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Thread: Dr. Young - question on bone care...

  1. #1

    Dr. Young - question on bone care...

    I know that over time...our bones will grow weaker...is there anything we can do to keep them as strong as possible in the hopeful event that we will be standing on them again? and are we at a higher risk for osteoporosis? thanks...

  2. #2
    Yes, people with SCI nearly always develop osteoporosis, generally within 24-36 months post injury. Those who have the ability to walk are at lower risk, as are those with incomplete injuries. Unfortunately standing and the use of drugs such as Fosamax have not been shown to be effective in either prevention or correction of this problem. Standing has other benefits though, and everyone with SCI should be standing 1-2 hours daily if at all possible.

    Some studies with animals and limited use in research with humans have found that standing on a vibrating plate (with a very specific range of vibration frequency and amplitude) may be helpful, and NASA is looking at this now. We hope this will be clinically availalble soon if further clinical trials show it is effective.

    Some have chosen to get DEXA bone density scans to monitor the severity of their osteoporosis, although without an effective treatment this may have limited usefulness. All people with SCI should assume that they are at risk for easy fractures, and take precautions to prevent falls or activities that twist or torque their legs, which is a common cause of fractures.

    Meanwhile it is a good idea to at least use calcium supplements and vitamin D, although there is no proof that this is effective either.

    You can do a search here using the word "osteoporosis" to find many previous discussions on this.

    (KLD)

  3. #3
    Is there a difference between osteoporosis and osteomalacia? What exactly is osteoporosis? If we are not able to stand then what is going to happen to our bones?

    Marie
    Unbroken by the grace of God

  4. #4
    Osteoporosis means that the bone become porous (filled with holes) and subject to fracture and slow healing. The term is usually applied to bones of women following menopause or bones of people who have paralysis and other causes of lack of use.

    Osteomalacia means "bad bones" and is generally used to refer to a condition where there is deficiency of vitamin D or calcium, and is characterized by softening of bone with accompanying pain and weakness.

    While most studies have suggested that standing will not reverse, functional electrical stimulation and exercise may retard bone loss. Alendronate may also reduce the progression of osteoporosis Here are some recent studies about the prevalence and treatment of osteoporosis in spinal cord injury.

    Wise.


    Moran de Brito CM, Battistella LR, Saito ET and Sakamoto H (2005). Effect of alendronate on bone mineral density in spinal cord injury patients: a pilot study. Spinal Cord STUDY DESIGN:: Prospective, randomised controlled trial. OBJECTIVE:: To evaluate the effect of alendronate on bone mineral density in chronic spinal cord injury (SCI) patients. SETTING:: University-based rehabilitation centre in Sao Paulo, Brazil. METHODS:: A total of 19 chronic SCI patients were evaluated, divided into a control group and an experimental group. Control group patients received 1000 mg of calcium daily, and experimental group patients received 1000 mg of calcium plus 10 mg of alendronate daily. The study duration was 6 months. In all, 12 densitometric parameters were analysed using whole-body dual-energy X-ray absorptiometry at baseline and after 6 months. RESULTS:: The experimental group presented increases in nine densitometric parameters, although statistical significance was attained in only two of those parameters. In the control group, an increase was observed in only one parameter, whereas the remaining 11 presented either no alteration or a decrease. CONCLUSION:: The use of alendronate had a positive effect on bone mineral density in SCI patients and therefore represents a potential tool for prevention and treatment of osteoporosis in this population.Spinal Cord advance online publication, 8 February 2005; doi:10.1038/sj.sc.3101725. 1Department of Rehabilitation Medicine of the University of Sao Paulo Hospital das Clinicas, Sao Paulo, Brazil. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15700052

    Khong S, Savic G, Gardner BP and Ashworth F (2005). Hormone replacement therapy in women with spinal cord injury - a survey with literature review. Spinal Cord 43: 67-73. STUDY DESIGN: Postal questionnaire survey. OBJECTIVE: To examine the current use of hormone replacement therapy (HRT) in a sample of menopausal women with spinal cord injury (SCI). SETTING: National Spinal Injuries Centre (NSIC), Stoke Mandeville Hospital, Aylesbury, UK. METHOD: A postal questionnaire was sent to 94 women from the NSIC patient database who met the study inclusion criteria (wheelchair dependent, aged 49 years and above, last seen or heard from within the last 3 years). RESULTS: A total of 59 valid questionnaires were analysed. At the time of the survey, 50 women were menopausal and 11 of them were using HRT, six for menopausal symptoms and five for osteoporosis prevention. Another 11 had used HRT, eight for menopausal symptoms and three for osteoporosis prevention, but had discontinued it. The main reasons for stopping HRT were side effects. Of the 28 women who had never been on HRT, 20 had either enquired about it, or had been offered HRT, but decided against it. Of the nine women who were still premenopausal at the time of the survey, four would consider using HRT. CONCLUSIONS: Results show that 44% of the menopausal women in our sample have used HRT at some point and 22% still do, mostly for treatment of menopausal symptoms and for osteoporosis prevention. In view of the latest literature findings in able-bodied women, use of HRT for osteoporosis prevention in women with SCI may have to be reconsidered. Department of Obstetrics and Gynaecology, Stoke Mandeville Hospital, Aylesbury, Bucks, UK. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15570321

    Bauman WA (2004). Risk factors for osteoporosis in persons with spinal cord injury: what we should know and what we should be doing. J Spinal Cord Med 27: 212-3. Spinal Cord Damage Research Center, Sinai Medical Center, New York, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15478522

    Garland DE, Adkins RH, Kushwaha V and Stewart C (2004). Risk factors for osteoporosis at the knee in the spinal cord injury population. J Spinal Cord Med 27: 202-6. BACKGROUND: The objective of this study was to determine modifiable and nonmodifiable risk factors for bone loss at the knee in individuals with spinal cord injury (SCI) by examining known risk factors for osteoporosis in the general population and additional, unique nonmodifiable SCI elements including age at injury onset, injury duration, and extent of neurologic injury (level and completeness). METHODS: Risk factors were examined by logistic regression in 152 individuals with chronic SCI. Knees were classified as osteoporotic based on whether bone mineral density (BMD) of the knee as assessed by dual-energy x-ray absorptiometry fell within the 95% confidence interval of the BMD of the knee of individuals who had experienced fractures at the knee. RESULTS: Accuracy for predicted membership in the osteoporotic group and nonosteoporotic group were 79.22% and 69.33%, respectively. Of all variables included in the analysis, 3 had a significant effect on predicted group membership: completeness of injury (P < 0.0001), body mass index [BMI) [P = 0.0035), and age [P = 0.0394). Individuals with complete injuries were 6.17 times [617%) more likely to have BMD of the knee low enough to place them in the osteoporotic category. The odds ratio for BMI indicated that every unit increase in BMI lowered the odds of being in the osteoporotic group by 11.29%. The odds ratio for age indicated that every 1-year increase in age increased the odds of being in the osteoporotic group by 3.54%. No other modifiable or nonmodifiable risk factors were significant predictors. CONCLUSION: Completeness of injury dictates and overrides most modifiable and nonmodifiable risk factors for bone loss at the knee leading to pathologic fractures in SCI. SCI osteoporosis may be classified more appropriately as neurogenic in origin. Neurotrauma Division, Rancho Los Amigos National Rehabilitation Center, Downey, California 90242, USA. dougarland@email.msn.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15478520

    Slade JM, Bickel CS, Modlesky CM, Majumdar S and Dudley GA (2005). Trabecular bone is more deteriorated in spinal cord injured versus estrogen-free postmenopausal women. Osteoporos Int 16: 263-72. The prevalence of osteoporosis is high among postmenopausal women and individuals sustaining a spinal cord injury (SCI). We assessed the effects of estrogen loss and unloading on the trabecular bone of the knee in women. Pre- and postmenopausal ambulatory women (n=17) were compared to pre- and postmenopausal women with SCI (n=20). High-resolution magnetic resonance imaging was used to compare groups on apparent measures of trabecular bone volume, trabecular number, trabecular spacing, and trabecular thickness in the distal femur and proximal tibia, regions with a high proportion of trabecular bone and the most common fracture site for SCI patients. Trabecular bone was deteriorated in women with SCI compared to ambulatory women. SCI groups had fewer, (-19 and -26% less) and thinner trabeculae (-6%) that were spaced further apart (40% and 62% more space between structures) resulting in less trabecular bone volume (-22% and -33%) compared to the ambulatory groups (tibia and femur, respectively). Postmenopausal women with SCI also had 34% greater trabecular spacing in the tibia compared to the 40-year-old premenopausal women with SCI, showing an interaction between unloading and estrogen loss. Middle-aged postmenopausal, ambulatory women, not taking estrogen or medications that affect bone, did not show the deteriorated trabeculae that were evident in women with SCI, nor did they show differences in distal femur and proximal tibia trabeculae compared to a premenopausal group. We conclude that the effect of unloading on bone architecture is greater than that of estrogen loss in middle-aged women. Department of Exercise Science, University of Georgia, 300 River Rd, Athens, GA, 30602, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15338112

    McDonald JW, Becker D, Sadowsky CL, Jane JA, Sr., Conturo TE and Schultz LM (2002). Late recovery following spinal cord injury. Case report and review of the literature. J Neurosurg Spine 97: 252-65. The authors of this prospective, single-case study evaluated the potential for functional recovery from chronic spinal cord injury (SCI). The patient was motor complete with minimal and transient sensory perception in the left hemibody. His condition was classified as C-2 American Spinal Injury Association (ASIA) Grade A and he had experienced no substantial recovery in the first 5 years after traumatic SCI. Clinical experience and evidence from the scientific literature suggest that further recovery would not take place. When the study began in 1999, the patient was tetraplegic and unable to breathe without assisted ventilation; his condition classification persisted as C-2 ASIA Grade A. Magnetic resonance imaging revealed severe injury at the C-2 level that had left a central fluid-filled cyst surrounded by a narrow donutlike rim of white matter. Five years after the injury a program known as "activity-based recovery" was instituted. The hypothesis was that patterned neural activity might stimulate the central nervous system to become more functional, as it does during development. Over a 3-year period (5-8 years after injury), the patient's condition improved from ASIA Grade A to ASIA Grade C, an improvement of two ASIA grades. Motor scores improved from 0/100 to 20/100, and sensory scores rose from 5-7/112 to 58-77/112. Using electromyography, the authors documented voluntary control over important muscle groups, including the right hemidiaphragm (C3-5), extensor carpi radialis (C-6), and vastus medialis (L2-4). Reversal of osteoporosis and an increase in muscle mass was associated with this recovery. Moreover, spasticity decreased, the incidence of medical complications fell dramatically, and the incidence of infections and use of antibiotic medications was reduced by over 90%. These improvements occurred despite the fact that less than 25 mm2 of tissue (approximately 25%) of the outer cord (presumably white matter) had survived at the injury level. The primary novelty of this report is the demonstration that substantial recovery of function (two ASIA grades) is possible in a patient with severe C-2 ASIA Grade A injury, long after the initial SCI. Less severely injured (lower injury level, clinically incomplete lesions) individuals might achieve even more meaningful recovery. The role of patterned neural activity in regeneration and recovery of function after SCI therefore appears a fruitful area for future investigation. Department of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri 63108, USA. mcdonald@neuro.wustl.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12296690

    Jones LM, Legge M and Goulding A (2002). Intensive exercise may preserve bone mass of the upper limbs in spinal cord injured males but does not retard demineralisation of the lower body. Spinal Cord 40: 230-5. STUDY DESIGN: Cross-sectional study comparing a group of active spinal cord injured (SCI) males carefully matched for age, height, and weight with active able-bodied male controls. OBJECTIVES: To compare bone mass of the total body, upper and lower limbs, hip, and spine regions in active SCI and able-bodied individuals. SETTING: Outpatient study undertaken in two centres in New Zealand. METHODS: Dual energy X-ray absorptiometry (DEXA) scanning was used to determine bone mass. Questionnaires were used to ascertain total time spent in weekly physical activity for each individual. The criterion for entry into the study was regular participation in physical activity of more than 60 min per week, over and above that required for rehabilitation. RESULTS: Seventeen SCI and their able-bodied controls met our required activity criterion. Bone mineral density (BMD) values of the total body and hip regions were significantly lower in the SCI group than in their controls (P=0.0001). Leg BMD and bone mineral content (BMC) were also significantly lower in the SCI group (P=0.0001). By contrast, lumbar spine BMD and arm BMD and BMC did not differ between the SCI and control groups. Arm BMD and BMC were greater (not significant) than the reference norms (LUNAR database) for both groups. CONCLUSION: Intensive exercise regimens may contribute to preservation of arm bone mass in SCI males, but does not prevent demineralisation in the lower body. The School of Physical Education, University of Otago, Dunedin, New Zealand. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11987005

    Sniger W and Garshick E (2002). Alendronate increases bone density in chronic spinal cord injury: a case report. Arch Phys Med Rehabil 83: 139-40. Over the first 6 to 16 months after spinal cord injury (SCI), up to a third of bone mass may be lost because of demineralization, resulting in an increased risk for fractures. Studies in postmenopausal women have shown the efficacy of oral alendronate, an aminobisphosphonate, in increasing bone mass. However, the efficacy of alendronate in reversing bone density loss has not been shown in patients with chronic SCI. This article reports on the efficacy of alendronate in increasing bone mass in a patient with neurologically incomplete American Spinal Injury Association class D SCI and Brown-Sequard's syndrome. Bone mass change over 2 years while taking alendronate is compared for a weak extremity (majority of muscles grade 2/5) and strong extremity (majority of muscles grade 4/5) and spine. There was a greater increase in bone mineral density in the weaker lower extremity compared with the stronger one; the spine had the greatest increase overall. Spinal Cord Injury Medicine Service, VA Boston Healthcare System, West Roxbury, MA, USA. drsniger@massmed.org http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11782844

    Garland DE, Adkins RH, Stewart CA, Ashford R and Vigil D (2001). Regional osteoporosis in women who have a complete spinal cord injury. J Bone Joint Surg Am 83-A: 1195-200. BACKGROUND: Regional bone loss in patients who have a spinal cord injury has been evaluated in males. In addition, there have been reports on groups of patients of both genders who had an acute or chronic complete or incomplete spinal cord injury. Regional bone loss in females who have a complete spinal cord injury has not been reported, to our knowledge. METHODS: In a study of thirty-one women who had a chronic, complete spinal cord injury, we assessed bone mineral density in relation to age, weight, and time since the injury. The results were compared with the bone mineral density in seventeen healthy, able-bodied women who had been age-matched by group (thirty years old and less, thirty-one to fifty years old, and more than fifty years old). Dual-energy x-ray absorptiometry was used to measure the bone mineral density of the lumbar spine, hip, and knee; Z-scores for the hip and spine were calculated. RESULTS: The mean bone mineral density in the spine in the youngest, middle, and oldest spinal-cord-injury groups was 98%, 108%, and 115% of the densities in the respective age-matched control groups (p < 0.0001), and the mean bone mineral density in the oldest spinal-cord-injury group was equal to that in the youngest control group. This gain in bone mineral density in the spine was reflected by the spine Z-scores, as the mean score in the oldest injured group averaged more than one standard deviation above both the norm and the mean score in the control group. The mean loss of bone mineral density in the knee in the youngest, middle, and oldest spinal-cord-injury groups was 38%, 41%, and 47% compared with the densities in the corresponding control age-groups [p < 0.0001). Furthermore, the oldest injured group had a mean reduction of knee bone mineral density of 54% compared with the youngest control group. The mean loss of bone mineral density in the hips of the injured patients was 18%, 25%, and 25% compared with the densities in the control subjects in the respective age-groups [p < 0.0001). CONCLUSIONS: The bone mineral density in the spine either was maintained or was increased in relation to the time since the injury. This finding is unlike that seen in healthy women, in whom bone mineral density decreases with age. The bone mineral density in the hips of the injured patients initially decreased approximately 25%; thereafter, the rate of loss was similar to that in the control group. The bone mineral density in the knees of the injured patients rapidly decreased 40% to 45% and then further decreased only minimally. Neurotrauma Division, Rehabilitation Research and Training Center on Aging with Spinal Cord Injury, CA, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11507128

    Lazo MG, Shirazi P, Sam M, Giobbie-Hurder A, Blacconiere MJ and Muppidi M (2001). Osteoporosis and risk of fracture in men with spinal cord injury. Spinal Cord 39: 208-14. STUDY DESIGN: Cross-sectional study to evaluate bone mineral density (BMD) and fracture history after spinal cord injury (SCI). OBJECTIVES: To determine frequency of osteoporosis and fractures after SCI, correlate extent of bone loss with frequency of fractures after SCI, and determine fracture risk in SCI patients. SETTING: The Hines Veterans Affairs Hospital in Hines, Illinois, USA. METHODS: Femoral neck BMD was measured in 41 individuals with a history of traumatic or ischemic SCI using dual-energy X-ray absorptiometry (DEXA Lunar Whole Body Densitometer Model). RESULTS: Twenty-five patients (61%) met the World Health Organization (WHO) criteria for osteoporosis, eight (19.5%) were osteopenic, and eight (19.5%) were normal. Fracture after SCI had occurred in 14 patients (34%). There were significant differences between the femoral neck BMD and SCI duration in patients with a fracture history compared to those without. For patients in the same age group, each 0.1 gm/cm(2) and each unit of standard deviation (SD) (t-value) decrement of BMD at the femoral neck increased the risk of fracture 2.2 and 2.8 times, respectively. Considered simultaneously with age, duration of SCI, and level of SCI, BMD was the only significant predictor of the number of fractures. CONCLUSION: Osteoporosis and an increased frequency of fractures occur after SCI. Measurement of femoral neck BMD can be used to quantify fracture risk in SCI patients. Spinal Cord Injury Service (128), Hines VA Hospital, Hines, Illinois 60141, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11420736

    Sabo D, Blaich S, Wenz W, Hohmann M, Loew M and Gerner HJ (2001). Osteoporosis in patients with paralysis after spinal cord injury. A cross sectional study in 46 male patients with dual-energy X-ray absorptiometry. Arch Orthop Trauma Surg 121: 75-8. In a cross-sectional study, 46 male patients with paralysis after spinal cord injury (average age 32 years; injuries sustained from 1 to 26 years ago; 33 Frankel A, 13 Frankel B, C, D) were examined clinically and by dual-energy X-ray absorptiometry (DEXA). Their bone mineral density (BMD) values were compared with age-related controls and correlated to clinical parameters. BMD was reduced in the proximal femur (p < 0.05) and the distal forearm [p < 0.05), but not in the lumbar spine. Demineralisation was influenced in the proximal femur [Z-score -2.95) by immobilisation after surgical treatment. Patients suffering from complete lesions had significantly lower BMD in the lumbar spine [-1.47) compared with patients with incomplete lesions [+0.02). BMD was not significantly influenced by the level of the lesion and the ambulatory status. Long-term monitoring showed significant demineralisation in the proximal femur [r = -0.36) and the distal forearm [r = -0.4), but not in the lumbar spine [r = -0.21). By correlating BMD with clinical parameters, it can be deduced that, firstly, immobilisation after surgical treatment should be reduced to a minimum; secondly, that every effort must be expended to prevent turning an incomplete into a complete lesion; and finally, that rehabilitation treatment should be lifelong. Stiftung Orthopadische Universitatsklinik Heidelberg, Abteilung Orthopadie I, Germany. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11195125

    Dauty M, Perrouin Verbe B, Maugars Y, Dubois C and Mathe JF (2000). Supralesional and sublesional bone mineral density in spinal cord-injured patients. Bone 27: 305-9. This study was performed to evaluate supra- and sublesional bone mineral density (BMD) in spinal cord-injured (SCI) patients after 1 year postinjury, and to correlate the BMD to the neurological level; to correlate the sublesional demineralization to functional parameters (duration postinjury, duration of the initial bedrest); and to assess the role of classic methods of prevention such as walking or standing. Thirty-one SCI patients, all male, were studied vs. 31 controls (age matched). The mean age of the population was 36 years (range 18-60 years). Eleven were tetraplegic and 20 were paraplegic. Twenty-six patients dysplayed a complete motor lesion. The BMD was measured by dual-photon absorptiometry on the lumbar spine and on the femoral neck, and the bone mineral content (BMC) on whole-body scans. Particular attention was paid to the distal femur and proximal tibia upper third. Blood samples and urine samples included phosphocalcic parameters, with determination of urinary hydroxyproline and deoxypyridinoline. SCI patients showed a decrease of sublesional BMD of 41% in comparison with controls. This loss of bone mass is higher at the distal femur (-52%) and proximal tibia (-70%), which are the most common sites of fracture. The degree of demineralization for the lumbar spine, the pelvis, and the lower limbs is independent of the neurological level. The duration of acute posttraumatic immobilization (mean 43.3 days) and the time postinjury increase the loss of bone mass for lower limbs (p = 0.04) and particularly for the proximal tibia (p = 0.02). The study of biomechanical stress (i.e., standing, walking, sitting) does not influence the sublesional BMC. This study underlines the major role of the neurological lesion on the decrease of sublesional BMC in SCI patients and the absence of influence of biomechanical stress. Rehabilitation Department, Hopital Saint Jacques, Nantes, France. marc.duaty@chu-nantes.fr http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10913927

    Stein RB (1999). Functional electrical stimulation after spinal cord injury. J Neurotrauma 16: 713-7. This article reviews work mainly from my own laboratory on the effects of electrical stimulation for therapy and function following spinal cord injury. One to two hours per day of intermittent stimulation can increase muscle strength and endurance and also reverse some of the osteoporosis in bones that are stressed by the stimulation. Stimulation during walking can also be used to improve speed and other parameters of the gait. Surface stimulation systems with 1-4 channels of stimulation were used in a multicenter study. Initial increases of almost 20% in walking speed were seen and overall increases of nearly 50% in subjects who continued to receive stimulation for a year on average. Some changes were due to improved strength and coordination with stimulation and additional walking, but a specific effect of stimulation persisted throughout the trial. Improved devices will soon be available commercially that were developed on the basis of feedback from users. Department of Physiology, University of Alberta, Edmonton, Canada. richard.stein@ualberta.ca http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10511244

  5. #5
    With all that said, what are we supposed to do if we can't stand? What meds should we take?

    Marie
    Unbroken by the grace of God

  6. #6
    Originally posted by Marie:

    With all that said, what are we supposed to do if we can't stand? What meds should we take?

    Marie
    Unbroken by the grace of God
    really.
    a question i'm interested in.
    i keep seeing it asked over and over, but no answers.
    maybe there are none?

  7. #7
    Senior Member poonsuzanne's Avatar
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    Originally posted by Nancie:

    Originally posted by Marie:
    With all that said, what are we supposed to do if we can't stand? What meds should we take?

    Marie
    Unbroken by the grace of God
    really.
    a question i'm interested in.
    i keep seeing it asked over and over, but no answers.
    maybe there are none?
    I also heard that there is nothing we can do to remedy or prevent the threat of higher risk of osteoporosis when you are having SCI. I am so worried for my son!

    Suzanne

  8. #8
    i think the only thing you can do is stand or do weight-bearing exercises. i started standing right after rehab and my bone density is normal.

  9. #9
    WHAT CAN BE DONE TO REVERSE BONE ATROPHY AFTER SCI?
    Wise Young, Ph.D., M.D.

    Spinal cord injury causes a loss of bone mass density (BMD) in bone below the injury level. Calcium is lost in the vertebral column, hip, and leg bones (femur, tibia). Wood, et al. (Wood, et al., 2001) measured BMD in 22 paraplegic patients and found bone loss sufficiently severe to increase the risk of femoral fracture in over 80% of the subjects. Garland, et al., (Garland, et al., 1992) measured BMD in 55 quadriplegic patients and found significant loss of bone throughout the entire skelton, except for the skull with most of the bone loss below the pelvis, stabilizing at two thirds of original bone mass, near fracture thresholds, by 16 months after injury. Can this be prevented? The following is a review of the medical literature on the subject.

    Preliminary data indicate that the aminobisphosphonate Alendronate improves calcium density in bones of people with spinal cord injury. This drug is used to treat osteoporosis in post-menopausal women. In 2002, Sniger & Garshick (Sniger and Garshick, 2002) studied one patient with incomplete spinal cord injury (ASIA Class D). The patient had Brown-Sequard's syndrome where one leg was weaker than the other. A two year treatment of the Alendronate (10 mg/day) resulted in a greater increase of BMD in the weaker lower extremity compared to the stronger one. The spine had the greatest overall increase of BMD. These results, however, may have resulted from progressive improvement in the overall activity of the patient from incomplete spinal cord injury. In 2004, Zehnder, et al. (Zehnder, et al., 2004) randomized 65 paraplegics with complete thoracic spinal cord injuries (ASIA A) or sensory incomplete (ASIA B) to either Alendronate with 500 mg of calcium or 500 mg of calcium alone; 55 of the subjects continued the treatment for 2 years. The study indicates the 10 mg of Alendronate daily completely stopped bone loss at all measured site. Moran de Brito, et al. (2005) from Brazil randomized 19 subjects with chronic SCI to 10 mg Alendronate plus 1000 mg calcium per day or 1000 mg calcium alone. They showed that Alendronate increased the amount of calcium in 9 of 12 measured bone sites after 6 months but only 2 of the sites was statistically different from controls. These results strongly suggest that daily Alendronate treatment will prevent bone loss after spinal cord injury and may even reverse bone loss in chronic spinal cord injury when given over a 6-24 month period.

    The cause of bone loss after spinal cord injury is often attributed to inactivity and lack of use. Some data suggest that the bone loss can be reversed with activity. Saltzstein, et al. (Saltzstein, et al., 1992) correlated the degree of osteoporosis to the an index of mobility in people with spinal cord injury, ranging from 1 for complete immobility to 9 for full mobility. They found that those patients who had more mobility had less loss of calcium, suggesting that standing and weight-support with the bones may prevent osteoporosis. They suggested that people with spinal cord injury may benefit from efforts to maintain a standing posture with some regularity. De Bruin, et al. (de Bruin, et al., 1999) assessed the effects of early weight-bearing and treadmill walking on 19 patients. They found that patients have had early weight-bearing training had little or no loss of bone, compared to severe losses in patients who did not have such training.

    Apparently, moderate activity alone is not sufficient to prevent bone loss. Dauty, et al. (Dauty, et al., 2000) compared 31 male patients with spinal cord injury with 31 age-matched non-injured controls. They found a 41% decrease in BMD in leg bones compared to controls but simple standing and walking activity did not seem to change the degree of bone loss. Likewise, Vlychou, et al. (Vlychou, et al., 2003) studied 57 paraplegics and found that the degree of demineralization did not depend on complete or incomplete injury, level of lesion, physiotherapy, and standing. Some investigators have hypothesized that spasticity may prevent osteoporosis. Frey-Rindova, et al. (Frey-Rindova, et al., 2000) studied 29 patients with spinal cord injury and found no correlation between the degree of spasticity on bone loss. However, more recently, Eser, et al. (Eser, et al., 2005) studied 54 patients with clinically complete spinal cord, finding no significant relationship between bone loss and lifestyle factors but they did find that subjects with higher spasticity scores had larger total and cortical cross-sectional bone areas.

    Several studies reported that electrical stimulation of muscles against resistance can reverse bone loss but the data is controversial. Bloomfield & Jackson (Bloomfield, et al., 1996) reported that exercise training with functional electrical stimulation for 9 months can improve bone mass density. Mohr, et al. (Mohr, et al., 1997) studied 10 patients that underwent stimulated (FES) upright cycling 30 minutes per day, 3 days per week, followed by six months of with only one weekly training session. After the period of intensive training, the bone mass density of the proximal tibia increased 10% from 0.49 to 0.54. However, after 6 months of reduced training the improvement of tibial bone mass density had receded. Belanger, et al. (Belanger, et al., 2000) studied 14 patients with SCI, stimulating their quadriceps against an isokinetic load. They found that this training increased the bone density by about 30% in the femur and proximal femur. Ott (Ott, 2001) suggested that weight-bearing and functional electrical stimulation may prevent some of the bone loss. Stein, et al. (Stein, et al., 2002) likewise reported that therapeutic stimulation of paralyzed muscles for one hour a day not only retarded muscle atrophy and increased endurance but improved their bone density.

    However, several groups were unable to show any improvement in bone density associated with exercise and FES stimulation. Leeds, et al. (Leeds, et al., 1990) studied six quadriplegic patients who trained 3 days a week for 6 months on a FES cycle ergometer. There was no statistically significant difference before and after 6 months of training. Solomonow, et al. (Solomonow, et al., 1997) examined 70 paraplegic patients who were training to walk with the reciprocal gait orthosis and functional electrical stimulation, but did not find any significant effect on bone more muscle. Eser, et al. (Eser, et al., 2003) from Switzerland reported that electrical stimulation-induced cycling started shortly after injury did not significantly attenuate bone loss in 19 patients, compared to 19 who did not have such exercise. The treatment consisted of 30-minute FES cycling 3 times a week for the duration of their primary rehabilitation time for 6 months. Thus, it seems that 30-minute training for 3 days a week is not sufficient to change bone mass densities over periods of 6 months. The difference between these studies and ones that show significant effects of FES-cycling on BMD may be related to intensity and length of training. Most of the studies showing beneficial effects had more intense training (one hour daily) and for 9 months or longer.

    In conclusion, preliminary data suggest that 10 mg of Alendronate plus calcium can significantly reduce osteoporosis when started early after injury and may even reverse osteoporosis in people with chronic spinal cord injury over a period of two years. Mobility in patients and intensive weight-bearing treadmill training appear to be associated with reduced osteoporosis. However, moderate activity and lifestyle differences do not appear to be associated with reduced osteoporosis. There is some disagreement about the effect of spasticity on osteoporosis. Several studies suggest that intensive functional electrical stimulation activated cycling against resistance will reduce osteoporosis but this appears to depend on the intensity and length of training.

    References Cited


    Eser P, de Bruin ED, Telley I, Lechner HE, Knecht H and Stussi E (2003). Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest 33: 412-9. BACKGROUND: Bone atrophy in spinal cord-injured people (SCI) is, among other factors, caused by immobilization and is initiated shortly after the injury. The present study measured the effect of an functional electrical stimulation (FES)-cycling intervention on bone mineral density (BMD) of the tibia in recently injured SCI people. METHODS: As soon as possible after the injury (mean 4.5 weeks), para- and tetraplegic patients were recruited into an intervention and control group comparable with regard to gender, age, and lesion level. The intervention consisted of 30-min functional electrical stimulation-cycling three times a week for the duration of their primary rehabilitation (mean = 6 months). Computed tomography (CT) scans of the right tibia diaphysis were taken at the beginning and at the end of the intervention. Bone mineral density of cortical bone was calculated from the CT scans. RESULTS: A total of 38 subjects (19 in each group) were included in the study. Both groups showed a reduction in tibial cortical BMD of 0-10% of initial values within 3-10 months. The mean decrease in BMD was 0.3% (+/- 0.6) per month in the intervention group and 0.7% (+/- 0.8) in the control group. This difference did not reach statistical significance. Decrease of BMD was linearly correlated to initial BMD and age in the pooled data of both groups; subjects who had a high initial BMD and/or were older lost more bone. In neither group was bone loss associated with duration of immobilization nor lesion level. CONCLUSIONS: Functional electrical stimulation-cycling applied shortly after SCI did not significantly attenuate bone loss. Swiss Paraplegic Centre, Nottwil, Swiss Federal Institute of Technology, Schlieren, Switzerland. prisca.eser@paranet.ch http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12713456


    Wood DE, Dunkerley AL and Tromans AM (2001). Results from bone mineral density scans in twenty-two complete lesion paraplegics. Spinal Cord 39: 145-8. STUDY DESIGN: The bone mineral density (BMD) in 22 male subjects with complete lesion paraplegia sustained 1.8 to 27 years previously was measured. The measurements were used in screening each subject for a research programme investigating the restoration of standing using functional electrical stimulation (FES). OBJECTIVES: To assess the extent of bone loss in this group of subjects and correlation to age, time post-injury and level of lesion. SETTING: District General Hospital in the UK. METHODS: BMD was measured by dual energy X-ray absorptiometry (DEXA) in the lumbar spine and femoral neck and expressed as an indirect index to an age matched 'normal' population. Fracture risk was described from this score using published data indicating that the risk increased with each standard deviation difference from the 'normal' mean. RESULTS: The bone density in the lumbar spine was better preserved than in the femoral neck. BMD in the lumbar spine was found to be greater than the mean from the age matched population in 57.1% of subjects. Bone loss at the femoral neck suggested that 81.8% of the subjects were at increased risk of fracture, but only 22.7% were at a high risk. No correlation was found between BMD at the lumbar spine or the femoral neck and age, lesion level or time post-injury. CONCLUSION: The study indicates that further investigation into baseline BMD values for the SCI population is required to improve information provided to patients and assessment of fracture risk on an individual basis. Department of Medical Physics and Biomedical Engineering, Salisbury District Hospital, Salisbury, Wiltshire, UK. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11326324

    Garland DE, Stewart CA, Adkins RH, Hu SS, Rosen C, Liotta FJ and Weinstein DA (1992). Osteoporosis after spinal cord injury. J Orthop Res 10: 371-8. Dual-photon absorptiometry characterized bone loss in males aged less than 40 years after complete traumatic paraplegic and quadriplegic spinal cord injury. Total bone mass of various regions and bone mineral density (BMD) of the knee were measured in 55 subjects. Three different populations were partitioned into four groups: 10 controls (healthy, age matched); 25 acutely injured (114 days after injury), with 12 reexamined 16 months after injury; and 20 chronic (greater than 5 years after injury). Significant differences (p less than 0.0001) in bone mass mineral between groups at the arms, pelvis, legs, distal femur, and proximal tibia were found, with no differences for the head or trunk. Post hoc analyses indicated no differences between the acutely injured at 16 months and the chronically injured. Paraplegic and quadriplegic subjects were significantly different only at the arms and trunk, but were highly similar at the pelvis and below. In the acutely injured, a slight but statistically insignificant rebound was noted above the pelvis. Regression techniques demonstrated early, rapid, linear (p less than 0.0001) decline of bone below the pelvis. Bone mineral loss occurs throughout the entire skeleton, except the skull. Most bone loss occurs rapidly and below the pelvis. Homeostasis is reached by 16 months at two thirds of original bone mass, near fracture threshold. Department of Neurotrauma, Rancho Los Amigos Medical Center, Downey, California 90242. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1569500

    Sniger W and Garshick E (2002). Alendronate increases bone density in chronic spinal cord injury: a case report. Arch Phys Med Rehabil 83: 139-40. Over the first 6 to 16 months after spinal cord injury (SCI), up to a third of bone mass may be lost because of demineralization, resulting in an increased risk for fractures. Studies in postmenopausal women have shown the efficacy of oral alendronate, an aminobisphosphonate, in increasing bone mass. However, the efficacy of alendronate in reversing bone density loss has not been shown in patients with chronic SCI. This article reports on the efficacy of alendronate in increasing bone mass in a patient with neurologically incomplete American Spinal Injury Association class D SCI and Brown-Sequard's syndrome. Bone mass change over 2 years while taking alendronate is compared for a weak extremity (majority of muscles grade 2/5) and strong extremity (majority of muscles grade 4/5) and spine. There was a greater increase in bone mineral density in the weaker lower extremity compared with the stronger one; the spine had the greatest increase overall. Spinal Cord Injury Medicine Service, VA Boston Healthcare System, West Roxbury, MA, USA. drsniger@massmed.org http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11782844

    Zehnder Y, Risi S, Michel D, Knecht H, Perrelet R, Kraenzlin M, Zach GA and Lippuner K (2004). Prevention of bone loss in paraplegics over 2 years with alendronate. J Bone Miner Res 19: 1067-74. To assess the effects of long-term treatment of bone loss with alendronate in a group of paraplegic men, 55 patients were evaluated in a prospective randomized controlled open label study that was 2 years in duration comparing alendronate and calcium with calcium alone. Bone loss was stopped at all cortical and trabecular infralesional sites (distal tibial epiphysis, tibial diaphysis, total hip) with alendronate 10 mg daily. INTRODUCTION: Bone loss after spinal cord injury (SCI) leads to increased fracture risk in the lower limbs of paraplegics. The aim of this study was to document long-term treatment of bone loss with alendronate in a group of paraplegic men with complete motor lesion after SCI. MATERIALS AND METHODS: Sixty-five men with complete motor post-traumatic medullary lesion between T1 and L2 with total motor and sensory loss (Frankel classification, stage A) or with total motor and partial sensory loss (Frankel classification, stage B) after SCI were included in this prospective randomized controlled open label study that was 2 years in duration. The patients were randomized to either the treatment group with alendronate 10 mg daily and elemental calcium 500 mg daily or to the control group with elemental calcium 500 mg daily alone. The primary endpoint was defined as the effect over 24 months of alendronate and calcium compared with calcium alone on the BMD values at the distal tibial epiphysis (as a surrogate for trabecular bone in the paralyzed zone). The secondary endpoints were changes in BMD at supra- and infralesional sites of measurement. Biochemical markers of bone turnover were assessed. RESULTS: Fifty-five subjects, 0.1-29.5 years post-SCI, completed the study over 24 months. BMD at the distal tibial epiphysis significantly decreased from baseline in the calcium group (-10.8 +/- 2.7% at 24 months, p < 0.001), whereas it remained stable in the alendronate plus calcium group [-2.0 +/- 2.9% at 24 months, p = not significant versus baseline), leading to a significant intergroup difference over time [p = 0.017). At the tibial diaphysis, similar significant results were observed. At the ultradistal radius and the radial shaft, BMD did not change significantly from baseline in either treatment group. At the total hip, BMD decreased significantly in the calcium group [-4.1 +/- 1.6%, p = 0.038) but remained stable in the alendronate plus calcium group [+0.43 +/- 1.2%), with a significant intergroup difference [p = 0.037). At the lumbar spine, BMD increased significantly [p < 0.0001) from baseline in both groups. Biochemical markers of bone resorption were significantly decreased with alendronate versus baseline and control. Alendronate and calcium were generally safe and well tolerated. CONCLUSIONS: In paraplegic men, SCI bone loss was stopped at all measured cortical and trabecular infralesional sites over 24 months with alendronate 10 mg daily. Osteoporosis Policlinic, University Hospital of Berne, Berne, Switzerland. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15176988

    Saltzstein RJ, Hardin S and Hastings J (1992). Osteoporosis in spinal cord injury: using an index of mobility and its relationship to bone density. J Am Paraplegia Soc 15: 232-4. This study was undertaken to improve quantification of the extent of osteoporosis that accompanies spinal cord injuries (SCI) of various types, using single photon densitometry. In this study, we evaluated subjects with complete and incomplete SCI to determine whether there is a correlation between mobility and bone density. We created an index to rank the various levels of mobility among SCI subjects. Mobility index parameters ranged from 1, for complete immobility, to 9, for the full mobility of the uninjured control population. Incomplete SCI subjects (motor and/or sensory) ranked from 2 to 8 on the mobility scale. We also attempted to define clearly the mechanism of osteoporosis in those with predominantly unilateral SCI (Brown-Sequard syndrome). Using single photon absorptiometry (SPA), we found a strong correlation between our mobility index and observed bone density. These observations clearly show that osteoporosis is affected by the subject's level of physical activity. These observations also support the hypothesis that SCI individuals benefit from efforts to maintain a standing posture with some regularity. This effort to improve bone density slows the development of osteoporosis, a process that results in physical impairments in the SCI population. VA Medical Center, Milwaukee, WI 53295. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1431871

    de Bruin ED, Frey-Rindova P, Herzog RE, Dietz V, Dambacher MA and Stussi E (1999). Changes of tibia bone properties after spinal cord injury: effects of early intervention. Arch Phys Med Rehabil 80: 214-20. OBJECTIVE: To evaluate the effectiveness of an early intervention program for attenuating bone mineral density loss after acute spinal cord injury (SCI) and to estimate the usefulness of a multimodality approach in diagnosing osteoporosis in SCI. DESIGN: A single-case, experimental, multiple-baseline design. SETTING: An SCI center in a university hospital. METHODS: Early loading intervention with weight-bearing by standing and treadmill walking. PATIENTS: Nineteen patients with acute SCI. OUTCOME MEASURES: (1) Bone density by peripheral computed tomography and (2) flexural wave propagation velocity with a biomechanical testing method. RESULTS: Analysis of the bone density data revealed a marked decrease of trabecular bone in the nonintervention subjects, whereas early mobilized subjects showed no or insignificant loss of trabecular bone. A significant change was observed in 3 of 10 subjects for maximal and minimal area moment of inertia. Measurements in 19 subjects 5 weeks postinjury revealed a significant correlation between the calculated bending stiffness of the tibia and the maximal and minimal area moment of inertia, respectively. CONCLUSION: A controlled, single-case, experimental design can contribute to an efficient tracing of the natural history of bone mineral density and can provide relevant information concerning the efficacy of early loading intervention in SCI. The combination of bone density and structural analysis could, in the long term, provide improved fracture risk prediction in patients with SCI and a refined understanding of the bone remodeling processes during initial immobilization after injury. Department of Material Sciences, Laboratory for Biomechanics ETH, Zurich, Switzerland. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10025500

    Dauty M, Perrouin Verbe B, Maugars Y, Dubois C and Mathe JF (2000). Supralesional and sublesional bone mineral density in spinal cord-injured patients. Bone 27: 305-9. This study was performed to evaluate supra- and sublesional bone mineral density (BMD) in spinal cord-injured (SCI) patients after 1 year postinjury, and to correlate the BMD to the neurological level; to correlate the sublesional demineralization to functional parameters (duration postinjury, duration of the initial bedrest); and to assess the role of classic methods of prevention such as walking or standing. Thirty-one SCI patients, all male, were studied vs. 31 controls (age matched). The mean age of the population was 36 years (range 18-60 years). Eleven were tetraplegic and 20 were paraplegic. Twenty-six patients dysplayed a complete motor lesion. The BMD was measured by dual-photon absorptiometry on the lumbar spine and on the femoral neck, and the bone mineral content (BMC) on whole-body scans. Particular attention was paid to the distal femur and proximal tibia upper third. Blood samples and urine samples included phosphocalcic parameters, with determination of urinary hydroxyproline and deoxypyridinoline. SCI patients showed a decrease of sublesional BMD of 41% in comparison with controls. This loss of bone mass is higher at the distal femur (-52%) and proximal tibia (-70%), which are the most common sites of fracture. The degree of demineralization for the lumbar spine, the pelvis, and the lower limbs is independent of the neurological level. The duration of acute posttraumatic immobilization (mean 43.3 days) and the time postinjury increase the loss of bone mass for lower limbs (p = 0.04) and particularly for the proximal tibia (p = 0.02). The study of biomechanical stress (i.e., standing, walking, sitting) does not influence the sublesional BMC. This study underlines the major role of the neurological lesion on the decrease of sublesional BMC in SCI patients and the absence of influence of biomechanical stress. Rehabilitation Department, Hopital Saint Jacques, Nantes, France. marc.duaty@chu-nantes.fr http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10913927

    Vlychou M, Papadaki PJ, Zavras GM, Vasiou K, Kelekis N, Malizos KN and Fezoulidis IB (2003). Paraplegia-related alterations of bone density in forearm and hip in Greek patients after spinal cord injury. Disabil Rehabil 25: 324-30. PURPOSE: Paraplegia due to spinal cord injury is related with sublesional bone demineralization with an increased incidence of pathologic fractures in lower extremities. This study was carried out in order to evaluate bone density alterations in forearm and hip in Greek paraplegic patients after spinal cord injury and to correlate the findings with the level of injury, the neurological status, the time interval from injury and the performing of physiotherapy and therapeutic standing. METHOD: Fifty-seven paraplegic patients (33 men and 24 women, with injuries sustained from 6 months to 27 years) and 36 able-bodied age-matched controls (25 men, 16 women) participated in the study. Bone mineral density (BMD) was measured by dual X-ray absorptiometry (DXA) in the proximal and distal forearm, the femoral neck, the greater trochanter and Ward's triangle. Results: The measurements revealed a significant reduction of BMD of femoral neck (p<0.001 in male, p<0.001 in female paraplegics), greater trochanter [p<0.001 and p=0.001, respectively) and Ward's triangle [p=0.001 and p=0.005, respectively). Proximal forearm depicted non-significantly decreased BMD values and distal forearm depicted a slight increase in BMD values. The degree of demineralization was independent of factors such as complete or incomplete spinal cord injury, level of the lesion, physiotherapy and performing of standing. In addition to that, BMD values in both hip and forearm showed no statistically significant correlation with time after injury. CONCLUSIONS: BMD measurements in Greek paraplegic patients reveal bone loss, which most dramatically occurs in the region of hip with a consequent increase of fracture risk. Forearm measurements depict a non-homogeneous response with limited proximal bone loss and slight distal increase of BMD, the latter being possibly attributed to daily activities. Department of Radiology, National Institute of Rehabilitation, Ilion 13122, Greece. mvlychou@hol.gr http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12745956

    Frey-Rindova P, de Bruin ED, Stussi E, Dambacher MA and Dietz V (2000). Bone mineral density in upper and lower extremities during 12 months after spinal cord injury measured by peripheral quantitative computed tomography. Spinal Cord 38: 26-32. OBJECTIVE: To evaluate the loss of trabecular and cortical bone mineral density in radius, ulna and tibia of spinal cord injured persons with different levels of neurologic lesion after 6, 12 and 24 months of spinal cord injury (SCI). DESIGN: Prospective study in a Paraplegic Centre of the University Hospital Balgrist, Zurich. SUBJECTS AND METHODS: Twenty-nine patients (27 males, two females) were examined by the highly precise peripheral quantitative computed tomography (pQCT) soon after injury and subsequently at 6, 12 and in some cases 24 months after SCI. Using analysis of the bone mineral density (BMD), various degrees of trabecular and cortical bone loss were recognised. A rehabilitation program was started as soon as possible (1-4 weeks) after SCI. The influence of the level of neurological lesion was determined by analysis of variance (ANOVA). Spasticity was assessed by the Ashworth Scale. RESULTS: The trabecular bone mineral density of radius and ulna was significantly reduced in subjects with tetraplegia 6 months (radius 19% less, P<0.01; ulna 6% less, P>0.05) and 12 months after SCI (radius 28% less, P<0.01; ulna 15% less, P<0.05). The cortical bone density was significantly reduced 12 months after SCI [radius 3% less, P<0.05; ulna 4% less, P<0.05). No changes in BMD of trabecular or cortical bone of radius and ulna were detected in subjects with paraplegia. The trabecular BMD of tibia was significantly reduced 6 months [5% less, P<0.05) and 12 months after SCI [15% less, P<0.05) in all subjects with SCI. The cortical bone density of the tibia only was decreased after a year following SCI [7% less, P<0.05). No significant difference between both groups, subjects with paraplegia and subjects with tetraplegia was found for tibia cortical or trabecular BMD. There was no significant influence for the physical activity level or the degree of spasticity on bone mineral density in all subjects with SCI. CONCLUSIONS: Twelve months after SCI a significant decrease of BMD was found in trabecular bone in radius and in tibia of subjects with tetraplegia. In subjects paraplegia, a decrease only in tibia BMD occurred. Intensity of physical activity did not significantly influence the loss of BMD in all subjects with para- and tetraplegia. However, in some subjects regular intensive loading exercise activity in early rehabilitation [tilt table, standing) can possibly attenuate the decrease of BMD of tibia. No influence was found for the degree of spasticity on the bone loss in all subjects with SCI. Paraplegic Centre, University Hospital Balgrist, Zurich, Switzerland. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10762194

    Eser P, Frotzler A, Zehnder Y, Schiessl H and Denoth J (2005). Assessment of anthropometric, systemic, and lifestyle factors influencing bone status in the legs of spinal cord injured individuals. Osteoporos Int 16: 26-34. The aim of the present study was to assess the influence of muscle spasms, systemic or lifestyle factors on bone mass and geometry of the femur and the tibia in people with long-standing spinal cord injury (SCI). Fifty-four motor complete SCI people with paralysis duration of between 5 and 50 years were included in the study. Spasticity was measured by means of the Ashworth scale. Distal epiphyses and mid shafts of the femur, tibia, and radius were measured by peripheral quantitative computed tomography. From the epiphyseal scans, trabecular and total bone mineral density (BMDtrab and BMDtot) were calculated, and from the shaft scans, cortical BMD (BMDcort), total and cortical cross-sectional area (CSAtot and CSAcort), and muscle cross-sectional areas (CSAmus) were determined. Personal characteristics, anthropometric, as well as life-style factors, were assessed by means of a questionnaire. A Spearman correlation matrix was produced with measured data. Correlation coefficients exceeding 0.3 were tested for significance by performing linear regression for parametric data and ANOVA for non-parametric data. Subjects with higher spasticity scores had significantly larger CSAmus in the upper and lower leg. Both spasticity and CSAmus were found to be significantly related to BMDtrab and BMDtot of the distal epiphysis of the femur and to CSAcort of the femoral shaft. In the lower leg, bone parameters of the tibia were found to be strongly related to corresponding bone parameters of the radius, which suggests a systemic origin. No significant relationships were found between bone parameters and any of the life-style factors. The extent of bone loss caused by disuse of the lower extremities in people with long-standing SCI is influenced by systemic factors. Additionally, spasticity has a positive effect on bone parameters of the femur. Institute for Clinical Research, Swiss Paraplegic Centre, 6207, Nottwil, Switzerland. peser@deakin.edu.au http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15138665

    Bloomfield SA, Mysiw WJ and Jackson RD (1996). Bone mass and endocrine adaptations to training in spinal cord injured individuals. Bone 19: 61-8. To investigate whether exercise training can produce increases in bone mass in spinal cord-injured (SCI) individuals with established disuse osteopenia, nine subjects (age 28.2 years, time since injury 6.0 years, level of injury C5-T7) were recruited for a 9-month training program using functional electrical stimulation cycle ergometry (FES-CE), which produces active muscle contractions in the paralyzed limb. After training, bone mineral density (BMD, by X-ray absorptiometry) increased by 0.047 +/- 0.010 g/cm2 at the lumbar spine; changes in BMD at the femoral neck, distal femur, and proximal tibia were not significant for the group as a whole. In a subset of subjects training at > or = 18 W for at least 3 months (n = 4), BMD increased by 0.095 +/- 0.026 g/cm2 (+18%) at the distal femur. By 6 months of training, a 78% increase in serum osteocalcin was observed, indicating an increase in bone turnover. Urinary calcium and hydroxyproline, indicators of resorptive activity, did not change over the same period. Serum PTH increased 75% over baseline values (from 2.98 +/- 0.15 to 5.22 +/- 0.62 pmol/L) after 6 months' training, with several individual values in hyperparathyroid range; PTH declined toward baseline values by 9 months. These data establish the feasibility of stimulating site-specific increases in bone mass in severely osteopenic bone with muscle contractions independent of weight-bearing for those subjects able to achieve a threshold power output of 18 W with FES-CE. Calcium supplementation from the outset of training in osteopenic individuals may be advisable to prevent training-induced increases in PTH. Department of Health & Kinesiology, Texas A&M University, College Station 77843-4243, USA. sbloom@acs.tamu.edu http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8830990

    Mohr T, Podenphant J, Biering-Sorensen F, Galbo H, Thamsborg G and Kjaer M (1997). Increased bone mineral density after prolonged electrically induced cycle training of paralyzed limbs in spinal cord injured man. Calcif Tissue Int 61: 22-5. Spinal cord injured (SCI) individuals have a substantial loss of bone mass in the lower limbs, equaling approximately 50% of normal values in the proximal tibia, and this has been associated with a high incidence of low impact fractures. To evaluate if this inactivity-associated condition in the SCI population can be reversed with prolonged physical training, ten SCI individuals [ages 35.3 +/- 2.3 years (mean +/- standard error [SE]); post injury time: 12.5 +/- 2.7 years, range 2-24 years; level of lesion: C6-Th4; weight: 78 +/- 3.8 kg] performed 12 months of Functional Electrical Stimulated (FES) upright cycling for 30 min per day, 3 days per week, followed by six months with only one weekly training session. Bone mineral density (BMD) was determined before training and 12 and 18 months later. BMD was measured in the lumbar spine, the femoral neck, and the proximal tibia by dual energy absorptiometry (DEXA, Nordland XR 26 MK1). Before training, BMD was in the proximal tibia (52%), as well as in the femoral neck, lower in SCI subjects than in controls of same age (P < 0.05). BMD of the lumbar spine did not differ between groups [P > 0.05). After 12 months of training, the BMD of the proximal tibia had increased 10%, from 0.49 +/- 0.04 to 0. 54 +/- 0.04 g/cm2 (P < 0.05). After a further 6 months with reduced training, the BMD in the proximal tibia no longer differed from the BMD before training [P > 0.05). No changes were observed in the lumbar spine or in the femoral neck in response to FES cycle training. It is concluded that in SCI, the loss of bone mass in the proximal tibia can be partially reversed by regular long-term FES cycle exercise. However, one exercise session per week is insufficient to maintain this increase. Department of Medical Physiology, Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen, Denmark. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9192506

    Belanger M, Stein RB, Wheeler GD, Gordon T and Leduc B (2000). Electrical stimulation: can it increase muscle strength and reverse osteopenia in spinal cord injured individuals? Arch Phys Med Rehabil 81: 1090-8. OBJECTIVE: To study the extent to which atrophy of muscle and progressive weakening of the long bones after spinal cord injury (SCI) can be reversed by functional electrical stimulation (FES) and resistance training. DESIGN: A within-subject, contralateral limb, and matching design. SETTING: Research laboratories in university settings. PARTICIPANTS: Fourteen patients with SCI (C5 to T5) and 14 control subjects volunteered for this study. INTERVENTIONS: The left quadriceps were stimulated to contract against an isokinetic load (resisted) while the right quadriceps contracted against gravity (unresisted) for 1 hour a day, 5 days a week, for 24 weeks. MAIN OUTCOME MEASURES: Bone mineral density (BMD) of the distal femur, proximal tibia, and mid-tibia obtained by dual energy x-ray absorptiometry, and torque (strength). RESULTS: Initially, the BMD of SCI subjects was lower than that of controls. After training, the distal femur and proximal tibia had recovered nearly 30% of the bone lost, compared with the controls. There was no difference in the mid-tibia or between the sides at any level. There was a large strength gain, with the rate of increase being substantially greater on the resisted side. CONCLUSION: Osteopenia of the distal femur and proximal tibia and the loss of strength of the quadriceps can be partly reversed by regular FES-assisted training. Departement de Kinanthropologie, Universite du Quebec a Montreal, Canada. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10943761

    Ott SM (2001). Osteoporosis in women with spinal cord injuries. Phys Med Rehabil Clin N Am 12: 111-31. Decreased bone density and increased fracture risk are seen in patients with SCI. The bone resorption rate is markedly increased. Hypercalciuria, low PTH, and low 1,25 (OH)2 vitamin D are commonly seen. Bed-rest studies show similar findings, but of lesser magnitude. Therapies to treat or prevent osteoporosis include optimal nutrition (with care to avoid exacerbating hypercalciuria). Weight-bearing or functional electrical stimulation cycle ergometry may prevent some of the bone loss, especially in acutely injured patients. Estrogen should be considered in postmenopausal or amenorrheic women, but not if they are at high risk of thromboembolism. More research on effects of estrogen is needed in this population. Bisphosphonates may also help prevent the acute bone loss; oral routes must not be used in recumbent patients. Thiazides could be useful as adjunct therapy. Department of Medicine, University of Washington, Seattle 98195-6426, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11853032

    Stein RB, Chong SL, James KB, Kido A, Bell GJ, Tubman LA and Belanger M (2002). Electrical stimulation for therapy and mobility after spinal cord injury. Prog Brain Res 137: 27-34. This article reviews the use of therapeutic and functional electrical stimulation in subjects after a spinal cord injury (SCI). Muscles become much weaker and more fatigable, while bone density decreases dramatically after SCI. Therapeutic stimulation of paralyzed muscles for about 1 h/day can reverse the atrophic changes and markedly increase muscle strength and endurance as well as bone density. Functional electrical stimulation can also improve the speed and efficiency of walking in people with an incomplete SCI. Finally, a modified wheelchair is described in which electrical stimulation or residual voluntary activation of leg muscles can produce movements of a footrest that is coupled to the wheels. The wheelchair can provide greater mobility and fitness to persons who are not functional walkers and currently use their arms to propel a wheelchair. Centre for Neuroscience, University of Alberta, Edmonton, AB T6G 2S2, Canada. richard.stein@ualberta.ca http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12440357

    Leeds EM, Klose KJ, Ganz W, Serafini A and Green BA (1990). Bone mineral density after bicycle ergometry training. Arch Phys Med Rehabil 71: 207-9. The effect of functional electrical stimulation (FES) cycle ergometry on bone mineral density (BMD) was investigated in six spinal cord injury (SCI) quadriplegic men. Each subject trained three days a week for six months on an FES cycle ergometer. Pretraining and posttraining BMD measurements of the proximal femur were performed using dual photon absorptiometry. Mean pretraining BMD (percent norm) for the femoral neck, Ward triangle, and trochanter were 66.65, 57.43, and 57.67, respectively. After six months of FES cycle ergometry, mean BMD measurements were 66.15, 57.07, and 55.13, respectively. There was no statistically significant difference between the pretraining and posttraining BMD measurements. All subjects were found to have osteoporotic proximal femurs when BMD was expressed as a percent of their age-matched controls. Bone mineral density measurements were subsequently performed on three additional men with SCI who had exercised for three years with the FES cycle ergometry modality. Their mean BMDs were not significantly different from the experimental group. This study demonstrated that six months of FES cycle ergometry did not produce an increase in BMD. University of Miami School of Medicine, FL. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=2317139

    Solomonow M, Reisin E, Aguilar E, Baratta RV, Best R and D'Ambrosia R (1997). Reciprocating gait orthosis powered with electrical muscle stimulation (RGO II). Part II: Medical evaluation of 70 paraplegic patients. Orthopedics 20: 411-8. Medical evaluation was performed on a group of paraplegics who were trained to walk with the Reciprocating Gait Orthosis powered with electrical muscle stimulation (RGO II). The evaluation included changes in spasticity, cholesterol level, bone metabolism, cardiac output and stroke volume, vital capacity, knee extensors torque, and heart rate at the end of a 30-meter walk. After an average of 14 weeks of training during which patients walked for 3 hours per week, significant reductions in spasticity, total cholesterol and low-density lipids, hydroxyproline/creatinine ratio, and increased knee extensor torque were evident. The data also showed that improvements occurred in the calcium/creatinine ratio, serum calcium and alkaline phosphatase levels, cardiac output and stroke volume, and vital capacity, yet these improvements were not statistically significant. The final heart rate at the end of a 30-meter walk showed that the RGO II required only a moderate level of exertion, which was found to be the lowest among the other mechanical or muscle stimulation orthoses available to paraplegics. It was concluded that the limited but reasonable level of functional regain provided by the RGO II is associated with a general improvement in the paraplegic's physiological condition if used for a minimum of 3 to 4 hours per week. Department of Orthopedic Surgery, State University Medical Center, New Orleans, La, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9172248

    Eser P, de Bruin ED, Telley I, Lechner HE, Knecht H and Stussi E (2003). Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest 33: 412-9. BACKGROUND: Bone atrophy in spinal cord-injured people (SCI) is, among other factors, caused by immobilization and is initiated shortly after the injury. The present study measured the effect of an functional electrical stimulation (FES)-cycling intervention on bone mineral density (BMD) of the tibia in recently injured SCI people. METHODS: As soon as possible after the injury (mean 4.5 weeks), para- and tetraplegic patients were recruited into an intervention and control group comparable with regard to gender, age, and lesion level. The intervention consisted of 30-min functional electrical stimulation-cycling three times a week for the duration of their primary rehabilitation (mean = 6 months). Computed tomography (CT) scans of the right tibia diaphysis were taken at the beginning and at the end of the intervention. Bone mineral density of cortical bone was calculated from the CT scans. RESULTS: A total of 38 subjects (19 in each group) were included in the study. Both groups showed a reduction in tibial cortical BMD of 0-10% of initial values within 3-10 months. The mean decrease in BMD was 0.3% (+/- 0.6) per month in the intervention group and 0.7% (+/- 0.8) in the control group. This difference did not reach statistical significance. Decrease of BMD was linearly correlated to initial BMD and age in the pooled data of both groups; subjects who had a high initial BMD and/or were older lost more bone. In neither group was bone loss associated with duration of immobilization nor lesion level. CONCLUSIONS: Functional electrical stimulation-cycling applied shortly after SCI did not significantly attenuate bone loss. Swiss Paraplegic Centre, Nottwil, Swiss Federal Institute of Technology, Schlieren, Switzerland. prisca.eser@paranet.ch http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12713456

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    Super Moderator Sue Pendleton's Avatar
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    Considering the range of countries these abstracts cover there is no mention of methylprednisolone (Solumedrol) being a factor or not in bone loss. Anyone know if there are any comparison studies?

    And I am curious if gritty urine soon after injury is a sign of bone loss. When I was still in the acute hospital in Germany as soon as I could maintain my blood pressure I was on a tilt table 4 to 5 days a week. During that month or so I had seriously clear pee. As soon as I arrived in the US for rehab at NRH we were told that standing and tilt tables added nothing that sitting upright 14 to 16 hours a day wouldn't do. (I have since learned to be rude and ask about the effect on their labor costs versus my health.) For several weeks I was still using a foley (waiting for urodynamics to be done). I had seriously gross pee. It was like bags of wet sand. UTIs were constant and one old school nurse (I liked her!) wanted to irrigate my bladder even with the risk to my kidneys it was so bad.

    I've been scheduled for a DEXA to go along with some other tests gals my age need. Just kind of curious even after all these years whether I was peeing away my tibias.

    Oh yea, a once a month form of Fosomax was announced yesterday. It means standing a bit more than an hour but hey 12 instead of 52 pills a year sounds good.

    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

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