A Conceptual Model of Pain: Treatment Modalities
In part one of this series,1 the author described a conceptual model of pain based on electrical principles: sensors (free nerve endings), wires (axons/nerves) and the perceptron (spinal cord and brain). Pain was described as either nociceptive (normal functioning of pain fibers), neuropathic (misfiring of axons/nerves), or central dysfunctions (central nervous system), the latter includes the pain pathways in the spinal cord and the brain. Part two of this series discussed methods to measure and quantify functioning of the pain nerve pathways with a view to understanding the underlying pathology causing the pain.2
The concept that pain results from mechanically- and chemically-caused physical changes that become more and more difficult to reverse is well-accepted throughout Medicine. With the passage of time, the reasons for the pain also become multi-factorial and overlapping, as well as more difficult to cure. Thus, early treatment is better to avoid permanent physiologic and structural changes and facilitate a cure.
While the pain mechanism(s) may become more complicated over time,1,2 as more than one of the basic mechanisms becomes active (i.e. nociceptive pain may progress to neuropathic pain and then to central pain), the physician can address one mechanism at a time by choosing treatment methods that are logically most effective and logistically most convenient. Patient perception of treatment “reasonableness” also plays a role in the initial treatment adopted.
Pain Patterns Related to Different Pathologies
Having pathology is not the same as having pain from that pathology. Without visible tissue changes, there may not be a peripheral pain generator, leaving neuropathic and/or central pain as the probable cause. There could also be a microscopic pathology and/or local metabolic reason. Ultimately, there must always be a mechanism whereby some pathology or dysfunction causes the perception of pain. There are, however, a multitude of pain-pathology referral patterns. Most physicians only recognize dermatomal patterns; there are also sclerotomal, myofascial, viscerotomal, thermatomal, myotomal, as well as other referral patterns.
Dermatomal pain suggests nerve root involvement from a herniated disc or other physical or chemical pathology at the nerve root exit from the spinal canal.3 While these distributions are usually unambiguous, specific mapping of the sensory distributions of thoracic dermatomes and the anatomic locations of the innervating nerves clearly show overlapping and highly individualized patterns.
Sclerotomal pain is deep bone pain referred from specific vertebral segments that may be interpreted as non-physiological. Bone pain may be either local or referred from ipsilateral spinal segments.3
Pain referred from tendinous and/or ligamentous interfaces with bone surfaces has no specific name that may also be interpreted as non-physiological. Hackett4 mapped pain referred from ligamentous and tendon attachments to bones.
Drs. Travel and Simons5,6 have provided physicians and patients with detailed maps of referred pain patterns from myofasical trigger points. While individual variations certainly occur, in general, these patterns of referred pain can be recognized in physician practice, and may sometimes be incorrectly referred to as “non-physiologic” pain patterns.
Likewise, the pain referral patterns of pathology in the internal organs are well-known across multiple field of medicine. Of course, there is an embryologic basis for these fairly consistent patterns of pain.5,6
There are also thermal patterns of pain, which are probably related to the distribution of sympathetic nerves (see Figure 1).7
Butler8 has mapped referred pain from the spinal dura, which is also probably related to stimulation/irritation of the sympathetic C-fibers on the dura. Pain referred from the spinal dura is reminiscent of thermatomes in being diffuse, but these referral patterns are unique.
Bonica and Loeser describe “myotomal” pain as involving problems with the fascial tissue planes that surround muscle groups.3 While “myotomal” may not be the correct description, when muscles were injected with hypertonic saline, which is an experimental substance known to produce pain, the above-mapped patterns of referred pain emerged.
Sometimes the myofascial pain referral patterns follow dermatomes, to some degree.9 Dermatomes are somatic sensory nerve distributions whereas trigger point pain referral patterns are more related to sympathetic C-fiber distributions.
There is much to be investigated and considered before an integrated theory really useful to pain management can be advanced.
These different pain referral patterns may even occur simultaneously. If the physician does not pick out the correct primary pathology, treatment is — at best — a hit-or-miss “shotgun” approach. This approach is demonstrated on a daily basis as many physicians routinely — but consistent with the standard of care and training they’ve received — prescribe muscle relaxants, pain-killers (opioid/acetaminophen), NSAIDs (non-steroidal anti-inflammatory drugs) and sleeping pills to patients in acute and chronic pain.
It is important to note that “curing” the pain, as opposed to “masking” it, requires a specially trained physician to precisely and effectively decide the primary cause of a patient’s pain problem and to pick the best and most effective treatment early in their care. This exercise is the essential first step in deciding on a theoretically-based and pragmatically-possible treatment plan.
Interestingly enough, these different pain etiologies and patterns are most directly helpful in dealing with nociceptive pain. In other words, these pain sources and referral patterns basically represent normal neurophysiologic functioning and, by and large, provide the patient and the physician with useful information in determining a good working diagnosis for nociceptive pain. However, actual clinical presentations are usually more complex.
While somewhat arbitrary, acute and chronic pain are concepts that must be considered and are useful in the sense that changes of real consequence occur over time. There are typically many, more complex, and permanent changes that do occur. Certainly, most physicians have seen the very visible changes that can occur in the natural progression of CRPS or RSD.
Neuropathic changes can also occur with CRPS and other pain conditions as illustrated in the 2nd of this series.2 If efferent pathways are either damaged or are responding in a reflex manner to aberrant afferent signals, then easily visible anatomic and structural changes can occur. These changes become more notable, complex, and difficult to cure over time. Anti-nociception can be a dysfunctional result in any type of pain.