Abstract
L-DOPA is still the most effective pharmacological therapy for the treatment of motor symptoms in Parkinson's disease (PD) almost four decades after it was first used. Deep brain stimulation (DBS) is a safe and highly effective treatment option in patients with PD. Even though a clear understanding of the mechanisms of both treatment methods is yet to be obtained, the combination of both treatments is the most effective standard evidenced-based therapy to date. Recent studies have demonstrated that DBS is a therapy option even in the early course of the disease, when first complications arise despite a rigorous adjustment of the pharmacological treatment. The unique feature of this therapeutic approach is the ability to preferentially modulate specific brain networks through the choice of stimulation site. The clinical effects have been unequivocally confirmed in recent studies; however, the impact of DBS and the supplementary effect of L-DOPA on the neuronal network are not yet fully understood. In this review, we present emerging data on the presumable mechanisms of DBS in patients with PD and discuss the pathophysiological similarities and differences in the effects of DBS in comparison to dopaminergic medication. Targeted, selective modulation of brain networks by DBS and pharmacodynamic effects of L-DOPA therapy on the central nervous system are presented. Moreover, we outline the perioperative algorithms for PD patients before and directly after the implantation of DBS electrodes and strategies for the reduction of side effects and optimization of motor and non-motor symptoms.
Highlights
The principal pathological characteristic of Parkinson’s disease (PD) is the progressive death of the pigmented neurons of the substantia nigra pars compacta (SNc) diagnosed by symptoms including bradykinesia/akinesia, rigidity, postural abnormalities and tremor [1]
The neural correlates of globus pallidus internus (GPi) stimulation in PD have been less investigated, some studies have shown an increase in anterior cingulate cortex (ACC) and supplementary motor area (SMA) activation during a motor task [94, 95]
Recent work has shown that in the distinct group of brain regions acting synchronously, segregated tremor clusters may relate to tremor activity in specific muscle groups, pointing to multiple tremor-related subloops within subcortical structures [158], which suggests the possible existence of multiple tremor oscillators within the basal gangliathalamo-cortical circuits
Summary
The principal pathological characteristic of Parkinson’s disease (PD) is the progressive death of the pigmented neurons of the substantia nigra pars compacta (SNc) diagnosed by symptoms including bradykinesia/akinesia, rigidity, postural abnormalities and tremor [1]. Several animal studies have shown support for the hypothesis of direct cortical activation during STN-DBS [61, 62]. Non-invasive brain stimulation studies using TMS have shown abnormal motor cortical plasticity in PD which has been investigated further for understanding the mechanism of DBS.
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