Pain associated with intervertebral disk disease
Animals with acute intervertebral disk extrusion are almost always painful. The spinal cord itself does not possess pain
receptors. Pain associated with intervertebral disk degeneration has been shown to be secondary to both biochemical mediators
and nervous tissue impingement. The ligaments, joint capsule and bone of the spinal column are highly innervated The external periosteum, articular facet joint capsule and longitudinal ligaments receive sensory innervation by way of the
medial branches of the dorsal rami of the spinal nerves. These rami form the recurrent sinuvertebral nerve. The dorsal longitudinal
ligament and the ventral meningeal surface is highly innervated by complex encapsulated nerve endings and as well as poorly
myelinated free nerve endings. These fibers also innervate the outer lamellae of the dorsal annulus fibrosus and direct stimulation
of the intervertebral disk has been shown to induce pain. While the innervation to these structures are diverse and include postganglionic efferent fibers from the thoracolumbar autonomic
ganglia (which mediate smooth muscle function of the vasculature of the spinal canal) and proprioceptive fibers (which modulate
postural reactions), the majority of these fibers are nociceptive in function. In fact, it has been shown experimentally,
that stimulation of tissues innervated by the sinuvertebral nerve elicits back pain. In the clinical setting, mechanical
impingement of the nerve roots (radiculopathy) and meninges by extruded disk material and hypertrophy of supporting structures
plays a role in generation of pain.
Disruption of the intervertebral disk and its ligaments and compression of nervous tissue leads to production of neuropeptides
and other algesic molecules can activate nociceptors in the dorsal longitudinal ligament and dorsal annulus. The somata of the dorsal root ganglia make various algesic neuropeptides transported to central and peripheral terminals. Neurogenically-derived cytokines implicated include substance P and calcitonin gene-related protein (CRGP). Substance P has
been shown be a part of the inflammatory cascade and generation of pain in radiculopathy. CGRP found in primary sensory neurons
has been shown to mediate nociception and mechanoreception. Non-neurogenic-derived chemicals released during tissue damage
(e.g. bradykinin, serotonin, histamine, and Pgs) also sensitize pain fibers. Extruded intervertebral disk material itself
has been implicated as a source of biochemical mediators in the pathophysiology of radicular pain. In an in vitro study of human herniated disk material removed during decompressive surgery, nitric oxide, prostaglandin E2a, and interleukin 6 concentrations were elevated compared to nonherniated control disks from patients undergoing spinal surgery
for other reasons (e.g. scoliosis correction). Nitric oxide is a novel mediator of inflammation and immune regulation. This
biochemical has been shown to have both proinflammatory and anti-inflammatory functions. As a proinflammatory agent, it exerts
strong vasodilatory effects promoting vascular leakiness resulting in edema. As an anti-inflammatory agent, it has been shown
to inhibit production of IL-6, PgE2, and thromboxane. The exact function of nitric oxide in the disk and disk degeneration is not known at this time, however.
Pain associated with spinal cord compression/injury
Pain that originates from the spinal cord or nervous tissue (also referred to as central pain syndrome) is reported primarily
in human patients following severe spinal cord injury. Following initial injury, the patient usually manifests acute pain
which is the result of spinal column and adjacent soft tissue injury. Pain associated with spinal cord injury tends to occur
months to years after the initial injury and is difficult to manage and treat. This type of pain should be considered a disease
in and of itself, rather than a clinical manifestation of some other problem. The incidence is reported between 10-90% of
all spinal cord injured patients and is often more of a concern to the patient than the residual functional disabilities.
What is interesting is that this is not commonly recognized phenomenon in veterinary patients that are managed long-term following
spinal cord injury but is reported in rodent models of spinal cord injury.