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Washington University Experience | NEURODEGENERATION | Lewy Body Disease (LBD) | 2 LBD - Gross Pathology - Cerebrum LBD -Dementia | 12B Case 12 Denoument
Final Neuropathologic Diagnoses: Diffuse Lewy Body Disease ---- Comment: The main neuropathological findings are Lewy bodies and Lewy neurites in brainstem nuclei, limbic areas, and neocortex. In the staging scheme proposed by Braak et al. the presence of Lewy bodies in brainstem, limbic and neocortical areas in this brain is consistent with Parkinson's disease stage 6 of a six-stage scale (range: 0, 1-6). The density and distribution of these lesions is also sufficient to meet the criteria for dementia with Lewy bodies and in the revised criteria, which takes account of coexisting Alzheimer's disease-type changes, there is a ‘high probability’ that the dementia is caused by Lewy body disease (McKeith et al, PMID: 16237129). The parkinsonism preceded the cognitive changes by more than one year. Neocortical areas showed generally few but occasional foci of frequent beta-amyloid plaques, no neuritic plaques, and only a few neurofibrillary tangles, mainly confined to the medial temporal lobe. The frequent neocortical beta-amyloid plaques are sufficient to meet the neuropathologic criteria for the diagnosis of Alzheimer's disease according to the criteria of Khachaturian, but the absence of neuritic plaques and tangles excludes a diagnosis of AD by CERAD and NIA-Reagan Institute criteria. In addition to the neurodegenerative lesions described above, there was also moderate vascular pathology with areas of hypoxia-ischemia which may also have contributed, in part, to the cognitive changes. In conclusion, the parkinsonian and cognitive symptoms may be explained largely by idiopathic Parkinson’s disease with dementia (LBD with dementia). The Alzheimer's disease-type changes and vascular pathology probably contributed only modestly, if at all, to the cognitive changes.
