Traumatic brain injury (TBI) is not a singular event with finite boundaries, but a complex and evolving pathology. While the initial mechanical insult may be fleeting, its consequences can ripple across physiological systems for months or years. One of the most underappreciated yet clinically significant consequences is the disruption of the hypothalamic-pituitary axis (HPA). Neuroendocrine dysfunction after TBI can present in various forms-some subtle, others life-altering-affecting metabolic regulation, sexual health, psychological wellbeing, and rehabilitation potential. This review explores the pathophysiology and clinical implications of HPA dysfunction in TBI, highlighting current gaps in diagnosis and proposing an approach that recognises the chronic nature of these sequelae.