Pain serves a protective role that alerts an individual to injury from the environment or from within. Based on what is known to date, all vertebrates, and some invertebrates, experience pain in response to actual or potential tissue damage. Many different types of pain are encountered, with the most common being acute, chronic, cancer, and neuropathic pain. Acute pain is the normal, predicted physiologic response to an adverse chemical, thermal, or mechanical stimulus. It may also be the initiation phase of an extensive, persistent nociceptive and behavioral cascade triggered by tissue injury. Acute pain generally improves within the first 3 days after an event such as surgery but may persist for weeks or months. Chronic pain may be defined as pain that persists longer than the expected time for tissue healing or pain associated with progressive nonmalignant disease (such as osteoarthritis). Cancer pain refers to pain that is the result of primary tumor growth, metastatic disease, or the toxic effects of chemotherapy and radiation. Neuropathic pain refers to a persistent syndrome resulting from damage to a peripheral nerve, dorsal root ganglion or dorsal root, or the CNS. Neuropathic pain is recognized in veterinary medicine much less often than in human medicine. It is not clear whether this represents a lower incidence or a deficiency in our ability to recognize such pain.
For an animal to experience pain, nociceptive information must be sent to higher centers in the CNS to be integrated, modulated, and interpreted into the conscious perception of pain. Noxious stimuli (heat, cold, mechanical, chemical) activate free sensory nerve endings known as nociceptors. A-δ and C-fibers transmit sensory information from nociceptors to the dorsal horn of the spinal cord, which directs and modulates input from the periphery and higher centers. Nociceptive information arriving in the dorsal horn of the spinal cord may activate motor neurons responsible for the reflex responses to noxious stimuli (such as withdrawing a limb). Importantly, nociceptive sensory input may be amplified or inhibited by spinal interneurons and glial cells.
Sensory information is relayed to higher centers in the CNS along a variety of pathways that differ according to species. In general, nociceptive information ascends the spinal cord along superficial and deep pathways to the brain stem with connections to the thalamus, reticular formation (responsible for level of arousal), and limbic system (responsible for emotions). From these areas of the brain, nociceptive information is relayed to the cortex where it is perceived as pain. Activity in spinal nociceptive pathways is strongly influenced by descending antinociceptive systems that originate in the brain stem. Endogenous antinociceptive neurotransmitters (eg, endorphin, enkephalin, dynorphin, serotonin, and norepinephrine) inhibit the transmission of nociceptive information in the spinal cord and brain.
The neuroanatomic components of the nociceptive/pain pathways and pain-suppressing systems can change in response to sustained sensory input. Peripheral sensitization of nociceptors and central sensitization of nociceptive pathways in the dorsal horn, spinal cord, and brain can develop as a result of extensive tissue trauma or nerve injury. The process of peripheral and central sensitization has been termed “wind-up” and refers to the neuroanatomic changes (plasticity) that result in heightened or exaggerated pain states. Additionally, these exaggerated pain states often do not respond to conventional analgesic therapy. Thus, changes in the CNS in response to repeated and sustained nociceptive input (ie, pain) complicate the clinical management of pain.
Last full review/revision July 2011 by Peter W. Hellyer, DVM, MS, DACVA; Patrice M. Mich, DVM, MS, DABVP (Canine/Feline), DACVA