Abstract

Deep brain stimulation has developed into an established treatment for movement disorders and is being actively investigated for numerous other neurological as well as psychiatric disorders. An accurate electrode placement in the target area and the effective programming of DBS devices are considered the most important factors for the individual outcome. Recent research in humans highlights the relevance of widespread networks connected to specific DBS targets. Improving the targeting of anatomical and functional networks involved in the generation of pathological neural activity will improve the clinical DBS effect and limit side-effects. Here, we offer a comprehensive overview over the latest research on target structures and targeting strategies in DBS. In addition, we provide a detailed synopsis of novel technologies that will support DBS programming and parameter selection in the future, with a particular focus on closed-loop stimulation and associated biofeedback signals.

Highlights

  • Deep brain stimulation (DBS) has become the treatment of choice for movement disorder, such as Parkinson’s disease (PD), medically intractable essential tremor (ET) and complicated segmental and generalized dystonia [1]

  • DBS is increasingly used in other neurological disorders like neuropathic pain and epilepsy, and is being investigated for psychiatric disorders [2], such as obsessive-compulsive disorder, depression and Tourette syndrome and neurodegenerative diseases like Alzheimer’s disease [3]

  • Local field potentials and network connectivity measures based on electrophysiological signals with their high temporal resolution can already be measured with sensing DBS electrodes or other implanted neural sensors and hold great promise as biomarkers

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Summary

Introduction

Deep brain stimulation (DBS) has become the treatment of choice for movement disorder, such as Parkinson’s disease (PD), medically intractable essential tremor (ET) and complicated segmental and generalized dystonia [1]. Improving the initial targeting and later stimulation of specific neural structures and pathways involved in the generation of pathological neural activity as well as avoiding others will be a crucial point for improving the clinical DBS effect and, at the same time, limiting side-effects.

Results
Conclusion

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