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THE PAIN PROCESS
Dave
Thompson
February
2004
Pain involves
an incredibly complicated myriad of physiochemical responses leading to
the perception of an unpleasant sensation arising from actual or potential
tissue damage. While the full complexities of the pain process are beyond
the scope of this discussion, an understanding of the terminology and
basic neurophysiology involved is helpful in preventing and treating
discomfort in our patients.
Pain can be classified as physiologic,
which refers to the body’s protective mechanism to avoid tissue injury,
or pathologic, which arises from tissue injury and inflammation or
damage to a portion of the nervous system. Pathologic pain can be further
divided into categories such as nociceptive (peripheral tissue
injury), neuropathic (damage to peripheral nerves or spinal cord), visceral (stimulation of pain receptors in the thoracic or abdominal viscera), and somatic (injury to tissues other than viscera, such as bones, joints, muscles and
skin). It can also be defined temporally as acute (arising from a
sudden stimulus such as surgery or trauma) or chronic (persisting
beyond the time normally associated with tissue injury).
Nociception refers to the processing of a noxious stimulus resulting in the perception
of pain by the brain. The components of nociception include transduction,
transmission, modulation and perception. Transduction is the
conversion of a noxious stimulus (mechanical, chemical or thermal) into
electrical energy by a peripheral nociceptor (free afferent nerve ending).
This is the first step in the pain process, and can be inhibited by
NSAID’s, opioids and local anesthetics. Transmission describes
the propagation through the peripheral nervous system via first-order
neurons. Nerve fibers involved include A-delta (fast) fibers responsible
for the initial sharp pain, C (slow) fibers that cause the secondary dull,
throbbing pain, and A-beta (tactile) fibers , which have a lower threshold
of stimulation. Transmission can be reduced by local anesthetics and
alpha-2 agonists. Modulation occurs when first-order neurons
synapse with second-order neurons in the dorsal horn cells of the spinal
cord. Excitatory neuropeptides (including, but not limited to, glutamate,
aspartate and substance P) can facilitate and amplify the pain signals in
ascending projection neurons. At the same time, endogenous (opioid,
serotonergic and noradrenergic) descending analgesic systems serve to
dampen the nociceptive response. Modulation can be influenced by local
anesthetics, alpha-2 agonists, opioids, NSAID’s, tricyclic
antidepressants (TCA’s), serotonin-selective reuptake inhibitors (SSRIs)
and NMDA receptor antagonists. Perception is the cerebral cortical response to nociceptive signals that are
projected by third-order neurons to the brain. It can be inhibited by
general anesthetics, opioids and alpha-2 agonists.
Hyper responsiveness (increased
sensitivity) is a hallmark feature of both acute and chronic pathologic
pain. This is a result of changes in the nervous system response (neuroplasticity) at peripheral and central locations. Peripheral sensitization occurs when tissue inflammation leads to the release of a complex array of
chemical mediators, resulting in reduced nociceptor thresholds. This
causes an increased response to painful stimuli (primary hyperalgesia). Central
sensitization refers to an increase in the excitability of spinal
neurons, mediated in part by the activation of NMDA receptors in dorsal
horn neurons. The net effect is expanded receptor fields (pain in
neighboring areas not subjected to injury, or secondary hyperalgesia) and
painful responses to normally innocuous stimuli (mediated by A-beta fibers
and referred to as allodynia). The combination of peripheral and central
sensitization results in an increase in the magnitude and duration of
pain.
Because the pain response is
extremely complex and can involve multiple mechanisms in the same animal
(inflammatory and neuropathic, acute and chronic), no one drug at one dose
can be expected to be effective in every patient. Two important concepts
should be kept in mind when treating pain. Preemptive analgesia involves initiating treatment before the nociceptive response is
triggered, in an effort to inhibit the development of peripheral and
central sensitization. Multimodal analgesia is the strategy of
combining two or more analgesic drugs to achieve an additive or
synergistic effect. This reduces the individual drug dosages (lowering the
risk of side effects) and works best when each drug has a different
mechanism of action (blocks a different portion of the nociceptive
response).
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