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

Abstract

Patients with extensive subcortical cerebrovascular disease may have impaired memory, often despite the absence of medial temporal or diencephalic strokes. In this group, episodic memory failure may arise from frontal lobe dysfunction based on disruption of frontosubcortical loops caused by lacunae. We tested this idea by studying cognitively impaired subcortical stroke (CIS) patients and Alzheimer's disease (AD) patients with [18F]-fluorodeoxyglucose positron emission tomography using a continuous verbal memory task during the period of tracer uptake. Patients were matched on severity of cognitive 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 prefrontal lobe metabolism, whereas in AD (but not in CIS), memory correlates with left hippocampal and temporal lobe metabolism. Analysis of memory subscores showed that CIS patients made more errors on short-delay trials, which is consistent with working memory failure. It seems that different pathogenic mechanisms underlie episodic memory failure in subcortical cerebrovascular disease and AD.

Fig 1

Effect plots of significant relations between metabolism and memory function in cognitively impaired stroke. Left dorsolateral and right orbital prefrontal count ratios are shown in relation to memory performance. As detailed in Table 3, neither region was significant in Alzheimer’s disease.

Fig 2

Effect plots of significant relations between metabolism and memory function in Alzheimer’s disease. Left hippocampal and left middle temporal gyrus count ratios are shown in relation to memory performance. As detailed in Table 3, neither region was significant in cognitively impaired stroke.