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在精神病风险综合征和早期精神分裂症患者的发声过程中,听觉预测编码不足:最终扩展样本。

Deficient auditory predictive coding during vocalization in the psychosis risk syndrome and in early illness schizophrenia: the final expanded sample.

机构信息

University of California, San Francisco (UCSF), San Francisco, CA,USA.

California School of Professional Psychology (CSPP), Alliant International University, San Diego, CA,USA.

出版信息

Psychol Med. 2019 Aug;49(11):1897-1904. doi: 10.1017/S0033291718002659. Epub 2018 Sep 25.

Abstract

BACKGROUND

During vocalization, efference copy/corollary discharge mechanisms suppress the auditory cortical response to self-generated sounds. Previously, we found attenuated vocalization-related auditory cortical suppression in psychosis and a similar trend in the psychosis risk syndrome. Here, we report data from the final sample of early illness schizophrenia patients (ESZ), individuals at clinical high risk for psychosis (CHR), and healthy controls (HC).

METHODS

Event-related potentials (ERP) were recorded from ESZ (n = 84), CHR (n = 71), and HC (n = 103) participants during a vocalization paradigm. The N1 ERP component was elicited during production (Talk) and playback (Listen) of vocalization. Age effects on N1 suppression (Talk-Listen), Talk N1, and Listen N1 were compared across groups. N1 measures were adjusted for normal aging before testing for group differences.

RESULTS

Both ESZ and CHR groups showed reduced Talk-Listen N1 suppression relative to HC, but did not differ from each other. Listen N1 was reduced in ESZ, but not in CHR, relative to HC. Deficient Talk-Listen N1 suppression was associated with greater unusual thought content in CHR individuals. N1 suppression increased with age in HC (12-36 years), and while CHR individuals showed a similar age-related increase, no such relationship was evident in ESZ.

CONCLUSIONS

Putative efference copy/corollary discharge-mediated auditory cortical suppression during vocalization is deficient in ESZ and precedes psychosis onset, particularly in CHR individuals with greater unusual thought content. Furthermore, this suppression increases from adolescence through early adulthood, likely reflecting the effects of normal brain maturation. This maturation effect is disrupted in ESZ, presumably due to countervailing illness effects.

摘要

背景

在发声过程中,传出副本/推论放电机制抑制了听觉皮质对自我产生声音的反应。此前,我们发现精神病患者的发声相关听觉皮质抑制减弱,精神病风险综合征也存在类似趋势。在这里,我们报告了早期精神病患者(ESZ)、精神病高危个体(CHR)和健康对照组(HC)的最终样本数据。

方法

在发声范式中,从 ESZ(n = 84)、CHR(n = 71)和 HC(n = 103)参与者中记录事件相关电位(ERP)。在发声产生(Talk)和播放(Listen)期间诱发 N1 ERP 成分。比较各组之间 N1 抑制(Talk-Listen)、Talk N1 和 Listen N1 的年龄效应。在测试组间差异之前,对 N1 测量值进行了正常老化调整。

结果

ESZ 和 CHR 组的 Talk-Listen N1 抑制均低于 HC,但彼此之间没有差异。与 HC 相比,ESZ 的 Listen N1 减少,但 CHR 则没有。CHR 个体的异常思维内容与 Talk-Listen N1 抑制不足有关。HC 中 N1 抑制随年龄增加(12-36 岁),而 CHR 个体也表现出类似的年龄相关增加,但在 ESZ 中则没有。

结论

发声时传出副本/推论放电介导的听觉皮质抑制在 ESZ 中不足,且在精神病发病前出现,特别是在异常思维内容较多的 CHR 个体中。此外,这种抑制从青春期到成年早期增加,可能反映了正常大脑成熟的影响。ESZ 中这种成熟效应被破坏,可能是由于疾病的拮抗作用。

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