A Country Doctor Writes:

Why would a toothache bring Ted Larson to the emergency room when he already takes half a dozen morphine tablets per day for his chronic back pain?

Why did Bridget Hall’s fibromyalgia pain seem to escalate after her last doctor gave her long-acting oxycodone?

Is Bob Bachman really in that much pain from his arthritis, or is he sharing or even selling his pills?

Taking care of patients with chronic pain is difficult. Physicians are at the same time told to recognize and treat pain better, and also to be more stringent with pain prescriptions to avoid drug diversion. Our understanding of the physiology and psychology of pain is evolving, as well as our knowledge of the science behind addiction.

As often before I see that some of the things I learned from my clinical professors in medical school were forgotten or even dismissed, only to come back into focus years later.

Thirty years ago I was taught that patients with ordinary low back pain would get better pain relief from modest doses of conventional pain medications if they were also prescribed a low dose of the antidepressant amitriptylene. The reason, as I remember it, was thought to be that amitriptylene made the brain interpret incoming pain signals differently.

Later, other authorities made a big distinction between mechanical low back pain and neuropathic or radicular pain, commonly referred to as sciatica. The focus shifted away from the brain’s interpretation of pain signals in general to whether a pain originated in the musculoskeletal system, like low back pain or arthritis, or in the peripheral nervous system, like sciatica.

When fibromyalgia was first recognized as a disease, there was a lot of confusion about where the pain came from. The name itself suggested that the pain originated in the musculoskeletal system. With the understanding at the time that such pains could be treated with narcotics, many fibromyalgia patients ended up on strong pain medications. We still used medications like amitriptylene and the more modern antidepressants with success, but the thinking was that these drugs worked mostly by improving sleep or treating unrecognized depression. Today we recognize fibromyalgia as a disease involving increased pain sensitivity of the nervous system, and we now have several medications targeting this mechanism.

We have also learned that patients who receive opiates for any kind of pain can develop a fibromyalgia-like intensification of nerve pain associated with ordinary touch, allodynia, or otherwise moderately painful stimuli. This phenomenon is called opioid-induced hyperalgesia. Paradoxically, decreasing such a patient’s pain medication dosage reduces their pain level.

More recently, even chronic musculoskeletal pain of arthritis has been shown to cause a nerve-mediated general pain sensitivity of a similar type. Patients with severe arthritis often experience aching and pain in areas without joint disease, such as skin or muscle tissue.

The practice of my early teachers, who treated most chronic pain as if it were at least in part nerve pain has found new respect and acceptance after many years of neglect as science has finally caught up with their clinical wisdom.

So when Ted Larson, already on chronic narcotics, complains of severe, nerve-mediated tooth pain, his pain is real and may actually be more severe than the same toothache in a person not on narcotics.

Bridget Hall’s fibromyalgia pain may actually have been made worse by the narcotics she was prescribed.

And Bob Bachman’s long-standing arthritis may indeed have made him increasingly pain sensitive. He has never failed a random urine drug screen or pill count. With the new data on neuropathic pain sensitization in patients with longstanding arthritis, it may be time to try him on something specifically for nerve pain, rather than increasing his regular pain medications.