Pain assessment and management strategies (Proceedings)


Pain assessment and management strategies (Proceedings)

Apr 01, 2008

Physiology of Pain

Pain is defined as an aversive sensory and emotional experience.1 Nociception is the neural response to the application of a noxious stimulus. It is observable and recordable, but does not necessarily equate to pain. Pain in animals can only be characterized by the observation of behavioral changes in response to a noxious stimulus which may be painful.

Nociception receptors are free nerve endings located in most tissues of the body. These receptors are sensitive to mechanical, thermal, or chemical stimulation. The primary afferents of the nociceptor pathways include the A-delta fibers and the C fibers. A-delta afferent pathways are responsible for the first, acute, fast, sharp pain associated with an injury; the conduction velocity of these pathways are very fast. The receptive area of these afferents is very discrete, enabling the animal to localize exactly the site of the stimulus. C afferent pathways are responsible for the second, dull, aching, burning, throbbing, chronic pain of an injury. The receptive area is relatively large and localization of the site of the stimulus is limited to general areas of the body. A-beta fibers are associated with the sensations of vibration, tickling, prickling, or tingling. These afferent fibers have a major role in ascending anti-nociception mechanisms of the spinal gate control mechanism (transcutaneous electrical nerve stimulation, acupuncture/acupressure, massage, and mechanical manipulation of the painful area). A-beta fibers exhibit lower stimulation thresholds than do A-delta and C fibers and therefore can be selectively stimulated.

The gate theory of pain control was introduced in 1965.2 Afferents of A-delta, C, and A-beta fibers synapse with neurons in the dorsal horns which send long axons upward to the brain.3,4 Prior to synapsing with these "central transmission cells", the nociceptor fibers give off branches which synapse with interneurons in laminae I and II (the substantia gelatinosa) of the dorsal horn. The substantia gelatinosa cells, in turn, presynaptically inhibit the release of neurotransmitter by the primary nociceptor fibers at the synapse to the central transmission cells. The A-delta and C fibers inhibit the substantia gelatinosa cells thereby facilitating the A-delta and C fiber stimulation of the central transmission cell and the secondary afferents to the brain. This positive feedback mechanism of A-delta and C fibers serve to enhance the magnitude of the nociceptive input from a given painful stimulus. The A-beta fibers activate the substantia gelatinosa cells and thereby inhibit neurotransmitter release and stimulation of the central transmission cell. This negative feedback system serves to minimize the nociceptive input to the central nervous system from a given painful stimulus. Several modes of pain therapy are based upon this ascending pain modulation mechanism since A-beta fibers can be stimulated at sub-pain thresholds.

Assessment and Recognition of Pain

Pain is herein defined as an aversive (perceptual) physical nociceptive stimulus, which threatens to, or does, cause tissue damage, and which would evoke protective motor actions and avoidance. Nociception is the neural response to a noxious stimulus and does not, per se, equate to pain. Discomfort encompasses a broad range of aversive sensory and emotional experiences, of which pain is only one form. When discomfort is great enough or prolonged enough so as to alter normal behavior or activity, the recipient is said to be suffering. The existence of pain in an animal and the need for analgesic therapy is dependent upon the observation of behavioral changes or abnormalities in the animal which can reasonably attributed to pain. It might be helpful to divide pain into levels of magnitude: severe, moderate, and mild. Severe pain might be defined as that which is intolerable; the kind of pain where the animal throws itself about its cage in a mindless frenzy because the pain is so severe that the animal simply cannot deal with it in any other way. Unprovoked vocalizing (crying, whimpering) in an animal that does not have CNS disease and is not recovering from anesthesia, and does have a disease which might be painful, is also taken as evidence of severe pain. Mild pain might be equated with that amount which is a nuisance; the animal is well able to tolerate it and to go about its daily activity since it does not interfere with behavior in any fashion.