Autonomic dysreflexia is a potentially life-threatening hypertensive syndrome following high thoracic (T) spinal cord injury (SCI). It is commonly triggered by noxious pelvic stimuli below the injury site that correlates with increased sprouting of primary afferent C-fibers into the lumbosacral (L/S) spinal cord. We have recently demonstrated that injury-induced plasticity of (L/S) propriospinal neurons, which relay pelvic visceral sensations to thoracolumbar sympathetic preganglionic neurons, is also correlated with the development of this syndrome. To determine the phenotype of pelvic afferent fiber sprouts after SCI, cholera toxin subunit beta (CTb) was injected into the distal colon 2 weeks post-T4 transection/sham to label colonic visceral afferents. After 1 week of transport, the (L/S) spinal cords were cryosectioned and immunohistochemically stained for CTb, the nociceptive-specific marker calcitonin gene-related peptide (CGRP), and the myelinated fiber marker RT97. Quantitative analysis showed that the density of CGRP(+) afferent fibers was significantly increased in the L/S dorsal horns of T4-transected versus sham rats, whereas RT97(+) afferent fiber density showed no change. Importantly, CTb-labeled pelvic afferent fibers were co-localized with CGRP(+) fibers, but not with RT97(+) fibers. These results suggest that the sprouting of unmyelinated nociceptive pelvic afferents following high thoracic SCI, but not myelinated fibers, contributes to hypertensive autonomic dysreflexia induced by pelvic visceral pain.