As discussed elsewhere in this text, spinal cord contusion and compression have their earliest and most deleterious effects on the myelin sheathing that surrounds neurons subserving ascending proprioceptive and descending motor pathways (see Chapter 15). Compromise of proprioception and/or voluntary motor function can therefore occur even though the axons themselves remain intact. Assessing these functions alone cannot determine the degree or reversibility of any underlying spinal cord injury, since we cannot easily distinguish between loss of saltatory conduction (myelin loss) and actual axonal transection. In contrast, those axons that subserve the conduction of deep pain are typically small diameter with minimal to no myelin sheathing. Consequently, the absence of deep pain caudal to the level of the spinal cord lesion suggests a more severe spinal cord injury, and possibly one that is irreversible.

In dogs with thoracolumbar disc extrusions, deep pain perception is the most important prognostic factor for neurologic recovery. For example, in one study, 92% of patients with intact deep pain perception regained the ability to walk after surgery, whereas only 69% of patients with absent or questionable deep pain perception became ambulatory postoperatively [2]. This study demonstrated a 1.7 times better chance for return to ambulation in dogs with preserved deep pain perception than in those dogs without deep pain perception. Therefore the accurate testing of deep pain perception is critical. However, the assessment of deep pain perception is subjective and requires the clinician understand the functional neuroanatomy and clinical techniques involved. Determining deep pain status is generally only germane to dogs with thoracic, thoracolumbar, or lumbar spinal cord lesions. Dogs with cervical spinal cord lesions and loss of nociception will usually suffer respiratory paralysis, and therefore die unless intubated and mechanically ventilated. The respiratory paralysis will provide much better prognostic information than determining if the animal retains sensation caudal to the lesion.

Pain versus nociception

The International Association for the Study of Pain (IASP) defines pain as an unpleasant sensory and emotional experience that is associated with actual or potential tissue damage or described in such terms [3]. Because sensory experiences and emotions are always subjective, pain can never be measured directly, even in human patients. Instead, the person’s communication of his or her own pain is used as a proxy measure. Therefore, assessing pain in veterinary patients that cannot express their subjective experiences is especially challenging [4].

The IASP defines nociception as the neural process of encoding noxious stimuli [3]. The term nociception was introduced over 100 years ago by Sherrington to distinguish between detection of a noxious stimulus and the psychological and emotional response to it. This was based on studies of laboratory cats in which the cerebral hemispheres and portions of the thalamus were ablated. In these decerebrate animals, pinching a foot elicited responses including turning the head toward the stimulus, dilation of the pupils, and crying or snarling [5]. De Lahunta reports similar findings in a newborn calf with congenital aplasia of the cerebrum and thalamus. Noxious stimuli applied to the hoof elicited signs of discomfort including turning the head toward the stimulus [6]. Certain regions of the forebrain are thought to be responsible for the conscious perception of pain, including the location of the stimulus, as well as the unpleasant, emotional aspects associated with pain. Because behavioral responses such as vocalization and turning the head toward the noxious stimulus may occur in animals without a functional forebrain, these responses may not indicate conscious pain. Accordingly, some authors suggest that it is most accurate to describe what we assess as “pain” in veterinary patients as nociception [3, 7, 8].

On the other hand, although a nonhuman animal cannot express in words the psychological and emotional consequences of a noxious stimulus, it is imperative to acknowledge that unless it is established to the contrary, we should assume that those procedures that produce pain in us might also produce pain in animals [7]. And veterinary patients with IVDH typically do not have a diffuse, severe forebrain lesion; they are not decerebrate. Therefore, one can argue that using the term “pain” in this circumstance is appropriate. In recognizing both sides of this semantic debate, the authors have made the editorial decision to use the phrase “deep pain” in this chapter when referring to the clinical assessment of veterinary patients because that is the phrase used in most veterinary literature concerning intervertebral disc disease. The term “nociception” is used in accordance with the IASP definition to refer to the unconscious neural process of encoding noxious stimuli. From a clinical perspective, the two terms can be used somewhat interchangeably and synonymously however.

Neuroanatomy

The first step in nociception is activation of receptors that respond to stimuli that are actually or potentially damaging to body tissue. Activation of nociceptors associated with fast-conducting nerve fibers (A-δ fibers) is associated with sharp, pricking pain. Nociceptors associated with slow-conducting fibers (C fibers) are associated with a slower, burning type of pain. Both types of receptors innervate the skin (superficial pain) and deep somatic or visceral structures (deep pain). The distinction between superficial and deep pain is not just based on location. Each is associated with an anatomically and functionally segregated pathway, varies in the susceptibility to damage, and is tested separately in the neurologic examination [9].

Superficial pain is transmitted primarily by the spinothalamic pathway. Axons ascend in the ipsilateral lateral funiculus of the spinal cord to the contralateral thalamus and somatosensory cortex. This pathway is discriminative in that the precise location of the stimulus is perceived [7].

Deep pain is conveyed primarily by the spinoreticular pathway. The primary sensory axons enter the spinal cord and immediately diverge to send collaterals across several spinal cord segments. The ascending pathway is located diffusely in the lateral and ventral funiculi on both sides of the spinal cord. This pathway projects to the cerebral cortex through diffuse projections from the reticular formation in the brain stem and thalamus. Activation of this pathway increases arousal and activates the limbic system, which is involved in the emotional component of pain. Due to the diffuse nature of this pathway, the perception of deep pain is poorly localized [7]. Because this pathway is so diffuse and involves small, unmyelinated fibers which are the least susceptible to damage by compression, deep pain perception is the last function to be lost in spinal cord injury caused by IVDH.

Testing pain perception

Because of the predictable pattern of functional loss associated with spinal cord compression, and the correlation of this pattern with degree of neuronal myelination, it is generally safe to conclude that a patient that retains some voluntary motor function must ipso facto retain nociception. It is therefore unnecessary to test sensation in such a patient, and one should expect preservation of both superficial and deep pain perception.

The superficial pain pathway is tested by lightly and briefly pinching the skin to preferentially activate the superficial pain pathway. Perception of the stimulus is assesses by observing for a response such as turning the head toward the stimulus. If there is no behavioral response to pinching the toes or the tail, start caudally and pinch the skin just lateral to each vertebra to determine if there is a level at which pain is perceived. This may allow more precise localization of the lesion.

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