Purpose Reports on long-term variations in pituitary function after traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH) diverge. The aim of the current study was to evaluate the prevalence and changes in pituitary function during the first year after moderate and severe TBI and SAH and to explore the relation between pituitary function and injury variables.MethodsAdults with moderate and severe TBI or SAH were evaluated at 10 days, 3, 6 and 12 months post-injury/illness. Demographic, clinical, radiological, laboratory, including hormonal data were collected.ResultsA total of 91 adults, 56 (15 women/41 men) with TBI and 35 (27 women/8 men) with SAH were included. Perturbations in pituitary function were frequent early after the event but declined during the first year of follow-up. The most frequent deficiency was hypogonadotrope hypogonadism which was seen in approximately 25 % of the patients. Most of the variations were transient and without clinical significance. At 12 months, two patients were on replacement with hydrocortisone, four men on testosterone and one man on replacement with growth hormone. No relations were seen between hormonal levels and injury variables.ConclusionsPerturbations in pituitary function continue to occur during the first year after TBI and SAH, but only a few patients need replacement therapy. Our study could not identify a marker of increased risk of pituitary dysfunction that could guide routine screening. However, data demonstrate the need for systematic follow-up of pituitary function after moderate or severe TBI or SAH.

Background: Pituitary insufficiencies after traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH) have been reported with very varying frequencies. The aim of this study was to describe the pituitary function in the acute phase after TBI and SAH in a cohort of adults and relate the results to injury variables. Methods: Adults admitted to the neurointensive care unit in our hospital after moderate and severe TBI or SAH were included prospectively. Demographic, clinical, laboratory, including ACTH stimulation test, and radiological data were collected. Results: A total of 130 adults, 84 (19 women/65 men) with TBI and 46 (38 women/8 men) with SAH were included. Nine patients with TBI and six patients with SAH responded insufficiently to ACTH stimulation; 14 patients with TBI and 9 patients with SAH had low fT4 and low-normal TSH levels. No relations were seen between hormonal levels and injury variables. Conclusions: Pituitary deficiencies occur after TBI and SAH, and a continuous endocrine evaluation of these patients is important. Our study could not define a marker for increased risk for pituitary deficiency. The long-term clinical outcome of the pathological hormone levels in the early phase after TBI and SAH is not known in detail and further studies to elucidate this are needed.

Cognitive improvements after SAH and TBI exhibit similarities and correlate with global function. GCS scores are associated with outcome after TBI but not after SAH.

A quality registry presents an opportunity to improve rehabilitation processes at participating units, provides data for use in benchmarking between units, and enables hospital management to utilize resources wisely.

Traumatic brain injury and aneurysmal subarachnoid haemorrhage are leading causes of physical, cognitive and behavioural disabilities. Traumatic brain injury and aneurysmal subarachnoid haemorrhage may affect the hypothalamus and pituitary gland, which are of major importance for our hormone balance. The purpose of the study was to investigate the relationship between the pituitary dysfunction after traumatic brain injury and aneurysmal aneurysmal subarachnoid haemorrhage, and cognitive and global outcomes at 12 months after the injury. In total, we included 127 patients during neurointensive care. Follow-up was at a rehabilitation medicine department. The study showed negative associations between high level of growth hormone and prolactin and behavioural and cognitive function; and between low gonadotropins and high prolactin and global outcome. We conclude that some pituitary dysfunctions during the first year after traumatic brain injury and aneurysmal subarachnoid haemorrhage may have clinically relevant, independent effects on clinical outcome at 12 months. Objective: To explore associations between pituitary dysfunction and clinical outcome at 12 months after traumatic brain injury and aneurysmal subarachnoid haemorrhage. Methods: Prospective cohort study of 82 patients with traumatic brain injury and 45 with aneurysmal subarachnoid haemorrhage, included at one neurointensive care unit. Baseline data comprised age, sex, Glasgow Coma Scale (GCS) score, S100B and pupil light reactions. Hormone data were collected in the neurointensive care unit and after 3, 6 and 12 months. Outcome was assessed with Barrow Neurological Institute Screen for Higher Cerebral Functions (BNIS), Rancho Los Amigos Cognitive Scale-Revised (RLAS-R) and Glasgow Outcome Scale Extended (GOSE). Results: The most frequent hormonal deviations were hypogonadotropic hypogonadism (38%) and hypercortisolism (52%). At 12 months, performance on BNIS was impaired in 54% and GOSE in 37%. Controlling for baseline variables, low levels of gonadal hormones were associated with lower GOSE score (b =-0.80, p = 0.033), high levels of prolactin with lower RLAS (b =-1.42, p = 0.034) and high levels of serum insulin-like growth factor I (S-IGF-I) with lower RLAS level (b =-1.78, p = 0.002) and lower GOSE score (b =-1.49, p = 0.006). Conclusion: These data suggest that pituitary dysfunctions during the first year after traumatic brain injury and aneurysmal subarachnoid haemorrhage may have clinically relevant, independent effects on clinical outcome at 12 months.