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Pain (defined by the International Association for the Study of Pain, IASP) is an unpleasant sensory and emotional experience associated with actual or potential tissue damage [1]. Pain is not merely the sensation or perception of it, but has an additional affective, emotional component. In other words, pain is said to be multidimensional (i.e., it is not just what you feel, but how it makes you feel). This is because pain pathways terminate not only in the frontal cortex (perception), but in deep, primitive parts of the brain (the limbic center) that control emotions such as anger, fear, anxiety, stress, even depression. And with this “stress response” comes a release of hormones such as cortisol, epinephrine, and proinflammatory cytokines; these very molecules actually then sensitize nociceptors, the specialized neurons that carry pain signals. In other words, a circular problem can be present: pain causes stress, and stress causes pain.

Chronic pain, furthermore, has been shown to elicit harmful cognitive changes: decreased learning, memory, and other features of mental acuity and agility; in humans it is also co‐morbid with clinical depression (and one must wonder if this element does not also exist in dogs and cats).

Nociception involves several neurons. The “first‐order” neuron transducts tissue damage (mechanical, thermal, chemical, etc.) into a signal that is transmitted via action potential up to the dorsal horn of the spinal cord (the largest cells in the body; its nucleus is in the dorsal root ganglion). There in the dorsal horn, excitatory neurotransmitters are released and carry the signal across a synapse to the “second‐order” neuron which then depolarizes and carries an action potential to the brain. The body has intrinsic ways of mitigating pain, through inhibitory neurons that reside in the dorsal horn and those that descend from the brain down to the dorsal horn. It is in the dorsal horn where pain signaling can be modulated; that is, like a rheostat, it can be dialed up or down – either by the body itself or through veterinary interventions.

When pain works correctly, it is both normal and protective; this is often referred to as “adaptive” pain. If pain becomes exaggerated in some way (duration, scope, character, field), it is then said to be “maladaptive.” Maladaptive pain occurs through a process called “hypersensitization”: a combination of cellular and molecular processes that include lowering firing thresholds of nociceptors, recruitment of “innocent bystander” nociceptors, “cross‐talk” with other neurons such as those responsible for touch, pressure, and sympathetic fibers, and diminished inhibitory control. The molecular and cellular changes of hypersensitization occur in both the peripheral tissue and the spinal cord. The result for the patient is pain that is worse than it should be (“hyperalgesia”), normally nonnoxious stimuli like touch now become painful (“allodynia”), odd sensations that accompany the pain (“dysthesias” like tingling, itch, burning, even numbness), a larger area than originally affected is now painful, pain present for longer than expected, and spontaneous pain without any obvious tissue damage present.

Maladaptive pain can occur through a variety of circumstances, but generally includes nerve injury of some type. This injury can be macroscopic and obvious, or microscopic and inobvious. Taken to the extreme, maladaptive pain of any origin becomes “neuropathic,” whereby permanent changes are encoded into the peripheral and central nervous system. At this point, pain can be said to be a disease unto itself.

Maladaptive pain and/or pain with a neuropathic component can occur under both heritable and acquired, and acute and chronic circumstances. A partial list of these includes but is not limited to the following.

 CNS injury, including heritable disorders such as Chiari‐like malformation (Cavalier King Charles spaniels) and acquired ones such as intervertebral disc disease and other spinal trauma, traumatic nerve injury, e.g., amputation, encephalitides.

 Any severe tissue trauma.

 Persistent postsurgical pain.

 Chronic inflammation: OA, lymphoplasmacytic gingivitis/stomatitis, otitis.

 Visceral: pancreatitis, feline interstitial cystitis (“Pandora syndrome”) [2], inflammatory bowel disease, glaucoma.

 Spontaneous/idiopathic: feline hyperesthesia syndrome, feline orofacial pain syndrome.

 In humans, microneuropathies may be caused by diabetes, herpesvirus, and some chemotherapy agents, especially vinca alkaloids; some dogs and cats probably also suffer thus).