Neuroendocrine responses following graded traumatic brain injury in male adults

Abstract

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.

Neurosurgical Hyponatremia

“…Hyponatremia was previously thought to be primarily due to SIADH [7,49], with acute ACTH deficiency felt to be a relatively rare entity. However, almost all previous studies relied on assessment of cortisol dynamics at a single time point, providing only a “snapshot” of patients’ pituitary function [50,51,52,53,54,55,56]. Plasma cortisol levels are highly dynamic in the days following TBI [51,52], so protocols with only a single time point for testing may underestimate the true incidence of pituitary dysfunction immediately following TBI.…”

The Pathophysiology of Concussions in Youth

“…As for the subacute period, studies suggest that plasma cortisol levels are dependent on the injury severity. Cortisol tends to increase after mild to moderate brain injury in the early post-injury period, whereas it is depressed after a severe injury [ 82, 83 ]. Although structural pituitary damage may be dependent on the severity of the injury [ 84 ], pituitary abnormalities have been reported in mild to moderate injuries.…”

“…Among these, a retrospective cohort study by Majerske found that high levels of cognitive and physical activity during the early postinjury period had a negative effect on cognitive function and were associated with worsened concussive symptoms and performance on cognitive testing [ 162 ] [Majerske J Athl Training 2008]. The occurrence of negative mood states and cognitive impairments may be associated with neuroendocrine alterations that are found in the early post-TBI weeks, such as elevated plasma cortisol levels [ 83 ].…”

Diffuse traumatic brain injury affects chronic corticosterone function in the rat

“…Injury-induced endocrine dysfunction can be concomitant with and potentially augment clinical symptoms commonly associated with postconcussive syndrome and post-traumatic stress disorder (PTSD) (22, 29). While the prevalence of endocrine dysfunction is reported in the clinical literature, few experimental models have elucidated the persistence and pathological basis of mild-moderate diffuse brain injury-induced endocrine dysfunction (9, 30). …”