ABSTRACT
Parkinson’s disease (PD) is a progressive disorder that produces tremor, slowness, rigidity, and postural instability. Pathologically there is selective neuronal loss in the substantia nigra with the presence of intraneuronal inclusions (Lewy bodies) containing abnormal deposition of alpha-synuclein, reduced nigrostriatal neuronal projections, and subsequent striatal dopamine deficiency (1). Symptomatic treatment focuses on replacing striatal dopamine; however, no treatment has been proven to slow or halt progression of the disease (2,3). Further, the etiology remains unknown, with ongoing controversy about the role of genetics versus environment (4-8). Other neurodegenerative diseases, like progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), directly damage striatum and may also cause bradykinesia, rigidity, and postural instability. Until recently, these diseases were distinguished from idiopathic PD by subtle clinical features, response to levodopa, or postmortem findings (9).
