Institute of Neurology, University Clinical Center, Belgrade, Serbia.
Eur J Neurol. 2010 May;17(5):696-702. doi: 10.1111/j.1468-1331.2009.02910.x. Epub 2009 Dec 30.
The objective of the study was to asses the possible influence of hypothalamo-pituitary deficiencies, and growth hormone (GH) deficiency in particular, on cognition in adult patients with traumatic brain injury (TBI). TBI is a recently identified risk factor for cognitive deficits and hypopituitarism. Even the patients with favorable outcome after TBI may present with persistent bodily, psychosocial, and cognitive impairments, resembling patients with untreated partial or complete pituitary insufficiency.
We performed retrospective and cross-sectional study of endocrine and cognitive function in TBI in 61 patients (aged 37.7 +/- 1.7 years) of both sexes (44 m,17 f), at least 1 year after TBI (3.9 +/- 0.6 years). Serum insulin-like growth factor 1 (IGF-I), thyroxin, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (in men), prolactin, and cortisol were measured, and GH secretion was assessed by growth hormone releasing hormone (GHRH) + growth hormone releasing peptide-6 (GHRP-6) test. Cognitive function was assessed by using a standard neuropsychological battery.
GH deficiency (GHD) and GH insufficiency (GHI) were found in 20 patients (32.8%). After adjustment for confounders [age, body mass index (BMI), education level, time elapsed from TBI], there were no significant differences in results of neuropsychological tests between patients with TBI with GHD, GHI, and normal GH secretion. There were no correlations of neuropsychological variables with stimulated peak GH secretion or IGF-I level.
GHD persists long after the TBI, independently of trauma severity and age at traumatic event. GH secretion is more sensitive to TBI than other pituitary hormones. No evidence is found for an association of cognitive function impairment and somatotropic axis impairment in adult patients tested more than 1 year after the TBI.
本研究旨在评估下丘脑-垂体功能减退，尤其是生长激素（GH）缺乏，对创伤性脑损伤（TBI）成年患者认知功能的可能影响。TBI 是认知功能障碍和垂体功能减退的新近确定的危险因素。即使 TBI 后预后良好的患者也可能存在持续的身体、心理社会和认知障碍，类似于未经治疗的部分或完全垂体功能不足的患者。
我们对 61 例（男 44 例，女 17 例；年龄 37.7 ± 1.7 岁）TBI 患者进行了内分泌和认知功能的回顾性和横断面研究，这些患者在 TBI 后至少 1 年（3.9 ± 0.6 年）进行了研究。测量了血清胰岛素样生长因子 1（IGF-1）、甲状腺素、促甲状腺激素（TSH）、卵泡刺激素（FSH）、黄体生成素（LH）、睾酮（男性）、催乳素和皮质醇，并通过生长激素释放激素（GHRH）+生长激素释放肽-6（GHRP-6）试验评估 GH 分泌情况。使用标准神经心理学成套测验评估认知功能。
发现 20 例（32.8%）患者存在 GH 缺乏（GHD）和 GH 不足（GHI）。在调整混杂因素[年龄、体重指数（BMI）、教育程度、TBI 后时间]后，GHD、GHI 和正常 GH 分泌的 TBI 患者神经心理学测试结果无显著差异。神经心理学变量与刺激后 GH 分泌峰值或 IGF-1 水平无相关性。
GHD 在 TBI 后长期存在，与创伤严重程度和创伤发生时的年龄无关。GH 分泌对 TBI 比其他垂体激素更敏感。在 TBI 后 1 年以上进行测试的成年患者中，未发现认知功能障碍与生长激素轴损害之间存在关联的证据。
