Author(s): Adithi Vemuri, DO, Anita Kou, MD
Originally published: October 22, 2013 Last updated: July 31, 2025
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Disease/Disorder

Definition

Osteoporosis by definition means “porous bones”. Osteoporosis is a disorder of bone and mineral metabolism characterized by low bone mineral density (BMD), altered bone micro-architecture and decreased bone strength. This disorder can often make patients more vulnerable to low energy fragility fractures. The World Health Organization defines osteoporosis as a BMD of 2.5 standard deviations (SDs) or more below the mean peak bone mass as measured by Dual-Energy X-ray Absorptiometry (DXA).1

Etiology

Osteoporosis is caused by an imbalance of bone formation and resorption. Patients with central nervous system (CNS) injury are at risk of osteoporosis. These patients include those living with brain injury, spinal cord injury (SCI), stroke, multiple sclerosis (MS), Parkinson’s disease (PD), cerebral palsy (CP) and spinal cord/brain tumors.

Epidemiology including risk factors and primary prevention

Osteoporosis is a major complication of CNS injury. In the United States there are at least 1.5 million osteoporosis-related fractures that occur annually. 2

Following CNS injury immobility is the greatest contributing factor to the development of osteoporosis.3 Other contributing factors include mechanical unloading and longer duration of immobilization since time of initial injury. Medications such as heparin, warfarin, glucocorticoids and anticonvulsants may also contribute to the development of osteoporosis.3

The incidence and risk factors vary in different CNS injury states. Following a brain injury individuals may face significant ambulation challenges and prolonged immobility. Accordingly, > 40% of these patients develop osteopenia and >20% develop osteoporosis. In this population contributing factors to development of osteopenia/osteoporosis include inflammatory stress, pituitary dysfunction and anti-epileptic medications. 5

The incidence of Spinal Cord Injury patients who develop osteoporosis is more than 50%.5 Those patients with higher neurological injury and complete injuries have a greater degree of bone loss. Individuals with paraplegia have 16% more bone density in their upper extremities than those with tetraplegia.6

Strokes can also lead to rapid bone loss and deterioration in skeletal architecture. In these patients, bone loss more commonly affects paretic limbs and occurs more commonly in older adults, in whom osteoporosis is more prevalent. Contributing factors include muscle imbalance, dysregulated bone modeling and the use of anticoagulants. 7,8,9 For example, warfarin (a vitamin K antagonist) could affect bone metabolism, potentially leading to reduced BMD. Other anticoagulants such as direct oral anticoagulants (DOACs) may be associated with a lower risk of osteoporosis when compared to warfarin.10  

Multiple Sclerosis is an autoimmune condition characterized by an inflammatory phase (with plaques formed) and a relapsing remitting phase (axonal damage occurs). Both phases are associated with bone loss. However, there is a notable increase in osteopenia and osteoporosis in the relapsing remitting phase. Contributing factors include decreased ambulation, steroid use and vitamin D deficiency.3

Parkinson’s Disease is a neurodegenerative basal ganglia syndrome. It has been associated with bone loss and increased risk of developing osteoporosis, particularly in women. Contributing factors include weight loss, poor nutrition, vitamin D deficiency, decreased muscle strength and the use of dopaminergic medications.3

In Cerebral Palsy results in difficulties with movement, posture and balance. More than 30% of these patients have difficulty walking. Up to 90% of individuals with CP have lower than normal bone density levels. Contributing factors include altered nutrition, non-weightbearing status, late-onset puberty and the use of anticonvulsants.11

Although, brain tumors are heterogeneous, and therefore it is difficult to estimate the incidence of osteoporosis in this affected population, factors that contribute to osteoporosis include the use of antiepileptic medications, glucocorticoids, anticoagulants, radiation therapy and hemiplegia.12

Primary prevention for these CNS conditions includes optimizing overall health and nutrition. Mobilization, including weight-bearing exercises should be included in a therapeutic plan as much as possible.4

Patho-anatomy/physiology

The skeleton is constantly remodeling in order 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. 3,4

As we age, net bone loss is due to increased osteoclasts or decreased osteoblast activity. Immobility and lack of normal weight-bearing forces on the body can hasten bone loss too. Calcium loss occurs during immobility and is another important contributing factor.4,5

In CNS injury decreased weight-bearing activity causes reduced mechanical stress on bone. 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 which leads to bone loss. CNS injury can affect cognition as well. This may put individuals at risk for falling, which in turn can affect bone health. Changes in nutritional status that can affect bone health also commonly occur in CNS injury.13

In patients with brain injury changes to the normal process of bone remodeling include alteration of growth hormone-insulin growth factor (GH-IGF-1) axis, impaired thyroid function and impaired gonadal function.4 Increased parathyroid hormone (PTH) levels can cause compensatory mobilization of calcium stores from bone.5 If PTH is suppressed, less calcium is absorbed in the gut and less vitamin D is produced.14 Low serum vitamin D levels also negatively affect bone formation. Medications such as anticonvulsants including phenytoin and carbamazepine can lead to increased conversion of vitamin D to its inactive form which leads to less biologically active vitamin D to help build new bone.5,13

Osteoporosis in SCI is also mediated by hormonal changes, including PTH, thyroid hormones and sympathetic activity. These autonomic changes cause dilation of bony intravenous shunts and vascular stasis, which contributes to an imbalance of bone formation and resorption.15

Bone loss after in the early phase of a stroke can be caused by increased bone resorption in the setting of muscle weakness on the paretic side. In the later phases of a stroke, bone loss is suspected to be related to the degree of paresis and vitamin D levels.7

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, however there are common trends amongst CNS injuries. For example, the rate of bone loss is greater soon after the initial injury and during periods of immobility. Bone loss is also more likely during periods of physiological stress, when nutrition status is sub-optimal and when patients are on medications that affect bone health.5

In the acute phase of SCI osteoclast activity outpaces osteoblast activity. This leads to rampant bone turnover leading to an imbalance between calcium absorption and excretion. Hypercalcemia and hypercalcinuria are generally seen 4-6 weeks post-injury. If left untreated, this increase in calcium can lead to complications such as dehydration, personality changes, calcium nephrolithiasis and renal insufficiency.14

Patients with SCI experience most of the bone loss in the first 12 months from the initial injury. 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 the upper extremities suffer approximately 21% bone demineralization. In contrast, there may be a net gain in the trunk.9

In stroke patients, bone loss reaches a maximum at 4 months. After 4 months, bone loss stabilizes. Bone density recovery has been seen in patients who regain ability to ambulate.7,16

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.3

Specific secondary or associated conditions and complications

Fractures are a major complication of osteoporosis. Decreases in BMD are directly linked to an increased risk for fractures. 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.25 Older adults experience bone loss related to age itself. As such, 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 compared to the general population.5 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. Lumbar fractures can change 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 patients. More than 50% of people with motor complete SCI experience an osteoporotic fracture at some point following their injury. Most fractures occur in the distal femur and proximal tibia.6 yes. The most common cause of fracture after SCI is falling from a wheelchair. People with SCI can sustain fractures during low impact activities including transferring from bed to chair, turning in a bed and low speed traffic crashes.9,17 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.6,9

Following stroke, in the setting of a non-ambulatory status, individuals have lower bone mass and a risk of fracture up to 7 times than 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 to home.7

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 compared to the general population. These patients have been noted to experience significant decline in functional independence after a fracture.2

Essentials of Assessment

History

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, and smoking and alcohol use should also be reviewed and addressed.

For individuals with CNS injury, it is important to pay attention to immobility, degree of motor impairment and duration of disability. Past and current medications should also be reviewed to determine if possibly contributing to osteoporosis. Finally, consideration should be made regarding pre-existing osteoporosis and history of low impact fractures.

Physical examination

There are no specific physical exam findings for osteoporosis. Body type, including body mass index and overall appearance are important to note. Those who are at 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, erythema, and changes in baseline spasticity may indicate an underlying fracture in asymptomatic insensate patients. Vertebral compression fractures can be painless, but patients can present with localized pain on palpation, paravertebral muscle spasms or 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

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.16 Ambulation with an inadequate assistive device, on uneven surfaces or using poor technique with transfer all 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.17

Laboratory studies

There is no single laboratory test for osteoporosis, but many tests may identify secondary causes. Clinicians can 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.18

Imaging

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.1,18 A T-score compares the BMD to healthy young adults while a Z-score compares BMD to adults of the same age and gender.

BMD measurement using DXA at any site is the single best predictor of fracture at that site.5 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.6

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.5

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.18

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.18

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.18

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.

Environmental

Home evaluation and modification are extremely important for fall prevention. Patients and families are asked to complete a self-assessment form or a formal evaluation is 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.

Professional issues

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.16,19

Rehabilitation Management and Treatments

Available or current treatment guidelines

Treatment of diagnosed osteoporosis should focus on treating or eliminating secondary causes of osteoporosis, modifying lifestyle factors, developing an appropriate exercise/rehabilitation program, dietary supplementation and specific pharmacological treatments. Patients should receive appropriate counseling regarding reducing alcohol intake, smoking cessation and modifying caffeine consumption.

The International Society of Clinical Densitometry’s official position recommends that all adults with SCI that have either permanent motor or sensory dysfunction should have a DXA scan of the total hip, proximal tibia and proximal femur as soon as they are medically stable enough to tolerate. This will ensure that they have a baseline DXA.6

There is not an established threshold BMD value below which weight bearing activities are absolutely contraindicated in SCI patients. It is recommended to use the BMD and evaluate clinical risk factors in order to appropriately assess fracture risk before planning weight-bearing activities.6,19

At different disease stages

Prevention of bone loss is more likely effective than treating diagnosed osteoporosis. After diagnosing a patient with CNS injury, clinicians should consider proper nutrition, lifestyle modifications, supplementation, and weight-bearing exercise.

Treatment with medications should be considered. 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. Zoledronic acid is given yearly by intravenous administration. The bisphosphates have been shown to increase BMD, most notably in the spine and hip. In post-menopausal women with osteoporosis bisphosphonates can decrease vertebral and hip fractures by at least 40% over three years. They can also be used after fractures to reduce subsequent risk. Taking bisphosphonates for over five years may increase the risk of having an atypical femur fracture. For women, limiting treatment to five years or less maximizes the benefits of taking bisphosphonates and reduces the risk of having typical osteoporotic fractures, while minimizing the risk of having typical femoral fractures.21

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. It is given biannually via subcutaneous route. It has been shown to increase BMD and decrease risk of hip fracture by 40%, with a near 70% reduction of relative risk for vertebral fracture at three years.1

Teriparatide is a recombinant version of a parathyroid hormone fragment, PTH 1-34. It is 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

Abaloparatide is a synthetic parathyroid hormone-related protein analogue. It is given daily via subcutaneous route. It has been shown to increase BMD at hip, femoral neck and lumbar spine.1

Non-pharmacologic interventions can also help decrease bone loss. Functional electrical stimulation (FES) applied to an affected limb may help prevent bone loss at that site. Protocols that have used 30 minutes of stimulation 3 times a week and isometric contraction have been shown to prevent muscle atrophy and increase muscle volume.15

In SCI patients, passive weight-bearing exercise such as standing and walking have not been definitively shown to prevent BMD loss or fractures but are generally well-tolerated. A caveat is in the case where BMD is low, and fracture risk is high. If this is the case, caution is warranted in order to prevent fractures.6

In older adults who suffered from a 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.7

A whole-health, individualized, biopsychosocial approach should be applied after CNS injury. It is important to help patients and their families find ways to optimize nutrition, engage in regular exercise and participate in activities that reduce stress in order improve overall health, and as it follows, better bone health.3

Coordination of care

Bone health after CNS injury is best approached by a multidisciplinary team. This team should include a physiatrist, a primary care provider, an occupational therapist, a physical therapist, the patient and family. An endocrine specialist may also be helpful. If the patient has had a fracture involving an orthopedist is also important.

 Osteoporosis is a common sequelae of CNS injury, but the diagnosis is often delayed until a fracture occurs. Treatment is widely available including anti-resorptive medications and supplements such as vitamin D and calcium. Treatment should be offered much earlier to prevent fractures. Coordination between providers and specialties may also help address this issue.

Patient & family education

Clinicians should discuss bone loss early after CNS injury with patients and their families. Emphasis should be placed on fall prevention and reducing fall risk. Increased risk of osteoporosis as an adverse effect of certain medications should also be discussed. Patients and families should be encouraged to ask for devices and exercise sessions where safe weight-bearing methods are included.

Emerging/unique interventions

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.26 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.9

A study published in 2022 found that acute and subacute SCI patients who underwent anti-gravity FES-assisted load-bearing exercises showed improvements in volumetric bone mass density in the proximal and distal tibia.2 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 bone loss is refractory to treatment, or development of fractures. Fractures in SCI patients may not require surgical intervention as precise reduction may not be necessary and the bones may be too fragile for internal fixation.

Patients with painful vertebral fractures and who have failed conservative management may benefit from interventional pain procedures such as a kyphoplasty or vertebroplasty.

It is important to note that most 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, may have cognitive impairment and may have diet restrictions 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.28 In SCI patients, sclerostin is both a mediator of bone loss and an osteoporosis biomarker.1,27 Emerging therapies include anti-sclerostin antibodies, inhibitors of members of the transforming growth factor β (TGF- β) family and inhibitors of cathepsin27. Inhibitors of TGF- β family are part of a class of osteoanabolic agents that help to preserve bone mass after paralysis.27 To date, two medications undergoing clinical trials are blosozumab and setrusumab. Recently, Romosozumab has been shown to increase bone mass and have favorable safety profile in postmenopausal women with osteoporosis when compared to placebo, alendronate and teriparatide.1,27 However, when it comes to skeletal fractures, alendronate, zoledronate and denosumab are associated with the greatest bone protection and therapeutic benefits.2

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 calcaneus 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.6

Another budding area of research involves the complex relationship between the brain and bones. It is possible that neuronal forces and 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 it is also possible that neural factors, and not the hormones, are the driving force in this system. Research is ongoing.3,20

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, even less research exists. Given the high incidence of osteoporosis in these patients and the devastating effects that fractures can have it is especially important to pursue additional research on prevention and treatment of osteoporosis after CNS injury.

References

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  2. Clynes MA, Harvey NC, Curtis EM, Fuggle NR, Dennison EM, Cooper C. The epidemiology of osteoporosis. Br Med Bull. 2020 May 15;133(1):105-117. doi: 10.1093/bmb/ldaa005. PMID: 32282039; PMCID: PMC7115830.
  3. Kelly RR, Sidles SJ, LaRue A. Effects of neurological disorders on bone health. Front Psychol. 2020; 11: 1-27.
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  10.  Huang H, Pin-Sung L, Lin S, Peng C, Wang J, Yeh J, Loh C. Risk of Osteoporosis in Patients With Atrial Fibrillation Using Non–Vitamin K Antagonist Oral Anticoagulants or Warfarin. Journal of American Heart Association. 2020; 9:2. https://doi.org/10.1161/JAHA.119.013845
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  28. Park SY, Ahn SH, Yoo JI, Chung YJ, Jeon YK, Yoon BH, Kim HY, Lee SH, Lee J, Hong S. Position Statement on the Use of Bone Turnover Markers for Osteoporosis Treatment. J Bone Metab. 2019 Nov;26(4):213-224. doi: 10.11005/jbm.2019.26.4.213. Epub 2019 Nov 30.

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, Diane Schretzman Mortimer, MD. Osteoporosis and Fractures after CNS Injury. 6/1/2021

Author Disclosures

Adithi Vemuri, DO
Nothing to Disclose

Anita Kou, MD
Nothing to Disclose