It has been suspected for almost a century that traumatic brain injury (TBI) can produce pituitary dysfunction, but only over the recent years/last decade have we completed prospective studies that document hypothalamic-pituitary axis damage occurs after TBI. An important aspect of TBI-induced hypopituitarism is the potential impact on brain recovery. For those who survive a TBI, the clinical manifestations vary depending on the type, site, and severity of the injury, including direct or indirect injury to the hypothalamus and pituitary. The probability of developing hypopituitarism has been based on the severity of the TBI,1,14 especially when associated with cranial fractures, cerebral damage, and a prolonged period of loss of consciousness (LOC). The most widely used clinical classification of TBI severity is the Glasgow Coma Scale (GCS). Other factors that define clinical severity of TBI include duration of LOC, posttraumatic amnesia, and intracranial lesion(s) on imaging studies. Endocrine evaluation should, therefore, be considered in spite of the absence of diabetes insipidus.