Introduction

Parkinson's disease (PD) is one of the most prevalent neurodegenerative diseases and affects between 100 and 200 persons per 100,000 (Schrag, 2002). The prevalence of PD increases with age to affect about 2% of those aged 65 years and above (de Rijk et al., 1997). In addition to idiopathic PD, the term “parkinsonism” is used to label a variety of diseases and syndromes related to different neurodegenerative processes, structural cerebral changes and environmental exposures. Dystonia, although less frequent than PD may also affect up to 700 patients per 100,000 in the population aged above 50 years (Muller et al., 2002). Considering the high prevalence of essential tremor (ET) of 0.4–4% in the overall population (Louis et al., 1998) and the idiopathic restless-legs syndrome affecting some 10% of the population above 65 years (Rothdach et al., 2000) there can be little doubt that movement disorders are among the most prevalent neurologic conditions in the community. In fact medical or surgical therapies are available for most of these but symptomatic efficacy is usually incomplete. This is particularly true for PD and dystonia which will be the focus of this chapter.

Functional organization of the basal ganglia

The current understanding of basal ganglia dysfunction in PD and other movement disorders is based on the model introduced by Alexander et al. (1986). This model postulates that striatal projections are segregated into discrete loops according to their projection targets. Within these circuits striatal output to the globus pallidus internus (GPi) and substantia nigra pars reticulata (SNr) involves a direct GABAergic (gamma aminobutyric acid) pathway and an indirect pathway via the globus pallidus externus (GPe) and the subthalamic nucleus (STN).