Page 36 - Veterinary Laser Therapy in Small Animal Practice

CHAPTER 4

Analgesic effect

The love for all living creatures is the most noble attribute myelinated fibers) and C fibers (polymodal receptors,
of man. slow conduction unmyelinated fibers), these get fired
— Charles Darwin (they translate or transduce biochemical and physi-
cal signals into an electric impulse) and conduct the
Pain is currently defined as “an unpleasant sensory information to the dorsal horn of the spinal cord; from
and emotional experience associated with actual or there, the spinothalamic tract carries the informa-
potential tissue damage, or described in terms of such tion into the brain. Different mechanisms can amplify
damage” (International Association for the Study of or reduce the signal in the spinal cord. For instance,
Pain). Note that pain is not just a physical stimulus or gamma-amino butyric acid (GABA) and serotonin act
sensation, but it is also how it makes the patient feel as signal inhibitors, but the inflammatory cascade that
about it. The psychological component is way more starts with the initial injury produces prostanoids and
recognized, studied, and treated in humans, while often other mediators, which make fiber discharge persist and
overlooked in veterinary science. This does not mean produce sensitization and primary hyperalgesia. Once
it does not exist: you are used to noticing how some the signal reaches the brain, pain is perceived and this
patients seem to do just fine with conditions that you triggers motor, endocrine, and biochemical responses.
know are moderately painful, while others become Acute pain arises to minimize tissue damage after
paralyzed, highly vocal, or seem to panic with manipu- a specific disease or injury; it has a warning and pro-
lations or conditions that you expect to elicit very little tecting function and should disappear once healing is
pain. completed. An example is pain during surgery or in the
Pain should be treated both for ethical and clinical postoperative period. The body has mechanisms to deal
reasons. As veterinarians, we must work to prevent with pain and modulate it; serotonin, norepinephrine,
and treat pain in the most proactive way we can; it is a and endogenous opioids are some of these neurotrans-
key component of our patients’ quality of life. Under- mitters that inhibit nociceptive transmission. When
treated pain leads to physiological changes such as the nociceptive information enters the brain, inhibitory
increased glycemia and arterial pressure, immunologi- descending pathways are activated. This may remind
cal compromise, delayed wound healing, and increased you of the anti-inflammatory mediators and mecha-
risk of self-trauma to a surgical area. Pain increases not nisms activated when the inflammatory cascade begins.
just morbidity, but mortality risk. Chronic pain, on the other hand, persists after what
Let’s review how the physical part happens. The would be considered the normal healing time for a
origin of the noxious stimulus can be somatic, visceral, particular injury, or remains because healing has not
or neuropathic (central or peripheral), but pain can also occurred; but it has no biological function and obvi-
be referred to distant sites. Once an injury or noxious ously affects quality of life. Think, for instance, about
stimulus activates nociceptors or free nerve endings of degenerative joint disease and the remodeling peri-
A-delta (mechanoreceptors and thin, fast-conduction osteum, oncological pain, or visceral pain in chronic

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