PS-36-7 Segmental potential and evoked thoracic spinal cord potential elicited by peripheral nerve stimulation in the leg

Author(s):  
Akira Miyauchi ◽  
Teruo Doi ◽  
Kazuhiko Hashimoto ◽  
Yasutaka Yoshinaka ◽  
Hideo Matsuda
2017 ◽  
Vol 41 (1) ◽  
pp. 119-124 ◽  
Author(s):  
Daniela Mehech ◽  
Melvin Mejia ◽  
Gregory A. Nemunaitis ◽  
John Chae ◽  
Richard D. Wilson

Pain ◽  
2011 ◽  
pp. 148-154
Author(s):  
Tabitha A. Washington ◽  
Khalilah M. Brown ◽  
Gilbert J. Fanciullo

2019 ◽  
Vol 35 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Christine H. Meyer-Frießem ◽  
Theresa Wiegand ◽  
Lynn Eitner ◽  
Christoph Maier ◽  
Tina Mainka ◽  
...  

2015 ◽  
Vol 113 (9) ◽  
pp. 3209-3218 ◽  
Author(s):  
Michael Lee ◽  
Matthew C. Kiernan ◽  
Vaughan G. Macefield ◽  
Bonne B. Lee ◽  
Cindy S.-Y. Lin

There is accumulating evidence that peripheral motor axons deteriorate following spinal cord injury (SCI). Secondary axonal dysfunction can exacerbate muscle atrophy, contribute to peripheral neuropathies and neuropathic pain, and lead to further functional impairment. In an attempt to ameliorate the adverse downstream effects that developed following SCI, we investigated the effects of a short-term peripheral nerve stimulation (PNS) program on motor axonal excitability in 22 SCI patients. Axonal excitability studies were undertaken in the median and common peroneal nerves (CPN) bilaterally before and after a 6-wk unilateral PNS program. PNS was delivered percutaneously over the median nerve at the wrist and CPN around the fibular head, and the compound muscle action potential (CMAP) from the abductor pollicis brevis and tibialis anterior was recorded. Stimulus intensity was above motor threshold, and pulses (450 μs) were delivered at 100 Hz with a 2-s on/off cycle for 30 min 5 days/wk. SCI patients had consistently high thresholds with a reduced CMAP consistent with axonal loss; in some patients the peripheral nerves were completely inexcitable. Nerve excitability studies revealed profound changes in membrane potential, with a “fanned-in” appearance in threshold electrotonus, consistent with membrane depolarization, and significantly reduced superexcitability during the recovery cycle. These membrane dysfunctions were ameliorated after 6 wk of PNS, which produced a significant hyperpolarizing effect. The contralateral, nonstimulated nerves remained depolarized. Short-term PNS reversed axonal dysfunction following SCI, may provide an opportunity to prevent chronic changes in axonal and muscular function, and may improve rehabilitation outcomes.


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