from Part one - Clinical issues
Published online by Cambridge University Press: 06 July 2010
Summary
The pathological correlate of parkinsonism and dementia (PD-dementia) may be diffuse Lewy body disease (DLBD), Alzheimer's disease (AD) or a combination of both pathologies. Positron emission tomography (PET) studies show a resting pattern of fronto-temporo-parietal hypometabolism in both AD and in PD-dementia patients. Diagnostic criteria have been recently devised to try and distinguish between AD and dementia of the Lewy body type. We have studied three PD-dementia patients fulfilling the clinical criteria for DLBD with 18F-fluorodeoxyglucose (FDG) PET. The results showed an AD pattern of fronto-temporo-parietal hypometabolism, although these patients had only mild cognitive dysfunction. These preliminary results suggest that metabolic PET studies are unable to distinguish the cortical deficit of PD-dementia from AD, though the PD-dementia patients may have relatively greater frontal hypometabolism. Further studies with postmortem confirmation will be required to establish whether DLBD is associated with a distinctive pattern of resting hypometabolism.
Introduction
Patients with postmortem evidence of diffuse Lewy body disease (DLBD) present clinically with either isolated parkinsonism, dementia or a combination of both (PD-dementia). PD-dementia may also be a manifestation of patients who show isolated Alzheimer's (AD) type changes at postmortem, or a mixture of both Alzheimer and Lewy body pathologies.
Initially, Lewy body disease was categorized according to its distribution in the central nervous system, diffuse (DLBD), transitional and iso-lated brainstem subtypes being recognized (Kosaka et al., 1984). Antiubiquitin staining however, has shown that cortical Lewy bodies are present in nearly all patients with clinically typical Parkinson's disease (PD) (Perry et al., 1991; Schmidt et al., 1991; Hughes et al., 1993).
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