Abstract

Despite advances in the pharmacological treatment of Parkinson’s disease (PD), there comes a time when symptoms can no longer be adequately controlled, alternating between freezing and dyskinesia, seemingly refractory to the entire panoply of the pharmacopeia at the disposal of neurologists. This has prompted a renewed interest in neurosurgical approaches to treatment, targets for lesions, or deep brain stimulation (DBS) having been identified on the basis of our current understanding of the functional organization of basal ganglia circuits in normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated subhuman primates (1, 2). As confirmed by neurophysiological recording in PD patients during surgery, the disease leads to excessive neuronal discharge in the internal division of the globus pallidus (GPi) and substantia nigra, pars reticulata (SNr), as well as in the subthalamic nucleus (STN). Accordingly, the neurosurgeon aims his intervention at either the GPi or STN. The goal is to reduce or eliminate the pathologically high levels of neuronal drive, which ultimately are responsible for excessive thalamic inhibition. The general clinical outcome is consistent with these models. Both posteroventral pallidotomy (PVP) (usually unilateral) and bilateral or unilateral DBS in the GPi are effective in reducing or eliminating drug-induced dyskinesias. The alternate strategy, STN-DBS, improves the symptoms of tremor and rigidity, permitting a reduction of about 50% of medication, and sometimes more in younger patients who are more responsive to levadopa (L-dopa). Rarely, bilateral lesions of the STN have also been effective, but there remains a danger of inducing ballismus, albeit usually transiently. Systematic clinical evaluation of patient symptoms is usually done with the Unified Parkinson’s Disease Rating Scale (UPDRS), following the Core Assessment Program for Surgical Interventional Therapies (CAPSIT) protocol (see refs. 3–7 for comprehensive reviews).

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