The relationship between Dementia with Lewy bodies (DLB) and Parkinson’s disease (PD) has received little scientific investigation. PD is characterized pathologically by neuronal loss of substantia nigra, with Lewy bodies in the remaining cells. The resulting dopaminergic loss in the basal ganglia causes the clinical syndrome of parkinsonism with resting tremor, rigidity, bradykinesia and postural instability. In nearly all PD patients, Lewy bodies are present in the cortex as well. In addition, other brain stem nuclei, such as locus coeruleus and raphe nuclei, cholinergic cell groups and prefrontal cortex are also involved. The majority of PD patients eventually develop dementia (PDD). DLB and PDD are differentiated by the sequence of symptoms. If dementia occurs before or within one year after appearance of parkinsonism, the diagnosis should be DLB, whereas a diagnosis of PDD is given when dementia develops later, usually after more than 10 years with pure motor symptoms.
Evidence suggests that the neuropsychiatric changes in PD are causally related to the extra-striatal pathologies. In particular, an association between cortical Lewy bodies and dementia has been demonstrated. PDD and DLB share many pathological, neurochemical and clinical features. There is currently no consensus regarding the nosological relationship between these two syndromes. However, the available evidence of similar brain changes and clinical features favours a unifying hypothesis, suggesting that DLB and PDD represent different aspects of a spectrum of Lewy body disease. The presentation will review recent pathological, clinical, genetic and prognostic studies comparing DLB and PDD.
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