Muscle and bone plasticity after spinal cord injury: review of adaptations to disuse and to electrical muscle stimulation

Abstract

The paralyzed musculoskeletal system retains a remarkable degree of plasticity after spinal cord injury (SCI). In response to reduced activity, muscle atrophies and shifts toward a fast-fatigable phenotype arising from numerous changes in histochemistry and metabolic enzymes. The loss of routine gravitational and muscular loads removes a critical stimulus for maintenance of bone mineral density (BMD), precipitating neurogenic osteoporosis in paralyzed limbs. The primary adaptations of bone to reduced use are demineralization of epiphyses and thinning of the diaphyseal cortical wall. Electrical stimulation of paralyzed muscle markedly reduces deleterious post-SCI adaptations. Recent studies demonstrate that physiological levels of electrically induced muscular loading hold promise for preventing post-SCI BMD decline. Rehabilitation specialists will be challenged to develop strategies to prevent or reverse musculoskeletal deterioration in anticipation of a future cure for SCI. Quantifying the precise dose of stress needed to efficiently induce a therapeutic effect on bone will be paramount to the advancement of rehabilitation strategies.

Figure 1

Magnetic resonance imaging of subject who performed >3 years of soleus electrical stimulation training. In stack of 20 such images, trained soleus was substantially larger (∼28%) than untrained soleus (“S” labels in image). Gastrocnemius area (“G”) did not appreciably differ between limbs. Because gastrocnemius is placed on slack during training in knee-bent position, it received electrical current but little isometric loading. Note that all single-joint muscles in deep posterior compartment (“D”) also hypertrophied (tibialis posterior, flexor hallicus longus, flexor digitorum longus). L = left, R = right.

Figure 2

(a) Peripheral quantitative computed tomography (pQCT) imaging of distal tibia of same subject in Figure 1. (Image is viewed from cephalad rather than caudad direction. In this subject, right leg underwent training.) Note extensive loss of trabecular lattice in untrained limb. L = left, R = right. (b) Distal tibia trabecular bone mineral density (BMD) for 3 subjects who trained >3 years was 30% higher in trained than untrained limbs (p < 0.05). Typical non-spinal cord injury BMD at this site is 250 mg/cm³. Source: Eser P, Frotzler A, Zehnder Y, Wick L, Knecht H, Denoth J, Schiessl H. Relationship between the duration of paralysis and bone structure: A pQCT study of spinal cord injured individuals. Bone. 2004;34(5):869–80 [PMID: 15121019]; Shields RK, Dudley-Javoroski S, Boaldin KM, Corey TA, Fog DB, Ruen JM. Peripheral quantitative computed tomography: Measurement sensitivity in persons with and without spinal cord injury. Arch Phys Med Rehabil. 2006;87(10):1376–81. [PMID: 17023249]