zones of cerebral cortex that appeared normal on x-ray computed tomography and technetium 99m pertechnetate scans. In its present state of development, the 18FDG ECT method should aid in defining the location and extent of altered brain in studies of disordered function after stroke. With improved knowledge of tracer behaviour in diseased brain, the method has promise for mapping the response to therapeutic intervention and increasing our understanding of how the human brain responds to stroke.