A clinical and pathophysiological approach to traumatic brain injury-induced pituitary dysfunction

This review aimed to evaluate the data underlying the pathophysiology of TBI-induced hypothalamo-pituitary dysfunction.

Recent literature about the pathophysiology of TBI-induced hypothalamo-pituitary dysfunction reviewed.

Traumatic brain injury (TBI) is a worldwide epidemic that frequently leads to death; TBI survivors tend to sustain cognitive, behavioral, psychological, social, and physical disabilities in the long term. The most common causes of TBI include road accidents, falls, assaults, sports, work and war injuries. From an endocrinological perspective, TBIs are important, because they can cause pituitary dysfunction. Although TBI-induced pituitary dysfunction was first reported a century ago, most of the studies that evaluate this disorder were published after 2000. TBI due to sports and blast injury-related pituitary dysfunction is generally underreported, due to limited recognition of the cases.

The underlying pathophysiology responsible for post-TBI pituitary dysfunction is not clear. The main proposed mechanisms are vascular injury, direct traumatic injury to the pituitary gland, genetic susceptibility, autoimmunity, and transient medication effects.