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Osteoporosis (Secondary): Treatment & Medication

Author: Alana C Serota, MD, Fellow in Metabolic Bone Disease and Osteoporosis, Department of Orthopedics, Hospital for Special Surgery
Coauthor(s): Joseph M Lane, MD, Professor of Orthopedic Surgery, Weill Medical College of Cornell University; Chief, Metabolic Bone Disease Service, Hospital for Special Surgery
Contributor Information and Disclosures

Updated: Jun 25, 2009

Treatment

Results from a literature review by Kastner and Straus suggested that the use of "reminders plus education targeted to physicians and patients" can lead to increased BMD testing and greater use of osteoporosis medications.12  In addition, the employment of a physician reminder along with the use of a patient risk assessment strategy apparently can result in a reduction in patient fractures and an increase in osteoporosis therapy. The authors concluded that multi-component tools aimed at doctors and patients may support clinical decision making in the management of osteoporosis.

A study by Majumdar et al indicated that the use of a case manager for the treatment of patients with hip fractures can, in comparison with a more commonly employed care strategy, lead to more frequent use of appropriate osteoporosis treatment and may result in fewer fractures, increased life expectancy, and significant health-care cost savings.2

Rehabilitation Program

Physical Therapy

The first goal of rehabilitation in osteoporosis patients is to control pain if a fracture has occurred. Physical therapy then focuses on improving function and reducing disability. Spinal compression fractures can be extremely painful and can cause short- and long-term morbidity. Oral analgesics on a regular schedule can be implemented. Pain-relieving modalities such as moist hot packs and transcutaneous electrical nerve stimulation should also be considered. During this period of acute pain management, monitoring the patient carefully for signs of constipation, urinary retention, and respiratory depression, which can occur with the use of narcotic analgesics, is essential.

A comfortable mechanical support for the spine and, in some cases, a thoracic orthosis, may need to be prescribed. The primary reason for the application of a thoracic orthosis is to limit motion in the spine. The length of time a patient should wear a rigid spinal orthosis is undetermined. What is well known is that immobilization contributes to bone demineralization.

During the early mobilization period, deep breathing exercises, pectoral and intercostal strengthening, and back conservation techniques need to be implemented.

As soon as the course of therapy allows, weightbearing exercises should be initiated. Weightbearing activities are essential for maintenance of bone mass (Wolff law). Aerobic low-impact exercises, such as walking and bicycling, generally are recommended. During these activities, ensure the patient maintains an upright spinal alignment. In 1984, Sinaki and Mikkelsen showed that exercises that place flexion forces on the vertebrae tend to cause an increase in the number of vertebral fractures in patients.13

Although swimming is not a weightbearing exercise that will improve BMD, it does provide chest expansion, spinal extension, and low-impact cardiopulmonary fitness.

Isometric exercises should be used to strengthen abdominal muscles, aiding in the prevention of a kyphosis.

Occupational Therapy

Home modification focuses on reducing the risk of falling by installing handrails and grab bars in hallways, stairs, and bathrooms. The use of a shower chair, tub bench, and adaptive bathing devices also can be beneficial. The application of nonskid tape to steps (indoors and outdoors), as well as the removal of throw rugs, greatly improves home safety.

Surgical Intervention

Percutaneous vertebroplasty (PVP) with polymethylmethacrylate (PMMA) was developed in 1984. The first indication for this treatment was aggressive vertebral angiomas. PVP with PMMA was then used for other lesions that weakened the vertebral body, such as malignant tumors. PMMA is the principal component of bone cements used for rapid stable fixation of implants, such as metal and plastic prosthetics placed in living bone during orthopedic procedures. PVP is one therapeutic alternative for the treatment of pain associated with compression fractures. PMMA is used in PVP to fortify a collapsed vertebral body and stabilize the vertebral column. Success with vertebroplasty is limited by the lack of significant height restoration and the high rate of cement extravasation. (See image below and Image 5.)

Percutaneous vertebroplasty, transpedicular appro...

Percutaneous vertebroplasty, transpedicular approach.

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Percutaneous vertebroplasty, transpedicular appro...

Percutaneous vertebroplasty, transpedicular approach.


The second therapeutic alternative for vertebral compression fractures is balloon kyphoplasty, whereby the vertebra is initially expanded with an inflatable balloon tamp. This reduces the fracture and restores height to the vertebral body. The balloon is then removed and cement is injected into the cavity under lower pressure than that used in PVP, thereby reducing the risk of cement extravasation. (See images below and Images 6-7.)

In kyphoplasty, a KyphX inflatable bone tamp is p...

In kyphoplasty, a KyphX inflatable bone tamp is percutaneously advanced into the collapsed vertebral body (A). It is then inflated, (B) elevating the depressed endplate, creating a central cavity, and compacting the remaining trabeculae to the periphery. Once the balloon tamp is deflated and withdrawn, the cavity (C) is filled under low pressure with a viscous preparation of methylmethacrylate (D).

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In kyphoplasty, a KyphX inflatable bone tamp is p...

In kyphoplasty, a KyphX inflatable bone tamp is percutaneously advanced into the collapsed vertebral body (A). It is then inflated, (B) elevating the depressed endplate, creating a central cavity, and compacting the remaining trabeculae to the periphery. Once the balloon tamp is deflated and withdrawn, the cavity (C) is filled under low pressure with a viscous preparation of methylmethacrylate (D).



Reduction in kyphotic angulation after kyphoplast...

Reduction in kyphotic angulation after kyphoplasty.

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Reduction in kyphotic angulation after kyphoplast...

Reduction in kyphotic angulation after kyphoplasty.


PVP and balloon kyphoplasty are indicated in patients with incapacitating and persistent severe focal back pain related to vertebral collapse. At the primary author's institution, vertebroplasty is used for lesions above T8 and kyphoplasty is used for the remainder.

In 1997, Jensen et al studied age-related or steroid-induced osteoporotic vertebrae with partial compression fractures in patients who underwent PVP with PMMA.14 A total of 48 vertebrae in 30 patients were injected, and 90% of the patients described marked improvement of pain within 1 week of treatment. All the patients who experienced pain relief noted increased mobility and decreased need for narcotics. The patients were tracked for an average of 9 months, and the rate of long-term pain relief was reported to be approximately 80%. Whether this pain relief was related to mechanical stabilization of the spine or was secondary to neurotoxic effects of PMMA remains to be determined.

Traditional operative management of vertebral compression fractures is uncommon and is usually reserved for gross spinal deformity or for threatened or existing neurologic impairment. Operative interventions include anterior and posterior decompression and stabilization with placement of such internal fixation devices as screws, plates, cages, or rods. Bone grafting is routinely performed to achieve bony union. The failure rate of spinal arthrodesis is significant because achieving adequate fixation of hardware in osteoporotic bone is difficult. Moreover, patients who are elderly have a reduced osteogenic potential.

Consultations

Consultation with a nonsurgical spine specialist is appropriate for a patient who is not a surgical candidate or whose symptoms persist despite surgical fixation. Consultation with a spine surgeon is appropriate for patients with intractable, severe, function-limiting symptomatology that has not been relieved by noninterventional techniques.

Medication

Currently, no treatment can completely reverse established osteoporosis. Early intervention can prevent osteoporosis in most people. For patients with established osteoporosis, medical intervention can halt its progression. If secondary osteoporosis is present, treatment for the primary disorder should be provided.

Prevention of osteoporosis has 2 components, behavior modification and pharmacologic interventions. In 1998, the National Osteoporosis Foundation outlined that the following factors should be modified to reduce the risk of development of osteoporosis: cigarette smoking; physical inactivity; and intake of alcohol, caffeine, sodium, animal protein, and calcium.15,16 The pharmacologic prevention methods include calcium supplementation and administration of estrogen, raloxifene, and bisphosphonates (with the exception of intravenous ibandronate).

Some of the preventative measures are also used in the treatment of osteoporosis. The goal of the current recommendations for daily calcium intake is to ensure that individuals maintain an adequate calcium balance. Several large studies have demonstrated that supplementation of calcium and vitamin D resulted in a 30-70% reduction of fracture rates over 2-4 years.

In 1994, the National Institutes of Health recommended the following daily calcium intake:

  • Birth to age 6 months - 400 mg/d
  • Age 6 months to 1 year - 600 mg/d
  • Age 1 to 10 years - 800-1200 mg/d
  • Age 11 to 24 years - 1200-1500 mg/d
  • Age 25 to 50 years - 1000 mg/d
  • Age 51 to 64 years - 1000 mg/d
  • Age 51 years and older (only women not on hormone replacement therapy [HRT]) - 1500 mg/d
  • Age 65 years and older - 1500 mg/d
  • Pregnant or lactating women - 1200-1500 mg/d

Vitamin D is increasingly being recognized as a key element in overall bone health and muscle function. The minimum daily requirement in patients with osteoporosis is 800 IU of vitamin D3, or cholecalciferol. Many patients require more, continuously or for a short period, to be considered vitamin D replete, defined as a serum 25-hydroxyvitamin D level of 32 ng/mL.

Although not currently recommended for the treatment of osteoporosis, HRT is important to mention because many osteoporosis patients in a typical practice still use it for controlling postmenopausal symptoms. The results of the Women's Health Initiative were distressing with respect to the adverse outcomes associated with combined estrogen and progesterone therapy (eg, risks for myocardial infarction, stroke, deep venous thrombosis, and breast cancer) and estrogen alone (eg, risks for stroke and deep venous thrombosis); however, it was the first randomized controlled trial that demonstrated that HRT was efficacious in preventing nonvertebral fractures, in the order of 35%.

US Food and Drug Administration–approved pharmacologic treatment options for osteoporosis include raloxifene, calcitonin, bisphosphonates, and teriparatide (human recombinant PTH 1-34).5

Raloxifene is part of a class of compounds termed selective estrogen receptor modulators (SERMs), which provide the beneficial effects of estrogen without the potentially adverse outcomes. Raloxifene has been shown to prevent bone loss, and data in females with osteoporosis have demonstrated that raloxifene causes a 35% reduction in the risk of vertebral fractures. It has also been shown to reduce the prevalence of invasive breast cancer. Raloxifene has been shown to increase the incidence of deep vein thrombosis and hot flashes. In 601 postmenopausal women who had daily therapy with raloxifene, BMD was increased, serum concentrations of total low-density lipoprotein cholesterol were lowered, and the endometrium was not stimulated.

Calcitonin is a hormone that decreases osteoclast activity, thereby impeding postmenopausal bone loss. Results from a single controlled clinical trial indicate that calcitonin may decrease osteoporotic vertebral fractures by approximately 30%. In the first 2 years, calcitonin has been found to increase spinal BMD by approximately 2%. Calcitonin also has an analgesic property that makes it ideally suited for the treatment of acute vertebral fractures. Calcitonin is delivered as a single daily intranasal spray that provides 200 U of the drug. The drug can be delivered subcutaneously, but this route is rarely used.

Bisphosphonates have been used for the prevention and treatment of osteoporosis. When used for prevention, the recommended dose of both alendronate and risedronate is 5 mg/d. In a study by Hosking et al, doses of 2.5 mg and 5 mg of alendronate were evaluated in postmenopausal women who did not have osteoporosis.17 They found that the women who received placebo lost BMD at all measured sites, whereas the women treated with 5 mg/d of alendronate had a mean increase in BMD of 3.5% ± 0.2% at the lumbar spine, 1.9% ± 0.1% at the hip, and 0.7% ± 0.1% for the total body (all, P <.001).

Alendronate has been shown to increase spinal and hip mineral density in postmenopausal women. Well-conducted controlled clinical trials using alendronate sodium indicate that treatment reduces the rate of fracture at the spine, hip, and wrist by 50% in patients with osteoporosis. The treatment dose of alendronate is 70 mg/wk, to be taken sitting upright with a large glass of water at least 30 minutes before eating in the morning. Newer bisphosphonates include risedronate, dosed at 35 mg every weekend, and ibandronate, dosed at 150 mg/mo. The latter has not shown efficacy in nonvertebral fractures in the clinical trials. Ibandronate is also available as an intravenous formulation that is given every 3 months. It is an excellent choice for patients intolerant to oral bisphosphonates or in those in whom adherence is an issue.

Over time, bisphosphonate therapy decreases bone turnover and, at very high levels in animals, decreases bone strength and resilience. Some limited reports, including that by Odvina et al from 2005, describe patients on long-term bisphosphonate therapy developing transverse stress fractures; biopsy specimens of these individuals have suggested extremely low turnover states.18 Therefore, while the bisphosphonates are outstanding in their efficacy, bone turnover markers should be monitored; if these become profoundly suppressed, the patient should be taken off the bisphosphonates and given a rest period until he or she can return to therapeutic levels (NTx, 20-40).

Teriparatide, human recombinant PTH 1-34, is the only available anabolic agent for the treatment of osteoporosis. When PTH is given continuously, it is associated with increased osteoclastic and osteoblastic turnover, leading to a net loss of bone. However, in an intermittent subcutaneous administration of 20 mcg/d, PTH has been demonstrated to lead to a very active anabolic phase, with bone mass increasing up to 13% over 2 years in the spine and to a lesser degree within the hip.19,20,21

Most studies with PTH have been performed on women. The medication decreases the risk of vertebral and nonvertebral fractures to the same extent as bisphosphonates. Teriparatide is given for a maximum of 2 years, after which time the gains in BMD achieved with PTH are secure and can even be augmented with bisphosphonate therapy, otherwise the BMD slowly deteriorates to pretreatment levels.22

According to Finkelstein et al in 2003, initial studies using a combination of concurrent PTH and bisphosphonate therapy showed decreased benefit compared with therapy with either agent alone; therefore, the general recommendation is that these drugs be given separately and in sequence.23 A 2005 study by Cosman and colleagues challenged this conclusion by giving 3-month-on, 3-month-off pulses of teriparatide while the subjects were on weekly alendronate; BMD in the spine increased above that of the alendronate-only arm.24 This pulsed regimen appears to take advantage of the 3- to 4-month so-called anabolic window, in which the markers of bone formation rise more quickly than the markers of bone resorption.

Studies by Deal et al from 2005 and Ste-Marie et al from 2006 on women have shown that the concurrent use of estrogen or raloxifene can enhance the bone-forming effects of teriparatide.25,26 Data on the use of PTH in men are much more limited, but they appear to have relatively comparable efficacy.

Indications for PTH in men and women are a bone density decline while on bisphosphonate therapy, bone density stabilization while on extremely low-level bisphosphonate therapy, a fracture occurring while on bisphosphonate therapy, or a very low initial bone turnover rate for which an anabolic effect is clearly warranted.

Denosumab is a novel agent that has been studied in cancer patients and in patients with postmenopausal osteoporosis. It is a fully human monoclonal antibody against RANKL (ie, receptor activator of nuclear factor kappa-B ligand). RANKL is a key mediator of the resorptive phase of bone remodeling. In patients with multiple myeloma or bone metastases from breast cancer, a single subcutaneous dose of denosumab decreases bone turnover markers within 1 day, and this effect is sustained through 84 days at the higher doses used in one study. Although no fracture data are available as yet, denosumab was shown to increase BMD and decrease bone resorption in postmenopausal women with osteoporosis over a 12-month period.

Denosumab is currently in phase 3 clinical studies for metastatic bone disease and postmenopausal osteoporosis. Because the overactivity of RANKL is a major factor in bone loss in patients with autoimmune and inflammatory disorders, such as ulcerative colitis, denosumab may become first-line therapy for these patients.

Hormone-replacement therapy agents

Restore effects of decreased steroid hormone levels. Estrogens may be administered orally or by transdermal (skin) patch (eg, estradiol [Vivelle, Climara, Estraderm, Esclim, Alora]).


Conjugated estrogens/medroxyprogesterone acetate (Prempro)

Estrogens reduce bone resorption and retard or halt postmenopausal bone loss.

Adult

0.625 mg/2.5 mg or 0.625 mg/5 mg tab PO qd

Pediatric

Not established

May decrease hypoprothrombinemic effects of anticoagulants; rifampin may decrease serum concentrations; aminoglutethimide may increase hepatic metabolism of medroxyprogesterone

Documented hypersensitivity; undiagnosed vaginal bleeding; thrombophlebitis; liver disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Estrogens and progestins may cause fluid retention; acute intermittent porphyria may be precipitated by estrogens


Ethinyl estradiol and norethindrone (FemHRT)

Used to treat moderate-to-severe vasomotor symptoms and to prevent osteoporosis associated with menopause.

Adult

1 tab PO qd

Pediatric

Not established

Phenobarbital, phenytoin, paramethadione, carbamazepine, troglitazone, rifampicin, and griseofulvin induce enzymes that decrease levels of contraceptive steroids; oral anticoagulants may increase thromboembolic potential

Documented hypersensitivity; endometrial and hepatic cancer; thromboembolic disorders; undiagnosed vaginal bleeding; persons >35 y who smoke; cardiovascular disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in patients diagnosed with hepatic impairment, migraines, seizure disorders, cerebrovascular disorders, breast cancer, or thromboembolic disease

Selective estrogen receptor modulators

Affect some of the receptors stimulated by estrogen but can selectively act as antagonist or agonist, depending on the organ system.


Raloxifene (Evista)

SERM that decreases bone loss.

Adult

60 mg PO qd

Pediatric

Not established

Documented hypersensitivity; active thromboembolic disorder

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in history of venous thromboembolism, pulmonary embolism, cardiovascular disease, renal or hepatic insufficiency, and cervical/uterine carcinoma; caution in persons concurrently taking estrogens

Calcitonin analogs

Inhibit osteoclastic bone resorption


Calcitonin (Miacalcin nasal spray)

Directly inhibits osteoclastic bone resorption and decreases tubular resorption of calcium, phosphate sodium, magnesium, and potassium.

Adult

200 U (1 puff)/d intranasally

Pediatric

Not established

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

Have epinephrine immediately available for possible anaphylactic reaction

Bisphosphonates

Analogs of pyrophosphate. Act by binding to hydroxyapatite in bone matrix, thereby inhibiting the dissolution of crystals. Prevent osteoclast attachment to the bone matrix, osteoclast recruitment, and viability.


Alendronate (Fosamax)

Inhibits bone resorption via actions on osteoclasts or osteoclast precursors.

Adult

70 mg PO qwk

Pediatric

Not established

Documented hypersensitivity; hypocalcemia; esophageal abnormalities; inability to stand upright for 30 min

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

Must be taken at least 30 min before first food, beverage, or medication of the day and should be taken with large amounts of water; caution in renal impairment


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
Alternatively, 150 mg PO once monthly on the same date each month or 3 mg IV push (infuse over 15-30 seconds) q3mo

Pediatric

Not established

Multivalent cations (eg, calcium, aluminum, magnesium, iron) decrease absorption (administer 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)


Risedronate (Actonel)

Potent aminobisphosphonate. Inhibits bone resorption via actions on osteoclasts or osteoclast precursors.
Has been shown to reduce bone resorption and increase BMD of spine by 5% and femoral neck by 1.6%. Also has been shown to reduce incidence of vertebral fracture by 41% and nonvertebral fracture by 39% over a period of 3 y in postmenopausal women.

Adult

Prevention or treatment: 5 mg PO qd; alternatively, 35 mg PO qwk

Pediatric

Not established

Patients with hypocalcemia, documented hypersensitivity to any component of the product; inability to remain upright for 30 min; not recommended for use in patients with severe renal impairment (CrCl <30 mL/min)

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 (eg, serum levels of calcium, phosphate, magnesium, potassium); maintain adequate intake of calcium and vitamin D to prevent severe hypocalcemia; caution if active upper GI problems; do not administer with alendronate for osteoporosis in postmenopausal women; adverse effects include diarrhea, headache, and arthralgia

Parathyroid hormones

Promote new bone formation, leading to increased BMD. Teriparatide is a biological product containing a portion of human PTH, which primarily regulates calcium and phosphate metabolism in bones. Teriparatide is approved for men or women at high risk of fracture due to primary or hypogonadal osteoporosis or postmenopausal osteoporosis, respectively.5


Teriparatide (Forteo)

Recombinant human PTH 1-34, which has identical sequence to 34 N-terminal amino acids (biologically active region) of 84-amino acid human PTH. Acts as endogenous PTH, thus regulating calcium and phosphate metabolism in bone and kidneys. 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 reabsorption of calcium and phosphate, and intestinal calcium absorption. When administered with calcium and vitamin D, teriparatide increases BMD and decreases risk of fractures in patients with osteoporosis.

Adult

20 mcg SC qd

Pediatric

Not for use in children

Documented hypersensitivity; increased risk for osteosarcoma (including those with Paget disease of bone or 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 those with metabolic bone diseases 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 (Secondary)

Overview: Osteoporosis (Secondary)
Differential Diagnoses & Workup: Osteoporosis (Secondary)
Treatment & Medication: Osteoporosis (Secondary)
Follow-up: Osteoporosis (Secondary)
Multimedia: Osteoporosis (Secondary)
References
Further Reading
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Keywords

secondary osteoporosis, osteoporosis, bone density, bone loss, bone disease, hip fracture, Forteo, alendronate, bisphosphonate, osteoporosis treatment, osteoporosis exercise, bone mass, bone densitometry, bone mineral density, broken hip, hip fractures, teriparatide, metabolic bone disease, vertebral compression fracture

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Contributor Information and Disclosures

Author

Alana C Serota, MD, Fellow in Metabolic Bone Disease and Osteoporosis, Department of Orthopedics, Hospital for Special Surgery
Alana C Serota, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph M Lane, MD, Professor of Orthopedic Surgery, Weill Medical College of Cornell University; Chief, Metabolic Bone Disease Service, Hospital for Special Surgery
Joseph M Lane, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of University Professors, American Federation for Aging Research, American Orthopaedic Association, American Society for Bone and Mineral Research, Association of Bone and Joint Surgeons, Medical Society of the State of New York, Musculoskeletal Tumor Society, National Osteoporosis Foundation, North American Spine Society, and Orthopaedic Research Society
Disclosure: P & G; Roche; Lilly: Aventis: Novartis: Spinewave; biomimetics; Zimmer; DFine; Innovative Solutions; Honoraria Speaking and teaching

Medical Editor

Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Pharmacy Editor

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

Managing Editor

Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
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
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: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
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