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Corticospinal modulation of vibration-induced H-reflex depression
Colleen L Bringman1,2, Richard K Shields3, Stacey L DeJong1
1Department of Physical Therapy and Rehabilitation Science, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, 1-252 Medical Education Building, Iowa City, Iowa, 52242-1190, USA.
Experimental Brain Research
|January 19, 2022
Summary
Transcranial magnetic stimulation (TMS) partially restored soleus H-reflexes suppressed by limb vibration. This disinhibition suggests corticospinal signals may reduce presynaptic inhibition during movement control.
Area of Science:
- Neuroscience
- Motor Control
- Human Physiology
Background:
- Spinal reflex excitability is modulated by descending corticospinal pathways.
- Presynaptic inhibition plays a crucial role in regulating sensory input to motoneurons.
- Understanding corticospinal modulation is key to deciphering motor control mechanisms.
Purpose of the Study:
- To investigate how transcranial magnetic stimulation (TMS) affects spinal reflex excitability.
- To determine the impact of TMS on soleus H-reflexes during vibration-induced suppression.
- To explore the role of corticospinal modulation in disinhibiting spinal reflexes.
Main Methods:
- 15 healthy adults participated in the study.
- Single-limb vibration was applied to the non-dominant leg (0.6 g, 30 Hz, 0.33 mm displacement).
- Soleus H-reflexes were measured under various conditions, including tibial nerve stimulation, vibration, and subthreshold TMS.
Main Results:
- Subthreshold TMS alone did not affect soleus electromyography or produce motor evoked potentials.
- In the absence of vibration, TMS did not alter H-reflex amplitudes.
- During vibration, TMS significantly increased nearly abolished H-reflexes (p < 0.008), indicating partial restoration.
Conclusions:
- Limb vibration alone did not alter corticospinal excitability.
- Subthreshold TMS partially restored suppressed soleus H-reflexes during vibration.
- This disinhibition suggests corticospinal signals may reduce presynaptic inhibition, aiding motor control.
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