Mechanisms for Pain and Injury in Musculoskeletal Disorders - Fundamentals and Assessment Tools for Occupational Ergonomics - page 389

PAIN
SYMPTOMS

Afferent
fibers

INJURY

CENTRAL
(CNS)

LOCAL
( periphery )

Dorsal Horn Excitability

Electrophysiologic
Signaling

Decreased threshold,
Increased response to stimuli,
Ongoing spontaneous activity

Structural & Material
Responses

Neuroimmune Activation & Inflammation

Neuromodulator Release
(SP, CGRP)

Glial activation,
Cytokine & chemokine upregulation/release,
Altered synaptic transmission,
Algesic Mediator Induction & Release

Inflammation
& Immune Responses

Edema

SP, CGRP, prostaglandins, glutamate, NO

FIGURE 16.3 This schematic illustrates the collection of physiologic mechanisms following an injury in
the periphery, which initiates and contributes to pain. Nociceptive responses are complicated and involve a
host of changes both locally and in the CNS. While the schematic suggests a simple linear cascade (from left to
right) of events following injury, which lead to pain, events are quite dynamic in nature and involve aspects of
electrophysiology, immunology and an interplay between both. Some changes occur both at the site of injury and
in the spinal cord and CNS. However, the degree to which these alterations occur is variable and dependent on
both the nature of the injury and the type of response. Moreover, many of these individual responses affect each
other (small arrows) and are themselves directly altered by confounding physiologic, anatomical and mechanical
factors.

by nociceptors, the nerve endings of the Adand C fibers. Conduction velocities of Adfibers are approxi-
mately 10 times those of C fibers (5-30 and 0.5-2 m sec, respectively) due to the saltatory conduction

resulting from the myelin sheathing. As a consequence of this difference in conduction velocity, a sharp
pain is first detected in response to a stimulus, followed by a second, longer lasting dull and burning pain
mediated by the C fibers.
Pain sensation and signaling begin at the injury site where Adand C fibers are activated by thermal,
chemical, mechanical, and electrical stimuli. These nociceptors can become sensitized; this both lowers
their thresholds for firing and increases their firing rates when stimulated at levels similar to those before
injury. 4 Following injury, inflammation is induced in an effort to promote healing and recovery. In this
process, inflammatory mediators such as prostaglandin E, serotonin, bradykinin and histamine, among
others, can have altering effects on fiber responses for a given mechanical stimulation. These and other
mediators activate nociceptors or further sensitize those nociceptors which are already responding to
stimuli — inducing increased activity. Specifically, bradykinin, serotonin, excitatory amino acids, and
hydrogen ions are all responsible for directly activating afferents. 4,31 Similarly, prostaglandins, serotonin,
noradrenaline, adenosine, NO, and nerve growth factor sensitize nociceptors.
In addition to altered electrical activity, injury initiates the local synthesis and release of inflammatory
mediators that induce inflammation and edema as part of the healing process (Figure 16.3). However,
these same processes that provide healing also sensitize nociceptors and recruit new nociceptors that
enhance pain. 17,19 Cytokines are also released in the periphery in association with tissue injury and
inflammation. These small proteins, in turn, contribute to the local inflammatory response, while
further affecting the electrophysiologic responses of nerve fibers in the region and altering nociception.

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