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An Urban Experience
B.D. Wright1
1Veterinary Anesthesiologist — Integrative Pain Management Specialist,
Know your enemy and know yourself and you can fight a hundred battles without disaster
Sun Tzu
There is no doubt that the experience of pain transforms an individual’s life, both while it is ongoing and after
the acute effects have passed. Pain alters healing, activity, social interactions and the kinesthetics of movement. Pain will always undergo some aspects of amplification and deamplification- allowing it to persist or gradually reduce over time.
While the subject of pain processing is startlingly complex, an understanding of the basic framework allows the clinician to design a more appropriate, individualized analgesic treatment for their patient in pain.
When contemplating the physiology of pain signaling there is a continuum between acute pain and chronic pain that defies attempts to confine these definitions to discrete time frames. Physiologists studying ‘acute pain’ define this as pain that does not actually cause damage to tissue. Clearly, this is a very different scenario from what a clinician would describe as acute pain, which very often involves surgical incisions, manipulation of deep, visceral type tissues and always, consequent inflammation. For this discussion, I will not attempt
to separate acute pain processing from chronic pain processing, but rather see acute pain as phasic, and chronic pain as a progress through the entire spectrum that becomes tonic, at least for a while.
In the complexity of clinical medicine, it is not possible
to predict where any given individual will land along the road of pain amplification. Many will fully recover from acute injury and return to a state indistinguishable from a non-injured counterpart (unless you were to investigate the pain map that was created on their glia). Others
will manifest life-long changes and these individuals
will tend to move differently and manifest accumulating dysfunction as their kinesthetics, myofascial system and nervous system find alternative methods of processing.
Simple pain begins at the site of injury, and may begin
as a proportional response to the level of stimulus (the pain reported is proportional to the intensity of the
injury). Peripheral nerve terminals are established in close association with resident mast cells and capillaries. These triads sense changes in pH, temperature and proteins
as well as transducing high intensity mechanical
stimuli. Unlike the other sensory receptors, pain receptors do not fatigue in response to repeated stimulation. Rather, with repeated stimulation, changes occur that include: increased sensitivity, budding of new receptive terminals, and recruitment of previously quiescent terminals
(silent nociceptors). Likewise, when significant neuronal activity occurs (with or without local tissue damage) the associated mast cells and capillaries escalate the release of inflammatory mediators, recruit white blood cells and promote metabolic activity in the region.
Once a signal is sufficient to trigger the high-intensity receptors (pain receptors) the signal travels up the
axon. The axon may be myelinated (A-delta fibers) or unmyelinated (c fibers). In the peripheral nervous system, the primary afferent will synapse in the dorsal horn of the spinal cord in lamina 1, 2, 3 or 5. Other sensory fibers synapse in similar regions (especially 3, 4 and 5), allowing interaction between signaling pathways carrying different types of sensory information.
Local Anesthetics/Na Channel blockers
Anti-inflammatories (NSAID or steroid- local or systemic)
Ice, heat, TRP channel modifiers Touch, acupuncture, laser
Before plunging into a discussion of the dorsal horn
it is important to recognize some major way-points
for pain signal modification along the path of axonal
flow. All along the axons of peripheral nerves are
ion channels, receptors and the cellular machinery
for energy production and electrical gradient maintenance. Contemplating the sheer magnitude of a nerve fiber (picture a horse sensory nerve body in the DRG extending up to the spinal cord and down to the coronary band) provides an understanding of how much activity occurs along this pathway. Imagine the amount of transportation that must occur along the filaments within the axon fibers. Thus, the axonal entity is not inert, but rather subject to modification during prolonged pain states.
Touch, acupuncture, laser
Local Anesthetics/Na Channel blockers Ice, heat, TRP channel modifiers
Likewise, the dorsal root ganglion (DRG) holds the cell bodies for peripheral pain fibers. There is a tendency
to think about these cell bodies as if they were fans
in the bleachers- watching the action go by without having any impact on the outcome. Not so, as becomes immediately evident when we consider the role of

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