ABSTRACT
Parkinson’s disease (PD) is a neurobehavioral disorder dened clinically by its motor features (Rowland 2000; Fahn 2003). Pathologically, it is dened by the loss of pigmented neurons in the brain stem, coupled with the presence of Lewy bodies in those degenerating centers (Rowland 2000; Hardy 2003). However, advances in histology have led to the recognition of pathological changes in regions far more widespread than recognized even a decade ago, such as the olfactory structures, enteric nuclei, preganglionic parasympathetic projection neurons and preganglionic and postganglionic sympathetic projection neurons, lower brain stem, midbrain, neocortex, and sensory association areas (Braak and Del Tredici 2008a,b). Correlations between pathology and clinical phenomena have yet to be made for most brain regions, leaving our understanding of the mechanisms of the clinical features of the disease incomplete. The behavioral and nonmotor aspects of PD are particularly difcult to understand because of the major overlap among problems due to neuronal degeneration, psychological responses to progressive disability, iatrogenic complications, and the secondary effects of primary disorders, such as excessive daytime somnolence due to sleep disorders (Friedman and Friedman 1993; Shulman et al. 2001, 2002).
