Memory failure has different mechanisms in subcortical stroke and Alzheimer's disease

Patients with extensive subcortical cerebrovascular disease may have impair ed memory, often despite the absence of medial temporal or diencephalic str okes. In this group, episodic memory failure may arise from frontal lobe dy sfunction based on disruption of frontosubcortical loops caused by lacunae. We tested this idea by studying cognitively impaired subcortical stroke (C IS) patients and Alzheimer's disease (AD) patients with [F-18]-fluorodeoxyg lucose positron emission tomography using a continuous verbal memory task d uring the period of tracer uptake. Patients were matched on severity of cog nitive impairment and overall memory task performance. As hypothesized, we found a double dissociation in the relations between metabolism and memory in these groups, such that memory in CIS (but not in AD) correlates with pr efrontal lobe metabolism, whereas in AD (but not in CIS), memory correlates with left hippocampal and temporal lobe metabolism. Analysis of memory sub scores showed that CIS patients made more errors on short-delay trials, whi ch is consistent with working memory failure. It seems that different patho genic mechanisms underlie episodic memory failure in subcortical cerebrovas cular disease and AD.