Clinical Recognition of Central Abnormal Neuroplasticity
Arguably the major scientific research finding in the Decade of Pain is that severe pain causes rearrangement or reconfiguration of nerve cells in the central nervous system.1-8 This rearrangement or transformation, called neuroplasticity, is a response to electronic impulses that arise from a peripheral pain site that is not healed by the body’s basic immune response to a painful injury.1,7
The ramifications of this finding are profound for clinical treatment, disability determination, epidemiologic outcomes, and even terminology. While the term ‘neuroplasticity’ simply means rearrangement or transformation without a positive or negative connotation, the result in this case is negative as it produces an abnormal cellular structure, altered electronic circuitry, and encoding of the memory of the initiating pain. Precisely how this occurs is unclear but it is essentially the mechanism of phantom limb pain.9 It is incumbent on all pain practitioners to understand the development of central abnormal neuroplasticity (CAN) and clinically recognize its probable existence in pain patients.
Presented here is a first time attempt to clinically characterize and profile the patient with CAN so we can begin to identify these unfortunate patients at the clinic level. We must now view patients with this condition as having a central brain disease in addition to a peripheral pain-initiating site. The clinical diagnosis must now be made by an old-fashioned history and physical exam. Although the scientific underpinning of this phenomenon has primarily been documented by sophisticated neuroimaging studies, there is no standard imaging technique yet available for routine clinical use. Consequently, the profile for probable or suspected diagnosis of CAN given here will demand refinement and advances as we learn more about it. The diagnosis of CAN should not replace current nomenclature, but be a secondary diagnosis such as “intractable pain with likely CAN.”
Evidence of Existence
The evidence that central abnormal plasticity develops and encodes the memory of pain is well documented by a large number of research and clinical studies.1-8 The model for understanding this phenomenon is phantom limb pain.9 The patient with severe hip, spine, or other pain condition may develop an encoded memory of pain in nerve cells just like the amputee.4,7,11 It’s just that the patient still has their spine, nerve, joint, hip or other initiating pain site.
The various neuroimaging studies and other clinically-related investigations clearly demonstrate the presence of CAN. Glial cell and neurons are affected as there may be loss of gray and white matter including opioid and dopamine receptors.2,3,6 There appears to be little consistency as to the site of the brain neuroplasticity. Various reports involve the cortex, thalamus, hippocampus, corpus callosum, amygdyla, and cingulate gyrus. The great variance in the brain imaging studies showing loss of tissue is puzzling and a concern to clinicians. Why? If the neuroimaging studies showed a uniform anatomic loss of tissue and neuroplasticity in chronic pain patients, it would make a clinical diagnosis more specific and treatment strategies could be more targeted.
At this time, the neuroimaging studies clearly document the presence of neuroplasticity as indicated by tissue loss, but there appears considerable variability among chronic pain patients. This fact leaves us with a limited ability to make a specific clinical diagnosis. Therefore, I recommend that pain practitioners simply state in their records, for example, that the patient has suspected, probable, or likely CAN.
At this time, it appears that the pain and disability that CAN may produce can be clinically graded by the medical standard of mild, moderate, or severe. CAN is strictly a clinical diagnosis at this point as there is no laboratory, radiologic, or electric wave assessment that has been correlated with severity. Additionally, the brain imaging studies used to determine neuroplasticity with tissue loss and restructuring are far from being available to routine clinical practice.
Known to all pain practitioners is the tragic severity of pain that is called Reflex Sympathetic Dystrophy or Chronic Regional Pain Syndrome. In some of these cases, CAN appears to cause paralysis or retardation of movement. CAN also appears to be related to reports of twitches, jerks, and restless legs commonly reported by chronic pain patients.
Major Historical Characteristics
A careful history will usually identify the patients with suspected CAN. They will clearly state that their pain is constant (“24/7”) unless asleep. Additionally, sleep will usually require a medical sleep aid. This is in contrast to the patient who describes their pain, for example, as being intermittent, varies in intensity, comes in waves, or exacerbates with certain physical activities.
The patient with constant pain will invariably date their pain to a certain point in time. Often they can identify the date and hour that their pain became constant. In most cases, they relate that they originally had an intermittent pattern of pain that abruptly converted to a constant state. Others relate that the constant pain started at the instant of an accident or surgery. They frequently report that surgery made their pain worse. In reality, the surgery, per se, was probably quite sound but the stressful event precipitated CAN with it’s encoding of the memory of their pain. The severe case will describe great impairment of social, vocational, and familial functions. They report being bed- or house-bound in the absence of medication. In addition, they relate loss of memory and attention span.
Peripheral Pain Site Responds Poorly
A second hallmark characteristic of CAN is that local, peripheral treatments do little, or nothing, for the pain. For example, the usual chronic arthritis patient with intermittent or non-constant pain will report local pain site treatments such as oral anti-inflammatory agents, topical analgesics, injections, electromagnetic measures, and physical therapies to be effective. This may not be the case with CAN because central-encoded pain will require agents that act in the spinal cord and central nervous system to reduce pain. Some patients with CAN will not even experience much pain relief if the peripheral pain site is anesthetized.
The initiating pain site may show little sign of inflammation, inadequate healing, or pain on physical manipulation such as pressure or stretching. The peripheral pain site may have what appears to be rather good healing following surgery or injury. As part of a diagnostic evaluation, the pain practitioner should attempt some peripheral pain treatments to determine if the peripheral pain site is active. This might include a topical analgesic, oral anti-inflammatory agent, or anesthetic injection. If there is little or no response to a peripheral treatment, one may then suspect the presence of CAN.