ABSTRACT
Parkinson’s disease (PD) is a neurobehavioral disorder defined clinically by its motor features.1,2 Pathologically, it is defined by the loss of pigmented neurons in the brain stem, coupled with the presence of Lewy bodies in those degenerating centers.1,3 However, advances in histology have led to the recognition of pathological changes in regions far more widespread than recognized even a decade ago, and there is every reason to believe that more surprises are in store in the near future.4,5 The 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 difficult 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 disorder.6-8
One of the most common nonmotor symptoms associated with Parkinson’s disease is fatigue.6,7 “Fatigue is a complex and enigmatic entity;”9 it is a symptom complex, rather than an isolated symptom or sign, and may be considered in a sense analogous to depression or even to the historical name of the disease itself, paralysis agitans. Patients with PD are never paralyzed, or even particularly weak, but they often feel weak and complain about it. Unlike weakness, which can be objectively measured, fatigue is, by its nature, an elusive concept.
