Spinal cord injury (SCI) patients develop allodynia and hyperalgesia in body regions distant from the injury site, called “above or below level” pain. Mechanisms underlying above level behavioral changes are unknown. We hypothesize that in a rat model of SCI, dorsal root reflexes (DRRs) are generated in the sensitized cervical cord and the antidromic activity leads to neurogenic inflammation in the forepaws. This could contribute to sensory abnormalities observed above level in SCI patients. We investigate the presence of DRRs and neurogenic inflammation in forelimbs of SCI rats. Following a T10 contusion using an Infinite Horizons impactor, rats demonstrate mechanical allodynia and heat hyperalgesia in the forepaws at 35 days. Using an in vivo DRR recording paradigm, unit recordings were made from proximal stumps of radial nerves. In anesthetized, paralyzed SCI rats, spontaneous DRR activity in C (1±0.21 imp/s, n=70) and A delta (0.47±0.11 imp/s, n=32) fibers was significantly increased compared to control (C = 0.16±0.07 imp/s, n=35; A delta = 0.16±0.1 imp/s, n=20, p<0.01, Mann-Whitney). The percentage of C (68%) and A delta (76%) fibers displaying evoked DRRs increased significantly in SCI rats compared to control (C and A delta = 20%; p<0.05, Chi square test). Intrathecal bicuculline (10uM, GABAA antagonist) blocked evoked DRRs in A delta and C fibers in SCI and control animals. IT bumetanide (10uM, NKCC1 co-transporter inhibitor), also blocked evoked DRRs but a KCC2 co-transporter inhibitor, (DIOA) did not. A consequence of DRRs is the generation of neurogenic inflammation and weekly measurements of forepaw volume using a plethysmometer demonstrated a significant increase in SCI forepaw volume compared to sham (measurements normalized to body weight). This study provides several lines of evidence that following a T10 injury, cervical DRR activity and forepaw neurogenic inflammation could contribute to above level pain in SCI patients.