The Sequence Effect Worsens Over Time in Parkinson’s Disease and Responds to Open and Closed-Loop Subthalamic Nucleus Deep Brain Stimulation

Kehnemouyi, Yasmine M.; Petrucci, Matthew N.; Wilkins, Kevin B.; Melbourne, Jillian A.; Brontë‐Stewart, Helen

doi:10.3233/jpd-223368

Cited by 5 publications

(2 citation statements)

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“…On the neural level, for instance, it has been shown that STN‐DBS can induce LTP‐like plasticity (Milosevic et al, 2018) and reshape and stabilize motor networks, as measured by fMRI, bringing them closer to the healthy state (Chu et al, 2023). On the behavioural level, it was found that STN‐DBS can restore motor learning that is lost in the absence of stimulation (De Almeida Marcelino et al, 2019) and counteract the sequence effect or decrement in amplitude and velocity (Kehnemouyi et al, 2023).…”

Section: Neural Reinforcement As a Target For Adaptive Deep Brain Sti...mentioning

confidence: 99%

Dopaminergic reinforcement in the motor system: Implications for Parkinson's disease and deep brain stimulation

Cavallo,

Neumann

2024

Eur J of Neuroscience

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Millions of people suffer from dopamine‐related disorders spanning disturbances in movement, cognition and emotion. These changes are often attributed to changes in striatal dopamine function. Thus, understanding how dopamine signalling in the striatum and basal ganglia shapes human behaviour is fundamental to advancing the treatment of affected patients. Dopaminergic neurons innervate large‐scale brain networks, and accordingly, many different roles for dopamine signals have been proposed, such as invigoration of movement and tracking of reward contingencies. The canonical circuit architecture of cortico‐striatal loops sparks the question, of whether dopamine signals in the basal ganglia serve an overarching computational principle. Such a holistic understanding of dopamine functioning could provide new insights into symptom generation in psychiatry to neurology. Here, we review the perspective that dopamine could bidirectionally control neural population dynamics, increasing or decreasing their strength and likelihood to reoccur in the future, a process previously termed neural reinforcement. We outline how the basal ganglia pathways could drive strengthening and weakening of circuit dynamics and discuss the implication of this hypothesis on the understanding of motor signs of Parkinson's disease (PD), the most frequent dopaminergic disorder. We propose that loss of dopamine in PD may lead to a pathological brain state where repetition of neural activity leads to weakening and instability, possibly explanatory for the fact that movement in PD deteriorates with repetition. Finally, we speculate on how therapeutic interventions such as deep brain stimulation may be able to reinstate reinforcement signals and thereby improve treatment strategies for PD in the future.

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Section: Neural Reinforcement As a Target For Adaptive Deep Brain Sti...mentioning

confidence: 99%

Dopaminergic reinforcement in the motor system: Implications for Parkinson's disease and deep brain stimulation

Cavallo,

Neumann

2024

Eur J of Neuroscience

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show abstract

“…While no scientific study has addressed this hypothesis specifically, some findings can corroborate this idea. On the neural level, for instance, it has been shown that STN-DBS can induce LTP-like plasticity (Milosevic et al, 2018) and on the behavioral level it was found that it can restore motor learning that is lost in the absence of stimulation (De Almeida Marcelino et al, 2019) and it can counteract the sequence effect or decrement in amplitude and velocity (Kehnemouyi et al, 2023).…”

Section: Neural Reinforcement As a Target For Adaptive Deep Brain Sti...mentioning

confidence: 99%

Dopaminergic reinforcement in the motor system: Implications for Parkinson’s disease and deep brain stimulation

Cavallo,

Wolf-Julian

2023

Preprint

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Millions of people suffer from dopamine-related disorders spanning disturbances in movement, cognition and emotion, often attributed to changes in striatal dopamine function. Understanding how dopamine signaling in the striatum and basal ganglia shapes human behavior is fundamental to advancing the treatment of affected patients. Dopaminergic neurons innervate large scale brain networks and many different roles for dopamine signals have been proposed, such as invigoration of movement and tracking of reward contingencies. The canonical circuit architecture of cortico-striatal loops sparks the question, whether dopamine signals in the basal ganglia serve an overarching computational principle which could provide new insights into symptom generation in psychiatry to neurology. Here, we review the perspective that dopamine could bidirectionally control neural population dynamics, increasing, or decreasing their strength and likelihood to reoccur in the future, a process previously termed neural reinforcement. We outline how the basal ganglia pathways could drive strengthening and weakening of circuit dynamics and discuss the implication of this hypothesis on the understanding of motor signs of Parkinson’s disease (PD), the most frequent dopaminergic disorder. We propose that loss of dopamine in PD may lead to a pathological brain state where repetition of neural activity leads to weakening and instability, possibly explanatory for the fact that movement in PD deteriorates with repetition, as defined by the sequence effect or decrement of movement. Finally, we speculate on how therapeutic interventions such as deep brain stimulation (DBS) may be able to reinstate reinforcement signals and thereby improve treatment strategies of PD in the future.

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Subthalamic stimulation modulates context-dependent effects of beta bursts during fine motor control

Bange,

Gonzalez-Escamilla,

Herz

et al. 2024

Nat Commun

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Increasing evidence suggests a considerable role of pre-movement beta bursts for motor control and its impairment in Parkinson’s disease. However, whether beta bursts occur during precise and prolonged movements and if they affect fine motor control remains unclear. To investigate the role of within-movement beta bursts for fine motor control, we here combine invasive electrophysiological recordings and clinical deep brain stimulation in the subthalamic nucleus in 19 patients with Parkinson’s disease performing a context-varying task that comprised template-guided and free spiral drawing. We determined beta bursts in narrow frequency bands around patient-specific peaks and assessed burst amplitude, duration, and their immediate impact on drawing speed. We reveal that beta bursts occur during the execution of drawing movements with reduced duration and amplitude in comparison to rest. Exclusively when drawing freely, they parallel reductions in acceleration. Deep brain stimulation increases the acceleration around beta bursts in addition to a general increase in drawing velocity and improvements of clinical function. These results provide evidence for a diverse and task-specific role of subthalamic beta bursts for fine motor control in Parkinson’s disease; suggesting that pathological beta bursts act in a context dependent manner, which can be targeted by clinical deep brain stimulation.

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The Sequence Effect Worsens Over Time in Parkinson’s Disease and Responds to Open and Closed-Loop Subthalamic Nucleus Deep Brain Stimulation

Cited by 5 publications

References 50 publications

Dopaminergic reinforcement in the motor system: Implications for Parkinson's disease and deep brain stimulation

Dopaminergic reinforcement in the motor system: Implications for Parkinson's disease and deep brain stimulation

Dopaminergic reinforcement in the motor system: Implications for Parkinson’s disease and deep brain stimulation

Subthalamic stimulation modulates context-dependent effects of beta bursts during fine motor control

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