Osteoporosis, the word that means “porous bones,” is a disorder of bone and mineral metabolism characterized by low bone mineral density (BMD), altered bone microarchitecture, and decreased bone strength. Osteoporosis makes patients more vulnerable to low energy or fragility fractures. The World Health Organization defines osteoporosis as a BMD of 2.5 standard deviations or more below the mean peak bone mass as measured by dual-energy X-ray absorptiometry (DXA).1
Osteoporosis results from the imbalance of bone formation and resorption. Many individuals with central nervous system (CNS) injury, including individuals with brain injury, spinal cord injury (SCI), stroke, multiple sclerosis (MS), Parkinson’s disease (PD), cerebral palsy (CP), and brain tumors, are at risk for osteoporosis.
Epidemiology including risk factors and primary prevention
Osteoporosis is a major complication of CNS injury. In the US, there are at least 1.5 million osteoporosis-related fractures each year.2 Following CNS injury, immobility is the greatest contributing factor to the development of osteoporosis.3 Other risk factors include mechanical unloading and longer duration since injury. Commonly used medications, including heparin, warfarin, glucocorticoids, and anticonvulsants, may also contribute.2
The incidence and risk factors vary in different CNS injury states. Following brain injury, among individuals who face significant ambulation challenges, over 40% develop osteopenia and over 20% osteoporosis. Factors include inflammatory stress, pituitary dysfunction, and anti-epileptic medications. 4
Most people with SCI develop osteoporosis, with the incidence well above 50%. The degree of bone loss is greater with higher neurological level and more complete injuries. Individuals with paraplegia have 16% more bone density in their upper extremities than do those with tetraplegia.5
Stroke can lead to rapid bone loss and deterioration in skeletal architecture. This bone loss, which more commonly affects paretic limbs, seems to occur more commonly in older adults in whom osteoporosis is also more common. Factors include muscle imbalances, dysregulated bone modeling, and use of anticoagulants. 6,7,8
MS, an autoimmune condition, is characterized by inflammatory phase (with plaques formed) then relapsing remitting phase (axon damage). Both phases are associated with bone loss, but there is a notable increase in osteopenia and osteoporosis in the relapsing remitting phase. Factors include decreased ambulation, steroid use, and vitamin D deficiency.2
PD, a neurodegenerative basal ganglia syndrome, has been associated with bone loss and increased osteoporosis risk, particularly in women. Factors include weight loss/ poor nutrition, vitamin D deficiency, decreased muscle strength, and use of dopaminergic medications.2
In CP, which can result in difficulties with movement, posture, and balance, more than 30% of people have difficulty walking. Up to 90% of individuals with CP have lower than normal bone density levels. Factors include altered nutrition, non-weightbearing status, late-onset puberty, and use of anticonvulsants.9
Brain tumors are heterogeneous, and it is difficult to estimate the incidence of osteoporosis in affected people. However, it but seems clear that bone health can be affected in this vulnerable population. Contributing factors include use of antiepileptic medications, glucocorticoids, anticoagulants, radiation therapy, and hemiplegia.10
For all these diverse CNS conditions, primary prevention includes optimizing overall health and nutrition. Mobilization, including weight-bearing exercises, should be included whenever possible.3
The skeleton is constantly remodeling, allowing us to maintain calcium homeostasis. During the normal remodeling process, new bone is laid down by osteoblasts, which synthesize and mineralize new bone. The new bone replaces the bone that is milled by osteoclasts, the cells that resorb mineralized bone matrices. This process is regulated by hormones, growth factors, response to mechanical forces, and overall physiological status. 2,3
With age there’s net bone loss due to increased osteoclasts or decreased osteoblast activity. Immobility, and associated changes in lack of normal weight-bearing forces on the body, can hasten bone loss too. Calcium loss, which occurs during immobility, is another important factor.3,4
In CNS injury, when there is decreased weight-bearing, reduced mechanical stress on bone results. This situation inhibits osteoblast-mediated bone formation and accelerates osteoclast-mediated bone resorption. CNS injuries can also trigger immune cells to release inflammatory mediators and activate osteoclasts, leading to bone loss. CNS injury can affect cognition and put individuals at risk for falling, which can affect bone health. Changes in nutritional status also occur commonly in CNS injury.11
In brain injury, changes to the normal process include alteration of growth hormone-insulin growth factor (GH-IGF-1) axis, impaired thyroid and gonadal function (Bell 2013). Increased parathyroid hormone (PTH) levels can cause compensatory mobilization of calcium stores from bone.4 If PTH is suppressed, less calcium is absorbed in the gut and less vitamin D is produced.12 Low serum vitamin D levels also negatively affect bone formation. Medications, such as anticonvulsants phenytoin and carbamezapine that affect cytochrome P450 system, like lead to increased conversion of vitamin D to inactive form, leaving less biologically active vitamin D to help build new bone.4,11
Osteoporosis in SCI is also mediated by hormonal changes, including PTH and thyroid hormones, and blunted sympathetic activity. These autonomic changes cause dilation of bony intravenous shunts and vascular stasis which is thought to contribute to an imbalance of bone formation and resorption.13
Bone loss after stroke in the early phase seems to be caused by increased bone resorption in the setting of muscle weakness, since it occurs on the paretic side. Later cases of bone loss seem related to the degree of paresis and vitamin D levels.6
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Disease progression differs by the type of CNS injury but there are some commonalities. The rate of bone loss is greater sooner after injury and during periods of immobility. Bone loss is also more likely during periods of physiologic stress, in times when nutrition status is sub-optimal, and when individuals are on medications that affect bone health.4
In the acute phase of SCI, when osteoclast activity far outpaces osteoblasts and bone turnover is rampant, imbalance between calcium absorption and excretion can occur. Hypercalcemia and hypercalcinuria are generally seen between weeks 4 and 8 post-injury. If left untreated, these can lead to complications like dehydration, personality changes, calcium nephrolithiasis, renal insufficiency.12
Patients with SCI experience most bone loss in the first 12 months. After that, bone loss continues but at a slower rate. Individuals with motor complete SCI have regional bone loss of almost 1% of bone mineral density per week for the first several months post injury. By 10-12 years after injury, the pelvis and lower extremities suffer approximately 50% bone demineralization, and 21% in the upper extremities, but there may be a net gain in the trunk.8
In stroke, bone loss reaches a maximum at 4 months and then stabilizes. Recovery of bone density has been seen in patients who recover ambulation.6,14
Individuals with progressive MS have more severe bone loss than those with a relapsing-remitting disease course. Their bone loss is also greater during acute flares of the disease.2
Specific secondary or associated conditions and complications
Fracture is the major complication of osteoporosis. Decreases in BMD are directly linked to an increased risk for fracture. Of note, for every decrease of one standard deviation below control subjects for BMD at the hip, the risk for hip fracture increases 2-3 times. Older adults experience bone loss related to age itself, so age is also a risk factor for osteoporosis. More than 50% of women and 20% of men over 50 will sustain a fragility fracture. 1 These numbers are compounded by the effects of CNS injury. Morbidity due to fractures is greater among people with disability than in rest of population.4 The total annual cost for osteoporotic fractures in the US has been estimated to be $20 billion dollars.1 It is possible that not every fracture, including those sustained by patients who also have CNS injuries, are counted and that this estimate is low.
Fractures can in turn lead to more morbidity, mortality, and health care costs. Pain and structural changes can result from one or multiple fragility fractures. Multiple thoracic fractures can cause restrictive lung disease and lumbar fractures can change the abdominal anatomy leading to pain and constipation.1 These can all present major setbacks to individuals with CNS injuries.
The situation is especially significant in SCI. More than 50% of people with motor complete SCI experience an osteoporotic fracture at some point following their injury, with most fractures occurring in distal femur and proximal tibia.5 Individuals with SCI are more than 100 times more likely to have a fracture by the age of 50 than the general population. The most common cause of fracture after SCI is falling from wheelchair. People with SCI can sustain fractures during low impact activities including transferring from bed to chair, being turned in bed, and low speed traffic crashes.8,15 The most common sites are the femoral shaft and proximal tibia. Fractures then put individuals with SCI at risk for more complications, including altered fracture healing, osteomyelitis, cellulitis, pressure ulcers, lower limb amputation, autonomic dysreflexia, and premature death.5,8
Following stroke, in the setting of non-ambulatory status, individuals have lower bone mass and a risk of fracture up to 7 times that of healthy individuals of comparable age. Fractures more commonly involve the plegic side and are associated with the development of additional strokes, increased mortality, increased hospital length of stay, and fewer discharges home.6
Individuals with multiple sclerosis experience more bone loss, and have 20-40% increased risk of fracture, particularly in the lumbar spine, femur, and hip, compared with healthy controls.2
Individuals with Parkinson’s disease have a higher incidence of fractures, notably in the hip, lumbar spine, and femoral neck, than the general population. They have noted to experience significant declines in functional independence after fracture.2
Essentials of Assessment
Assessment consists of a comprehensive evaluation of current health status and osteoporosis risk factors. This includes a thorough assessment of nutritional intake, medication use, and any weight-bearing difficulties.
It is necessary to identify any additional secondary causes of osteoporosis, including vitamin D deficiency, thyroid disease, parathyroid disease, renal failure, chronic liver disease, inflammatory bowel disease, anorexia, amenorrhea/menopause, hypogonadism, and any cancer managed with chemotherapy or radiation.
Other risk factors, including hereditary disposition, low body mass index, smoking and alcohol use, should be reviewed.
For individuals with CNS injury, particular attention should also be paid to immobility, degree of motor impairment, and duration of disability. Past and current medications should be reviewed to determine possible contributing factors. Finally, consideration should be made regarding pre-existing osteoporosis and history of low impact fractures.
There are no specific physical exam findings for osteoporosis. Body type, including body mass index, and overall appearance are important to note. Those are risk for falls present with poor balance, impaired proprioception, or muscle deconditioning.
The musculoskeletal examination is essential. It is important to check muscle strength, tone, and bulk. Manual muscle testing should be used when that is possible, or passive testing in cases of impaired movement. Joints should be assessed for the potential presence of contractures or heterotopic ossification.
Clinicians can also look for signs of fracture. Localized edema and erythema may indicate an underlying fracture in asymptomatic insensate patients. The majority of vertebral fractures are painless, but patients can present with localized pain on palpation, paravertebral muscle spasms, kyphosis. There may be limited active or passive range of motion in the fractured limbs.
Vision, balance, coordination, and sensation, including proprioception, should be checked.
Functional assessment should focus on evaluation of fall risk. Factors to consider include mobility, balance, urinary incontinence, visual problems, polypharmacy, and environmental safety. Falls are extremely common after CNS injury and greatly increase the likelihood of fracture. For example, in one community sample, 73% of individuals with a stroke experienced a fall within 6 months of hospital discharge.14 Ambulation with an inadequate assistive device or on uneven surfaces, as well as poor technique with transfers, increase fall risk.
For wheelchair users, fall risk can be lowered by ensuring that the wheelchair is regularly maintained and fits the user appropriately. Other strategies include use of grip gloves, anti-tippers, seatbelt, or chest straps. Any transfer devices should also be evaluated to minimize falls during use.15
There is no single laboratory test for osteoporosis, but many tests may identify secondary causes. Clinicians should consider obtaining a complete blood count, chemistry panel, thyroid stimulating hormone (TSH), PTH, ionized calcium, liver function tests, bone specific alkaline phosphatase, 24-hour urinary calcium, vitamin D, and gonadal hormones. Hydroxyproline, a urinary marker of bone resorption, may be useful for early identification.16
DXA is currently the criterion standard for the evaluation of BMD. DXA consists of 2 x-ray beams with different energy levels focused on a specific area of bone. Soft tissue is subtracted out and the BMD can be determined by the absorption of each beam by the bone. BMD is reported as a T- or Z-score as appropriate.1,16
BMD measurement using DXA at any site is the single best predictor of fracture at that site.4 BMD measurement using DXA has been shown to be the single best predictor of fracture at a particular site. Traditionally, DXA measurements are obtained at the lumbar spine, femoral neck, total hip, and distal radius. In individuals with SCI, measurements at the distal femur and proximal tibia are also recommended, as these are the most common areas of fracture. DXA can also be used to monitor disease progression and response to therapy. The International Society of Clinical Densitometry (ISCD) recommends monitoring response to treatment every 1-2 years at the same facility, with the same densitometer, using the same acquisition, and analysis protocols.5
T-score: compared to control subjects at peak BMD
- 1 to 2.5 standard deviation (SD) lower than control subjects indicates osteopenia
- Less than 2.5 SD lower than control subjects than indicates osteoporosis
- Less than 2.5 SD lower than control subjects, with the presence of one or more fragility fractures, indicates severe osteoporosis
Z-score: compared to patients matched for age and gender
- < 2.0 SD is below the expected range for age
- 2.0 SD is within the expected range for age
Of note, heterotopic ossification can falsely elevate the BMD. Plus, clinicians need to ensure that the DXA is being compared to other people of similar age.4
Plain x-rays are used regularly to visualize fractures, but are less helpful for detection of bone loss, as 30% of bone density must be lost before changes can be detected. They are also used to diagnose quiescent fractures, particularly in patients with decreased or absent sensation.
Quantitative ultrasound densitometry (QUS) can be used if DXA scan is not available. Assessment at the heel produces a T-score that can be predictive of fracture risk. However, this technique does not measure BMD directly and results are not equivalent to DXA results, so comparison between the two tests is difficult.16
Supplemental assessment tools
Combining clinical risk factors with DXA score is thought to provide a better estimate of fracture risk than each assessment alone.1
The Fracture Risk Assessment Tool (FRAX) can predict the 10-year probability of developing an osteoporotic fracture. Its use is limited to individuals 50 or older with low BMD who have not received any osteoporosis treatment.16
Quantitative computed tomography (QCT) can be used to assess bone architecture but is mostly a research tool and is not routinely available in the clinical setting.16
A comprehensive nutrition evaluation, including a food diary for at least a few days, provides crucial information about eating habits, which can affect osteoporosis risk significantly.
Early predictions of outcomes
Risk factors for fractures should be minimized. Methods include prevention and treatment of osteoporosis, detailed assessment of fall risk, and mitigating risk of fall whenever possible.
Home evaluation and modification are extremely important for fall prevention. Patients and families can be asked to complete a self-assessment form, or a formal evaluation can be performed by a member of the therapy team. The home evaluation can occur in-person or virtually.
Patients and caregivers can advocate for a safer and more accessible community which can also reduce fall risk.
Social role and social support system
Awareness of the possibility of bone loss and fracture by the patient, family, clinician, and other members of the rehabilitation team is essential for the development of a comprehensive prevention and treatment approach.
Osteopenia and osteoporosis are very common in adults with CNS injury who are participating in rehabilitation. Focusing on prevention and treatment during their stay could be beneficial but is not universally done. Even in a study of a specialized stroke management center, relatively few patients were taking osteoporosis medications and supplements. This may be due to lack of knowledge or another system issue and might improve with more attention to the problem.14,17
Rehabilitation Management and Treatments
Available or current treatment guidelines
Treatment of established osteoporosis should focus on treating or eliminating secondary causes of osteoporosis, modifying lifestyle factors, developing an appropriate exercise/rehabilitation program, dietary supplementation, and specific pharmacologic treatments. Individuals should receive counseling regarding reducing alcohol intake, smoking cessation, and modifying caffeine consumption, if appropriate.
The International Society of Clinical Densiometry’s official position about DXA in individuals with SCI recommends that all adults with SCI resulting in permanent motor or sensory dysfunction should have a DXA scan of the total hip, proximal tibia, and proximally femur as soon as they are medically stable enough to tolerate. This will ensure that they have a baseline DXA.5
For SCI, there’s no established threshold BMD value below which weight bearing activities are absolutely contraindicated. Use BMD and clinical risk factors to assess fracture risk before planning weight-bearing activities.5,17
At different disease stages
Prevention of bone loss is likely more effective than treatment of established osteoporosis. Clinicians should consider proper nutrition, lifestyle modifications, supplementation, and weight-bearing exercise in individuals with CNS injury early after diagnosis.
Treatment with medications should be considered. Some options are described here. Bisphosphonates are the most widely used medications for osteoporosis. They work by preventing bone resorption. They block osteoclast activity, thus decreasing the rate of bone remodeling and resorption. Options include alendronate and risedronate which are given weekly by mouth. Ibandronate is given monthly by mouth. Zolendronic acid is given yearly by intravenous administration. The bisphosphates have been shown to increase BMD, most notably at the spine and hip. In post-menopausal women with osteoporosis, bisphosphonates can decrease the vertebral and hip fractures by at least 40% over three years. They can be also used after fractures to reduce subsequent risk. The optimal duration of treatment is not yet certain.1
Denosumab is a very potent anti-resorptive agent. It is a monoclonal antibody to the receptor activation of nuclear factor-kB ligand (RANKL). Rankl has effects on osteoclast development and function, which allow it to regulate bone resorption. Given biannually via subcutaneous route, it has been shown to increase BMD and decrease risk of hip fracture by 40%, with a near 70% of reduction of relative risk for vertebral fracture, at three years.1
Teriparatide is a recombinant version of a parathyroid hormone fragment, PTH 1-34. Given daily via subcutaneous route, it leads to bone formation and increased bone mass. Its anabolic effect on bone is the result of increasing bone resorption markers at the PTH receptor 1 to a larger extent than it increases bone resorption markers. It has been shown to decrease fracture risk at 2 years and beyond.1
Abalopartide is a synthetic parathyroid hormone-related protein analogue. It is given daily via subcutaneous route, and has been shown to increase BMD at hip, femoral neck, and lumbar spine.1
Non-pharmacologic interventions are also available. Functional electrical stimulation (FES), applied to an affected limb, may help prevent bone loss there. Protocols using 30 minutes of stimulation 3 times weekly, involving isometric contractions, have been shown to prevent muscle atrophy and increase muscle volume, which can help prevent bone loss as well.13
In SCI, passive weight-bearing, including standing and walking activities, have not been definitively shown to prevent BMD loss or fractures but are generally well-tolerated. A caveat is that in case where BMD is low and fracture risk is high, caution is warranted.5
In older adults with stroke, early return to walking and bisphosphonate treatment within a few days to 5 weeks after the onset of stroke may prevent bone loss, particularly on the paretic side.6
A whole-health, individualized, biopsychosocial approach can be applied after CNS injury. Helping patients and families find ways to optimize nutrition, engage in regular exercise, participate in activities that lead to stress reduction, and other integrative strategies can lead to better overall health, and it follows, better bone health.2
Coordination of care
Bone health after CNS injury is best approached by a multidisciplinary team including of a physiatrist, primary care provider, occupational therapist, physical therapist, the patient and family. An endocrine specialist can also be helpful. If the individual has had a fracture, then involving an orthopedist is also important.
It is clear that osteoporosis is a common sequelae of CNS injury, but it is also notable that diagnosis is often delayed until a fracture occurs. Treatment, with widely available anti-resorptive medications and supplements such as vitamin D and calcium, could be offered much earlier and possibly before fractures occur. Coordination between providers and specialties could help address this issue.
Patient & family education
Clinicians should discuss bone loss early after CNS injury, both with patients and their families. Particular emphasis should be placed on fall prevention and reducing fall risk. Increased risk of osteoporosis as an adverse effect of medications should also be discussed, so families can monitor for this effect.
Patients and families should be encouraged to ask for devices and exercise sessions where safe weight-bearing is included.
Researchers are looking into exercises that might help prevent bone loss and build up muscles and bones. There is increasing research that combining FES with another activity, such as cycling, can be helpful. In addition, exercises that include weight-bearing, and particularly loading exercises, seem beneficial. Use of passive ambulation devices, like exoskeletons and assisted treadmills, are being trialed as well.8
From a medication perspective, there is ongoing research about potentially treating high-risk patients prophylactically. For instance, it is possible that administering bisphosphonate early after SCI could prevent osteoporosis and its effects.12
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Referral to a specialist should be considered when osteoporosis leads to uncontrolled pain, if significant bone loss is refractory to treatment, or with development of fractures. Fractures in SCI patients, in particular, may not require surgical intervention, as precise reduction may not be necessary, and the bones may be too fragile for internal fixation.
Vertebral fractures causing pain and failing conservative management can benefit from procedures like kyphoplasty or vertebroplasty.
It is important to note that the large majority of osteoporosis studies involve post-menopausal women. The literature needs to be carefully interpreted when we apply findings to individual patients with CNS disorders. The latter are often younger, have chronic mobility challenges, are on bone-damaging medications, can have cognitive impairment, and may have diet or swallowing challenges that affect treatment.4
Cutting Edge/ Emerging and Unique Concepts and Practice
Recent research has been focused on using bone turnover markers to monitor disease progression and response to treatment in osteoporosis. Examples of these markers include bone-specific alkaline phosphatase, osteocalcin, and c-telopeptide. In SCI, sclerostin is both a mediator of bone loss and an osteoporosis biomarker. Fat-bone interactions may contribute. Emerging therapies include anti-sclerostin antibodies, inhibitors of members of the transforming growth factor β family, and inhibitors of cathepsin. Inhibitors of transforming growth factor β family, part of a class of osteoanabolic agents, to preserve bone mass after paralysis. To date, three medications undergoing clinical trials are belsozumab, setrusumab, and romosozumab. Romosozumab, the subject of a phase three trial, has been shown to increase bone mass and have favorable safety profile in postmenopausal women with osteoporosis, when compared to placebo, alendronate, and teriparatide.
Clinical trials for cathepsin K inhibitors in postmenopausal osteoporosis are also occurring. These inhibitors are critical to resorption of bone by the osteoclast, therefore, may slow bone loss after CNS injury. However, a study of one of these, Odanacatib, was discontinued in 2016 due to increased risk of stroke in the trial. More research is needed.1
Gaps in the Evidence- Based Knowledge
It has been postulated that knee and calcaneous measurements could be added to routine DXA. Low values at these sites can possibly be predictors for fractures, particularly in individuals with SCI. This is not yet standard but might be in the future.5
Another budding area of research involves the complex relationship between the brain and bones. It is possible that some neuronal forces and neural elements, including beta adrenergic receptors functioning within the sympathetic nervous system, have a role in regulating bone formation and turnover. Early evidence for this theory includes the observation that psychological stress can be associated with hastened bone loss. It is already known that the endocrine system is intimately involved, but also possible that neural factors, and not the hormones, are the driving force in this system. Research is ongoing.2,18
Lastly, it is notable that there is very little research on osteoporosis in the setting of CNS injury. Individuals with SCI are the subject of some studies, but the amount of research pales in comparison to the importance of this problem. In other CNS conditions, including brain injury, stroke, MS, PD, CP, and brain tumors, there is even less research. Given the high incidence of osteoporosis in these patients, and the devastating effects that a fracture can have, it is especially important to pursue additional research, particularly about prevention and treatment, of osteoporosis after CNS injury.
- Lorentzon M. Treating osteoporosis to prevent fractures: Current concepts and future developments. J Intern Med. 2019; 285: 381-394.
- Kelly RR, Sidles SJ, LaRue A. Effects of neurological disorders on bone health. Front Psychol. 2020; 11: 1-27.
- Bell KR, Shenouda CN. Complications associated with immobility. In Zasler ND, Katz DI, Zafonte RD (Eds). Brain Injury Medicine: Principles and Practice, 2nd Ed. 2013. Demos: New York.
- Smith E, Comisky C, Carrroll A. Prevalence and risk factors for osteoporosis in adults with acquired brain injury. Ir J Med Sci. 2016; 185: 473-481.
- Morse LR, Biering-Sorensen F, Carbone LD. Bone mineral density in spinal cord injury: 2019 ISCD official position. J Clin Densitom. 2019; 22: 554-566.
- Kapoor E, Austin PC, Alibhai SM, et al. Screening and treatment for osteoporosis after stroke: Results from the Ontario stroke registry. Stroke. 2019; 50: 1564-1566.
- Smith E. Treatment of osteoporosis for people with a disability. PMR. 2011;3: 143-152.
- Soleyman-Jahi S, Yousefian A, Maberonnaghsh R et al. Evidence-based prevention and treatment of osteoporosis after spinal cord injury: A systematic review. Eur Spine J. 2018; 27: 1978-1814.
- Vitrikas K, Dalton H, Breisch D. Cerebral palsy: An overview. Am Fam Physician. 2020; 101:213-220.
- DaSilva AN, Heras-Herzig A, Schiff D. Bone health in patients with brain tumors. Surg Neurol. 2007;68: 525-533.
- Bajwa NM, Kesavan C, Mohan S. Long-term consequences of traumatic brain injury in bone metabolism. Front Neurol. 2018; 9: 115.
- Dionyssiotis Y. Is prophylaxis indicated after acute spinal cord injury? Spinal Cord Ser Cases. 2019; 5: 24-27.
- Biering-Sorensen F, Hansen B, Lee BSB. Non-pharmacological treatment and prevention of bone loss after spinal cord injury: A systematic review. Spinal Cord. 2009; 47: 508-518.
- Beaupre GS, Lew HL. Bone density changes after stroke. Am J Phys Med Rehabil. 2006;85: 464-472.
- Singh H, Scovil CY, Yoshida et al. Factors that influence the risk of falling after spinal cord injury. BMJ Open. 2020; 2: e034279.
- Cosman F, DeBeur SJ, LeBoff MS. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014; 25: 2359-2381.
- Bauman, WA, Cardozo CP. Osteoporosis in individuals with spinal cord injury. PMR. 2015;7: 188-201.
- Otto E, Knapstein PR, Jahn D et al. Crosstalk of brain and bone: Clinical observations and their molecular bases. Int J Mol Sci. 2020; 21; 4946-4984.
Original Version of the Topic
Marika Hess, MD, Timothy Tiu, MD, Jayne Donovan, MD. Osteoporosis and fractures after CNS injury. 10/22/2013
Previous Revision(s) of the Topic
Diane Schretzman Mortimer, MD, Kerri Chung, DO. Osteoporosis and fractures after CNS injury. 8/18/2016
Sarah Mahasin, MBBS
Nothing to Disclose
Diane Schretzman Mortimer, MD
Nothing to Disclose