Brazilian epidemiological profile of spinal cord trauma has male individuals aged between 10 and 30 years old as the injury predominance 1. The profile observed in this study matches male prevalence, although differing about the age of spinal cord injured individuals which varies from 31 to 73 years old (average of 45.3 years old).
Trauma is the main cause of spinal cord injury, with the principal etiologies being automobile accident, firearm injury and falls 1. In this study, the 13 injuries by traffic accident, two by fall from height and four by firearm are compatible with the literature. Other mechanisms of trauma are also involved, such as four injuries by dive in shallow water and one bone tumor.
Studies show that spinal cord injury is associated with higher prevalence of cervical-level injury 14,15,16,17. However, the present study differs from those, presenting 13 individuals (54%) with thoracic-level injury and 11 (44%) with cervical-level injury.
The literature points out that the higher increase of FIM scores occurs in the first years after injury and, after approximately five years, the scores stabilizes, existing little improvement in independence level, because it is understood that the maximum level of independence was obtained according to the level injury 18. Data obtained from the study agree with literature, because there was stabilization of the scores of most individuals.
Regarding bone mass quality, in this study, it was found 79% of osteopenia prevalence and 21% of osteoporosis, on any of the structures analyzed (lumbar spine and femoral neck). These data illustrate how much this population is affected by high degrees of bone loss. Some studies point out that these individuals lose up to 50% of bone density in the first year of injury, which tends to stabilize after the second year 19.
Although the pathophysiological mechanisms of this process are not yet totally elucidated, sublesionals central and peripheral neural denervations seem to have strong influence on bone mass loss, once they act on osteoanabolic metabolism 4. Other possible mechanisms which may be responsible for this event include the gravity change due to immobilization, the loss of anabolic factors (for example, testosterone and/or circulating growth hormones), the factors in bone local environment (paracrine influences of muscle atrophy) and the presence of catabolic factors at the time of injury (such as administration of high doses of methylprednisolone within a few hours after the acute and/or systemic event and/or the local production of inflammatory mediators or cytokines) 4,19.
In this study, it was also evidenced that femur is the most affected region by bone loss, with the prevalence of osteopenia approximately 75% and of osteoporosis 17% for femoral neck; and 8% of osteopenia and 4% of osteoporosis for lumbar spine.
In the study of Sabo et al 20, the authors also found BMD reduced in proximal femur, but not in lumbar spine. This is justified because, in order to avoid bone loss, it is necessary to have normal muscular function and load, variables practically absent in the femur and partially present in the lumbar spine, which supports the load of individual’s body while using the wheelchair 21.
In relation to the effects of NMES treatment on bone density of spinal cord injured individuals, literature does not show a consensus. Studies that investigated its effects on bone are conflicting 22. Several methodological limitations restrict the capability to confirm the utility of this intervention in order to improve the skeletal status 22. In Forrest et al 23 the authors observed a decrease of total BMD (1.54%) and regional BMD (legs: 6.72%).
In Giangregorio et al’s study 24, authors concluded that this intervention is not enough to prevent bone loss, as it was evidenced by BMD reduction for all individuals varying in magnitude from 1.2 to 26.7% for lower limb and 0.2 to 7.4% for lumbar spinal.
On the other hand, in the study carried out by Mohr et al 25, a 10% increase of BMD for proximal tibia was described, but no difference for femoral neck and spine. In the study of Coupaud et al 13, it was also verified an increase of BMD for distal tibia (5% for right leg and 20% for left leg). However, the results were insignificant for proximal tibia and for the femur. In this study, improvement of BMD of the femoral neck and worsening of BMD of the lumbar spine were found. Even though, data obtained were not statistically significant, preventing us from making statements and comparisons with other studies.
Limitations of this study include the small sample of 24 individuals and their difficulty to maintain 10-years follow-up treatment because of socioeconomic and psychological reasons, functional dependence and comorbidities due to the level of the spinal cord injury. Larger studies should be carried out for better future analysis and adjustments in these factors would help to continue the treatment of these patients.
The demographic profile of patients was compatible to the one found in literature in the characteristics analyzed, except for the age, which is higher among patients in this study. About functional independence measure score and bone mineral density, they remained similar to the beginning of the treatment with neuromuscular electrical stimulation (NMES), concluding that there has been stabilization of these parameters during 10 years of treatment.. Our long term results do show that it is feasible to preserve BMD thus avoiding bone fractures, due to disuse osteoporosis in spinal cord injury subjects.