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3 Articles in Volume 2, Issue #5
A Conceptual Model of Pain
Taxonomy of Pain Patient Behavior
Whiplash Injuries in Motor Vehicle Accidents

A Conceptual Model of Pain

The practicing physician's guide to the causative mechanisms of pain and how to translate these basic principles into diagnoses and treatments.

Pain, as a concept and symptom, is discussed and described throughout professional and lay medical literature. “Pain" is the reason for initial contact with any physician for the vast majority of medical problems, e.g. abdominal pain, chest pain, limb pain, low back pain, etc. Understanding pain mechanisms, however, is often hampered by the complex neural interconnections involved in pain. Any one, or combination, of the following mechanisms can contribute to pain: neural “sensor" stimulation, neural “wire” misfiring, and “perceptron” dysfunction.

The general public often righteously complains about the lack of recognition and help for their pain and discomfort — aside from direct treatment of the underlying medical pathology. On the other hand, many physicians feel helpless, in the face of the onslaught of public indignation, to help with pain that is not supported by “standard” laboratory and/or radiological evidence, or even by “physiologically” consistent behavior; someone just can’t hurt overall!

Medical doctors depend on knowledge of the pathophysiology or at least a diagnosis to decide on treatment. Thus, to maximize success, physicians need to understand how pain is perceived. Certainly, knowing where and what the problem is, increases the likelihood of a positive outcome. Present categories of pain mentioned in medical literature are helpful, but these concepts are not organized to provide the practicing physician with handles that can help the physician more effectively treat those patients presenting with pain — particularly chronic pain.

While the Joint Commission1 now recognizes and mandates pain as the “fifth vital sign,” the present focus of Pain Medicine is “cover-up” rather than “cure.” Even with an abundance of detailed Pain Medicine literature, there appears to be a limited understanding of the basic mechanisms of pain, even within the research world. Obviously, without a reasonably detailed diagnosis reflecting the underlying pathophysiology of a given pain, treatment is no more than “hit and miss.”

In the defense of physicians, we only know what we know and cannot be expected to be omniscient in our understanding and insight of all medical problems. If we cannot “cure,” then it is good medicine to “cover-up” to reduce suffering. In either case, good medical care must be based on “diagnosis, diagnosis, diagnosis,” and a mechanistic understanding of the underlying pain pathophysiology.

Furthermore, in light of the apparent epidemic of under-treatment of pain — which can have serious legal consequences (i.e., a recent misdemeanor conviction in California) — and the sometimes necessary prescription of socially-unacceptable narcotics in treating chronic pain, the treating physician must understand the basic pathophysiology of pain to provide both optimal and medically-justifiable treatment. For all these reasons, there is an urgent need to clarify, organize and synthesize the abundance of information about pain, and apply these conclusions as simply as possible to the practical treatment of patients.

The Present State of Pain Theory and Thought

Pain is described in a myriad of ways:

  • in temporal terms: chronic pain, subacute pain and acute pain
  • in characterizations: intermittent pain, intractable pain, lancinating pain, referred pain, burning pain and dull pain
  • in acceptable diagnoses (which are all basically syndromes): phantom pain, cancer pain, vascular pain, arthritic pain, nerve pain, muscle pain, fibromyalgia, myofascial pain, sympathetically maintained pain, and complex regional pain syndrome
  • in mechanistic terms: neuropathic and nociceptive pain
  • in anatomic perceptional terms: headache, back pain, neck pain, facial pain, limb pain, abdominal pain, etc.
  • in source of origin terms: central pain as originating in the spinal cord or brain
  • in psychiatric/psychogenic terms: psychosomatic “in-the-head” pain, etc.

These descriptors variously imply the chronicity, the character, the cause or the location of this type of unpleasant sensation. To add complexity, many factors, such as culture, personality, psychosocial stressors and nutritional status, can be involved to influence the degree of pain and to confound the causal factors of the pain.

Caudill2 analyzed pain from different angles to emphasize its complexity, where pain:

  • biologically — serves as a signal that the body has been harmed,
  • psychologically — is experienced as emotional suffering,
  • behaviorally — alters the way a person moves and acts,
  • cognitively — calls for thinking about its meaning, its cause, and possible remedies,
  • spiritually — serves as a reminder of mortality,
  • culturally — tests a people’s fortitude or forces their submission.

Pain disorders are categorized in the DSM-IV-TR3 (coded for the medical condition) as follows:

  • 307.80 Pain Disorder Associated with Psychological Factors
  • 307.89 Pain Disorder Associated with both Psychological Factors anda General Pain Condition

Elsewhere, the DSM-IV-TR3 attributes neural dysfunction to pain. Again, these are only descriptive categories.

The simplest traditional categorization of pain has been “acute” and “chronic.” Acute pain is really just a result of the stimulation of a normally-functioning pain detection system and serves to alert us to avoid or minimize tissue damage. Chronic pain merely means that pain is perceived over a long period of time, which has been arbitrarily set at 6 months.

Descartes showed a basic understanding of the pain pathways in 1664.4 However, this schematic (see Figure 1) suggests that he only appreciated nociceptive pain, which implies normally functioning pain pathways. A more recent rendering of the details of pain pathways is presented in Figure 2.5

Formal classification systems (see Table 1) do exist and provide some insight into what we are trying to accomplish in this article.

The most advanced concepts are expressed by Craig,6 who states that pain is just one manifestation of the mind-body’s homeostasis system. From the patient’s point of view, the spectrum of pain control spans temporary treatments (usually pharmaceutical) in suppressing pain to permanent remission or cure of the underlying pathology/disease.

While these are all very useful concepts, they are generally academic in nature and do not provide much practical help to a physician. Concepts of pain pathophysiology, and thus classification, are abundantly available in the scientific and medical literatures. There is a need to refine and clarify all of this information and apply it as simply as possible to the treatment of pain in the physician’s office.

Dallel and Voisin recognized the need for a clear roadmap: “once pain-generating mechanisms are known, it becomes possible to establish the appropriate treatment of pain.”7 We suggest that refining these concepts are a giant step in the right direction and propose to present a simple, clear pathophysiologically-based classification model. We contend that pain treatment should primarily focus on reversing pathologic mechanisms that cause the pain in the first place.

Neuroanatomy and Neurophysiology

Nerves, or neurons, are long tubes of protoplasm (rather than a series of “sausage links”) and which may, or may not, be surrounded by poor conducting myelin (insulation). Nerves generally present themselves in various sizes and characteristics and have numerous branches to other neurons. Neurons interact/communicate via numerous electrical (gap junction) and chemical synapses. There are motor (efferent) neurons, which primarily carry signals from the brain to muscles, and sensory (afferent) neurons, which primarily carry signals from the periphery to the brain.8

Figure 1. Descartes4 depicted the passage of pain signals from the source of the insult to the brain.. Figure 2. A 1998 presentation of details of pain pathways.5 . Figure 3. Variety of nerve endings. In this context, we are primarily interested in those that sense stimuli that are transmitted as pain, i.e. mainly free nerve endings.5,8.

The primary focus in Pain Medicine are the small sensory nerves, which carry unpleasant signals to the brain and may or may not be perceived by the brain. Descartes4 depicted exactly that: a noxious stimulus causes information to be conveyed to the brain which is then perceived as pain (see Figure 1).

Neural signals are conveyed by potassium and sodium ions moving into and out of neurons via voltage-gated channels, in specific patterns, to form a relatively slow moving wave of information to, from, and within the central nervous system. These voltage-gated channels are concentrated in “holes” in the myelin (nodes of Ranvier), but are more evenly distributed in the more primitive unmyelinated nerve fibers (C-fibers).

In the absence of neural wire damage, there is a continuum across various numbers of synapses (switching stations) from the source or place of stimulation to the site of perception. At the distal end of sensory nerves, there are various types of nerve endings. When it comes to pain nerves, those endings are so-called “free” nerve endings (see Figure 3). At the proximal end is the “perceptor” areas of the brain.8

There are three types of fibers that carry pain signals to the brain — A-beta, A-delta and C-fibers. The first two are evolutionarily modern fibers that are myelinated (insulated) and carry nerve impulses rapidly to the cortical regions of the brain (refer to a basic neurophysiology textbook).

Figure 4. Stained nerve fibers that coat the skin around the spinal cord.11 We expect that a similar distribution occurs on other tissue surfaces throughout the body..

The A-beta are probably reserved for deep, lancinating pain; certainly these carry vibratory signals. The A-delta fibers are somatic, myelinated fibers that have primary connections to the cortical regions of the brain. These fibers convey sharp, lancinating, easily localized pain signals; this pain sensation usually quickly passes. The C-fibers are relatively primitive, are unmyelinated and conduct rather slowly to the subcortical part of the brain. The brain perceives a more generalized burning, aching pain sensation, and this pain takes longer to pass. Thus, when one experiences a paper cut, you quickly appreciate a “zing” followed by a “burning” pain. You know exactly where the “zing” comes from, but the brain sees the burning pain through “fogged glass.”

Different nerves, when it comes to function, have different characteristics. These characteristics may overlap between function (see Table 2). There is no absolute scientific agreement as to how features and function are related, but to facilitate discussion and understanding, generalization is desirable (see Table 3).

Pain Classification System Table
Categories I II III IV V
Traditional Acute Subacute Chronic  
Pathogenetic Primary Secondary Tx. Effect (chemotherapy, tissue trauma, edema, etc.)
ICD-9 Disease process Pain location Secondary
IASP9 Region System Chronology Intensity Etiology
Biopsychosocial Acute Recurrent acute Condition related    
Dickerson Neuropathic Inflammatory Long-term    

Now that we know generally how these small nerves work, we need to know where these nerve endings and small pain nerves occur. Our standard anatomy books, such as Netter,12 do not depict or describe these networks of nerves. Dr. Fishman,13 an insightful pain doctor, has described in his book entitled, “The War on Pain," that these nerve fibers cover and line most of the tissue plane surfaces throughout the body. Figure 4 presents stained nerve fibers coating the skin around the spinal cord and provides a general impression of how the nerves cover other tissue planes/surfaces.

Proposed Model of Pain Neurophysiology

Nociceptive pain is merely normal functioning of the neural sensor/wire/perceptron system. This system serves useful purposes in alerting the brain to bodily injury. Neuropathic and central pain, however, are manifestations of true dysfunction, and can be the “disease" itself.

If one considers a bundle of axons (see Glossary), neuropraxia, axonotmesis and neurotmesis represent points along a complex continuum of damage to axons and nerves. The three possibilities for individual axons are normal function, hyperfunction (hyperesthesia, hyperalgesia, hyperpathia, and allodynia) and hypofunction (hypoesthesia, hypoalgesia, conduction block, and death). Hyperfunction can also be thought of as sensitization or irritation. The ultimate hypofunction is axon death without regrowth. Free nerve endings can also be sensitized or irritated, but is considered here to be in the neuropathic category.

Understanding neurophysiology of pain pathways is helpful. Further, we propose that all pain can be understood by considering problems of stimulation of sensors, conduction along nerves and/or perception in the spinal cord and brain. The perception then may involve feedback, either positive or negative (i.e. release — or not — of native painkillers, e.g. endorphins). If negative, the result is, by and large, a dysfunction that conceptually could stand alone.

Table 1. The “traditional" classification scheme merely addresses chronology. The “pathogenetic" system grossly indicates the cause. “ICD-9" coding is as listed above. The IASP system provides a detailed description of the pain, but fails to approach the cause, except generally in Etiology; the IASP definition of pain avoids linking pain to a specific stimulus or cause. “Biopsychosocial" considerations is one step up from the “traditional." Dickerson starts in the right direction, but still misses a direct approach to pathophysiology.

Peripheral Nerve Fiber Types/Characteristics
class\units stimuli/function perception conduct velocity m/sec diameter microns myelination
A-alpha fibers motor contraction efferent transmission none direct 30-85 12-22 +++
A-beta fibers vibration and pressure afferent transmission vibration and pressure 30-70 5-12 +++
A-delta fibers cold sensation and pain fast pain and localized touch afferent transmission cold sensation and pain localized touch 5-25 1-4 ++
C fibers hot sensation and pain slow pain and generalized touch afferent transmission hot sensation and pain generalized touch 0.7-2.0 0.3-1.3 -*
* C-fibers can still be clumped and embedded in other non-conducting tissue.

 

Last updated on: December 20, 2011
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