Abstract
We investigated the effects of intermittent theta-burst stimulation (iTBS) on locomotor function, motor plasticity, and axonal regeneration in an animal model of incomplete spinal cord injury (SCI). Aneurysm clips with different compression forces were applied extradurally around the spinal cord at T10. Motor plasticity was evaluated by examining the motor evoked potentials (MEPs). Long-term iTBS treatment was given at the post-SCI 5th week and continued for 2 weeks (5 consecutive days/week). Time-course changes in locomotor function and the axonal regeneration level were measured by the Basso Beattie Bresnahan (BBB) scale, and growth-associated protein (GAP)-43 expression was detected in brain and spinal cord tissues. iTBS-induced potentiation was reduced at post-1-week SCI lesion and had recovered by 4 weeks post-SCI lesion, except in the severe group. Multiple sessions of iTBS treatment enhanced the motor plasticity in all SCI rats. The locomotor function revealed no significant changes between pre- and post-iTBS treatment in SCI rats. The GAP-43 expression level in the spinal cord increased following 2 weeks of iTBS treatment compared to the sham-treatment group. This preclinical model may provide a translational platform to further investigate therapeutic mechanisms of transcranial magnetic stimulation and enhance the possibility of the potential use of TMS with the iTBS scheme for treating SCIs.
Highlights
Spinal cord injuries (SCIs) lead to changes in motor, sensory, and autonomic functions of the spinal cord [1]
Following an spinal cord injury (SCI), there was a change in the motor evoked potentials (MEPs) amplitude at all three different severities
There was no significant difference revealed by an independent t-test between pre- and post-intermittent theta-burst stimulation (iTBS) in the severe-SCI group at PO 4W (p = 0.24)
Summary
Spinal cord injuries (SCIs) lead to changes in motor, sensory, and autonomic functions of the spinal cord [1]. In the initial stage (a few seconds to a minute) after spinal damage occurs, termed the acute phase, the primary injury mechanism leads to physiological alterations, including hemorrhaging, spinal shock, systemic hypotension, cell death, reduced blood flow, edema, and neurotransmitter accumulation [4]. In the secondary stage (minutes to weeks) after the spinal cord is damaged, termed the sub-acute phase, necrotic cell death, edema, electrolyte shifts, free-radical production, delayed calcium influx, and apoptosis continue to occur [5]. In the last stage (months to years) after spinal cord damage, termed the chronic phase, apoptosis, demyelination, glial scar formation, and alteration of neuronal circuits continue to occur [4, 5]. Cortical areas are invaded which causes axonal disintegration and reductions in the dendritic spine density and angiogenesis, and information is not conveyed along the central pathway [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
