Objective: To compare the clinical and pathological features of Alzheimer’s d isease (AD) patients with and without associated cerebral infarcts (CI). Methods : The consecutive records of 57 prospectively studied dem...Objective: To compare the clinical and pathological features of Alzheimer’s d isease (AD) patients with and without associated cerebral infarcts (CI). Methods : The consecutive records of 57 prospectively studied demented patients fulfilli ng the CERAD criteria for the pathological diagnosis of AD were reviewed.Cases w ith cortical Lewy bodies were excluded. CI were found in 22 cases (39%) (AD+CI group): large infarcts (5), lacunes(13) and/or hip pocampal sclerosis (4), and were absent in 35cases (AD group). Microscopic inf arcts, cribiform change,amyloid angiopathy, and white matter rarefaction were no t considered in this classification, but were quantified. Corticalatrophy, neuro fibrillary tangle and senile plaque (diffuse and neuritic) load were also measur ed. Pathological evaluation was independent of clinical information. Clinical an d pathological data were compared between both groups. Results: AD+CI cases wer e significantly older, more commonly female, less educated, and more often had b lue collar occupations, sleep disturbances, frontal release signs, and EEG spike s than AD cases. Other differences found (acute/subacute onset, behavioral distu rbances, and leukoaraiosis on CT scan) disappeared after controlling for age. Th e frequency of known vascular risk factors and focal motor and sensory signs did not differ between the groups, which showed remarkable clinical similarity over all. The only significant differences on pathological exam were hippocampal micr oinfarcts and white matter lesions,although there was a trend for lower neurodeg enerative lesion load in the AD+CI group. The ischemic lesions were located in temporal lobe in 50%of AD+CI patients; these cases had a significantly lower n eocortical neurodegenerative lesion load than those with CI in other sites. Conc lusions: The presence of CI in AD increases significantly with age, but has scar ce influence on the clinical features, and cannot be predicted from common vascu lar risk factors. In spite of a trend, there are no major differences in neurode generative lesion load between AD and AD+CI groups, except when CI are located in the temporal lobe (including hippocampus), suggesting that this location mayb e important in the physiopathology of mixed vascular and AD dementia.展开更多
文摘Objective: To compare the clinical and pathological features of Alzheimer’s d isease (AD) patients with and without associated cerebral infarcts (CI). Methods : The consecutive records of 57 prospectively studied demented patients fulfilli ng the CERAD criteria for the pathological diagnosis of AD were reviewed.Cases w ith cortical Lewy bodies were excluded. CI were found in 22 cases (39%) (AD+CI group): large infarcts (5), lacunes(13) and/or hip pocampal sclerosis (4), and were absent in 35cases (AD group). Microscopic inf arcts, cribiform change,amyloid angiopathy, and white matter rarefaction were no t considered in this classification, but were quantified. Corticalatrophy, neuro fibrillary tangle and senile plaque (diffuse and neuritic) load were also measur ed. Pathological evaluation was independent of clinical information. Clinical an d pathological data were compared between both groups. Results: AD+CI cases wer e significantly older, more commonly female, less educated, and more often had b lue collar occupations, sleep disturbances, frontal release signs, and EEG spike s than AD cases. Other differences found (acute/subacute onset, behavioral distu rbances, and leukoaraiosis on CT scan) disappeared after controlling for age. Th e frequency of known vascular risk factors and focal motor and sensory signs did not differ between the groups, which showed remarkable clinical similarity over all. The only significant differences on pathological exam were hippocampal micr oinfarcts and white matter lesions,although there was a trend for lower neurodeg enerative lesion load in the AD+CI group. The ischemic lesions were located in temporal lobe in 50%of AD+CI patients; these cases had a significantly lower n eocortical neurodegenerative lesion load than those with CI in other sites. Conc lusions: The presence of CI in AD increases significantly with age, but has scar ce influence on the clinical features, and cannot be predicted from common vascu lar risk factors. In spite of a trend, there are no major differences in neurode generative lesion load between AD and AD+CI groups, except when CI are located in the temporal lobe (including hippocampus), suggesting that this location mayb e important in the physiopathology of mixed vascular and AD dementia.
