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leading to persistent pain is radiculopathy, which results from nerve root compression or impingement
and is a common source of low back pain. This painful syndrome is used here as an example to provide a
context for presenting immune mechanisms of chronic pain and their relationship to specific injury
parameters. Measures of injury biomechanics are presented for work with these models, including beha-
vioral sensitivity, local structural changes, and cellular and molecular changes in the CNS, as they apply
to kinematics, kinetics, and injury. Incorporating effects of injury parameters on mechanisms of persist-
ent pain, the text discusses implication of these and other factors confounding pain in MSD. Lastly, based
on these findings and others, a discussion is provided highlighting areas of future work to help elucidate
methods of injury prevention, diagnosis and development of therapeutic treatments.
It is important to define, at the outset, relevant distinctions in terminology. “Pain” is a complex per-
ception that is influenced by prior experience and by the context within which the noxious stimulus
occurs. Likewise, “nociception” is the physiologic response to tissue damage or prior tissue damage.
Similarly, for discussion in this chapter, “hyperalgesia” is defined as enhanced pain to a noxious stimu-
lus.
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Strictly speaking, this is a leftward-shift of the stimulus-response function relating pain to intensity.
The corresponding pain threshold is lowered and there is enhanced response to a given stimulus. Hyper-
algesia is mediated by nociceptor sensitization, where “sensitization” describes a corresponding shift in
the neural response curve for stimulation. Sensitization is characterized by a decrease in threshold, an
increased response to suprathreshold stimulus and spontaneous neural activity.
For this chapter, many of the examples are drawn from painful injuries related to the spine. These
include both low back and neck pain from radiculopathy. While it is recognized that these examples
are by no means all-inclusive of the painful musculoskeletal injuries, they do provide an ideal context
for discussing many of the pain mechanisms presented here. Certainly, syndromes such as those affecting
the carpal tunnel are important injuries in their own right, yet many of the same issues apply regarding
neural tissue damage, mechanical injury and inflammation. In addition, in this regard, within these
examples comments are made in this text to delineate the differences between persistent and resolving
(acute) pain syndromes.
16.1 Neurophysiologic Mechanisms of Pain
There are a host of physiologic mechanisms by which tissue injury leads to nociception, and ultimately
pain. In persistent pain, CNS signals can result in a hypersensitivity of neurons in the CNS. In addition to
alterations in electrical signaling, neuroimmune responses are initiated both locally at the site of injury
and in the spinal cord due to the altered neuronal function from perceived injury. Together, these changes
can further contribute to sensitization and persistent pain symptoms. Findings with regard to both neur-
onal signaling and neuroimmunity are reviewed here to form a basis for discussing more recent views of
nociceptive mechanisms of persistent pain.
16.1.1 Neural Anatomy Relevant to Pain
In order to provide a context for presentation and discussion of pain mechanisms, it is first necessary to
describe the relevant anatomical structures, connections and relationships of neural sensory and proces-
sing components. These are reviewed only briefly here and are described in much greater detail in texts
specializing in neural science and pain.
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Primary afferents, which are either directly injured or which relay pain signals from injured tissues,
terminate in the dorsal horn of the spinal cord (Figure 16.1). At each spinal level, dorsal nerve roots
carry sensory information from the periphery into the spinal cord. Dorsal roots contain sensory
neurons with cell bodies housed in the enlarged dorsal root ganglion (DRG) outside the spinal
column. In contrast, the ventral root contains the axons of neurons whose cell bodies are within the
ventral horn of the spinal cord and transmits efferent signals. Outside of the spinal column, the dorsal
and ventral nerve roots come together distal to the DRG at each spinal level and combine to form a
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