Etiology

• Trauma, eg head injury, surgery.

• Skin disease/ear disease.
• Degenerative joint disease.
• Periodontal disease.
• Neoplasia.

Pathophysiology

• Noxious stimulus → transmission of impulses in response, even if animal unconscious.

• Awareness if conscious, not if unconscious/anesthetized.
• Specific receptors for each stimulus/sensation (touch, sight, hearing) → structurally distinct pathways (but pain pathways less distinct), viz. small myelinated A-delta and unmyelinated C fibers, with other pathways co-opted.

• Normal protective transient sensation → localized injury → uses 'pain pathways' (high threshold nociceptors).

• Pain without stimulus, from normally innocuous stimulation (allodynia).
• More widespread injury/inflammatory response.
• No specific receptors - depends on changes in the nervous system induced by the nociceptive activity.

• Disruption of normal selectivity of nervous system.
• Nociception/pain sensation occurring through activity of nerve tracts that normally transmit only mechanical pressure, for example.
• Occurs as a result of physical changes to the nociceptive system and other sensory pathways.
• Nervous system is plastic - not hard-wired.
• Sensitization - same stimulus produces more neuronal activity.

• Decreased threshold in A-delta and C nociceptors.
• Increased sensitivity of sensory receptors.
• Release of chemicals from injury - excite nerve endings and increase sensitivity.
• Release of excitatory chemicals from efferent sympathetic nerve endings.

• Input from C fibers changes response of spinal cord dorsal horn cells.
• Receptor fields expand, dorsal horns respond to other stimuli.
• Increased excitability of dorsal horn cells.
• Sympathetic reflexes affected - drive injured afferents - vicious circle.