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  4. Electrical Stimulation Prevents Muscular Atrophy and the Decrease of Interleukin-6 in Paralyzed Muscles after Spinal Cord Injury in Rats

Electrical Stimulation Prevents Muscular Atrophy and the Decrease of Interleukin-6 in Paralyzed Muscles after Spinal Cord Injury in Rats

Rev Bras Ortop, 2024 · DOI: https://doi.org/10.1055/s-0044-1787767 · Published: September 4, 2024

Spinal Cord InjuryNeurologyMusculoskeletal Medicine

Simple Explanation

Spinal cord injury disrupts neural inputs, leading to muscle paralysis and imbalance between protein anabolism and catabolism, causing muscle loss. Neuromuscular electrical stimulation (NMES) is a treatment with the highest level of evidence for paralyzed muscles. This study analyzes if NMES can prevent atrophy following cervical SCI by analyzing muscular trophism and expression of IL-6.

Study Duration
5 weeks
Participants
15 adult female Wistar rats
Evidence Level
Not specified

Key Findings

  • 1
    NMES prevents biceps brachii muscle atrophy after incomplete cervical SCI in rats.
  • 2
    NMES prevents loss in IL-6 levels, a potential stimulation factor of muscular trophism.
  • 3
    NMES partially recovered the size of sarcomeres, which were reduced in the untreated SCI group, indicating prevention of muscle atrophy.

Research Summary

This study showed that applying NMES for 5 weeks prevents biceps brachii muscle atrophy after incomplete cervical SCI. Additionally, this therapy prevents loss in IL-6 levels, a potential stimulation factor of muscular trophism. The NMES partially maintained the reduction of IL-6 levels after injury in this muscle.

Practical Implications

Therapeutic Potential

Early NMES can be used as a therapeutic tool to prevent muscle atrophy following SCI.

Mechanism of Action

NMES likely induces IL-6 release, potentially activating satellite cells and increasing phosphorylated Akt levels.

Future Research

Further studies are required to elucidate the subsequent mechanisms of NMES on paralyzed muscles after SCI.

Study Limitations

  • 1
    The possibility of IL-6 being released by electrically induced muscle contraction inhibiting the catabolic pathway of trophism.
  • 2
    Whether there is an association between IL-6 levels and the number of type I muscle fibers.
  • 3
    Whether another myosin participates in the process of maintaining muscle trophism and the characteristics of muscle fibers and their underlying mechanisms.

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