Abstract
Spinal cord injury (SCI) produces paralysis and a unique form of neurogenic disuse osteoporosis that dramatically increases fracture risk at the distal femur and proximal tibia. This bone loss is driven by heightened bone resorption and near-absent bone formation during the acute post-SCI recovery phase and by a more traditional high-turnover osteopenia that emerges more chronically, which is likely influenced by the continual neural impairment and musculoskeletal unloading. These observations have stimulated interest in specialized exercise or activity-based physical therapy (ABPT) modalities (e.g., neuromuscular or functional electrical stimulation cycling, rowing, or resistance training, as well as other standing, walking, or partial weight-bearing interventions) that reload the paralyzed limbs and promote muscle recovery and use-dependent neuroplasticity. However, only sparse and relatively inconsistent evidence supports the ability of these physical rehabilitation regimens to influence bone metabolism or to increase bone mineral density (BMD) at the most fracture-prone sites in persons with severe SCI. This review discusses the pathophysiology and cellular/molecular mechanisms that influence bone loss after SCI, describes studies evaluating bone turnover and BMD responses to ABPTs during acute versus chronic SCI, identifies factors that may impact the bone responses to ABPT, and provides recommendations to optimize ABPTs for bone recovery.
Highlights
An estimated 250,000 to 500,000 new spinal cord injuries (SCI) occur worldwide each year [1], with males representing ~80% of the population [2]
Case studies or case series that enrolled participants with chronic SCI ranged from 10-weeks to 8-years in duration, instituted training frequencies of two- to five-days/week, and utilized the following modalities (Table 3): passive standing in a frame that was combined with leg or whole-body vibration [117], overground walking that was assisted by reciprocating gait orthosis [118], bodyweight-supported treadmill training (BWSTT) alone [119] or in combination with epidural electrical stimulation [120] or nerve stimulation [121], or functional electrical stimulation (FES)-based cycling [122,123] or rowing [124] that was delivered alone or after FES resistance training (RT) [106,125,126]
G, group; BWSTT, bodyweight supported treadmill training; FES, functional electrical stimulation; RT, resistance training; ZA, zoledronic acid; TA, teriparatide F, female; M, male; C, cervical; T, thoracic; L, lumbar; AIS, American Spinal Injury Association Impairment Scale; SCI Duration: time since SCI in relation to intervention reported as range, mean ± SD, or mean and; avg, average; min, minute; h, hour; d, day; wk, week; mo, month; yr, year; N/R, not reported; FEA, finite element analysis; F/U, follow-up after intervention complete; Note: % change was reported in individual papers or was manually calculated from data in tables and/or figures; † indicates
Summary
An estimated 250,000 to 500,000 new spinal cord injuries (SCI) occur worldwide each year [1], with males representing ~80% of the population [2]. Bone loss after SCI is termed neurogenic or disuse osteoporosis and is confined to the sublesional skeleton [10,11,12], with the most rapid and prevalent bone deficits occurring at the distal femur and proximal tibia regions [11,13,14]. At these sites, 50–100% lower trabecular bone mineral density (BMD) develops in individuals within the first two to three years of SCI [11,13,14], and 40–80% lower cortical bone mass exists several years after injury [14]. The severe bone loss, high fracture incidence, and the associated morbidity and mortality indicate the need to improve osteoporosis screening and to develop evidence-based guidelines to prevent and treat osteoporosis in the SCI population [21,22]
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