The most prevalent comorbidity of cerebral palsy (CP) is pain. In order to investigate the relationship between perinatal injuries that cause CP and nociception, we investigated mechanical and thermal sensitivity of New Zealand White rabbit kits after prenatal hypoxia-ischemia (HI), sham surgery without hypoxia, and after a typical, unperturbed gestation. A range of motor deficits were observed in kits born naturally after HI (40 minutes at 70-80% gestation) as previously described. We found that HI caused mechanical and thermal allodynia at postnatal day 5, which was accompanied by an expansion of peptidergic afferents (marked by expression of calcitonin gene related peptide; CGRP) in both the superficial and deep dorsal horn. Non-peptidergic afferents (marked by expression of isolectin B4; IB4) were unaltered in HI kits but overlap of the two populations (peptidergic and nonpeptidergic nociceptors) was increased by HI. Interestingly, HI-subjected rabbits exhibited allodynia, even in the absence of motor deficits. HI motor affected and unaffected kits had similar thermal sensitivity but affected kits had less mechanical sensitivity than HI unaffected kits. These findings suggest that prenatal neural injuries impact sensory and motor networks independently and that developing sensory circuits may be more vulnerable than motor circuits to perturbation by prenatal hypoxic-ischemic injury. In conclusion, pain experienced by individuals with CP could arise from developmental insults capable of causing the condition, and therapeutics that specifically target altered nociception in these individuals could be beneficial for treating and preventing chronic pain.