Aim: To elucidate neurohormonal mechanisms underlying the development of higher-order behavioral and cognitive disturbances after traumatic brain injury and to substantiate a pathogenetic approach to their correction using carbacetam. Materials and Methods: We examined neuroendocrine dynamics after closedhead TBI in rats and assessed pathogenetically oriented correction with carbacetam – an endogenous modulator of the Type-A γ-aminobutyric acid (GABA-A)-benzodiazepine receptor complex – compared with deproteinized calf blood hemoderivative (DCBH). One hundred seventy adult male outbred rats were used. Results: TBI caused a 5.4-5.9fold rise in neurological deficit on Day 1 with incomplete spontaneous recovery (still 3.4fold above intact on Day 7). Carbacetam accelerated recovery (57% reduction by Day 7 vs 43% in vehicle; p < 0.05) and improved orienting-exploratory behavior and eightarm maze performance; DCBH improved most behavioral outcomes but was less effective for exploratory activity. Endocrine profiling revealed an acute hyperreactive response (ACTH, corticosterone and vasopressin surges on Day 1) followed by delayed central depletion at Day 14 and persistent suppression of growth hormone (to 48% of intact at Day 30; p < 0.05). Conclusions: Carbacetam attenuated early hyperactivation, prevented delayed depletion and preserved somatotropic signaling, whereas DCBH primarily mitigated the delayed depletion phase. Mortality was 50% in vehicle, 16% with carbacetam and 36% with DCBH (p = 0.002). Immunohistochemistry on Day 7 showed reduced GFAP/S100 and increased NSE under carbacetam, consistent with attenuation of degenerative changes and preservation of neuronal metabolic activity.