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In Parkinson’s disease pallidal deep brain stimulation speeds up response initiation but has no effect on reactive inhibition

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Abstract

The fronto-striatal circuits are considered to mediate inhibitory control over action. The aim of this study was to investigate the contribution of the internal segment of the pallidum (GPi), one of the final output pathways from the basal ganglia to the cortex, in inhibition. We examined the effect of deep brain stimulation (DBS) of the GPi (GPi-DBS) in patients with Parkinson’s disease who performed a conditional stop signal task, with DBS on and off. Modulation of GPi activity was associated with significantly faster Go reaction times with DBS on than off, but stop signal reaction times were not altered. Application of the drift diffusion model indicated that GPi-DBS was associated with significantly lower response thresholds compared to GPi-DBS off. However, the drift rate was significantly lower than healthy controls with both GPi-DBS on and off. These results suggest that the GPi plays a crucial role in the ‘Go’ pathway, perhaps facilitating reaching the required threshold to initiate actions. However, GPi-DBS does not alter the functioning of the indirect ‘NoGo’ pathway, and other basal ganglia nuclei, such as the STN, may play a greater role in reactive response inhibition and conflict resolution.

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Abbreviations

PD:

Parkinson’s disease

DBS:

Deep brain stimulation

GPi:

Internal segment of the globus pallidus

STN:

Subthalamic nucleus

RT:

Reaction time

SSRT:

Stop signal reaction time

CIS:

Conflict-induced slowing

RDE:

Response delay effect

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Acknowledgments

We would like to thank the patients for their participation. This work was supported by the Marga and Walter Boll Foundation.

Conflict of interest

All authors declare that they have no conflict of interest.

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Correspondence to M. Jahanshahi.

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Kohl, S., Aggeli, K., Obeso, I. et al. In Parkinson’s disease pallidal deep brain stimulation speeds up response initiation but has no effect on reactive inhibition. J Neurol 262, 1741–1750 (2015). https://doi.org/10.1007/s00415-015-7768-6

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  • DOI: https://doi.org/10.1007/s00415-015-7768-6

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