Pain without nociception?

We describe a young woman with complete cervical spinal cord transsection, who developed significant abdominal pain, triggered by gastric distension and deep abdominal palpation. On the basis of the nature of her spinal cord injury, her brain-gut axis was limited to vagal pathways. Studies in mammalian models of human visceral sensation consistently showed that the subdiaphragmatic vagus contains a homogeneous population of afferents that are activated by low-intensity stimuli, which are generally believed to be important in regulating autonomic function and perhaps contributing to visceral sensory experiences triggered by such low-intensity stimuli (e.g. fullness, nausea), but not pain, although many fibers encode stimuli well into the noxious range. In contrast, spinal afferent pathways include fibers with high-activation thresholds that are thought to represent specialized nociceptors. This illustrative case argues against an exclusive role of specialized nociceptive pathways in visceral pain, but supports a concept of intensity coding with the composite of vagal and spinal input contributing to conscious perception and pain.