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Washington University Experience | NEURODEGENERATION | Lewy Body Disease (LBD) | 6 LBD - Microscopic Pathology - Cerebral Cortex | 13B Case 13 Denoument
Neuro Final Diagnoses: Idiopathic Parkinson’s disease with diffuse Lewy body disease; Alzheimer's disease; Remote infarcts, left occipital and temporal lobes. ---- Neuro Diagnosis Comment: The main neuropathological findings in this case are Lewy bodies and Lewy neurites in brainstem nuclei, limbic areas, and neocortex. In the staging scheme proposed by Braak et al. (PMID: 12498954) the distribution of Lewy bodies in brainstem, limbic and neocortical areas in this brain is consistent with Parkinson's disease stage 6 on 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; in the revised criteria (McKeith et al. criteria, PMID: 16237129, which take into account coexisting Alzheimer's pathology, there is a ‘high probability’ that the patient’s dementia is caused by Lewy body disease. In addition to Lewy body pathology, this brain shows evidence of Alzheimer’s disease (AD). Neocortical areas show widespread frequent diffuse beta-amyloid plaques. Neuritic plaques and neurofibrillary tangles are largely restricted to the mesial temporal lobe, amygdala and hippocampus, with only meager representation in the superior temporal gyrus and basal forebrain. This distribution of AD pathology is sufficient to meet the neuropathological criteria for the diagnosis of Alzheimer's disease according to the criteria of Khachaturian but only support a diagnosis of, at best, ‘possible AD’ by neuropathological CERAD criteria. By NIA-Reagan Institute criteria, these features suggest a ‘low probability’ that the patient’s dementia can be attributed to AD pathology. When the observed AD and Lewy body pathologies are considered together, the revised McKeith et al. criteria (PMID: 16237129) suggest a 'high probability' that the dementia in this patient was caused by Lewy body disease. In addition to the neurodegenerative lesions, remote infarcts were identified in the left temporal and left occipital lobes, consistent with lesions observed radiographically and through macroscopic pathological examination. These lesions are thought likely to have contributed to the patient’s clinical impairments. In conclusion, the patient’s parkinsonism and cognitive symptoms may be explained largely by Lewy body pathology (idiopathic Parkinson’s disease with diffuse Lewy body disease). However, the observed macroscopic infarcts and Alzheimer’s disease pathology also likely contributed somewhat to the patient’s cognitive impairment.
