Last updated: Mon, Oct 21, 2024
Multiple parts to pain are acknowledged in the experience of acute injury:
I propose that we think in terms of three varieties of pain:
Type A pain: The fast, sharp pain is well-localized. It alerts you to damage or at least to a threat. It may trigger a strong SNS response that helps you to cope with the damage or the threat. It results from the activation of A-delta sensory neurons.
Type C pain: This slow aching pain is less well-localized. It indicates a tissue problem but is not as clear or salient as Type A pain. It tends to involve a larger area than any Type A pain that accompanies it. It may be accompanied/caused by local inflammation and be considered a part of the normal response to injury. It may be a signal of tissue damage or irritation that occurs without fast, sharp pain in situations in which A-delta receptors are not triggered, or, as in the fascia and some other tissues, where A-delta receptors are lacking. It results from the activation of C sensory neurons
Type H pain: A very slow aching pain that is again less well-localized than Type C pain. It may be experienced as involving a much larger part of the body than Type C pain, and may be sensed not as associated with an injury but as a mood or state of motivation. (Also see A Rational Model of Emotion and Pain.) So, I propose an additional part to pain:
This very slow Type H pain is therefore not "pain" as defined by the IASP. It does, however, look, walk, and quack like slow IASP (Type C) pain, and is often caused by the same mechanisms as the slow aching pain. It can be caused by the chronic presence in the body of pro-inflammatory chemicals and/or by "learning" or allostatic processes within the nervous system such as long-term potentiation, damage to neurons, expansion of sensory fields, and the other pain-related phenomena described in Pain Phenomena of the Spine and Periphery and elsewhere.
Both Type C and Type H pains are accompanied by tenderness, prolonged hyperalgesia, and a motivation (a felt need) to withdraw, rest, and recuperate. Pain is intimately interwoven with the body's illness and healing systems. Many of the mechanisms of pain, from chemical messengers to processing networks in the brain, are shared with the immune system. Pain can usefully be viewed as a part of the body's reaction to injury or illness.
(My designation of the third type of pain as type "H" is meant as an acronym for "humoral," a reference to the humoral understanding that, until modern times, explained mood in terms of humors that inhabit the body. Circulating pro-inflammatory chemicals take the place of the classical humors, and potentiation and sensitization of the neural system is experienced in many ways in a similar fashion.)
My definitions are not clean and clear. I propose them not for a scientific but for a didactic purpose. My reading of pain understandings in light of the evidence is that the failure to clearly distinguish the type of pain leads to false generalizations about pain. I propose that what is true about Type A pain is not necessarily true of Type C nor or Type H. I doubt that this assertion would be seriously contested, yet scientific and medical generalizations about pain very commonly fail to make the necessary distinctions.
[Pain is] an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.1
As I've noted previously, the IASP had its reasons and its understandings when it defined "pain" the way it did. I haven't spent the time needed to infer their motivations, but it appears to me that they were trying to stake out the territory of their concern and to satisfy the interests of both physiological and behaviorist researchers. Whatever may be the explanation behind their definition, they defined boundaries to their attention that don't seem to follow the boundaries of the systems that they are studying.
The IASP say that pain is an experience, and I wouldn't deny that, but if pain is an "experience," so equally are any healthy or pathological states of human existence. Requiring pain to be "associated with actual or potential tissue damage" may be helpful in limiting the scope of study, or in other ways, yet the mechanisms of pain extend far beyond response to injury. Why should study of the "experience" be limited to those aspects that (some unspecified arbiter) associates with tissue damage? Certainly what I've labeled Type H pain is worthy of being dealt with as itself.
A tenet of systems science is that, to understand a system, you must also consider how it interacts with the system that constitutes the system's environment, and then to go on to that super-system's supersystem, in order to understand the role and function of the system of interest. [A REFERENCE WOULD BE NICE HERE.].
The IASP circumscribes pain in several ways. It limits pain to sensory and emotional experiences, for example. But pain is known to coincide with physiological and morphological changes. We know that pain is accompanied by increased sympathetic tone and by observable morphological changes and that those changes have significant implications for quality of life.
The IASP definition limits pain to what is sensed, but doesn't specify what it means to be "sensed." Yet we know that we respond to noxious signals that are well below the threshold of conscious awareness. This occurs automatically, for example, when we sit. Our nervous system monitors for signs of local ischemia caused by pressure on the sit-down, and we respond by shifting position without awareness or conscious effort. There is not evidence that sub-conscious irritation and damage are free from effects.
The IASP definition limits pain to that which is "associated with" or "described in term of" tissue damage. Yet we know that some of the effects of pain, particularly the emotional or mood components, do not necessarily meet those restrictions.
It is an error of analysis to limit the study of pain to the sensations and experiences that are delimited by the IASP definition. It is important to expand the scope of study to include all the ramifications of the specified sensations and experiences. These ramifications aren't "caused by," "mediated by," or "associated with" pain. They are as much a part of the process as are the sensory and emotional experiences referred to in that definition.
It is an error to limit the study of pain to only the specific and salient sensory and emotional experiences that are "associated" with tissue damage. It is important to expand the scope of study to include all the functioning of the elements of the pain system.
It is another error of analysis to treat all the phenomenon that are delimited by the IASP definition as if they also delimit a physiological/neurological system. It is instead important to recognize that Type A, C, and H pains (and perhaps more types) use different neurological networks and have different physiologies of operation and different sets of effects on human welfare.