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Adhesive Capsulitis in Physical Medicine and Rehabilitation Medication

  • Author: André Roy, MD, FRCPC; Chief Editor: Stephen Kishner, MD, MHA  more...
Updated: Apr 26, 2016

Medication Summary

The goal of pharmacologic intervention in FS is uniquely the control of pain in the 2 first stages of the disease because no drug affects the underlying disease process. Medication does not affect the duration of disease or the severity or duration of glenohumeral joint contracture. Most of the time, patients with FS can manage their pain with analgesics, such as acetaminophen, as needed. However, during the most painful months of the condition, when rest pain and night pain are most bothersome, appropriate use of narcotic agents is warranted.

Pain control should be aimed at relieving pain in the following order of priority:

  1. Rest pain and night pain: The preferred agent should be a long-acting, centrally acting agent (eg, calcitonin) or a sustained-release narcotic preparation (eg, low-dose oxycodone HCl [OxyContin]).
  2. Activity-related pain: Some physicians advocate the use of short-acting analgesic agents, such as oxycodone, before sessions of physical therapy to improve shoulder mobilization. The authors' opinion is that this regimen should be used with care because of the risk of causing a flare-up after physiotherapeutic mobilization due to an excessively vigorous mobilization session.

Attaining the favorable prognosis requires patience on the part of the physician and the patient.


Endocrine metabolic agents

Class Summary

Agents in this class may have analgesic effects.

Calcitonin (Miacalcin, Osteocalcin)


Can relieve some back pain associated with adhesive capsulitis. A prospective, randomized study was conducted to compare calcitonin SC for 3 wk with manual therapy and physical therapy with physical therapy alone. Pain decreased more in patients with posttraumatic capsulitis who were receiving calcitonin, manual therapy, and physical therapy than it did in others. The speed of recovery was comparable in both groups.



Class Summary

Given the absence of histopathologic evidence of capsular inflammation, NSAIDs must be used for their analgesic effects. To our knowledge, no researchers have compared the efficacy of NSAIDs with that of placebo in adhesive capsulitis. Comparisons of the efficacy of different NSAIDs in the treatment of adhesive capsulitis show a positive effect regardless of the NSAID used.

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well; examples are inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

COX-2 – selective NSAIDs are recommended in cases of FS. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than it is with traditional NSAIDs. Ongoing analysis of the cost of preventing GI bleeds will help in further defining the patient populations who are most likely to benefit from COX-2 inhibitors.

Two randomized, controlled studies were conducted to compare oral (PO) corticosteroids with placebo. One study showed an improvement only of night pain at 4 weeks. The other study showed an improvement of pain and function at 3 weeks. Therapeutic effects of PO corticosteroids after these periods have not been demonstrated.

PO corticosteroid therapy is significantly less effective than intra-articular corticosteroid injection in the short term.

Given the systemic adverse effects, one should question the indication for PO corticosteroids in the treatment of FS. Other drugs with fewer adverse effects are available; alternatively, corticosteroids can be administered intra-articularly with fewer adverse effects.

Celecoxib (Celebrex)


Inhibits primarily COX-2, an isoenzyme induced during pain and by inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; therefore, GI toxicity may be decreased. Seek the lowest dose for each patient.


Analgesic agents

Class Summary

In rare cases, narcotic analgesia may be needed for adequate pain control if the patient's condition is refractory to the judicious use of bupivacaine or bupivacaine suprascapular nerve blocks or in situations in which these nerve-block procedures and/or steroid injections (which are most often performed with fluoroscopic guidance) are not readily available. When combined with anti-inflammatory agents and physical modalities, analgesics should result in good pain control.

In the occasional patient whose condition does not respond to the aforementioned therapies, the use of a long-acting narcotic agent, such as codeine, morphine sulfate (MS Contin), oxycodone HCl (OxyContin), or hydromorphone, should be considered, along with rescue doses of short-acting drugs every 4-6 hours.

Acetaminophen (Tylenol, Feverall, Tempra, Aspirin Free Anacin)


Should be first-line drug of choice. In most patients, 3 g/d suffices to control the pain of FS during all but the most painful months. Narcotics and NSAIDs should be used only if the regular use of acetaminophen 1 g tid fails to adequately control pain. The authors prefer to be conservative and limit the prescription to 75% of the maximal daily dosage because patients may be prone to liver toxicity if they take the maximal dosage for many consecutive months.

Oxycodone (OxyContin, OxyIR, Roxicodone)


Indicated for relief of moderate to severe pain.

Contributor Information and Disclosures

André Roy, MD, FRCPC Consulting Staff, Department of Physiatry, Montreal University Hospital Center and Montreal Rehabilitation Institute

André Roy, MD, FRCPC is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.


Thierry HM Adahan, MD LMCC, CCFP, FRCPC, FABPMR, Head, Pain Rehabilitation Center, Haim Sheba Medical Center, Tel Hashomer, Israel

Thierry HM Adahan, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Patrick M Foye, MD Director of Coccyx Pain Center, Professor and Interim Chair of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School; Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Curtis W Slipman, MD Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center

Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, North American Spine Society

Disclosure: Nothing to disclose.


The editors wish to thank Luc Fortin, MD, for his previous contributions to this article.

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