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Thread: Keeping your body in shape for the cure

  1. #1

    Keeping your body in shape for the cure

    I just received the following question:

    Quote Originally Posted by royals80
    Hello Dr. Young,

    I was wondering what I have to do to keep my body ready for the cure. I have read in other post that using the standing frame does not benefit bone density. Also what exactly can FES do to benefit my body? also anything else I can do to benefit my body and its chances to be most ready for a cure. I am committed to staying as healthy and ready as possible.

    Thank you,
    John
    John,

    Let me answer this question in the forums since I am sure that a lot of other people have similar questions. I think that it is important to stand to place stress on the bones and to activate your muscles. We know that if one does not put stress on the muscles, they lose strength. If the muscles are not used, they undergo atrophy.

    Osteoporosis. The standard measure of osteoporosis is calcium concentration. However, it is not necessarily the best measure because the strength of bone is not only calcium but also cells and proteins that hold the calcium. For example, one might have a lot of calcium but without enough protein, the bone is brittle and may break just as easily. So, I think that investigators should also assess bone stength by the number of fractures that occur in people. It is true that standing 30 minutes a day 3 days a week for 3-6 months does not significantly increase calcium levels in bone. One interpretation may be that one needs more than 30 minutes a day, perhaps an hour or more per day every day. Also, the fact that calcium does not increase does not necessarily mean that the bone is not stronger. Finally, standing up has other benefits, including taking weight off your butt and creating some callouses on your feet. There are reports that it improves the regularity of bowel movements and also inmproves blood flow in the legs. Finally, I believe that standing stimulates some muscle activity, particular the anti-gravity extensor muscles.

    Muscle Atrophy. We know that muscle shrink when they are inactive. This occurs even if the muscles are innervated, in people with casexts for broken bones. I have long said that spasticity is a great and free form of exercise. For those that don't have strong spasticity, FES will help.

    Exercise is important for another reason. Muscle activity increase metabolism and improves cardiovascular fitness. Finally, much evidence suggests that exercise increases neurotrophin production in the brain and spinal cord.

    So, there are many reasons to exercise.

    Wise.

  2. #2
    Thank you very much Dr. Wise for your response and explanation on each category. I personally was starting to neglect using the standing frame because of post saying that doctors said it did not benefit bone density at all but could damage.

    I am lucky enough to be able to own the BioFlex which is a FES body suit and am glad to hear of the benefits it can have for me.

    I just want to thank you for your constant work and time to provide a better future for all SCI affected people...

  3. #3
    Sorry I did not get to finish my reply because Dragon messed up a 30 minute response I tried to post about 15 minutes ago so I just posted that quickly.

    To continue on what I was going to say, I have been reading a lot of negativity in many post recently which has caused to me to stop reading some post and I just want to say PEOPLE it starts with us.. we are falling into the traps set by the congressman and people with no clinical background who say spinal cord injury is forever.. for us hope is ALL we have and WE as a unit have to unite and fight to get funding so that one day in the foreseeable future I and we can hug a beloved family member once again, and we can have children that we can hold and look into the eyes of and know that we will be able to some physical task with them.. to me it is a smack in the face of Dr. Wise Young to say cure is impossible.. people I am asking everyone to push to get funding so that one day we will stand from these chairs and live normal lives again.. there is an upcoming presidential election in 08 and I know for a FACT that presidential candidate Hillary Clinton supports stem cell research and the CDRPA so please let us all come Republican or democratic and support her because she supports US.. if we push today it will lead for a better tomorrow.

  4. #4
    Dr. Young ,
    hi , i have a question . have you ever heard of this company NEUROCARE ?
    would you please, if you get a chance , go to their web site NEUROCARE.COM and read the article at the top of the page ,left side "BREAKTHROUGH IN SPINAL CORD INJURY " .thanks .
    they claim that their stimulator is different (because of the amount of electricity , etc, etc, etc) and by accident they found that when people using their eleterical stimulator , they start regaining some feeling, function even bowel and bledder control . and they charge too too much money for it , i don't know why it is so expensive ?
    i talked with someone from the compnay over the phone , and they sent me some reports about some of the cases , and i am going to see my doctor and aske him about it and see what he thinks of this .
    again, if you can, go to this site and see what you think of it , make sure you read that paper article . thanks . i did send you PM about this few days ago , but i assume you did not get it , or you did not have time to reply . is anybody using their stimulator? if so , please post your experince with it . thanks
    thanks for your time
    Last edited by kz; 10-07-2007 at 06:18 AM.

  5. #5
    Quote Originally Posted by kz
    Dr. Young ,
    hi , i have a question . have you ever heard of this company NEUROCARE ?
    would you please, if you get a chance , go to their web site NEUROCARE.COM and read the article at the top of the page ,left side "BREAKTHROUGH IN SPINAL CORD INJURY " .thanks .
    they claim that their stimulator is different (because of the amount of electricity , etc, etc, etc) and by accident they found that when people using their eleterical stimulator , they start regaining some feeling, function even bowel and bledder control . and they charge too too much money for it , i don't know why it is so expensive ?
    i talked with someone from the compnay over the phone , and they sent me some reports about some of the cases , and i am going to see my doctor and aske him about it and see what he thinks of this .
    again, if you can, go to this site and see what you think of it , make sure you read that paper article . thanks . i did send you PM about this few days ago , but i assume you did not get it , or you did not have time to reply . is anybody using their stimulator? if so , please post your experince with it . thanks
    thanks for your time
    kz,

    I don't know enough about neurocare to comment specifically. However, I am not aware of any technique of stimulation that is better than others and I don't think that any of the FES techniques restore function. I get hundreds of questions such as yours, many claims regarding treatments that are too good to be true and for which little or no evidence is available to support the claims. I am skeptical.

    Wise.

  6. #6
    Quote Originally Posted by Wise Young
    I just received the following question:



    John,

    Let me answer this question in the forums since I am sure that a lot of other people have similar questions. I think that it is important to stand to place stress on the bones and to activate your muscles. We know that if one does not put stress on the muscles, they lose strength. If the muscles are not used, they undergo atrophy.

    Osteoporosis. The standard measure of osteoporosis is calcium concentration. However, it is not necessarily the best measure because the strength of bone is not only calcium but also cells and proteins that hold the calcium. For example, one might have a lot of calcium but without enough protein, the bone is brittle and may break just as easily. So, I think that investigators should also assess bone stength by the number of fractures that occur in people. It is true that standing 30 minutes a day 3 days a week for 3-6 months does not significantly increase calcium levels in bone. One interpretation may be that one needs more than 30 minutes a day, perhaps an hour or more per day every day. Also, the fact that calcium does not increase does not necessarily mean that the bone is not stronger...

    Wise.
    Wise was right yet again. Bone strength and health hinges on more than just calcium content.
    Bone Structure 'Vastly Different' Than Previously Believed

  7. #7

    osteoporosis references

    Couple of points to bear in mind:

    -Osteoporosis due to SCI differs from the usual post-menopausal variety- eg SCI causes disproportionate loss of trabecular bone at the distal femur/proximal tibia, thus the so-called "paraplegic fracture" frequently occurs in those areas

    -Advertised benefits of standing frames are often inconsistent with published results of scientific studies. Long-term, frequent use may have a modest effect on bone density - the jury is still out.

    For those interested, here's an excellent technical review
    http://www.icord.org/scire/pdf/SCIRE_CH9.pdf

    Bottom line - seek a thorough medical evaluation before weight-bearing, eg bone density, vitamin D, testosterone level for men, etc, and ask your doctor to consider medication as appropriate

    [see also - Bauman WA. Risk factors for osteoporosis in persons with spinal cord injury: what we should know and what we should be doing.
    J Spinal Cord Med. 2004;27(3):212-3. No abstract available.
    PMID: 15478522 [PubMed - indexed for MEDLINE]
    Ed from Detroit

  8. #8
    I agree with Dr. Nieshoff. The jury is still out regarding the effects of standing on bone density and bone strength. As I had earlier pointed out, the degree and duration of exercise and standing may not be sufficient to change bone density significantly. Recent studies suggest that the preventing musculoskeletal changes may be more effective that reversing chronic changes (Shields & Dudley-Javoroski, 2007). A new term has been coined for the phenomenon: "immobilization osteoporosis" (Reiter, et al., 2007). A recent prospectively controlled study indicates the alendronate is useful in preventing bone loss and appears to be free of serious side-effects (GilChrist, et al. 2007). Functional electrical stimulation does not seem to prevent bone loss in one study (Clark, et al., 2007) but may have had some effect in another study (Shields, et al., 2006). Early axial loading may reduce bone mineral density loss (Can, et al., 2007). There is some evidence that spasms and spasticity may mitigate bone mineral density loss (Rittweger, et al., 2006).

    • Shields RK and Dudley-Javoroski S (2007). Musculoskeletal adaptations in chronic spinal cord injury: effects of long-term soleus electrical stimulation training. Neurorehabil Neural Repair. 21: 169-79. Graduate Program in Physical Therapy and Rehabilitation Science, The University of Iowa, Iowa City, IA 52242-1190, USA. richard-shields@uiowa.edu. OBJECTIVE: The purpose of this study was to determine whether long-term electrical stimulation training of the paralyzed soleus could change this muscle's physiological properties (torque, fatigue index, potentiation index, torque-time integral) and increase tibia bone mineral density. METHODS: Four men with chronic (>2 years) complete spinal cord injury (SCI; American Spinal Injury Association classification A) trained 1 soleus muscle using an isometric plantar flexion electrical stimulation protocol. The untrained limb served as a within-subject control. The protocol involved ~ 30 minutes of training each day, 5 days a week, for a period of 6 to 11 months. Mean compliance over 11 months of training was 91% for 3 subjects. A fourth subject achieved high compliance after only 5 months of training. Mean estimated compressive loads delivered to the tibia were approximately 110% of body weight. Over the 11 months of training, the muscle plantar flexion torque, fatigue index, potentiation index, and torque-time integral were evaluated periodically. Bone mineral density (dual-energy x-ray absorptiometry) was evaluated before and after the training program. RESULTS: The trained limb fatigue index, potentiation index, and torque-time integral showed rapid and robust training effects (P<.05). Soleus electrical stimulation training yielded no changes to the proximal tibia bone mineral density, as measured by dual-energy x-ray absorptiometry. The subject with low compliance experienced fatigue index and torque-time integral improvements only when his compliance surpassed 80%. In contrast, his potentiation index showed adaptations even when compliance was low. CONCLUSIONS: These findings highlight the persistent adaptive capabilities of chronically paralyzed muscle but suggest that preventing musculoskeletal adaptations after SCI may be more effective than reversing changes in the chronic condition.
    • Reiter AL, Volk A, Vollmar J, Fromm B and Gerner HJ (2007). Changes of basic bone turnover parameters in short-term and long-term patients with spinal cord injury. Eur Spine J. 16: 771-6. Department of Orthopedics, Vulpius Klinik Bad Rappenau, Bad Rappenau, Baden-Wurttemberg, Germany. areiter@vulpiusklinik.de. The bone mineral density (BMD), the cross- links (PYD, DPD and NTx) and the bone specific alcaline phosphatase (BAP) was investigated in a cross-sectional study in 62 male patients with spinal cord injury (SCI), n = 28 short-term (0-1 year after SCI) and n = 34 long-term SCI patients (> 5 years after SCI). Knowledge about this parameters are necessary to find an adequate therapy for this special kind of osteoporosis. Immobilisation osteoporosis in SCI patients is a well-known problem that may lead to pathological fractures. Little is known regarding the extend of the osteoporosis as well as the causative factors. Measurements of the BMD in the proximal femur and the lumbar spine were performed with dual-energy-X-ray-absorptiometry (DEXA), of the osteoblast marker BAP (bone specific alkaline phosphatase) from serum and the osteoclast markers PYD (pyridinoline), DPD (desoxy-pyridinoline) and NTx (N-telopeptide of collagen type I) from urine. We found a significant decrease of BMD in the proximal femur and no relevant change in the lumbar spine compared to an age- and sex correlated control group (Z-score) in short-term and long-term SCI patients. There was a significant bone loss at the proximal femur between short and long-term SCI patients, whereas at the lumbar spine the BMD even slightly increases. Bone resorption (cross-links) was increased in both groups, though in long-term SCI patients it is significantly decreased compared to short-term SCI patients (DPD from 211.7 micro/g creatinine to 118.1 micro/g creatinine; NTx from 215.1 nmol/mmol creatinine to 83,6 nmol/mmol creatinine). The bone formation marker BAP is slightly below normal range in both groups (12.3 U/l in short-term, 9.7 U/l in long- term SCI patients). Only the proximal femur is affected by the immobilisation osteoporosis of SCI patients, therefore the BMD measurements in these patients should be performed at the lower limb. The problem of the immobilisation osteoporosis in SCI patients is the striking increase of bone resorption and the missing reaction of the bone formation.
    • Gilchrist NL, Frampton CM, Acland RH, Nicholls MG, March RL, Maguire P, Heard A, Reilly P and Marshall K (2007). Alendronate prevents bone loss in patients with acute spinal cord injury: a randomized, double-blind, placebo-controlled study. J Clin Endocrinol Metab. 92: 1385-90. Canterbury Geriatric Medical Research Trust, The Princess Margaret Hospital, and Department of Medicine, Christchurch School of Medicine and Health Sciences, New Zealand. NigelG@cdhb.govt.nz. CONTEXT: Patients who sustain an acute spinal cord injury (SCI) experience rapid dramatic reductions in bone mineral density (BMD), especially marked in sublesional areas and sometimes leading to hypercalcemia and hypercalciuria, as well as increased fracture risk. OBJECTIVE: In this prospective, double-blind, randomized, placebo-controlled study, we evaluated the hypothesis that oral alendronate administration would preserve BMD when administered soon after acute SCI. PATIENTS AND INTERVENTION: Thirty-one patients with acute SCI were randomly allocated to receive oral alendronate 70 mg/wk or placebo, within 10 d of acute SCI, for 12 months. MAIN OUTCOME MEASUREMENTS: At entry and at 3, 6, 12, and 18 months, total body bone density, lumbar and hip BMD, ultrasound of the calcaneus, 24-h urinary calcium, and serum C-telopeptide (betaCTX) were measured. RESULTS: At study entry, patients in the two groups were well matched for age, gender, severity of neurological deficit, BMD, urinary calcium, and betaCTX. BMD indices declined steadily in the placebo group, and this effect was attenuated significantly by alendronate. After 12 months, there was a 5.3% difference (P<0.001) in total body BMD and a 17.6% difference (P<0.001) in the total hip BMD between the two groups. Alendronate compared with placebo induced significant (P<0.001) reductions in urinary calcium excretion and serum betaCTX. No treatment-related side effects were noted. CONCLUSIONS: We conclude that alendronate therapy, 70 mg/wk, initiated soon after acute SCI, prevents bone loss and is not associated with side effects.
    • Clark JM, Jelbart M, Rischbieth H, Strayer J, Chatterton B, Schultz C and Marshall R (2007). Physiological effects of lower extremity functional electrical stimulation in early spinal cord injury: lack of efficacy to prevent bone loss. Spinal Cord. 45: 78-85. Division of Orthopaedics and Trauma Service, Faculty of Health Sciences, University of Adelaide, Adelaide, SA, Australia. STUDY DESIGN: Controlled, repeat-measures study. OBJECTIVES: To determine if functional electrical stimulation (FES) can affect bone atrophy in early spinal cord injury (SCI), and the safety, tolerance and feasibility of this modality in bone loss remediation. SETTING: Spinal Injuries Units, Royal Adelaide Hospital and Hampstead Rehabilitation Centre, South Australia. METHODS: Patients with acute SCI (ASIA A-D) were allocated to FES (n=23, 28+/-9 years, C4-T10, 13 Tetra) and control groups (CON, n=10, 31+/-11 years, C5-T12, four Tetra). The intervention group received discontinuous FES to lower limb muscles (15 min sessions to each leg twice daily, over a 5-day week, for 5 months). Dual energy X-ray absorptiometry (DEXA) measured total body bone mineral density (tbBMD), hip, spine BMD and fat mass (FM) within 3 weeks, and 3 and 6 months postinjury. RESULTS: FES and CON groups' tbBMD differed significantly at 3 months postinjury (P<0.01), but not thereafter. Other DEXA measures (hip, spine BMD, FM) did not differ between groups at any time. No adverse events were identified. CONCLUSION: Electrically stimulated muscle activation was elicited, and tetanic effects were reproducible; however, there were no convincing trends to suggest that FES can play a clinically relevant role in osteoporosis prevention (or subsequent fracture risk) in the recently injured patient. The lack of an osteogenic response in paralysed extremities to electrically evoked exercise during subacute and rehabilitation/recovery phases cannot be fully explained, and may warrant further evaluation.
    • Shields RK, Dudley-Javoroski S and Law LA (2006). Electrically induced muscle contractions influence bone density decline after spinal cord injury. Spine. 31: 548-53. Graduate Program in Physical Therapy and Rehabilitation Science, University of Iowa, Iowa City, IA 52242-1190, USA. richard-shields@uiowa.edu. STUDY DESIGN: Longitudinal repeated-measures; within-subject control. OBJECTIVE: We examined the extent to which an isometric plantar flexion training protocol attenuates bone loss longitudinally after SCI. SUMMARY OF BACKGROUND DATA: After spinal cord injury (SCI), bone mineral density (BMD) of paralyzed extremities rapidly declines, likely because of loss of mechanical loading of bone via muscle contractions. METHODS: Six individuals with complete paralysis began a 3-year unilateral plantar flexor muscle activation program within 4.5 months after SCI. The opposite limb served as a control. Compliance with recommended dose was > 80%. Tibia compressive force was > 140% of body weight. RESULTS: Bilateral hip and untrained tibia BMD declined significantly over the course of the training. Lumbar spine BMD showed minimal change. Percent decline in BMD (from the baseline condition) for the trained tibia (approximately 10%) was significantly less than the untrained tibia (approximately 25%) (P < 0.05). Trained limb percent decline in BMD remained steady over the first 1.5 years of the study (P < 0.05). CONCLUSIONS: Compressive loads of approximately 1 to 2 times body weight, induced by muscle contractions, partially prevent the loss of BMD after SCI. Future studies should establish dose-response curves for attenuation of bone loss after SCI.
    • Can A, Dosoglu MS, Karacan I and Karamehmetoglu S (2007). [Effect of axial loading on bone mineral density in patients with traumatic spinal cord injury]. Ulus Travma Acil Cerrahi Derg. 13: 101-5. Deparment of Neurosurgery, Abant Izzet Baysal University, Duzce Medical Faculty, Duzce, Turkey. BACKGROUND: Osteoporosis occurs in paralyzed extremities secondary to immobilization following spinal cord injury (SCI). Bone mineral density (BMD) is rapidly lost after SCI. Loss of BMD may reach fracture threshold although it slows with time. This study was planned to investigate the option of impediment of osteoporosis by early axial loading in immobilized patients. METHODS: Fifteen patients with complete paraplegia having spinal cord lesion between T4-L1 and 15 normal volunteers were included into the study. Time, mechanism and type of injury, BMD, serum calcium, phosphorus and alkaline phosphatase levels were undertaken as variables. BMD was measured by dual energy X-ray absorbtiometry (DEXA) in the femoral neck, trochanteric region and T1 and L3 spine. RESULTS: The BMD values were lower in the femoral neck and trochanteric region, but there were no significant differences at T1 and L3 spine in paraplegics. CONCLUSION: BMD decreases in the femoral neck and trochanteric region, secondary to immobilization. Absence of significant differences of BMD values at T1 and L3 spine in the study and control groups might be due to early rehabilitation. Sitting exercises early after stabilization might impede of the loss of BMD by axial loading to the spine. Thus, complications such as osteoporosis and pathological fractures can be prevented.
    • Rittweger J, Gerrits K, Altenburg T, Reeves N, Maganaris CN and de Haan A (2006). Bone adaptation to altered loading after spinal cord injury: a study of bone and muscle strength. J Musculoskelet Neuronal Interact. 6: 269-76. Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Cheshire, UK. j.rittweger@mmu.ac.uk. Bone loss from the paralysed limbs after spinal cord injury (SCI) is well documented. Under physiological conditions, bones are adapted to forces which mainly emerge from muscle pull. After spinal cord injury (SCI), muscles can no longer contract voluntarily and are merely activated during spasms. Based on the Ashworth scale, previous research has suggested that these spasms may mitigate bone losses. We therefore wished to assess muscle forces after SCI with a more direct measure and compare it to measures of bone strength. We hypothesized that the bones in SCI patients would be in relation to the loss of muscle forces. Six male patients with SCI 6.4 (SD 4.3) years earlier and 6 age-matched, able-bodied control subjects were investigated. Bone scans from the right knee were obtained by pQCT. The knee extensor muscles were electrically stimulated via the femoral nerve, isometric knee extension torque was measured and patellar tendon force was estimated. Tendon force upon electrical stimulation in the SCI group was 75% lower than in the control subjects (p<0.01). Volumetric bone mineral density of the patella and of the proximal tibia epiphysis were 50% lower in the SCI group than in the control subjects (p<0.01). Cortical area was lower by 43% in the SCI patients at the proximal tibia metaphysis, and by 33% at the distal femur metaphysis. No group differences were found in volumetric cortical density. Close curvilinear relationships were found between stress and volumetric density for the tibia epiphysis (r(2)=0.90) and for the patella (r(2)=0.91). A weaker correlation with the tendon force was found for the cortical area of the proximal tibia metaphysis (r(2)=0.63), and none for the distal femur metaphysis. These data suggest that, under steady state conditions after SCI, epiphyseal bones are well adapted to the muscular forces. For the metaphysis of the long bones, such an adaptation appears to be less evident. The reason for this remains unclear.








    Quote Originally Posted by enieshoff
    Couple of points to bear in mind:

    -Osteoporosis due to SCI differs from the usual post-menopausal variety- eg SCI causes disproportionate loss of trabecular bone at the distal femur/proximal tibia, thus the so-called "paraplegic fracture" frequently occurs in those areas

    -Advertised benefits of standing frames are often inconsistent with published results of scientific studies. Long-term, frequent use may have a modest effect on bone density - the jury is still out.

    For those interested, here's an excellent technical review
    http://www.icord.org/scire/pdf/SCIRE_CH9.pdf

    Bottom line - seek a thorough medical evaluation before weight-bearing, eg bone density, vitamin D, testosterone level for men, etc, and ask your doctor to consider medication as appropriate

    [see also - Bauman WA. Risk factors for osteoporosis in persons with spinal cord injury: what we should know and what we should be doing.
    J Spinal Cord Med. 2004;27(3):212-3. No abstract available.
    PMID: 15478522 [PubMed - indexed for MEDLINE]
    Last edited by Wise Young; 10-20-2007 at 11:21 AM.

  9. #9
    Thanks for the thorough literature update, I was particularly encouraged by McGuire et al's paper. Hope to see a similarly positive result in chronic SCI when the Toronto group publishes their study using risendronate in chronic SCI (>18mos.) - http://clinicaltrials.gov/ct/show/NCT00138866?order=1 - nothing on PubMed yet. Even so, some of us are inclined to go ahead and use this class of drugs in the clinic now, based on the available data.
    Ed from Detroit

  10. #10
    All this bone problems could being reversed if person recover mobility(cure)?
    -Ramps in buildings are necessary, but it would be usefull to have another ones for people (mind/heart).....

    -Hoc non pereo habebo fortior me

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