scholarly journals The Role of Peripheral Nerve Electrotherapy in Functional Recovery of Muscle Motor Units in Patients after Incomplete Spinal Cord Injury

2021 ◽  
Vol 11 (20) ◽  
pp. 9764
Author(s):  
Juliusz Huber ◽  
Katarzyna Leszczyńska ◽  
Agnieszka Wincek ◽  
Agnieszka Szymankiewicz-Szukała ◽  
Wojciech Fortuna ◽  
...  

Functional electrical nerve stimulation (FES) is a non-invasive technique for neuromodulation and may have the potential for motor rehabilitation following incomplete spinal cord injury (iSCI). Axonal degeneration in motor fibers of lower extremity nerves is an inevitable secondary pathological change in iSCI subjects, despite no direct damage to lumbosacral neuromeres. This study evaluated the role of FES with individual parameters based on results of comparative neurophysiological studies. Forty-two participants with C4 to Th12 iSCI received repetitive sessions of electrostimulations applied to peroneal and tibial motor fibers, performed five times a week from 6 to 14 months, and the uniform system of kinesiotherapeutic treatment. The average duration of one electrostimulation session was 17 min, stimulation frequency of a train 20–70 Hz, duration of 2–3 s, intervals 2–3 s, pulses intensity 18–45 mA. The algorithm change was based on objective tests of subsequent surface electromyography (sEMG), and electroneurography (ENG) recordings. The same neurophysiological studies were also performed in patients after C2-Th12 iSCI treated with kinesiotherapy only (K group, N = 25) and compared with patients treated with both kinesiotherapy and electrostimulation (K + E, N = 42). The study revealed improvements in sEMG parameters recorded from tibialis anterior, gastrocnemius, extensor digitorum brevis muscles, and ENG evoked a compound muscle action potential recorded following bilateral stimulation of more peroneal than tibial nerves. Neurophysiological recordings had significantly better parameters in the K + E group of patients after therapy but not in the K group patients. The improvement of the motor transmission peripherally may reflect the specific neuromodulatory effect of FES algorithm evaluated with sEMG and ENG. FES may inhibit degeneration of axons and support functional recovery after iSCI.

2020 ◽  
Vol 37 (21) ◽  
pp. 2302-2314 ◽  
Author(s):  
Christian Meyer ◽  
Linard Filli ◽  
Stephanie A. Stalder ◽  
Christopher Awai Easthope ◽  
Tim Killeen ◽  
...  

Life Sciences ◽  
2019 ◽  
Vol 232 ◽  
pp. 116627 ◽  
Author(s):  
Jocemar Ilha ◽  
Anamaria Meireles ◽  
Gabriel Ribeiro de Freitas ◽  
Caroline C. do Espírito Santo ◽  
Nicolas A.M.M. Machado-Pereira ◽  
...  

2006 ◽  
Vol 23 (6) ◽  
pp. 908-919 ◽  
Author(s):  
Rebecca R. Smith ◽  
Alice Shum-Siu ◽  
Ryan Baltzley ◽  
Michelle Bunger ◽  
Angela Baldini ◽  
...  

Author(s):  
Liangjie Bai ◽  
Xifan Mei ◽  
Yanfeng Wang ◽  
Yajiang Yuan ◽  
Yunlong Bi ◽  
...  

Author(s):  
Ziying Zhang ◽  
Lifang Shen ◽  
Yingying Yan

Spinal cord injury (SCI) is a neurological trauma that causes loss of locomotor function and sensory deficit. Previous studies showed that miRNAs play a crucial role in SCI. This study further evaluated the potential role of miR-139-5p in the neural cell apoptosis after SCI in rats. A rat SCI model was successfully established and miR-139-5p expression level in SCI rats was down-regulated compared to the sham group (sham operation group) determined by qRT-PCR. MiR-139-5p overexpression via administration with miR-139-5p agomir improved locomotor functional recovery, attenuated allodynia and hyperalgesia and alleviated neural cell apoptosis in SCI rats. In addition, TRAF3 (TNF receptor-associated factor 3 ) was identified to be a target of miR-139-5p by searching the proposed target genes in TargetScan 7.1 database. Co-transfection of miR-139-5p agomir and adenovirus of TRAF3 plasmids significantly improved functional recovery and alleviated neural cell apoptosis. Therefore, TRAF3 mediated the anti-apoptosis effect of miR-139-5p in SCI rats and miR-139-5p could be a promising candidate for SCI therapy by alleviating neural cell apoptosis through targeting TRAF3.


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