Psychiatry Department, School of Medicine, University of Valladolid, Valladolid, Spain.
Psychiatry Service, University Clinical Hospital of Valladolid, Valladolid, Spain.
Schizophr Bull. 2024 Aug 27;50(5):1137-1146. doi: 10.1093/schbul/sbad157.
Corollary discharge mechanism suppresses the conscious auditory sensory perception of self-generated speech and attenuates electrophysiological markers such as the auditory N1 Event-Related Potential (ERP) during Electroencephalographic (EEG) recordings. This phenomenon contributes to self-identification and seems to be altered in people with schizophrenia. Therefore, its alteration could be related to the anomalous self-experiences (ASEs) frequently found in these patients.
To analyze corollary discharge dysfunction as a possible substrate of ASEs, we recorded EEG ERP from 43 participants with schizophrenia and 43 healthy controls and scored ASEs with the 'Inventory of Psychotic-Like Anomalous Self-Experiences' (IPASE). Positive and negative symptoms were also scored with the 'Positive and Negative Syndrome Scale for Schizophrenia' (PANSS) and with the 'Brief Negative Symptom Scale' (BNSS) respectively. The N1 components were elicited by two task conditions: (1) concurrent listening to self-pronounced vowels (talk condition) and (2) subsequent non-concurrent listening to the same previously self-uttered vowels (listen condition).
The amplitude of the N1 component elicited by the talk condition was lower compared to the listen condition in people with schizophrenia and healthy controls. However, the difference in N1 amplitude between both conditions was significantly higher in controls than in schizophrenia patients. The values of these differences in patients correlated significantly and negatively with the IPASE, PANSS, and BNSS scores.
These results corroborate previous data relating auditory N1 ERP amplitude with altered corollary discharge mechanisms in schizophrenia and support corollary discharge dysfunction as a possible underpinning of ASEs in this illness.
旁流放电机制抑制了自我产生的言语的有意识听觉感知,并削弱了脑电图(EEG)记录期间的听觉 N1 事件相关电位(ERP)等电生理标记。这种现象有助于自我识别,并且似乎在精神分裂症患者中发生了改变。因此,其改变可能与这些患者中经常发现的异常自我体验(ASE)有关。
为了分析旁流放电功能障碍作为 ASE 的可能基础,我们从 43 名精神分裂症患者和 43 名健康对照者中记录了 EEG ERP,并使用“精神病样异常自我体验清单”(IPASE)对 ASE 进行了评分。阳性和阴性症状也分别使用“精神分裂症阳性和阴性症状量表”(PANSS)和“简短阴性症状量表”(BNSS)进行了评分。通过两种任务条件诱发 N1 成分:(1)同时聆听自我发音的元音(说话条件)和(2)随后非同时聆听先前自我发出的相同元音(聆听条件)。
与健康对照组相比,精神分裂症患者在说话条件下诱发的 N1 成分的振幅较低。但是,在两种条件下 N1 振幅的差异在对照组中明显高于精神分裂症患者。患者中这些差异的值与 IPASE、PANSS 和 BNSS 评分显著负相关。
这些结果证实了先前的数据,即听觉 N1 ERP 振幅与精神分裂症中改变的旁流放电机制有关,并支持旁流放电功能障碍作为该疾病中 ASE 的可能基础。