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Objectives

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OBJECTIVES

After reading this chapter, the reader will be able to:

  • Enumerate the protein categories that underlie the plastic potential of skeletal muscle

  • Summarize the major muscular adaptations to reduced use after SCI

  • Discuss the adaptations of paralyzed muscle to the reintroduction of loads via electrical stimulation

  • Describe how mechanotransduction and osteoclast/osteoblast activity underlie skeletal plasticity

  • Summarize the adaptations of trabecular versus cortical bone to reduced use after SCI, along with consequences for bone strength and fracture risk

  • Discuss the concept of dose of loading in research protocols designed to preserve bone density after SCI

  • Discuss the subject-safety considerations of using electrical muscle stimulation to preserve musculoskeletal integrity after SCI (especially autonomic dysreflexia and fractures)

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Introduction

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Musculoskeletal Deterioration After SCI

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Given the catastrophic nature of traumatic spinal cord injury (SCI), the degree of adaptation made by many people with paralysis is remarkable. Despite sensory and motor loss, secondary medical complications, social adjustments, and financial and emotional challenges, many people with SCI regain partial or complete functional independence. Some individuals with SCI return to their former vocations or begin new occupations, and many return to busy, productive lives. Even individuals with high quadriplegia may, with the necessary adaptive assistance, fully participate in a broad range of vocational, academic, and social activities. People with SCI today can expect to live full lives, a credit to the resilience of people with SCI and to the success of modern rehabilitation interventions. In the broadest view, it would appear that the contemporary standard of SCI rehabilitation care has greatly advanced over time.

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However, even very high-functioning people with SCI will be the first to remark on the difficulty of living with the secondary complications of paralysis. Joint contractures, spasms, pain, and urinary and bowel complications can be inconvenient, health limiting, or even life threatening. Muscle atrophy below the level of the lesion impairs weight distribution over bony prominences, leading to pressure ulcers even in people who try to conscientiously perform pressure-relief measures. As paralyzed muscles atrophy, the loss of muscular loading through the skeleton precipitates severe osteoporosis in paralyzed limbs. Fractures reportedly occur in the paralyzed extremities of 1% to 6% of people with SCI,1,2,3 but this figure may be grossly underestimated because many fractures may go undetected.4 Undetected fractures likely lead to increased spasms, functional limitations, and decreased independence. These interrelated secondary complications represent various levels of musculoskeletal deterioration.5 Modern rehabilitation has yet to devise therapeutic interventions to fully prevent the wide range of secondary complications that emerge after complete SCI.

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Both individuals with SCI and the rehabilitation community eagerly await the development of a cure for SCI, which may reasonably emerge within the life spans of people living with SCI today. However, people with severe musculoskeletal deterioration may miss opportunities for reintroduction to standing mobility if bone and muscle deterioration are ...

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