Neuromuscular Electrical Stimulation is of benefit in the treatment of animals that have:

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1.   A peripheral nerve injury

2.   Disuse atrophy of an individual/group of muscles”

 

Neuromuscular electrical stimulation (NMES) is used for many purposes but was initially just used in elite sport for muscle strengthening and muscle retraining, as well as maintenance of muscle mass during periods of immobilisation. In recent years it has become utilised more often in national health settings to help increase muscle firing and strength and reduce atrophy. It works via application of an electrical stimulation to the percutaneous peripheral nerves, which therefore results in contraction of the desired skeletal muscle. (Lake, 1992 and Neuromuscular Electrical Stimulation, 2013).

 

NMES has been shown to accelerate axon regeneration after nerve injury when used for an hour period on a low frequency setting. It has been shown that re-innervation of motor and sensory pathways is evident after 56 days but not apparent before 14 days. However, by using electrical stimulation in those first 14 days, the motor nerve branch of axons had regenerated showing accelerated outgrowth and crossing of the repair site. This results in earlier functional recovery and muscle re-innervation. (Gordon and English, 2016).

 

When an injury occurs it is sometimes vital for a patient to undergo a period of immobilisation or bed rest in order for the injury to heal, for example fracture healing. When a limb is immobilised due to a fracture there is rapid loss of surrounding skeletal muscle mass and loss of strength, in the area that is immobilised. This muscle atrophy occurs due to imbalances between the breakdown and synthesis of muscle proteins. (Dirks et al, 2013).

 

NMES has been shown to increase protein synthesis rates for a few hours post a single administration (Wall et al, 2012). If used long term and self-administered by the patient during immobilisation, it can maintain homeostatic protein synthesis rates. NMES helps to regulate the ubiquitin-proteasome pathway which controls muscle protein breakdown, ubiquitin ligases are known to increase during periods of immobilisation resulting in loss of muscle mass. However, NMES prevents the increase in ubiquitin ligases (Dirks et al, 2013).

 

The loss of strength and muscle mass during periods of immobilisation are clinically correlated with the recovery time and outcomes. NMES can be used to prevent skeletal muscle atrophy during short periods of immobilisation, by recruiting type II muscle fibres. However, NMES does not seem to have an effect on the loss of muscle strength and this may be due to neuromuscular deconditioning that occurs in early immobilisation (Dirks et al, 2013).

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References:

 

• Dirks, M., Wall, B., Snijders, T., Ottenbros, C., Verdijk, L. and van Loon, L. (2013) ‘Neuromuscular electrical stimulation prevents muscle disuse atrophy during leg immobilization in humans,’ Acta Physiologica, 210(3), pp.628-641.

• Gordon, T., and English, A.W. (2016) ‘Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise,’European Journal of Neuroscience, 43, pp. 336-350.

• Neuromuscular Electrical Stimulation (NMES), (2013), Available at: http://www.electrotherapy.org/assets/Downloads/NMES%20Muscle%20Stimulation%20march%202013.pdf, Accessed: 4thJuly 2017.

• Lake, D.A. (1992) ‘Neuromuscular Electrical Stimulation: An overview and its Application in the Treatment of Sports Injuries,’ Sports Medicine, 13(5), pp. 320-336.

• Wall, B., Dirks, M., Verdijk, L., Snijders, T., Hansen, D., Vranckx, P., Burd, N., Dendale, P. and van Loon, L. (2012) ‘Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men,’ AJP: Endocrinology and Metabolism, 303(5), pp.E614-E623.