Abstract

Deep brain stimulation (DBS) is considered a safe and well tolerated surgical procedure to alleviate Parkinson’s disease (PD) and other movement disorders symptoms along with some psychiatric conditions. Over the last few decades DBS has been shown to provide remarkable therapeutic effect on carefully selected patients. Although its precise mechanism of action is still unknown, DBS improves motor functions and therefore quality of life. To date, two main targets have emerged in PD patients: the globus pallidus pars interna and the subthalamic nucleus. Two other targets, the ventralis intermedius and zona incerta have also been selectively used, especially in tremor-dominant PD patients. The main indications for PD DBS have traditionally been motor fluctuations, debilitating medication induced dyskinesias, unpredictable “off time” state, and medication refractory tremor. Medication refractory tremor and intolerable dyskinesia are potential palliative indications. Besides aforementioned targets, the brainstem pedunculopontine nucleus (PPN) is under investigation for the treatment of ON-state freezing of gait and postural instability. In this article, we will review the most recent literature on DBS therapy for PD, including cutting-edge advances and data supporting the role of DBS in advanced neural-network modulation.

Highlights

  • Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder affecting multiple brain circuits leading to motor symptoms such as bradykinesia, rigidity, resting tremor, and loss of postural reflexes [1]

  • A recent study found that the electrical stimulation of the subthalamic nucleus (STN) in PD patients using therapeutic parameters and a Deep brain stimulation (DBS) electrode did not result in a profound or long-lasting inhibition of surrounding neurons, partially normalizing or “jamming” the pathological signal in the basal ganglia-thalamocortical network [32,33,34]

  • This study provides evidence that improvement in motor symptoms could possibly remain stable for several years post-DBS in a subset of patients

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Summary

Introduction

Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder affecting multiple brain circuits leading to motor symptoms such as bradykinesia, rigidity, resting tremor, and loss of postural reflexes [1]. A recent study found that the electrical stimulation of the STN in PD patients using therapeutic parameters and a DBS electrode did not result in a profound or long-lasting inhibition of surrounding neurons, partially normalizing or “jamming” the pathological signal in the basal ganglia-thalamocortical network [32,33,34].

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