| Pain serves a protective role to alert an individual to injury from the environment or from within the individual. 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 following an event such as surgery, but may persist for weeks or months. Chronic pain may be defined as pain that persists for longer than the expected time frame for 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 pain 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. |
| For an animal to experience pain, nociceptive information must be sent to the higher centers in the CNS to be integrated and interpreted into the sensory experience 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 the nociceptors to the dorsal horn of the spinal cord, which directs and modulates the input from sensory neurons. 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, the nociceptive sensory input may be amplified or inhibited by spinal interneurons. 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 limbus (responsible for emotions). From these areas of the brain, nociceptive information is relayed to the cortex where it is recognized 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, and dynorphin) 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 neurons and pathways in the 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 that result in heightened
or exaggerated pain states. Additionally, chronic pain sometimes does not respond to conventional analgesic therapy due to changes in the CNS processing of nociceptive input. Thus, changes in the CNS in response to repeated and sustained nociceptive input (ie, pain) complicate the clinical management of pain. |
