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Bench to Bedside: Clinical Tips from APS Poster Presentations

Editor's Memo from June 2016
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First, it is important for practitioners to know that the American Pain Society (APS) has progressively pursued research as its primary goal and mission in recent years. This point is noted here because of the outstanding research that was presented in this year’s annual meeting, held May 11-14, in Austin, Texas.

To their considerable credit, the leaders of APS want their research to be “translational”—meaning the investigatory findings are transferred from “bench to bedside” or from the laboratory to the clinic. This highlight is designed to “translate” some research information from the meeting that may have some practical application.


Pain practitioners have long observed that pain patients who can obtain a few hours of sleep each night have less pain the next day. In a well-done study involving 139 participants with central sensitization and pain from knee osteoarthritis, fragmented sleep was associated with more pain.1 This supports medical treatment of insomnia in chronic pain patients. (see APS Highlights).

Complex Regional Pain Syndrome (CRPS)

This relatively rare, debilitating, and difficult-to-treat condition is being studied by many groups to hopefully improve our limited menu of options.2,3 Although no new treatment breakthroughs were reported, a better understanding of CRPS was put forward.

First, abnormal brain structures were found among pediatric patients with CRPS who did not respond to traditional treatments (n=10) compared to CRPS treatment responders (n=19).2 The structural changes included alterations in cortical thickness, subcortical volume, and dendritic atrophy. Much of our current literature implies that CRPS is a pathologic entity of the dorsal horn in the spinal cord. Now we know that the brain and spinal cord are both involved.

The dread of CRPS at the clinical level is that the condition will start in one extremity and spread to others. In a study of 150 patients, researchers found that the longer the condition existed, the more likely it was to spread to more than one extremity.3 They, therefore, recommend early and aggressive therapy to hopefully prevent the condition from spreading.

Traumatic Brain Injury (TBI)

Chronic pain as a result of  TBI has become increasingly common in pain practice. While it may manifest as trunk, neck, or extremity pain, constant headache is the most common result. This is no accident. A research team from the University of Maryland Department of Neural and Pain Sciences found cerebral grey matter changes in these individuals.4

The investigators found an “inverse relationship in the change in left S1 and thalamus grey matter volume between MRIs conducted immediately after TBI and post-traumatic headache and after 592 days, on average, with an increase in S1 and a decrease in thalamus.” Previous studies have reported decreased thalamus grey matter in TBI patients and an increased S1 in migraine patients. The current findings may be specific for patients with post-traumatic headache, noted the authors.

Therefore, don’t expect the usual and simplistic treatments for migraine and tension headaches to do the job.

Genetic Disorders

The collective research on genetics at this meeting was top notch. First, pain, usually lower back pain, was found to be present in 89% of Marfan syndrome patients.5 Anyone who has tried to deal with the pain flares of sickle cell disease knows it can be a frustrating experience. No wonder. This genetic disease has an extremely high percentage (over 80%) of patients who demonstrate cytochrome P450 genetic metabolic defects.6,7 The message here is to use the opioids morphine, hydromorphone, and tapentadol (Nucynta), which are not dependent upon the cytochrome system.

Not only do sickle cell patients have cytochrome P450 defects, they also have gene polymorphism in their adrenergic receptors.7 Some of these patients will likely require an adrenergic agent (amphetamine, methylphenidate, etc.) to control chronic pain and prevent pain flares.

Studies continue to show that certain polymorphisms of cytochrome P450 enzymes, opioid receptors, and other enzymes can identify patients who are at a higher-than-normal risk for opioid addiction and abuse.8 To date, there are no published studies on these addiction and abuse genetic predictors, but several are in process. It’s time for pain practitioners to start talking and thinking about the clinical and ethical activity we should undertake when we identify a patient who has a high genetic risk for addiction and abuse.

There is an accumulating body of research that links chronic pain conditions with decreased expression of the enzyme catechol-O-methyltransferase (COMT).9-11 A genetic deficiency of COMT increases central nervous system (CNS) levels of catecholamine, helps maintain a chronic pain state, and increases opioid requirements.10,11 Physicians are starting to test for COMT enzymes and are making clinical decisions based on COMT enzyme activity.

We urgently need a consensus effort on the real, practical meaning and actions to take with COMT testing. Forget what the labs tell us. We need facts and science. Put another way, is COMT testing friend or foe?

Opioid Resistance

It seems like everyone has a different theory as to why a patient does not respond well to opioids. Tolerance, genetics, hyperalgesia? Now there is another reason. A research team from the National Center for Complementary and Integrative Health, part of the National Institutes of Health, has found that there is decreased CNS opioid receptor availability 3 months after a peripheral nerve injury.12

Last updated on: July 5, 2016
First published on: June 1, 2016

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1 comment.

By Kricket on 06/23/2016
Is this another scheme that is adding to reasons that opioids shouldn't be used for chronic pain patients, according to our government, or is this real? Link??