San Francisco VA Healthcare System, United States of America.
University of California at San Francisco, United States of America; San Francisco VA Healthcare System, United States of America.
Int J Psychophysiol. 2019 Nov;145:91-98. doi: 10.1016/j.ijpsycho.2018.12.015. Epub 2018 Dec 29.
During vocalization, efference copy/corollary discharge mechanisms suppress the auditory cortical response to self-generated sounds as reflected in the N1 component of the auditory event-related potential (ERP). N1 suppression during talking is reduced in patients with schizophrenia. We hypothesized that these deficits would recover with auditory training that targets the speech processing system.
Forty-nine individuals early in the course of a schizophrenia-spectrum illness (ESZ) were randomly assigned to 40 h of Targeted Auditory Training (TAT; n = 23) or Computer Games (CG; n = 26). The N1 ERP component was elicited during production (Talk) and playback (Listen) of vocalization. Effects of Treatment on Global Cognition, N1 suppression (Talk-Listen), N1 during Talking and Listening were assessed. Simple effects of the passage of time were also assessed in the HC after 28 weeks.
There was a Treatment × Time interaction revealing that N1 suppression was improved with TAT, but not with CG. TAT, but not CG, also improved Global Cognition. However, TAT and CG groups differed in their pre-treatment N1 suppression, and greater N1-suppression abnormalities were strongly associated with greater improvement in N1 suppression.
In this sample of ESZ individuals, targeted auditory training appeared to improve the function of the efference copy/corollary discharge mechanism which tended to deteriorate with computer games. It remains to be determined if baseline N1 suppression abnormalities are necessary for TAT treatment to have a positive effect on efference copy/corollary discharge function or if improvements observed in this study represent a regression to the mean N1 suppression in ESZ.
ClinicalTrials.govNCT00694889. Registered 1 August 2007.
在发声过程中，传出/传出放电机制会抑制听觉皮层对自我产生声音的反应，这反映在听觉事件相关电位（ERP）的 N1 成分中。精神分裂症患者在说话时，N1 抑制会降低。我们假设，这些缺陷会随着针对言语处理系统的听觉训练而恢复。
49 名处于精神分裂症谱系疾病早期的个体（ESZ）被随机分配到 40 小时的靶向听觉训练（TAT；n=23）或计算机游戏（CG；n=26）。在发声（说话）和发声回放（听）期间引出 N1 ERP 成分。评估治疗对整体认知、N1 抑制（说话-听）、说话和听时的 N1 的影响。还评估了健康对照组在 28 周后时间推移的简单效应。
存在治疗×时间的交互作用，表明 TAT 可改善 N1 抑制，但 CG 则不能。TAT 可改善整体认知，但 CG 则不能。然而，TAT 和 CG 组在治疗前的 N1 抑制存在差异，并且更大的 N1 抑制异常与 N1 抑制的更大改善密切相关。
在本 ESZ 个体样本中，靶向听觉训练似乎改善了传出/传出放电机制的功能，而这种功能随着计算机游戏而恶化。尚不确定基线 N1 抑制异常是否是 TAT 治疗对传出/传出放电功能产生积极影响的必要条件，或者在这项研究中观察到的改善是否代表 ESZ 中 N1 抑制的回归均值。
ClinicalTrials.govNCT00694889。2007 年 8 月 1 日注册。
