Using monkey hand exoskeleton to explore finger passive joint movement response in primary motor cortex

The execution of voluntary muscular activity is controlled by the primary motor cortex, together with the cerebellum and basal ganglia. The synchronization of neural activity in the intracortical network is crucial for the regulation of movements. In certain motor diseases, such as dystonia, this synchrony can be altered in any node of the cerebello-cortical network. Questions remain about how the cerebellum influences the motor cortex and interhemispheric communication. This research aims to study the interhemispheric cortical communication between the motor cortices during dystonia, a neurological movement syndrome consisting of sustained or repetitive involuntary muscle contractions. We pharmacologically induced lateralized dystonia to adult male albino mice by administering low doses of kainic acid on the left cerebellar hemisphere. Using electrocorticography and electromyography, we investigated the power spectral densities, cortico-muscular, and interhemispheric coherence between the right and left motor cortices, before and during dystonia, for five consecutive days. Mice displayed lateralized abnormal motor signs, a reduced general locomotor activity, and a high score of dystonia. The results showed a progressive interhemispheric coherence decrease in low-frequency bands (delta, theta, beta) during the first 3 days. The cortico-muscular coherence of the affected side had a significant increase in gamma bands on days 3 and 4. In conclusion, lateralized cerebellar dysfunction during dystonia was associated with a loss of connectivity in the motor cortices, suggesting a possible cortical compensation to the initial disturbances induced by cerebellar left hemisphere kainate activation by blocking the propagation of abnormal oscillations to the healthy hemisphere. However, the cerebellum is part of several overly complex circuits, therefore other mechanisms can still be involved in this phenomenon.

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Multifocal Noninvasive Magnetic Stimulation of the Primary Motor Cortex in Type 1 Myotonic Dystrophy –A Proof of Concept Pilot Study

Journal of Neuromuscular Diseases ◽

10.3233/jnd-210690 ◽

2021 ◽

pp. 1-10

Author(s):

Ericka Greene ◽

Jason Thonhoff ◽

Blessy S. John ◽

David B. Rosenfield ◽

Santosh A. Helekar

Keyword(s):

Motor Cortex ◽

Myotonic Dystrophy ◽

Muscle Function ◽

Magnetic Stimulation ◽

Primary Motor Cortex ◽

Repetitive Transcranial Magnetic Stimulation ◽

Compound Muscle Action Potential ◽

Sham Stimulation ◽

Stimulation Of

Background: Repeated neuromuscular electrical stimulation in type 1 Myotonic Dystrophy (DM1) has previously been shown to cause an increase in strength and a decrease in hyperexcitability of the tibialis anterior muscle. Objective: In this proof-of-principle study our objective was to test the hypothesis that noninvasive repetitive transcranial magnetic stimulation of the primary motor cortex (M1) with a new portable wearable multifocal stimulator causes improvement in muscle function in DM1 patients. Methods: We performed repetitive stimulation of M1, localized by magnetic resonance imaging, with a newly developed Transcranial Rotating Permanent Magnet Stimulator (TRPMS). Using a randomized within-patient placebo-controlled double-blind TRPMS protocol, we performed unilateral active stimulation along with contralateral sham stimulation every weekday for two weeks in 6 adults. Methods for evaluation of muscle function involved electromyography (EMG), hand dynamometry and clinical assessment using the Medical Research Council scale. Results: All participants tolerated the treatment well. While there were no significant changes clinically, EMG showed significant improvement in nerve stimulus-evoked compound muscle action potential amplitude of the first dorsal interosseous muscle and a similar but non-significant trend in the trapezius muscle, after a short exercise test, with active but not sham stimulation. Conclusions: We conclude that two-week repeated multifocal cortical stimulation with a new wearable transcranial magnetic stimulator can be safely conducted in DM1 patients to investigate potential improvement of muscle strength and activity. The results obtained, if confirmed and extended by future safety and efficacy trials with larger patient samples, could offer a potential supportive TRPMS treatment in DM1.

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Effects of transcranial static magnetic stimulation over the primary motor cortex on local and network spontaneous electroencephalogram oscillations

Scientific Reports ◽

10.1038/s41598-021-87746-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Sumiya Shibata ◽

Tatsunori Watanabe ◽

Yoshihiro Yukawa ◽

Masatoshi Minakuchi ◽

Ryota Shimomura ◽

...

Keyword(s):

Motor Cortex ◽

Power Spectrum ◽

Magnetic Stimulation ◽

Primary Motor Cortex ◽

Cortical Excitability ◽

Controlled Study ◽

Functional Coupling ◽

Phase Lag ◽

Theta Band ◽

Double Blind

AbstractTranscranial static magnetic stimulation (tSMS) is a novel non-invasive brain stimulation technique that reduces cortical excitability at the stimulation site. We investigated the effects of tSMS over the left primary motor cortex (M1) for 20 min on the local electroencephalogram (EEG) power spectrum and interregional EEG coupling. Twelve right-handed healthy subjects participated in this crossover, double-blind, sham-controlled study. Resting-state EEG data were recorded for 3 min before the intervention and 17 min after the beginning of the intervention. The power spectrum at the left central electrode (C3) and the weighted phase lag index (wPLI) between C3 and the other electrodes was calculated for theta (4–8 Hz), alpha (8–12 Hz), and beta (12–30 Hz) frequencies. The tSMS significantly increased theta power at C3 and the functional coupling in the theta band between C3 and the parietal midline electrodes. The tSMS over the left M1 for 20 min exhibited modulatory effects on local cortical activity and interregional functional coupling in the theta band. The neural oscillations in the theta band may have an important role in the neurophysiological effects induced by tSMS over the frontal cortex.

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