Neonatal brachial plexus avulsion injury (BPAI) commonly occurs as a consequence of birth trauma and can result in lifetime morbidity; however, little is known regarding the evolving neuropathological processes it induces. In particular, mechanical forces during BPAI can concomittantly damage the spinal cord and may contribute to outcome. Here, we describe the functional and neuropathological outcome following BPAI, with or without spinal cord injury, in a novel pediatric animal model. Twenty-eight-day-old piglets underwent unilateral C5–C7 BPAI with and without limited myelotomy. Following avulsion, all animals demonstrated right forelimb monoparesis. Injury extending into the spinal cord conferred greater motor deficit, including long tract signs. Consistent with clinical observations, avulsion with myelotomy resulted in more severe neuropathological changes with greater motor neuron death, progressive axonopathy, and persistent glial activation. These data demonstrate neuropathological features of BPAI associated with poor functional outcome. Interestingly, in contrast to adult small animal models of BPAI, a degree of motor neuron survival was observed, even following severe injury in this neonatal model. If this is also the case in human neonatal BPAI, repair may permit functional restoration. This model also provides a clinically relevant platform for exploring the complex postavulsion neuropathological responses that may inform therapeutic strategies.