Deep brain stimulation for Parkinson’s disease: how to select candidates for pallidal or subthalamic stimulation

2000 ◽  
Vol 9 (6) ◽  
pp. 355-366
Author(s):  
Takashi Tsubokawa ◽  
Yoichi Katayama
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Subthalamic Stimulation ◽  
Deep Brain

scholarly journals Subthalamic stimulation impairs stopping of ongoing movements

Brain ◽  
2020 ◽  
Author(s):  
Roxanne Lofredi ◽  
Georg Cem Auernig ◽  
Friederike Irmen ◽  
Johanna Nieweler ◽  
Wolf-Julian Neumann ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Right Hemisphere ◽  
Inferior Frontal Gyrus ◽  
Motor Area ◽  
Subthalamic Stimulation ◽  
The Right ◽  
Deep Brain

Abstract The subthalamic nucleus is part of a global stopping network that also includes the presupplementary motor area and inferior frontal gyrus of the right hemisphere. In Parkinson’s disease, subthalamic deep brain stimulation improves movement initiation and velocity, but its effect on stopping of ongoing movement is unknown. Here, we examine the relation between movement stopping and connectivity of stimulation volumes to the stopping network. Stop and go times were collected in 17 patients with Parkinson’s disease on and off subthalamic stimulation during visually cued initiation and termination of continuous, rotational movements. Deep brain stimulation contacts were localized; the stimulation volume computed and connectivity profiles estimated using an openly available, normative structural connectome. Subthalamic stimulation significantly increased stop times, which correlated with the connectivity of the stimulation volume to presupplementary motor area and inferior frontal gyrus of the right hemisphere. The robustness of this finding was validated using three separate analysis streams: voxel-wise whole-brain connectivity, region of interest connectivity and a tract-centred method. Our study sheds light on the role of the fronto-subthalamic inhibitory triangle in stopping of ongoing movements and may inspire circuit based adaptive stimulation strategies for control of stopping impairment, possibly reflected in stimulation-induced dyskinesia.

Influence of deep brain stimulation and levodopa on signs and symptoms in Parkinson's disease

2009 ◽  
Vol 36 (S 02) ◽  
Author(s):  
J Gierthmühlen ◽  
P Arning ◽  
G Wasner ◽  
A Binder ◽  
J Herzog ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Signs And Symptoms ◽  
Deep Brain

The effects of subthalamic nucleus deep brain stimulation on precision grip abnormalities in Parkinson's disease

2005 ◽  
Vol 32 (S 4) ◽  
Author(s):  
S Fellows ◽  
M Kronenbürger ◽  
N Allert ◽  
C Fromm ◽  
J Noth ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Subthalamic Nucleus ◽  
Brain Stimulation ◽  
Precision Grip ◽  
Deep Brain

Visual Effects of Deep Brain Stimulation in a Patient with Parkinson’s Disease

2019 ◽  
pp. 158-173
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Visual System ◽  
Brain Stimulation ◽  
Neurodegenerative Disorder ◽  
Initial Examination ◽  
Before And After ◽  
Deep Brain ◽  
Cover Test

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder caused by a dopamine deficiency that presents with motor symptoms. Visual disorders can occur concomitantly but are frequently overlooked. Deep brain stimulation (DBS) has been an effective treatment to improve tremors, stiffness and overall mobility, but little is known about its effects on the visual system. Case Report: A 75-year-old Caucasian male with PD presented with longstanding binocular diplopia. On baseline examination, the best-corrected visual acuity was 20/25 in each eye. On observation, he had noticeable tremors with an unsteady gait. Distance alternating cover test showed exophoria with a right hyperphoria. Near alternating cover test revealed a significantly larger exophoria accompanied by a reduced near point of convergence. Additional testing with a 24-2 Humphrey visual field and optical coherence tomography (OCT) of the nerve and macula were unremarkable. The patient underwent DBS implantation five weeks after initial examination, and the device was activated four weeks thereafter. At follow up, the patient still complained of intermittent diplopia. There was no significant change in the manifest refraction or prism correction. On observation, the patient had remarkably improved tremors with a steady gait. All parameters measured were unchanged. The patient was evaluated again seven months after device activation. Although vergence ranges at all distances were improved, the patient was still symptomatic for intermittent diplopia. OCT scans of the optic nerve showed borderline but symmetric thinning in each eye. All other parameters measured were unchanged. Conclusion: The case found no significant changes on ophthalmic examination after DBS implantation and activation in a patient with PD. To the best of the authors’ knowledge, there are no other cases in the literature that investigated the effects of DBS on the visual system pathway in a patient with PD before and after DBS implantation and activation.

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