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Event-related brain potentials in male hypogonadism.

机译:男性性腺功能减退症中与事件相关的脑电位。

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摘要

Several studies based on psychometric tests have determined an impairment of cognitive functions in patients with androgen deficiency. However, little is known about event-related potentials (ERPs) alterations in male hypogonadism. We investigated alterations of ERP in male hypogonadism before and 3 months after gonadotropin treatment. ERPs were elicited in 20 untreated male patients with idiopathic hypogonadotropic hypogonadism (IHH) (mean age: 21.1+/-1.4 years) and in a group of 30 male controls with comparable mean age and educational level. ERP recordings were repeated 3 months after hCG/hMG treatment. Untreated hypogonadal patients had longer mean P300 latencies and increased P300 amplitudes when compared to those in controls (321.6+/-18.5 vs 299.3+/-20.1 msec, p=0.0002; 12.15+/-4.47 vs 9.38+/-3.02 microV, p=0.011, respectively). The mean P300 latencies did not change significantly 3 months after gonadotropin treatment, while P300 amplitudes were decreased significantly. P300 latencies did not correlate with serum testosterone and other hormone levels. We conclude that prolongation of P300 latencies and increased P300 amplitudes are associated with male hypogonadism, but P300 prolongation is not reversed 3 months after gonadotropin treatment. These findings confirm the occurrence of cognitive defects in hypogonadal patients and would support the hypothesis that perinatal androgen deficiency contributes to an insufficient cognitive development.
机译:几项基于心理测试的研究已经确定了雄激素缺乏症患者的认知功能受损。然而,人们对男性性腺功能减退症中事件相关电位 (ERP) 的改变知之甚少。我们研究了促性腺激素治疗前和治疗后 3 个月男性性腺功能减退症中 ERP 的改变。在 20 例未经治疗的特发性低促性腺激素性性腺功能减退症 (IHH) 男性患者(平均年龄:21.1+/-1.4 岁)和一组 30 例平均年龄和教育水平相当的男性对照组中引发了 ERP。hCG/hMG 治疗后 3 个月重复 ERP 记录。与对照组相比,未经治疗的性腺功能减退患者的平均 P300 潜伏期更长,P300 振幅增加(分别为 321.6+/-18.5 vs 299.3+/-20.1 毫秒,p=0.0002;12.15+/-4.47 vs 9.38+/-3.02 μV,p=0.011)。促性腺激素治疗后 3 个月,平均 P300 潜伏期无明显变化,而 P300 振幅显着降低。P300潜伏期与血清睾酮和其他激素水平无关。我们得出结论,P300潜伏期的延长和P300振幅的增加与男性性腺功能减退有关,但促性腺激素治疗后3个月P300的延长并未逆转。这些发现证实了性腺功能减退患者认知缺陷的发生,并将支持围产期雄激素缺乏导致认知发育不足的假设。

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