Answer
Lewy body dementia (LBD) refers to pathologic changes that underlie several closely related syndromes. Most manifest with a movement disorder component, and the clinical diagnosis received in life often depends on the interval between the diagnosis of dementia and the onset of movement disorder symptoms. If a clinical diagnosis of Parkinson disease is followed by dementia a minimum of 1 year later, then a diagnosis of Parkinson disease dementia is assigned. [19] If the onset of dementia precedes or is roughly concurrent with the onset of Parkinson disease, then the clinical diagnosis of dementia with Lewy bodies (not to be confused with LBD) is used.
By the time the postmortem diagnosis of LBD can be confirmed, years would have passed since the initial clinical diagnosis, making Parkinson disease dementia and LBD difficult to distinguish. Most LBDs are sporadic and are frequently associated with increased age and the male sex. Organophosphate pesticide exposure is a known risk factor. Of interest, several lines of evidence suggest that a history of cigarette smoking may protect from the processes that lead to LBD.
LBD and Parkinson disease dementia share characteristic neuropathologic changes, such as "deposition of alpha-synuclein in Lewy bodies and neurites, and loss of tegmental dopamine cell populations and basal forebrain cholinergic populations." [19]
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Dementia pathology. Bielschowsky silver staining of the cortex at 400× magnification demonstrates a neurofibrillary tangle (black arrow) and a neuritic plaque (white arrow).
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Dementia pathology. Congo red staining of a small cortical artery at 400× magnification demonstrates salmon-colored amyloid deposition in the media of the vessel.
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Dementia pathology. A: Hematoxylin-eosin-Luxol fast blue staining of the basal ganglia at 100× magnification demonstrates a cavitary infarct. Calcific medial sclerosis of small arteries is also present. B: At 400× magnification, numerous foamy macrophages are present within the center of the infarcted tissue.
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Dementia pathology. A: Hematoxylin and eosin staining of the substantia nigra at 400× magnification demonstrates multiple Lewy bodies within a pigmented neuron. The Lewy bodies are round with a densely eosinophilic core surrounded by a clear halo. B: Immunohistochemical staining (brown) against alpha-synuclein at 400× magnification reveals a round Lewy body within the soma of a neuron.
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Dementia pathology. Comorbid brain pathologies are common in the elderly population. This Venn diagram demonstrates the co-occurrence of brain pathologies as evident from population-based autopsy studies of brain aging.
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Dementia pathology. A: Hematoxylin and eosin staining at 400× magnification of the dentate fascia of the hippocampus reveals round eosinophilic Pick bodies (arrows) in the soma of granular neurons. B: Immunohistochemical staining (brown) against tau at 400× magnification reveals round intraneuronal Pick bodies in cortical neurons.
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Dementia pathology. A: Hematoxylin and eosin staining at 400× magnification of the cerebral cortex reveals the coalescent clear vesicles characteristic of spongiform encephalopathy. B: Immunohistochemical staining (brown) against protease-resistant prion protein reveals the granular immunoreactivity seen in Creutzfeldt-Jakob disease.
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Dementia pathology. Immunohistochemical staining (brown) against tau at 400× magnification reveals glial immunoreactivity that is characteristic of this case of cortico-basal ganglionic degeneration.
