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Referred Pain vs.Origin of Pain Pathology

Understanding the organic and physiological patterns of referred pain helps to identify the true origin of pathology and inform proper treatment.
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Referred pain, as defined by Anderson, is “pain felt at a site different from the injured or diseased organ or body part.”1 Radiating pain, however, is not defined by Anderson; radiating pain is more commonly used in connection with pain perceived in somatic nerve and spinal nerve root distributions (i.e. the dermatomes that all physicians learn early in their training). Merskey and Bogduk specify that “referred pain is pain perceived in a region that has a nerve supply different from that of the source of pain,”2 which indicates that radiating pain is completely different (the author does not find that excluding radiating pain from referred pain useful; radiating pain is just a subcategory of referred pain).

Bellenir adds “Antidromic” into the definition, noting that visceral and somatic nerve cells may synapse on the same neuron at the spinal cord.3 With chronic stimulation, “the impulse will spill over. . . . into the somatic nerve.” Warfield and Fausett also calls it “heterotopic” pain and state that “referred pain is a phenomenon that is frequently encountered and is most baffling.”4 Added meaning is conveyed by Khalsa, who defines referred pain as “pain that exists in a location other than the immediate area of the spasm”5 without defining limits, or specific distributions. However, according to Khalsa, the range of the main pain should not be larger than the receptive field, which varies in size depending on the area of the body

It has been said by the IASP Subcommittee on Classification that “Pain is always subjective. . .”2 Yet if the clinician does not understand a presenting pain pattern, where the pain is already considered “subjective,” the chances of justly handling and treating the patient are limited. Indeed, if psychogenic (eg. “subjective”) pain and referred pain become synonymous, then the physician may stop looking for the originating pathology and not provide proper treatment or any treatment at all. The patient is likely to slip into a downward spiral of “doctor shopping.”

However, it must be said that all pain “is always real.” Thus, diagnosing pain pathology — in the face of referred pain that may be perceived as worse than the origin of the pain — becomes a daunting challenge. An understanding of the pain pathophysiology with familiarity of referred pain possibilities, coupled with a thorough history and physical examination, is essential in making an appropriate and potentially correct diagnosis.

Figure 1. Note that the pain pathways from the skin surface and from an internal organ pass very close to each other at the dorsal horn. Via ephatic transmission (analogous to an electrical short) causes the brain to mistake pain from the internal organ for pain from the skin (Smith, 2000).13

Referred Pain Characteristics

The best known referred pain patterns originate from viscera and myofascial trigger points. Each type is presented in more detail below.

Ombregt has provided more precise principles limiting and defining referred pain.6 These principles are paraphrased as follows:

  1. radiation is related to spinal segmental
  2. perceived pain site and pathology are on the same side of midline
  3. usually felt deeply
  4. referred distally within a dermatome, but not necessarily throughout the whole dermatome (the author has agreed with this interpretation above)
  5. may be contiguous with or may be separated from pain origin

The author proposes a sixth principle: namely that the site of perceived pain is not tender, whereas the site of pathology is tender. Central pain phenomena do not necessarily fit completely within these criteria, but it is still useful to understand the similarities.

Kosek and Hansson have specifically found that, “referred pain is most likely a consequence of misinterpretation [by the perceptron] of the origin of input from the stimulated focal pain area, due to excitation of neurons somewhere along the neuroaxis with projected fields in the referred pain area. . . . [and] suggests that the divergence of the input is not reciprocally arranged.”7

Before enumerating and describing the various known referred pain patterns, the complexity of pain generation and propagation needs to be reviewed.

Pain Generators

The author, in a prior article,8 gives a detailed description of nociceptive, neuropathic and central pain and the neural pathways involved. For nociceptive pain, stimulation must occur at the free nerve endings with various types of signals being transmitted along several basic nerve fiber types. Neuropathic pain, on the other hand, is generated by the dysfunctioning pain nerves themselves. Central (“perceptron”) pain describes dysfunctional perception of pain by neurons in the spinal cord and/or brain. One superficially easy way to distinguish nociceptive and local neuropathic pain from psychosomatic, central, and referred pain is local tenderness, hyperalgesia and/or allodynia.

Above and beyond their identity, there are some basic principles of nerve distribution and anatomy that must be understood to follow the concepts presented here. To understand the generation of nociceptive pain, one must first identify the location of free nerve endings of the sympathetic C-fibers and the A-delta fibers, since the associated free nerve endings are really the only places were nociceptive pain is generated. Radiculopathy is a special case where sensory and motor nerve dysfunction may occur, but we are only concerned with the sensory portion of the radicular dysfunction that presents pain.

Butler presented photographic proof of myriad distribution of fine nerves on the spinal dura.9 Such evidence strongly implies similar patterns of different densities of these nerves occurring on many tissue planes or interfaces throughout the body. Distribution of nerve fibers on the spinal dura does not specifically assure us that free nerve endings also occur there. On the other hand, it is highly likely that such free nerve endings do, in fact, occur in this potential space, or more generically this tissue plane, as they do in tissue planes throughout the body.

Therefore, it is reasonable to expect that insults (mechanical, chemical or thermal) to the free nerve endings in tissue planes throughout the body may result in pain patterns that are completely consistent with the specific location of the impact on those nerve endings and, therefore, considered to be anatomically and physiologically valid.

There must be an origin of pain pathology before referred pain can be perceived. Some of these patterns of referred pain are well recognized, while others seem rather esoteric.

Factors Favoring Referred Pain

Ombregt, in describing “factors favouring reference of pain,” concluded that, from pooled experience, stronger central and/or proximal deep (vs. superficial) stimuli more likely cause the perception of pain beyond the pathology.6 Sclerotomal referred pain is more likely to occur than myotomal referred pain, and much more likely than bone pain to occur. This order of occurrence may be generally inversely related to intensity and pain-related dysfunction.

Last updated on: December 27, 2011
First published on: November 1, 2003