People with chronic pain are often challenged or misunderstood. They’re frequently asked to prove objectively that they have an ongoing potentially disabling problem. Without a dramatic test result, they may be considered to be overreacting to their difficulty. This can cause trouble in interactions with physicians, family members and other relevant contacts.
Sure, there are malingerers exaggerating their symptoms for a free ride on disability insurance, a payout in a case of liability, or those seeking controlled drugs. There’s a large group, however, of individuals experiencing pain and associated disability who are denied benefits or even simple validation due to lack of objective proof.
Many institutions are now considering “pain” as the fifth vital sign, (after pulse, blood pressure, respiration, and temperature). We don’t have a test which is easily and readily available to measure pain like we do for blood pressure or serum chemistry parameters. Thus, we’re left to measure pain by the subjective description of the patient who experiences it.
I believe we’re about 40 years behind in our knowledge and understanding of pain compared to the science of depression and mood disorders. For those of us old enough to remember 40 years back, if someone was depressed it was considered something of an embarrassment, it was hush-hush, and others thought of these individuals as feeble minded and overly focused on their problems instead of just picking themselves up and getting on with life.
Everyone now knows that, although there may be environmental stress triggers, depression is a biochemical “disease.” There’s an imbalance of neurotransmitters in the brain, i.e. serotonin. We use meds to help restore the neurotransmitter balance.
A physiological disease
Chronic pain is also a physiological disease. There are biochemical changes in the nervous system and actual physical architectural alterations that occur in patients whose acute pain progresses to chronic.
Peripheral receptors may become overly sensitized by these chemical changes resulting in a reduced stimulus threshold for afferent input of pain to the CNS. Similarly, in the brain and spinal cord, alterations in multiple neurotransmitters will affect hyperexcitability of the relevant neurons and also reduce the effects of inhibitory pathways.
Neuroplasticity, the reorganization of neurons, is a positive physiological process of ongoing rewiring in the CNS, which can also go awry and cause increased pain reception and feedback in prolonged pain syndromes.
The physical “disease” model is as relevant for chronic pain syndromes as it is for depression, and patients should be treated accordingly.
Steve Blitzer, MD, DAAPM practices family medicine in Thornhill, ON, and has a special interest in medical rehabilitation and pain management. He is on staff at York Central Hospital, Richmond Hill, and at St. Joseph’s Health Centre in Toronto.