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The conceptualization of clinical aspects of Parkinson disease (PD) and its pathophysiology has changed considerably since Braak's description of a “bottom-up” progression of Lewy body pathology from the lower medulla and the olfactory bundle.1 Substantia nigra involvement, once the hallmark of PD pathology, is now recognized to occur at a substantially later stage, with nonmotor symptoms (NMS) occurring before classical motor signs are evident. Recent diagnostic criteria have been devised to predict prodromal PD2 in which PD NMS underpin the prodromal stage. The phenotypic heterogeneity of PD reflects the convergence of deficits in multiple transmitter systems and non-dopamine pathways, including the cholinergic, noradrenergic, and serotonergic systems.3–5 This formulation has now been translated to clinical practice with the recent description of several nonmotor subtypes of PD.6
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- © 2016 American Academy of Neurology
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