Chapter

Brain and Behavior Deficits in De Novo Parkinson Disease

David E. Vaillancourt and Janey Prodoehl

in Motor Control

Published in print December 2010 | ISBN: 9780195395273
Published online January 2011 | e-ISBN: 9780199863518 | DOI: http://dx.doi.org/10.1093/acprof:oso/9780195395273.003.0015
Brain and Behavior Deficits in De Novo Parkinson Disease

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Over the past several decades, models of basal ganglia function that describe the pathophysiology of Parkinson disease (PD) have emerged from studies in both nonhuman primates and rodents. One influential experimental paradigm has relied upon infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a piperidine derivative, to acutely induce irreversible symptoms of Parkinsonism, including bradykinesia and rigidity, in animals. Investigators then use electrophysiological recordings in specific basal ganglia nuclei and cortical areas to relate behavioral deficits with electrophysiological recordings. Based on this experimental paradigm, clinically relevant models of basal ganglia and cortical function have been developed, and these models have led to new therapeutic interventions in humans with PD, such as deep brain stimulation. However, since the MPTP model causes a rapid degeneration of most of the cells in the substantia nigra, its significance for early-stage PD is less clear, because the development of PD symptoms in humans occurs more gradually. In addition, these models typically characterize the motor deficits of PD, with less focus on the nonmotor deficits of PD. In humans, most behavioral and brain imaging studies in PD have focused on patients with the disease who are more advanced in their symptomology, and who have already received symptomatic treatment. This can make it difficult to isolate the effects of the disease itself from the effects of the treatment on brain activation and behavior. As such, this chapter focuses on what is currently known regarding the motor and nonmotor features of patients with early-stage PD who have not yet started any symptomatic treatment (i.e., de novo PD). A substantial part of the chapter examines brain imaging studies of de novo PD.

Keywords: Parkinson disease; bradykinesia; rigidity; deep brain stimulation; early-state PD; de novo PD

Chapter.  10747 words.  Illustrated.

Subjects: Neuroscience

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