Chiun-Fan Chen1, Yin-Tsong Lin2, Wen-Shiang Chen3, Felipe Fregni4. 1. Spaulding Neuromodulation Center, Department of Physical Medicine & Rehabilitation, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Health Science and Wellness Center, National Taiwan University, Taipei, Taiwan. 2. Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan. 3. Department of Physical Medicine and Rehabilitation, National Taiwan University Hospital, Taipei, Taiwan. 4. Spaulding Neuromodulation Center, Department of Physical Medicine & Rehabilitation, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: Fregni.Felipe@mgh.harvard.edu.
Abstract
BACKGROUND: Protocols to induce motor related neuroplasticity are usually directed to central neural structures such as the motor cortex or the spinal cord. OBJECTIVE: Herein, we aimed to evaluate the effects of peripheral nerve stimulation using a current intensity (stimulation intensity) approach to understand the contribution of the corticospinal system and total energy to electrically-induced neuroplasticity. METHODS: Electrical stimulation trains of lower intensity, interlaced with 2-s bursts of higher intensity, were applied to anesthetized rabbits. Nerve blocks were applied to the proximal side of the stimulation site with identical stimulation trains in a different session to block the contribution of corticospinal volleys during intensity-modulated electrical stimulation. RESULTS: Additional force corresponding to additional recruitment of motoneurons was observed when a 2-s burst of high intensity was present (burst/constant: 24.7 ± 3.6%/2.09 ± 4.8%; p < .001). Additional force was absent in sessions when the neural pathway to the spinal cord was blocked (unblocked/blocked: 29.3 ± 3.8%/-2.49 ± 4.8%; p < .001). CONCLUSIONS: The results suggest that induced neuroplasticity indexed by the additional force is dependent on the total energy applied and connectivity to central structures. These results give additional evidence for the contribution of two factors for induced neuroplasticity: (i) modulation by corticospinal structures and (ii) total energy of stimulation. Further protocols should explore simultaneous peripheral and central stimulation.
BACKGROUND: Protocols to induce motor related neuroplasticity are usually directed to central neural structures such as the motor cortex or the spinal cord. OBJECTIVE: Herein, we aimed to evaluate the effects of peripheral nerve stimulation using a current intensity (stimulation intensity) approach to understand the contribution of the corticospinal system and total energy to electrically-induced neuroplasticity. METHODS: Electrical stimulation trains of lower intensity, interlaced with 2-s bursts of higher intensity, were applied to anesthetized rabbits. Nerve blocks were applied to the proximal side of the stimulation site with identical stimulation trains in a different session to block the contribution of corticospinal volleys during intensity-modulated electrical stimulation. RESULTS: Additional force corresponding to additional recruitment of motoneurons was observed when a 2-s burst of high intensity was present (burst/constant: 24.7 ± 3.6%/2.09 ± 4.8%; p < .001). Additional force was absent in sessions when the neural pathway to the spinal cord was blocked (unblocked/blocked: 29.3 ± 3.8%/-2.49 ± 4.8%; p < .001). CONCLUSIONS: The results suggest that induced neuroplasticity indexed by the additional force is dependent on the total energy applied and connectivity to central structures. These results give additional evidence for the contribution of two factors for induced neuroplasticity: (i) modulation by corticospinal structures and (ii) total energy of stimulation. Further protocols should explore simultaneous peripheral and central stimulation.