Neuroendocrine responses following graded traumatic brain injury in male adults

In an effort to characterize thyroid, gonadal and adrenal function following neurotrauma, the present study determined serum concentrations of thyroid-stimulating hormone (TSH), total triiodothyronine (T3), thyroxine (T4), testosterone and cortisol over a 7 day period in 31 patients with traumatic brain injury. The study group consisted of eight patients with mild closed head injury (Glasgow Coma Scale--GCS 13-15), 10 patients with extensive penetrating head injury (GCS 4-6) and 13 patients with blast injuries but without direct head trauma. The latter group was included in the study because the development of indirect brain trauma has previously been implicated in blast injuries. Patients with multiple injuries were not included. Following mild injury (GCS 13-15), TSH was increased up until day 3 after injury. T3 levels were elevated on days 1, 5 and 7 after injury while T4 remained unchanged throughout. While testosterone was decreased over only the first 2 days post-trauma, cortisol was increased over these first 2 days after injury. In contrast, following severe penetrating injury (GCS 4-6), there were significant declines in TSH, T3 and testosterone over the 7 day observation period post-trauma. Serum cortisol also declined in these patients between 1-3 days after injury, before increasing again on days 5 and 7 after injury. Following indirect neurotrauma, TSH was slightly decreased immediately after trauma but increased to above normal levels on days 5 and 7 post-trauma. Similarly, T3 initially declined after injury, but then increased to above normal levels between 5 and 7 days after injury. T4 and testosterone remained unchanged over the entire post-traumatic period. Serum cortisol was significantly increased after indirect neurotrauma but only up to day 2 post-trauma. In summary, patients with both direct and indirect traumatic brain injury demonstrated endocrine alterations after trauma, the dynamics of which may be a reflection of the severity of brain damage.