ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P396

The effects of growth hormone deficiency following moderate and severe traumatic brain injury on cognitive functions

Marko Stojanovic1, Sandra Pekic1, Dragan Pavlovic2, Vladimir Zivkovic1, Branko Djurovic3, Vladimir Jovanovic3, Milica Medic-Stojanoska4, Mirjana Doknic1, Dragana Miljic1, Marina Djurovic1, Carlos Dieguez5, Felipe Casanueva6 & Vera Popovic1

1Institute of Endocrinology, University Clinical Center, Belgrade, Serbia; 2Institute of Neurology, University Clinical Center, Belgrade, Serbia; 3Institute of Neurosurgery, University Clinical Center, Belgrade, Serbia; 4Institute of Endocrinology, University of Novi Sad, Novi Sad, Serbia; 5Department of Physiology, University Santiago de Compostela, Santiago de Compostela, Spain; 6Endocrine Section, Complejo Hospitalario, University Santiago de Compostela, Santiago de Compostela, Spain.

Hypopituitarism, in particular growth hormone (GH) deficiency, is common among survivors of traumatic brain injury (TBI). We investigated neurobehavioral consequences of TBI-induced GH deficiency (GHD) in 61 patients (aged 37.7±1.7 years, 44 male/17 female) at least one year (mean, 3.9±0.6 years) after moderate and severe TBI (mean GCS score 10.6). All patients were tested with standard neuropsychological battery (MMSE, TMT, RAVLT, RCF, BNT and WCST for executive cognitive functions). Serum samples for IGF-I, T4, testosterone (in males), prolactin and cortisol were taken at baseline and the GH/IGF-1 axis was evaluated by GHRH+GHRP-6 test. Three TBI patients with multiple pituitary hormone deficiencies were adequately replaced (except for GH). According to the established peak GH cut-off for normality >20 mcg/l and cut-off for severe GHD <10 mcg/l, TBI patients were divided in two groups: severely GHD (n=9, mean GH peak: 5.4±1.0 mcg/l) and those with normal GH secretory capacity (GHS, n=52, mean GH peak: 34.4±2.5 mcg/l). GHD TBI patients performed on WCST with significantly lower number of achieved WCST categories compared to GHS TBI patients (2.9±0.5 vs 5.1±1.0, P<0.05). Furthermore, GHD TBI patients have performed with more perseverative responses compared to GHS TBI patients (38.1±2.1 vs 31.6±3.9, P<0.05). In other tested cognitive variables there were no significant differences between GHD and GHS TBI patients. A significant inverse correlation was observed between GH peak response to the GHRH+GHRP-6 test and number of perseverative responses on WCST (P=0.05). In conclusion, GHD is a frequent consequence of TBI and can substantially influence executive cognitive functions, as demonstrated by neuropsychological testing.