PAIN SENSATION IS A PHYSIOLOGIC NECESSITY. Animals lacking the ability to sense or respond to noxious stimulation are doomed to a short, pitiable existence. Pain is best classified functionally and anatomically using a numerical system. Type I pain is sharp and intense. It is really an alarm system signaling actual or impending tissue damage and initiating responses to limit or prevent that damage. Type I pain is triggered by very hot, very cold, or very strong mechanical stimulation. The signals are carried from the periphery to the brain along a well-organized, high-speed neural pathway that permits recognition of affected peripheral areas and fast, appropriate, avoidance response. Type II pain often follows Type I pain after injury. It is not only triggered by intense thermal and mechanical stimuli, but also by chemical changes occurring in and around damaged tissues. Type II pain is carried by a slower speed neural pathway that is less well organized. As a result, this type pain is perceived as diffuse and difficult to locate. It is often described as dull, often aching or burning, sometimes with a throbbing quality. Type II pain normally persists until damaged tissues heal; its purpose seems to be one of encouraging immobility and rest to promote healing and to discourage further injury.
Painful sensory information is carried from the tips of peripheral nerve fibers (for example, in skin, connective tissue, and organs) to specific regions within the spinal cord. Here, the signals are modulated (either amplified or suppressed), and the processed pain signals, if strong enough, are sent to higher centers in the brain. Under certain conditions these processing centers in the spinal cord and brain can change, both in structure and in function. These regions initially become hyper-responsive to incoming signals, and normally non-painful sensations may be interpreted and passed on as painful. This is Type III pain. Actual damage to the sensory nerve axons often leads to Type III pain, but evidence is building that persistent pain (usually Type II with or without Type I) can do so as well. Type III pain is not easy to diagnose and extremely difficult to manage. In cases of severe Type III pain, euthanization of the animal often becomes necessary.
Persistent pain is not merely a symptom of another disease process; it is a disease in and of itself, putting the persistent pain patient on a slippery slope. The patient will self-splint and immobilize painful areas. These areas cease normal, symmetric, coordinated movement and de-condition. Muscle atrophy, muscle contracture, joint weakness, and neuropathies can ensue. Abnormal posture and gait can lead to overuse of ancillary musculature with resulting further overall degeneration. Severe pain is a potent stimulant of the hypothalamic-pituitary-adrenal axis, and the impact of persistent pain may be profound. Excess catecholamine production, glucocorticoid excesses and deficiencies, hypotestosteronemia, insulin-lipid abnormalities, and immune suppression have been recognized as complications of persistent pain in several species. In both animal models and in human clinical cases, problems of insomnia, attention deficit, memory loss, and cognitive deficiencies are often associated with persistent pain. Though the mechanisms by which these complications occur are unclear, they likely involve multiple effects, including neuroanatomical degeneration, neural synaptic depletion, and hormonal imbalances. Without adequate pain management, the persistent pain patient can slip into the abyss that is Type III pain.
Therapeutic approaches and modalities for managing the persistent pain patient will be discussed in the next issue of the Equine Disease Quarterly.
Tomasic, (505) 466-0151, email@example.com,
Veterinary Pain Management, Santa Fe, New Mexico