Guest Blog: Dr. Steve Blitzer
Those individuals with chronic pain are often challenged or misunderstood. They are often asked to prove they have an ongoing potentially disabling problem objectively, and without a dramatic test result, may be considered to be overreacting to their problem. This can leads to difficult situations with interactions with physicians, family members and other relevant contacts.
Sure, there are malingerers exaggerating their symptoms for a free ride on the train of disability insurance, a payout in a case of liability, or those seeking controlled drugs. However there is a large group of individuals experiencing pain and associated disability who are denied benefits or even just a validation of their problem because of 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 are left to measure pain by the subjective description of the patient who experiences it.
I believe we are about 40 years behind in the science of understanding pain and its acceptability as 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.
Now everybody knows even though there may be environmental stress triggers, depression is a biochemical “disease”. There is an imbalance of neurotransmitters in the brain especially serotonin. The treatment often involves medications to help restore the neurotransmitter balance. This reflects physiology and not just “attitude”.
Chronic pain is also a physiologic disease. There are biochemical changes in the nervous system and actual physical architectural changes which occur in these individuals where 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 towards the central nervous system. Similarly in the brain and spinal cord alterations in multiple neurotransmitters will effect hyperexcitability of the relevant neurons and additionally reduce the effects of inhibitory pathways.
Neuroplasticity, the reorganization of neurons physical structure, is a positive adaptive physiologic process of ongoing rewiring in the central nervous system. However, this can also go awry and cause increased pain reception and feedback as a pathological adverse consequence of this remodeling in prolonged pain syndromes.
Thus the physical “disease” model is relevant for chronic pain syndromes and patients should be treated accordingly.
Steve Blitzer MD DAAPM DCAPM