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Decreased resting gamma activity in adult attention deficit/hyperactivity disorder

机译:在成人注意力/多动障碍中减少静息γ活性

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摘要

Objectives: To delineate task-free gamma activity in adult ADHD and healthy control subjects based on high-density EEG recordings. Relationship of gamma activity with symptom severity was also examined, since gamma activity is considered to be an index of network functions in the brain that underlie higher-order cognitive processes. Methods: Spontaneous EEG was recorded in adult ADHD subjects (N = 42; 25 methylphenidate-naive and 17 on methylphenidate treatment) and controls (N = 59) with eyes open. EEG absolute power gamma was investigated in the gamma(1) (30.25-39 Hz) and gamma(2) (39.25-48 Hz) frequency bands. Results: Gamma(1) and gamma(2) activity was diminished in ADHD compared with healthy control subjects. The difference between ADHD and controls was the most pronounced in the right centroparietal region for both gamma(1) and gamma(2). Inverse associations were found between gamma(1) and gamma(2) activity and ADHD symptoms in centroparietal scalp regions. Conclusions: Gamma activity is reduced in adult ADHD, and the reduction has a predominantly right centroparietal distribution. Our findings are consistent with childhood ADHD literature with respect to diminished posterior gamma activity in patients, which may reflect altered dorsal attention network functions. Gamma abnormalities might provide a link between neurophysiological functioning and neuropsychological deficiencies, thereby offering an opportunity to investigate the neurobiological mechanisms that underlie the clinical symptoms of ADHD.
机译:目标:根据高密度EEG录音,描绘成人ADHD和健康控制主题的无任务伽玛活动。还研究了γ活性与症状严重程度的关系,因为伽玛活动被认为是大脑中的网络功能指标,使得高阶认知过程下降。方法:在成人ADHD受试者中记录自发性脑电图(n = 42; 25甲基苯甲酸盐 - 幼稚和17甲基苯胺处理),并用眼睛对照(n = 59)。在γ(1)(30.25-39Hz)和γ(2)(39.25-48Hz)频带中研究了EEG绝对功率γ。结果:与健康对照对象相比,ADHD中γ(1)和γ(2)活性降低。 ADHD和对照之间的差异是γ(1)和伽马(2)的右心观区域中最明显的。在γ(1)和γ(2)活性与中心马头皮地区的γ症状和ADHD症状之间发现反相。结论:成人ADHD中γ活性降低,减少具有主要的右心观分布。我们的研究结果与儿童时期的ADHD文献一致,在患者中减少后γ活性减少,这可能反映了越来越多的背部注意力网络功能。 γ异常可能提供神经生理功能和神经心理学缺陷之间的联系,从而提供了探讨基于ADHD的临床症状的神经生物学机制的机会。

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