2.16.1 Terms Defined
Allodynia: A pain response to nonnoxious stimuli such as touch and light pressure.
Dysthesia: Unpleasant or abnormal sensation, e.g., tingling, burning, itching, numbness.
Hyperalgesia: An exaggerated pain response to a noxious stimulus.
Hypersensitization: The molecular and cellular “wind‐up” in peripheral tissue and dorsal horn of the spinal cord, characterized by decreased neuron firing threshold, decreased descending inhibition, recruitment of bystanding neurons and more; results in maladaptive pain.
Nociception: Pain processing with peripheral neuronal activation, transmission in the primary afferent neuron, modulation in the spinal cord, and perception in various centers throughout the brain.
Osteoarthritis (OA): A subset of degenerative joint disease that occurs when the protecting cartilage on the ends of bones wears down over time.
Pain: Multidimensional unpleasant sensory and emotional experience associated with actual or potential tissue damage. Chronic pain occurs when the pain persists for three months or longer.
Pain, Adaptive: Normal and protective pain.
Pain, Acute: Pain experienced during the expected time of posttrauma inflammation and healing.
Pain, Chronic: Pain experienced past the expected time of posttrauma inflammation and healing (in humans, defined as pain still present 2–3 months or longer after initial tissue damage).
Pain, Maladaptive: Peripheral and central hypersensitization‐induced abnormal pain, characterized by increased scope, character, and field of pain: hyperalgesia, allodynia, dysthesias.
Pain, Neuropathic: Hypersensitization and maladaptive pain that has progressed to gene expression and permanent morphological and functional changes in the peripheral and central nervous system (CNS); pain as a disease at this point.
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).
2.16.2 Recognition/Assessment of Pain
The IASP stipulates that the inability to communicate (e.g., neonates, the cognitively impaired) does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain‐relieving treatment. In humans, pain is what the patient says it is; in animals (as in human neonates and the cognitively impaired), the pain is what we (the veterinary team) say it is.
The astute veterinary team can prompt pet owners' awareness and recognition that their pets are exhibiting either obvious or subtle clinical (or even historical) signs of pain (see 8.13 Team Approach to Pain Management). Observations of poor patient conformation, body position, gait and mobility, or a client report – even just over the phone or other communication – of “stiffness,” lameness, or reluctance to perform activities of daily living (including just getting up and down on or off furniture, etc.) can be enough to say “Sounds (or looks) like she may be uncomfortable,” followed by one or more of the following.
We'll have the doctor take a look at that.
Tell