eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Osteoporosis and Spinal Cord Injury: Treatment & Medication

Author: David Weiss, MD, Medical Director of Physical Medicine and Rehabilitation, Assistant Professor, Internal Medicine, Marianjoy Medical Group
Contributor Information and Disclosures

Updated: Apr 1, 2008

Treatment

Rehabilitation Program

Physical Therapy

The effect of remobilization on SCI-induced osteoporosis has been fairly well studied. Weight-bearing exercises with standing frames and bikes, using forms of functional electrical stimulation (FES), have been shown to be effective when started within 6 weeks of injury. These same programs in the population with chronic SCI, however, are ineffective in preventing osteoporosis or restoring bone mineral.17,18,19,20,21,22

Medical Issues/Complications

For more discussion on complications of osteoporosis following SCI see Mortality/Morbidity.

Surgical Intervention

Typically, conservative treatment is pursued, with healing reported in 3-4 weeks. Soft splints may be required. Hard splints and materials should not be used. With deformity of the extremity from fracture (eg, displacement of bones), surgical intervention of open reduction and internal fixation may be required.

Consultations

An orthopedic consultation may be warranted in cases of the above-described deformities.

Other Treatment

FES-induced lower extremity cycling has not been shown to increase bone density in the hip parameters of patients with chronic SCI.17,18,19,22

Medication

Changes occur rapidly in the skeleton of a patient with SCI, and interventions must be undertaken quickly. The fact that there are no effective treatments to restore bone mineral once it has been lost makes early treatment even more imperative. Thus, early prevention is the main focus in treating SCI-induced osteoporosis.8,23,24,25,26,27,28

See also the following related Medscape topic:
CME Advances in Osteoporosis Management: Clinical Insights

Bisphosphonate derivatives

To date, the bisphosphonates are the most well-studied class of medications to prevent demineralization following SCI. They are potent inhibitors of osteoclastic bone resorption and have been found to have a positive effect in preventing SCI-induced osteoporosis. The studies on bisphosphonates in persons with SCI, however, are preliminary, and there is no consensus on drug of choice or a dosing regimen. In addition, the effectiveness and side effects of other drug therapies oriented to the more common forms of osteoporosis have not been studied well in this population.


Pamidronate (Aredia)

Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.

Adult

Moderate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h

Pediatric

Not established

Documented hypersensitivity; hypocalcemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women


Etidronate disodium (Didronel)

Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.

Adult

Moderate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h

Pediatric

Not established

Documented hypersensitivity; hypocalcemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women


Clodronate (Bonefos)

Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.

Adult

Moderate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h

Pediatric

Not established

Documented hypersensitivity; hypocalcemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women


Ibandronate (BONIVA)

Inhibits osteoclast-mediated bone resorption. In postmenopausal women, reduces bone turnover rate, leading to a net gain in bone mass.

Adult

2.5 mg PO qd; administer with water at least 1 h prior to first food or beverages (other than water) of the day

Pediatric

Not established

Multivalent cations (eg, calcium, aluminum, magnesium, iron) decrease absorption, administer ibandronate at least 1 h prior to vitamin and mineral supplements; NSAIDs may aggravate GI irritation

Documented hypersensitivity; uncorrected hypocalcemia; inability to stand or sit upright for at least 60 min following drug administration

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause upper GI disorders (eg, dysphagia, esophagitis, ulceration), minimize GI risk by standing or sitting upright 1 h following dose; calcium and vitamin D supplementation required; not recommended with severe renal impairment (ie, CrCl <30 mL/min)

Parathyroid hormone

Promotes new bone formation, leading to increased bone mineral density. Teriparatide is a biological product containing a portion of human parathyroid hormone, which primarily regulates calcium and phosphate metabolism in bones. Teriparatide is approved for patients at high risk of fracture due to primary osteoporosis, hypogonadal osteoporosis (men), or postmenopausal osteoporosis (women).

See also the following related eMedicine topic:
CME Teriparatide Effective for Osteoporosis Following Prior Antiresorptive Therapy


Teriparatide (Forteo)

Recombinant human parathyroid hormone rh-PTH (1-34), which has identical sequence to 34 N-terminal amino acids (biologically active region) of 84 – amino acid human parathyroid hormone (PTH). Acts as endogenous PTH, thus regulating calcium and phosphate metabolism in bone and kidney. Works primarily to stimulate new bone by increasing number and activity of osteoblasts (bone-forming cells). Additional physiological actions include regulation of bone metabolism, renal tubular re-absorption of calcium and phosphate, and intestinal calcium absorption. When administered with calcium and vitamin D, teriparatide increases bone mineral density and decreases risk of fractures in patients with osteoporosis.

Adult

20 mcg SC qd

Pediatric

Not established

Documented hypersensitivity; increased risk for osteosarcoma (including patients with Paget disease of bone or with unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving the skeleton); children or growing adults; patients with bone metastases or history of skeletal malignancies, and persons with metabolic bone disease other than osteoporosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for hypercalcemia; may cause orthostatic hypotension (particularly following first several doses), dizziness, or leg cramps

More on Osteoporosis and Spinal Cord Injury

Overview: Osteoporosis and Spinal Cord Injury
Differential Diagnoses & Workup: Osteoporosis and Spinal Cord Injury
Treatment & Medication: Osteoporosis and Spinal Cord Injury
Follow-up: Osteoporosis and Spinal Cord Injury
Multimedia: Osteoporosis and Spinal Cord Injury
References
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Further Reading

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Keywords

spinal cord injury, osteoporosis, osteoporosis and SCI, SCI-induced osteoporosis, functional electrical stimulation, FES, dual-energy radiographic absorptiometry scan, dual-energy X-ray absorptiometry scan, DRA, DXA

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Contributor Information and Disclosures

Author

David Weiss, MD, Medical Director of Physical Medicine and Rehabilitation, Assistant Professor, Internal Medicine, Marianjoy Medical Group
David Weiss, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers, Phoenix
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Nothing to disclose.

 
 
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