Shields, Richard K., and Shauna Dudley-Javoroski. Musculoskeletal plasticity after acute spinal cord injury: effects of long-term neuromuscular electrical stimulation training. J Neurophysiol 95: 2380 -2390, 2006. First published January 11, 2006 doi:10.1152/jn.01181.2005. Maintaining the physiologic integrity of paralyzed limbs may be critical for those with spinal cord injury (SCI) to be viable candidates for a future cure. No long-term intervention has been tested to attempt to prevent the severe musculoskeletal deterioration that occurs after SCI. The purposes of this study were to determine whether a long-term neuromuscular electrical stimulation training program can preserve the physiological properties of the plantar flexor muscles (peak torque, fatigue index, torque-time integral, and contractile speed) as well as influence distal tibia trabecular bone mineral density (BMD). Subjects began unilateral plantar flexion electrical stimulation training within 6 wk after SCI while the untrained leg served as a control. Mean compliance for the 2-yr training program was 83%. Mean estimated compressive loads delivered to the tibia were ϳ1-1.5 times body weight. The training protocol yielded significant trained versus untrained limb differences for torque (ϩ24%), torque-time integral (ϩ27%), fatigue index (ϩ50%), torque rise time (ϩ45%), and between-twitch fusion (ϩ15%). These betweenlimb differences were even greater when measured at the end of a repetitive stimulation protocol (125 contractions). Peripheral quantitative computed tomography revealed 31% higher distal tibia trabecular BMD in trained limbs than in untrained limbs. The intervention used in this study was sufficient to limit many of the deleterious muscular and skeletal adaptations that normally occur after SCI. Importantly, this method of load delivery was feasible and may serve as the basis for an intervention to preserve the musculoskeletal properties of individuals with SCI.

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.

Objective-The purpose of this study was to determine whether long-term electrical stimulation training of the paralyzed soleus could change this muscle's physiological properties (torque, fatigue index, potentiation index, torque-time integral) and increase tibia bone mineral density. Methods-Four men with chronic (>2 years) complete spinal cord injury (SCI; American SpinalInjury Association classification A) trained 1 soleus muscle using an isometric plantar flexion electrical stimulation protocol. The untrained limb served as a within-subject control. The protocol involved ~30 minutes of training each day, 5 days a week, for a period of 6 to 11 months. Mean compliance over 11 months of training was 91% for 3 subjects. A fourth subject achieved high compliance after only 5 months of training. Mean estimated compressive loads delivered to the tibia were ~110% of body weight. Over the 11 months of training, the muscle plantar flexion torque, fatigue index, potentiation index, and torque-time integral were evaluated periodically. Bone mineral density (dual-energy x-ray absorptiometry) was evaluated before and after the training program.Results-The trained limb fatigue index, potentiation index, and torque-time integral showed rapid and robust training effects (P < .05). Soleus electrical stimulation training yielded no changes to the proximal tibia bone mineral density, as measured by dual-energy x-ray absorptiometry. The subject with low compliance experienced fatigue index and torque-time integral improvements only when his compliance surpassed 80%. In contrast, his potentiation index showed adaptations even when compliance was low.Conclusions-These findings highlight the persistent adaptive capabilities of chronically paralyzed muscle but suggest that preventing musculoskeletal adaptations after SCI may be more effective than reversing changes in the chronic condition. KeywordsParalysis; Bone density; Muscle; Plasticity; Fatigue The musculoskeletal system experiences extensive physiologic changes after spinal cord injury (SCI). Muscle paralyzed by an upper motor neuron lesion undergoes profound atrophy and gradual transformation to a fast-fatigable phenotype. 1,2 In the chronically paralyzed state (>2 years), the soleus muscle demonstrates decreased oxidative enzymes (SDH, NADH), 1 extensive fatigue, 2,3 and decreased cross-sectional area. 4 Deprived of its principal source of loading (voluntary muscle contraction 5 ), bone rapidly demineralizes and © 2007 American Society of Neurorehabilitation. All rights reserved.Address correspondence to Richard K. Shields, PhD, PT, Graduate Program in Physical Therapy and Rehabilitation Science, The University of Iowa, 1-252 Medical Education Building, Iowa City, IA 52242-1190. richard-shields@uiowa.edu. Despite the extensive changes that occur after SCI, evidence is accumulating that paralyzed tissues still adapt according to the overload principle and the specificity of training principle. Electrical stimulation training can improve the torque output 11-13 and fa...

Introduction In humans, spinal cord injury (SCI) induces deleterious changes in skeletal muscle that may be prevented or reversed by electrical stimulation muscle training. The molecular mechanisms underlying muscle stimulation training remain unknown. Methods We studied two unique SCI subjects whose right soleus received >6 years of training (30 minutes/day, 5 days/week). Results Training preserved torque, fatigue index, contractile speed and cross-sectional area in the trained, but not the untrained leg. Training decreased 10 mRNAs required for fast twitch contractions and mRNA that encodes for myostatin, an autocrine/paracrine hormone that inhibits muscle growth. Conversely, training increased 69 mRNAs that mediate the slow twitch, oxidative phenotype, including PGC-1α, a transcriptional co-activator that inhibits muscle atrophy. When we discontinued right soleus training, training-induced effects diminished slowly; some persisted >6 months. Discussion Training of paralyzed muscle induces localized and long-lasting changes in skeletal muscle mRNA expression that improve muscle mass and function.

Study Design-Longitudinal repeated-measures; within-subject control.Objective-We examined the extent to which an isometric plantar flexion training protocol attenuates bone loss longitudinally after SCI.Summary of Background Data-After spinal cord injury (SCI), bone mineral density (BMD) of paralyzed extremities rapidly declines, likely because of loss of mechanical loading of bone via muscle contractions.Methods-Six individuals with complete paralysis began a 3-year unilateral plantar flexor muscle activation program within 4.5 months after SCI. The opposite limb served as a control. Compliance with recommended dose was >80%. Tibia compressive force was >140% of body weight.Results-Bilateral hip and untrained tibia BMD declined significantly over the course of the training. Lumbar spine BMD showed minimal change. Percent decline in BMD (from the baseline condition) for the trained tibia (~10%) was significantly less than the untrained tibia (~25%) (P < 0.05). Trained limb percent decline in BMD remained steady over the first 1.5 years of the study (P < 0.05).Conclusions-Compressive loads of ~1 to 2 times body weight, induced by muscle contractions, partially prevent the loss of BMD after SCI. Future studies should establish doseresponse curves for attenuation of bone loss after SCI. Keywordsspine cord injury; osteoporosis; compressive load; electrical stimulation; dose-response After spinal cord injury (SCI), paralyzed extremities experience a precipitous loss of bone mineral density (BMD). Shortly after SCI, BMD begins to decline at a rate of 2% to 4% per month, 1 reaching equilibrium between 12 and 24 months at a level near fracture threshold. [2][3][4] At this stage, fractures can occur with trivial injuries to the limbs, often during routine transfers and activities of daily living. 5 Between 1% and 6% of people with SCI will sustain fractures in their paralyzed extremities, [6][7][8] NIH Public AccessAuthor Manuscript Spine (Phila Pa 1976 It remains unknown whether bone loss after SCI is due to insufficient osteogenic loads or if it is the result of neurogenic changes. Rehabilitation strategies to preserve BMD after SCI have been elusive. Strategies that involve loading of the extremities, such as electrically stimulated cycling and suspended treadmill walking, have shown limited effects on BMD. 9-11 These methods may not deliver a sufficient load to provide an osteogenic stimulus to the skeletal system. Bone is in a state of activity-dependent flux, and biomechanical stresses help determine the shape, size, and composition of bone. 12,13 Moreover, in the neurologically intact human model, bone density responds in a dosagedependent manner to strain magnitude. 14 It is plausible that this principle is still in operation after SCI. However, to our knowledge, no previous report has assessed compressive loads placed on bone as part of a long-term intervention to limit bone loss after SCI in humans.In the paralyzed human model, it is difficult to deliver loads that exceed an osteogenic threshold withou...

Understanding the torque output behavior of paralyzed muscle has important implications for the use of functional neuromuscular electrical stimulation systems. Postfatigue potentiation is an augmentation of peak muscle torque during repetitive activation after a fatigue protocol. The purposes of this study were 1) to quantify postfatigue potentiation in the acutely and chronically paralyzed soleus and 2) to determine the effect of long-term soleus electrical stimulation training on the potentiation characteristics of recently paralyzed soleus muscle. Five subjects with chronic paralysis (>2 yr) demonstrated significant postfatigue potentiation during a repetitive soleus activation protocol that induced low-frequency fatigue. Ten subjects with acute paralysis (<6 mo) demonstrated no torque potentiation in response to repetitive stimulation. Seven of these acute subjects completed 2 yr of home-based isometric soleus electrical stimulation training of one limb (compliance = 83%; 8,300 contractions/wk). With the early implementation of electrically stimulated training, potentiation characteristics of trained soleus muscles were preserved as in the acute postinjury state. In contrast, untrained limbs showed marked postfatigue potentiation at 2 yr after spinal cord injury (SCI). A single acute SCI subject who was followed longitudinally developed potentiation characteristics very similar to the untrained limbs of the training subjects. The results of the present investigation support that postfatigue potentiation is a characteristic of fast-fatigable muscle and can be prevented by timely neuromuscular electrical stimulation training. Potentiation is an important consideration in the design of functional electrical stimulation control systems for people with SCI.

Summary People with spinal cord injury (SCI) lose bone and muscle integrity after their injury. Early doses of stress, applied through electrically induced muscle contractions, preserved bone density at high-risk sites. Appropriately prescribed stress early after the injury may be an important consideration to prevent bone loss after SCI. Introduction Skeletal muscle force can deliver high compressive loads to bones of people with spinal cord injury (SCI). The effective osteogenic dose of load for the distal femur, a chief site of fracture, is unknown. The purpose of this study is to compare three doses of bone compressive loads at the distal femur in individuals with complete SCI who receive a novel stand training intervention. Methods Seven participants performed unilateral quadriceps stimulation in supported stance [150% body weight (BW) compressive load—“High Dose” while opposite leg received 40% BW—“Low Dose”]. Five participants stood passively without applying quadriceps electrical stimulation to either leg (40% BW load—“Low Dose”). Fifteen participants performed no standing (0% BW load—“Untrained”) and 14 individuals without SCI provided normative data. Participants underwent bone mineral density (BMD) assessment between one and six times over a 3-year training protocol. Results BMD for the High Dose group significantly exceeded BMD for both the Low Dose and the Untrained groups (p<0.05). No significant difference existed between the Low Dose and Untrained groups (p>0.05), indicating that BMD for participants performing passive stance did not differ from individuals who performed no standing. High-resolution CT imaging of one High Dose participant revealed 86% higher BMD and 67% higher trabecular width in the High Dose limb. Conclusion Over 3 years of training, 150% BW compressive load in upright stance significantly attenuated BMD decline when compared to passive standing or to no standing. High-resolution CT indicated that trabecular architecture was preserved by the 150% BW dose of load.

The purpose of this report is to describe student satisfaction with a near-peer interprofessional education (IPE) session for physical therapy and medical students. Ten senior physical therapy students worked in peer-groups to develop a musculoskeletal anatomy demonstration for first-semester medical students. Together with their classmates, they demonstrated observation, palpation, and musculoskeletal assessment of the shoulder and scapular-thoracic articulation to medical student dissection groups in the Gross Anatomy laboratory. The medical students were encouraged to consider the synergistic function of shoulder structures and the potential impact of a selected pathology: rotator cuff injury. The session provided the medical students with an opportunity to integrate their new anatomical knowledge into a framework for clinical musculoskeletal evaluation. The experience offered senior physical therapy students an opportunity to work in teams with their peers, internalize and adapt to constructive feedback, and seek common ground with members of another profession. Both student groups reported a high degree of satisfaction with the sessions and expressed a desire for further interaction. These positive perceptions by student stakeholders have prompted us to consider additional IPE exchanges for the anatomy course in the upcoming school year. Given the positive outcome of this descriptive study, we now plan to systematically test whether near-peer IPE interactions can enhance the degree that students learn key anatomical concepts.