Exploring the perception and physiology of pain in horses - DVM
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Exploring the perception and physiology of pain in horses


DVM360 MAGAZINE


Visceral pain arises from the distension of the viscera, and is associated with conditions of the GI tract and other internal organs. Compared to the skin, the viscera have a lower density of nociceptors, so that the pain tends to be not as well localized. Therefore it is more generalized, as opposed to a sharp or stabbing pain. It may be a gnawing or aching associated with gut torsion, distension or obstruction.

Allodynia and hyperalgesia

Though both acute and chronic pain vary in intensity, allodynia and hyperalgesia are unusual, exaggerated pain sensations.

Allodynia is an exaggerated response to otherwise non-noxious stimuli and may occur in areas other than the one stimulated. It can be either static or mechanical. For example, a person with a severely sunburned arm may perceive light pressure on that area, even from a feather touch or shirtsleeve, as pain radiating up the entire arm.

"I don't know of any specific case reports of allodynia in horses," says Smith. "I suppose one could imagine some types of clinical situation that could be analogous. One example that comes to mind is a horse with chronic back pain that may respond negatively to the saddle pad being placed on its back," says Smith, "but is that allodynia or negative anticipation of pain to come?"

Hyperalgesia is a severe pain response to a mild stimulus, such as extreme sensitivity accompanying inflammation, or a horse's surgical incision becoming tender during healing. Light pressure to the region then becomes painful to an exaggerated degree, with increasingly dramatic response as input increases.

Hyperalgesia is produced by mediator substances in response to tissue damage, including bradykinin, substance P, leukotrienes, tumor necrosis factor alpha (TNF?), interleukins (IL) 1 and 8 and prostaglandins.

Hyperalgesia can be experienced in focal, discrete areas, or in a more diffuse form involving the entire body. The focal form is typically associated with injury, and is divided into two subtypes, primary, which describes pain sensitivity that occurs directly in the damaged tissues, and secondary, which describes pain sensitivity that occurs in surrounding undamaged tissue.

Hyperalgesia is induced by a platelet-aggregating factor, which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (i.e., cytokines).

From trauma to pain sensation

"In people, the pain experience is separated into three components: nociception (transduction, transmission, and spinal cord modulation), perception (perceiving the unpleasant experience) and cognition (the behavioral response to pain)," Smith explains.

"We know that there probably are three or four fairly discrete, but interdigitating, processes that take place to provide for the experience of pain," Pettifer explains.

The peripheral nociceptors transduce the stimulus into an electrical signal that is then transmitted from the periphery up to the spinal chord. Some processing occurs there, and the information then is transmitted further up the spinal chord to the (cerebral) cortex.

In the human experience, it's not until there is a perception of a potentially damaging event that we ascribe the notion of pain. There is an experiential component. Prior to its being experienced, it's called nociception. There is a notion of transduction of the stimulus, transmission of it and perception of it.

There also are some events that allow for modulation of the input that is eventually experienced as pain.

From the point of origin of the initial noxious insult or injury to the tissues, nociception, the initial pain stimulus, is encoded as an electrical-action potential, an impulse transmitted to the dorsal horn of the spinal chord, then transmitted via ascending neural pathways to the CNS, including the cerebral cortex, where the awareness of the presence of pain occurs.

The first step in pain processing is the transduction of the stimulus by nociceptors, specialized pain-detecting nerve cells activated by mechanical (touch or pressure), thermal (hot or cold) or chemical (endogenous or exogenous) stimuli.

The nociceptors, found in skin, muscles, joint capsule, visceral organs, pleural membranes and arterial walls, are free nerve endings with cell bodies in dorsal-root ganglia that terminate/synapse in the dorsal horn of the spinal cord.


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Source: DVM360 MAGAZINE,
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