{"title":"精神分裂症和双相情感障碍中的必然放电和异常自我体验:特异性分析。","authors":"","doi":"10.1016/j.clinph.2024.07.014","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p>The Corollary Discharge (CD) mechanism inhibits self-generated speech sound perception, appearing disrupted in schizophrenia and potentially contributing to Anomalous Self-Experiences (ASEs). However, it remains unclear if this alteration and its correlation with ASEs extend to other psychotic disorders.</p></div><div><h3>Methods</h3><p>Electroencephalography was used to study the N1 Event-Related Potential (ERP) as an index of CD-mediated suppression in the auditory cortex across thirty-five participants with schizophrenia, twenty-six with bipolar disorder, and thirty healthy controls. Auditory N1 was elicited by two conditions: real-time listening to self-pronounced vowels while speaking through connected microphone and earphones (<em>listen/talk</em> −or <em>talk</em> condition in previous literature-) and passive listening to the same previously recorded self-uttered vowels (<em>listen/no talk</em> −or <em>listen</em> condition-).</p></div><div><h3>Results</h3><p>N1 ERP amplitude was lower in the <em>listen/talk</em> condition compared to <em>listen/no talk</em> across all groups. However, N1 suppression was significantly reduced in schizophrenia, with bipolar patients showing intermediate attenuation between both groups (i.e., non-significantly different from controls). Furthermore, N1 suppression inversely correlated with ASEs severity only in schizophrenia.</p></div><div><h3>Conclusions</h3><p>Dysfunction of the CD mechanism may be a defining feature of schizophrenia, where it is connected to ASEs.</p></div><div><h3>Significance</h3><p>These results corroborate previous findings linking auditory N1 ERP suppression with disrupted CD mechanism in schizophrenia, but not in bipolar disorder.</p></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":null,"pages":null},"PeriodicalIF":3.7000,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1388245724002153/pdfft?md5=83edb2b8ea549e026b707e557be060db&pid=1-s2.0-S1388245724002153-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Corollary discharge and anomalous self-experiences in schizophrenia and bipolar disorder: A specificity analysis\",\"authors\":\"\",\"doi\":\"10.1016/j.clinph.2024.07.014\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><p>The Corollary Discharge (CD) mechanism inhibits self-generated speech sound perception, appearing disrupted in schizophrenia and potentially contributing to Anomalous Self-Experiences (ASEs). However, it remains unclear if this alteration and its correlation with ASEs extend to other psychotic disorders.</p></div><div><h3>Methods</h3><p>Electroencephalography was used to study the N1 Event-Related Potential (ERP) as an index of CD-mediated suppression in the auditory cortex across thirty-five participants with schizophrenia, twenty-six with bipolar disorder, and thirty healthy controls. Auditory N1 was elicited by two conditions: real-time listening to self-pronounced vowels while speaking through connected microphone and earphones (<em>listen/talk</em> −or <em>talk</em> condition in previous literature-) and passive listening to the same previously recorded self-uttered vowels (<em>listen/no talk</em> −or <em>listen</em> condition-).</p></div><div><h3>Results</h3><p>N1 ERP amplitude was lower in the <em>listen/talk</em> condition compared to <em>listen/no talk</em> across all groups. However, N1 suppression was significantly reduced in schizophrenia, with bipolar patients showing intermediate attenuation between both groups (i.e., non-significantly different from controls). Furthermore, N1 suppression inversely correlated with ASEs severity only in schizophrenia.</p></div><div><h3>Conclusions</h3><p>Dysfunction of the CD mechanism may be a defining feature of schizophrenia, where it is connected to ASEs.</p></div><div><h3>Significance</h3><p>These results corroborate previous findings linking auditory N1 ERP suppression with disrupted CD mechanism in schizophrenia, but not in bipolar disorder.</p></div>\",\"PeriodicalId\":10671,\"journal\":{\"name\":\"Clinical Neurophysiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2024-08-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S1388245724002153/pdfft?md5=83edb2b8ea549e026b707e557be060db&pid=1-s2.0-S1388245724002153-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical Neurophysiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1388245724002153\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Neurophysiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1388245724002153","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Corollary discharge and anomalous self-experiences in schizophrenia and bipolar disorder: A specificity analysis
Objective
The Corollary Discharge (CD) mechanism inhibits self-generated speech sound perception, appearing disrupted in schizophrenia and potentially contributing to Anomalous Self-Experiences (ASEs). However, it remains unclear if this alteration and its correlation with ASEs extend to other psychotic disorders.
Methods
Electroencephalography was used to study the N1 Event-Related Potential (ERP) as an index of CD-mediated suppression in the auditory cortex across thirty-five participants with schizophrenia, twenty-six with bipolar disorder, and thirty healthy controls. Auditory N1 was elicited by two conditions: real-time listening to self-pronounced vowels while speaking through connected microphone and earphones (listen/talk −or talk condition in previous literature-) and passive listening to the same previously recorded self-uttered vowels (listen/no talk −or listen condition-).
Results
N1 ERP amplitude was lower in the listen/talk condition compared to listen/no talk across all groups. However, N1 suppression was significantly reduced in schizophrenia, with bipolar patients showing intermediate attenuation between both groups (i.e., non-significantly different from controls). Furthermore, N1 suppression inversely correlated with ASEs severity only in schizophrenia.
Conclusions
Dysfunction of the CD mechanism may be a defining feature of schizophrenia, where it is connected to ASEs.
Significance
These results corroborate previous findings linking auditory N1 ERP suppression with disrupted CD mechanism in schizophrenia, but not in bipolar disorder.
期刊介绍:
As of January 1999, The journal Electroencephalography and Clinical Neurophysiology, and its two sections Electromyography and Motor Control and Evoked Potentials have amalgamated to become this journal - Clinical Neurophysiology.
Clinical Neurophysiology is the official journal of the International Federation of Clinical Neurophysiology, the Brazilian Society of Clinical Neurophysiology, the Czech Society of Clinical Neurophysiology, the Italian Clinical Neurophysiology Society and the International Society of Intraoperative Neurophysiology.The journal is dedicated to fostering research and disseminating information on all aspects of both normal and abnormal functioning of the nervous system. The key aim of the publication is to disseminate scholarly reports on the pathophysiology underlying diseases of the central and peripheral nervous system of human patients. Clinical trials that use neurophysiological measures to document change are encouraged, as are manuscripts reporting data on integrated neuroimaging of central nervous function including, but not limited to, functional MRI, MEG, EEG, PET and other neuroimaging modalities.