What’s New in Orthopaedic Rehabilitation – Spinal Cord Injury

Harish Hosalkar, MD, MBMS(Orth), FCPS(Orth), DNB(Orth)1, Jason Hsu, MD1, Nirav K. Pandya, MD1 and Mary Ann Keenan, MD1

The use of systemic Hypothermia for spinal cord injury has received much attention in the past year, in large part because of the substantial neurologic recovery after the use of moderate hypothermia in the case of a professional football player who had sustained an incomplete Cervical spinal cord injury19. Whether the neurologic recovery was spontaneous, was due to hypothermia, or was due to early surgical decompression is uncertain. The current theory is that decreased temperatures will minimize metabolic demands and Edema during periods of spinal cord Ischemia.

The results from multiple studies investigating the use of hypothermia in animal models of spinal cord injury have been mixed. Morochovic et al.20 studied local transcutaneous cooling of the spinal cord. An animal model of spinal cord compression involving epidural balloon inflation was utilized in a study of forty rats. Twenty-five minutes after cord compression, the paravertebral temperature of twenty animals was maintained at 28.5°C for an hour, whereas the remaining twenty animals were kept normothermic. Functional recovery was monitored weekly for four weeks. Although there was more white matter in portions of the spinal cord in the hypothermic group, the overall volume of preserved spinal cord tissue and the overall functional improvement were not significantly different between the two groups.

Nishi et al.21 studied the effect of hypothermia on experimental ischemia in spinal ventral horn neurons, which previously have been found to be vulnerable to ischemia22. Lumbosacral spinal cord slices were prepared, and an oxygen and glucose-deprived solution was superfused to simulate ischemia in the ventral horn neurons. The frequency of spontaneous excitatory postsynaptic currents was significantly decreased in a hypothermic Environment, suggesting that glutamate release from presynaptic terminals onto these ventral horn neurons was inhibited by hypothermia. Because ischemia can disrupt synaptic function and can result in the accumulation of glutamate in the extracellular space, spinal ventral horn neurons can be excessively stimulated, initiating intracellular events leading to apoptosis and necrosis; hypothermia can reduce this excessive stimulation. The authors concluded that one mechanism of the neuroprotective effects of hypothermia may be through suppression of excitatory synaptic transmission and, therefore, eventual neuronal death. Other laboratory and animal studies have been inconclusive with regard to this neuroprotective effect of hypothermia; in addition, there have been no clinical case reports in the last three decades. Prospective clinical trials evaluating the effectiveness of hypothermia for the treatment of spinal cord injury are encouraged.

Surgical as compared with nonsurgical treatment for acute cervical spine injury continues to be investigated. In a retrospective review over a period of nine years, Singhal et al.23 evaluated the neurologic outcomes for patients who had had surgical treatment of incomplete closed traumatic cervical spinal cord injuries; these results were then compared with those of an earlier study of conservatively managed patients. Thirty-seven patients who had been followed for at least twelve months after the surgical treatment of a traumatic closed cervical spine injury with a Frankel grade of B or better were included in the study. No significant difference was noted between the two groups with regard to the neurologic outcome or the Motor recovery rate. The duration of hospital stay was also not significantly different between the groups. The results of that investigation concurred with the results of a prospective study by Vaccaro et al.24, which demonstrated no significant benefit when decompression performed earlier than seventy-two hours after the injury was compared with decompression performed more than five days after the injury.

The efficacy and safety of methylprednisolone for the treatment of acute spinal cord injury continue to be controversial as the complications stemming from its use cannot be ignored. Hurlbert and Hamilton25 recently reported a reversal of practice patterns related to the use of steroids for the treatment of spinal cord injury in the past five years. At a national meeting, a total of forty-six neurosurgeons and orthopaedic surgeons actively participating in the care of patients with spinal cord injury responded to a questionnaire. Eighty-five percent reported that their view on steroid administration had changed in the last five years. When the results of those questionnaires were compared with the results of questionnaires that had been completed five years earlier, only 24% of the spinal surgeons reported that they currently prescribed steroids for spinal cord injury, in contrast to 76% in 2001. Although not as prevalent as it was five years ago, litigation is still a major factor for surgeons who choose to prescribe steroids. Review articles still present contrasting conclusions regarding the use of steroids for the treatment of acute spinal cord injury, making it difficult for clinicians to make confident evidence-based decisions.

Immobilization arising from spinal cord injury leads to general bone loss, reported to be anywhere from 30% to 50%, which predisposes these patients to a high frequency of fractures. Alekna et al.26, in a prospective study, investigated the effect of weight-bearing on bone mineral density in patients with spinal cord injury. Fifty-four subjects were split evenly among two groups: one in which standing exercises were performed for more than one hour daily and one in which they were not. Bone mineral density was measured at the one-year and two-year time points. At two years after the injury, significant differences were noted between the two groups in terms of the bone mineral density of the leg (1.018 compared with 0.91 g/cm2; p = 0.0004), pelvis (1.002 compared with 0.91 g/cm2; p = 0.0144), and total body (1.116 compared with 1.077 g/cm2; p = 0.016). Age, sex, and the level of injury did not have an impact on bone mineral density. No significant difference was found between Paraplegic and tetraplegic patients with regard to bone mineral density. The authors concluded that standing for more than one hour daily for at least five days a week can decrease the loss of bone mineral density in patients with a spinal cord injury.

Multiple studies have suggested that substantial activity-dependent neuroplasticity is present following a spinal cord injury and that it warrants the use of locomotor training. Various strategies exist, including body weight-supported treadmill training and functional electrical stimulation. Mehrholz et al.27 systematically reviewed strategies for locomotor training in an attempt to find a superior method for improving walking function. Four randomized controlled trials involving 222 patients were included in the review; all studies compared body weight-supported treadmill training with other types of training approaches. One study also investigated robotic-assisted locomotor training, and one study included a combination of body weight-supported treadmill training along with functional electrical stimulation. Walking speed, walking capacity, and the chance of walking independently did not significantly improve in association with any of the methods. The safety of the exercises, measured on the basis of the prevalence of adverse events, was not significantly different in any of the trials. The authors concluded that there is insufficient evidence to support the use of one locomotor training strategy over another.
Griffin et al.28 investigated functional electrical stimulation cycling and its effect on the metabolic, body composition, and neurologic profile of patients with paralysis resulting from spinal cord injury. Eighteen patients with a spinal cord injury were enrolled in the study. After thirty minutes of functional electrical stimulation cycling three times per week for ten weeks, a comprehensive profile, including body composition and bone mass, motor and sensory American Spinal Injury Association (ASIA) scores, plasma glucose and insulin levels, and serum inflammatory marker levels, was compiled. Lean muscle mass increased, but there was no change in bone or Adipose tissue at ten weeks. Lower extremity motor, sensory, and total ASIA scores were significantly higher after functional electrical stimulation. Glucose levels were significantly lower at thirty, sixty, and ninety minutes after dextrose consumption following functional electrical stimulation cycling, and insulin levels were significantly lower. Although plasma lipid levels did not change, except for a slight increase in high-density lipoprotein levels, selected inflammatory markers were all significantly reduced after ten weeks. Significant improvements in motor and sensory ability, along with improvements in blood glucose control and lean muscle mass, are indicative of the health benefits of functional electrical stimulation cycling in patients with spinal cord injury.

Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

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