Erb's palsy, or brachial plexus birth injury (BPBI), is an injury sustained at birth to a vulnerable nervous system which even with the best care leaves many children with permanent impairments, growth retardation and pain. Established risk factors include maternal diabetes, increased foetal weight, shoulder dystocia and instrumental delivery. Yet these variables do not reliably predict which individual children will sustain injury. We propose an additional, largely neglected factor: developmental anatomical predisposition of the neonatal brachial plexus, with anomalies similar to those implicated in neurogenic thoracic outlet syndrome (nTOS) later in life. These include cervical ribs, aberrant scalene attachments and variant plexus branching - each capable of narrowing the supraclavicular corridor and concentrating mechanical strain during delivery. Such anatomical variants may lower the injury threshold and confer a 'neurologic vulnerability' when exposed to the forces of delivery. This may help explain why some infants sustain injury under normal obstetric conditions while others do not. We further propose that neonatal BPBI and adolescent nTOS represent distinct phenotypic expressions of a shared anatomical vulnerability, with a patterned molecular basis involving Hox gene regulation of axial skeletal patterning during embryogenesis. These insights carry direct clinical implications: in neonates undergoing brachial plexus exploration, recognition and decompression of anatomical compression may complement or replace standard nerve grafting strategies. We outline a research agenda including anatomical phenotyping, familial screening, biomarkers and prospective cohort studies to quantify this predisposition and integrate it into peripartum decision-making alongside conventional risk factors.Level of Evidence: Level V.