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Athletes’ injuries require effective, individualized treatment strategies.


Published 6/1/2011
Jennie McKee

When pain is part of the game

Aggressive pain management can reduce the risk of permanent CNS changes

Fractured bones, torn ligaments, and other injuries—some of which can result in chronic, debilitating pain—are a fact of life for many athletes. Treating the pain that accompanies these injuries can be challenging, Mark A. Harrast, MD, clinical associate professor of rehabilitation medicine and orthopaedic sports medicine at the University of Washington, told members of the American Orthopaedic Society for Sports Medicine during his 2011 Specialty Day presentation.

To avoid long-term impact on the central nervous system (CNS), he advised aggressive pain management.

Acute vs. chronic pain
The pain an athlete experiences right after an anterior cruciate ligament tear is much different than chronic pain that has been endured for several seasons.

Acute pain, explained Dr. Har-rast, is a time-limited response to a noxious stimulus that activates sensory receptors called nocioceptors. Treatment for acute pain is aimed at removing the underlying pathologic process or pain generator.

“Chronic pain is different,” he said. “There’s less correlation between the underlying tissue pathology or injury and the level of pain reported.”

In part, this is due to changes within the CNS and peripheral nervous system related to the pain. According to Dr. Harrast, research conducted in the last 15 years using magnetic resonance imaging has found discrete CNS changes in patients with chronic pain, including atrophy of areas in the brain and its gray matter.

“Changes to the CNS can occur within 6 weeks,” he said, “so it is important to treat pain appropriately and aggressively to potentially prevent long-term or permanent CNS changes.”

Treatment options
Physical rehabilitation, manual mobilization/manipulation, and ultrasound are commonly used to treat pain, as are both oral and topical nonsteroidal anti-inflammatory drugs (NSAIDs)—including traditional Cox-1 and Cox-2 inhibitors. These drugs, however, can have side effects, including delayed healing of fractures and increased risk of ulcers and subsequent hospitalization, and cardiovascular events.

“Short-term topical NSAID use immediately after injury can be considered a relatively well-justified treatment of muscle injuries without an apparent risk of delayed healing,” he said.

A review of 47 randomized controlled trials on the use of topical NSAIDs covering 3,455 participants with acute musculoskeletal pain, for example, found that the topical NSAIDs were significantly more effective than placebo in relieving pain.

Dr. Harrast cautioned, however, that prolonged NSAID use can cause significant side effects. Because basic science studies have shown that NSAIDs impair bone healing, they should be used cautiously after a fracture.

“Clinical significance in various patient groups still needs to be assessed for proper patient selection to understand who is at the highest risk of NSAID-induced delayed fracture healing,” he said.

Proton pump inhibitors (PPIs), which are commonly used in patients with gastrointestinal issues, may be helpful in patients on NSAIDs, said Dr. Harrast. PPIs must be used with caution, however, because although data show that they can reduce rates of ulcers and hospitalizations for ulcers related to NSAID use, they have also been linked to increased fracture risk.

Because cardiovascular risks have also been associated with NSAID use, said Dr. Harrast, “we need to be very careful with long-term use of these drugs and counsel our patients about potential side effects.”

Other pharmacologic treatments
According to Dr. Harrast, muscle relaxers have a sedative effect on the CNS, but do not have a direct effect on muscle.

“Muscle relaxers really just calm the patient while nature takes its course,” he said.

Cyclobenzaprine, which is in the family of tricyclic antidepressants, may be helpful, because a side effect is increased sleepiness.

“If patients can get at least 6 hours of sleep each night, research studies have found that their visual analog pain scores improve by as much as 40 percent,” he said.

Neuromodulating agents, including antidepressants and anticonvulsants, are helpful in the treatment of neuropathic pain, said Dr. Harrast. He pointed out that selective serotonin and norepinephrine reuptake inhibitors, such as venlafaxine, can be effective in treating pain and depression.

According to Dr. Harrast, the use of short-acting opiates for acute pain is appropriate in the right patient. He cautioned the audience, however, to be careful when prescribing acetaminophen with other combination drugs that contain acetaminophen.

“Percocet is oxycodone plus acetaminophen, and vicodin is hydrocodone mixed with acetaminophen,” he noted, cautioning that because the total recommended daily dose of acetaminophen is 4,000 mg in patients with normal liver and kidney function, it might be possible for a patient being treated for pain to overdose.

Looking to the literature
The impact of anti-inflammatory medications on muscle has been studied, but with mixed results. As a result, said Dr. Harrast, “the jury is still out regarding anti-inflammatory use in acute muscle injury.”

In the last few years, several studies have examined the effects of local anesthetic on cartilage.

“Many recent studies have highlighted the chondrotoxicity of local anesthetics in vitro, with truly conflicting results,” he said. “Clinical effects may be different than those found in studies using chondrocytes or osteochondral tissue in experimental culture.”

Dr. Harrast added that “the local anesthetics typically used for joint injections have all been linked to chondrotoxicity in at least one study.”

A recent study compared different concentrations of lidocaine and ropivacaine and found that lower concentrations seemed to be the least toxic, but “further investigation is definitely needed,” he concluded.

Disclosure information—Dr. Harrast reports no conflicts.

Jennie McKee is a staff writer for AAOS Now. She can be reached at

Bottom Line

  • According to Dr. Harrast, short-term topical NSAID use immediately after injury provides “a relatively well-justified treatment of muscle injuries without an apparent risk of delayed healing.”
  • Physical rehabilitation, manual mobilization/manipulation, and ultrasound are commonly used to treat pain, as are NSAIDs.
  • Because chronic pain may cause CNS changes within 6 weeks, it is important to treat pain appropriately and aggressively to potentially prevent these long-term or permanent changes.


  1. Massey T, Derry S, Moore, RA, McQuay HJ: Topical NSAIDs for acute pain in adults. Cochrane Database Syst Rev 2010;16(6):CD007402.
  2. Boursinos LA, Karachalios T, Poultsides, Malizos KN: Do steroids, conventional non-steroidal anti-inflammatory drug and selective Cox-2 inhibitors adversely affect fracture healing? J Musculoskelet Neuronal Interact 2009;9(1):44-52.
  3. McGettigan P, Henry D: Cardiovascular risk and inhibition of cyclooxygenase: A systematic review of the observational studies of selective and nonselective inhibitors of cyclooxygenase 2. JAMA 2006;296(13):1633-1644. Epub Sep 12, 2006.
  4. Mishra DK, Fridén J, Schmitz MC, Lieber RL: Anti-inflammatory medication after muscle injury: A treatment resulting in short-term improvement but subsequent loss of muscle function. J Bone Joint Surg Am 1995; 77(10): 1510-1519.
  5. Obremsky WT, Seaber AV, Ribbeck BM, Garrett WE Jr.: Biomechanical and histologic assessment of a controlled muscle strain injury treated with piroxicam. Am J Sports Med 1994:22(4):558-561.
  6. O’Grady M, Hackney AC, Schneider K, et al: Diclofenac sodium (Voltaren) reduced exercise-induced injury in human skeletal muscle. Med Sci Sports Exerc 2000;32(7):1191-1196.
  7. Shen W, Prisk V, Li Y, Foster W, Huard J: Inhibited skeletal muscle healing in cyclooxygenase-2 gene-deficient mice: The role of PGE2 and PGF2alpha. J Appl Physiol 2006;101(4):1215-1221.
  8. Bogatch MT, Ferachi DG, Kyle B, et al: Is chemical incompatibility responsible for chondrocyte death induced by local anesthetics? Am J Sports Med 2010;38(3): 520-526.
  9. Grishko V, Xu M, Wilson G, Pearsall AW 4th: Apoptosis and mitochondrial dysfunction in human chondrocytes following exposure to lidocaine, bupivacaine, and ropivacaine. J Bone Joint Surg Am 2010;92(3): 609-618.