The Biology of Brachial Plexus Birth Injuries

The provider caring for the child with brachial plexus birth injury (BPBI) must be familiar with both the normal neonatal neuromuscular system and the biological perturbations caused by BPBI. In the normal nervous system, synaptogenesis and myelination occur postnatally in an activity-dependent manner. Neonatal peripheral nerve pathways have redundancy that is pruned during infancy but can be maintained following BPBI, producing atypical motor patterns that confound patient assessment. Primitive reflexes can assist in neurologic evaluation following BPBI and can be a clue to neuropathology when abnormal. Neonates have delayed Wallerian degeneration of axons compared to adults but worse motor and sensory neuron cell death in the spinal cord and dorsal root ganglia following peripheral axotomy. Following BPBI, the brain increases activation and connectivity of multiple cortical regions, highlighting the importance of brain remodeling. Contractures following BPBI, once thought to be a purely mechanical consequence of altered limb mobility, have been recently proven to result from a denervation-induced increase in muscle protein degradation that impairs postnatal longitudinal muscle growth. Finally, bone homeostasis depends on signaling from sensory and sympathetic neurons, although the role of bone neuroregulation in the glenohumeral dysplasia and limb length discrepancy caused by BPBI is unknown.