Can neuromodulation techniques optimally exploit cerebello-thalamo-cortical circuit properties to enhance motor learning post-stroke?

2019 ◽  
Vol 30 (8) ◽  
pp. 821-837 ◽  
Author(s):  
Sharon Israely ◽  
Gerry Leisman
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Animal Studies ◽  
Motor Recovery ◽  
Motor Deficits ◽  
Post Stroke ◽  
Non Invasive ◽  
Deep Brain

Abstract Individuals post-stroke sustain motor deficits years after the stroke. Despite recent advancements in the applications of non-invasive brain stimulation techniques and Deep Brain Stimulation in humans, there is a lack of evidence supporting their use for rehabilitation after brain lesions. Non-invasive brain stimulation is already in use for treating motor deficits in individuals with Parkinson’s disease and post-stroke. Deep Brain Stimulation has become an established treatment for individuals with movement disorders, such as Parkinson’s disease, essential tremor, epilepsy, cerebral palsy and dystonia. It has also been utilized for the treatment of Tourette’s syndrome, Alzheimer’s disease and neuropsychiatric conditions such as obsessive-compulsive disorder, major depression and anorexia nervosa. There exists growing scientific knowledge from animal studies supporting the use of Deep Brain Stimulation to enhance motor recovery after brain damage. Nevertheless, these results are currently not applicable to humans. This review details the current literature supporting the use of these techniques to enhance motor recovery, both from human and animal studies, aiming to encourage development in this domain.

scholarly journals Deep Brain Stimulation Does Not Silence Neurons in Subthalamic Nucleus in Parkinson's Patients

2010 ◽  
Vol 103 (2) ◽  
pp. 962-967 ◽  
Author(s):  
Jonathan D. Carlson ◽  
Daniel R. Cleary ◽  
Justin S. Cetas ◽  
Mary M. Heinricher ◽  
Kim J. Burchiel
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Firing Rate ◽  
Subthalamic Nucleus ◽  
Brain Stimulation ◽  
Animal Studies ◽  
Stimulation Parameters ◽  
Deep Brain

Two broad hypotheses have been advanced to explain the clinical efficacy of deep brain stimulation (DBS) in the subthalamic nucleus (STN) for treatment of Parkinson's disease. One is that stimulation inactivates STN neurons, producing a functional lesion. The other is that electrical stimulation activates the STN output, thus “jamming” pathological activity in basal ganglia-corticothalamic circuits. Evidence consistent with both concepts has been adduced from modeling and animal studies, as well as from recordings in patients. However, the stimulation parameters used in many recording studies have not been well matched to those used clinically. In this study, we recorded STN activity in patients with Parkinson's disease during stimulation delivered through a clinical DBS electrode using standard therapeutic stimulus parameters. A microelectrode was used to record the firing of a single STN neuron during DBS (3–5 V, 80–200 Hz, 90- to 200-μs pulses; 33 neurons/11 patients). Firing rate was unchanged during the stimulus trains, and the recorded neurons did not show prolonged (s) changes in firing rate on termination of the stimulation. However, a brief (∼1 ms), short-latency (6 ms) postpulse inhibition was seen in 10 of 14 neurons analyzed. A subset of neurons displayed altered firing patterns, with a predominant shift toward random firing. These data do not support the idea that DBS inactivates the STN and are instead more consistent with the hypothesis that this stimulation provides a null signal to basal ganglia-corticothalamic circuitry that has been altered as part of Parkinson's disease.

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

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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