Effects of olanzapine on auditory P300 and mismatch negativity (MMN) in schizophrenia spectrum disorders

Korostenskaja, Milena; Dapšys, Kastytis; Šiurkutė, Aldona; Mačiulis, Valentinas; Rukšėnas, Osvaldas; Kähkönen, Seppo

doi:10.1016/j.pnpbp.2005.01.019

Cited by 66 publications

(34 citation statements)

References 37 publications

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“…However, glycine, which augments the NMDA receptor function by stimulating the glycine modulatory site of the NMDA receptor, attenuated the duration-MMN amplitude in normal subjects (Leung et al, 2008). Further, antipsychotics such as clozapine (Schall et al, 1998;Umbricht at al., 1998), risperidone (Umbricht et al, 1999), and olanzapine (Korostenskaja et al, 2005) did not enhance MMN amplitude in schizophrenia patients. However, very recently, a 6-wk administration of N-acetyl-cysteine, a glutathione precursor that can potentiate the activity of NMDA receptors, increased the MMN amplitude for frequency change in schizophrenia patients (Lavoie et al, 2007).…”

Section: Mmn In Separating First-episode and Chronic Patientsmentioning

confidence: 76%

“…As previously mentioned, medication did not abolish MMN abnormality in schizophrenia patients (Catts et al, 1995;Kasai et al, 2002c ;Kawakubo et al, 2006;Korostenskaja et al, 2005;Umbricht et al, 1998Umbricht et al, , 1999. Furthermore, this abnormality was present irrespective of the inter-stimulus interval (ISI), the deviant-stimulus probability, and the magnitude of stimulus change .…”

Section: Mmn Amplitude Reduction In Schizophreniamentioning

confidence: 84%

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Central auditory dysfunction in schizophrenia as revealed by the mismatch negativity (MMN) and its magnetic equivalent MMNm: a review

Näätänen

Kähkönen

2008

Int. J. Neuropsychopharm.

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215

137

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Since the early 1990s, the auditory change-detection response, mismatch negativity (MMN) and its magnetoencephalographic (MEG) equivalent MMNm have been applied in a large number of studies on schizophrenia. These studies have enhanced our understanding of the central auditory dysfunction underlying schizophrenia. The attenuation of the MMN amplitude is a systematic and robust neurophysiological finding in these patients. The gradual attenuation of the MMN amplitude resulting from frequency change reflects the progress of the disease, particularly the impairment occurring as a function of illness duration, whereas the MMN deficiency for duration change may be more closely linked to the genetic aspect of the illness. Electroencephalographic (EEG) and magnetoencephalographic (MEG) studies, together, suggest that both the temporal and frontal cortices contributing to MMN generation are affected in schizophrenia patients. Furthermore, abnormalities in auditory perception and discrimination revealed by a deficient temporal MMN generator process might be associated with patients' positive symptoms, whereas the dampened frontal attention-switching function, suggested by the attenuated responses of the frontal MMN generator, might contribute to the negative symptoms such as social withdrawal. In addition, gradual MMN amplitude reduction, in particular that for frequency change, reflects cognitive and functional impairment occurring as a function of illness duration. Finally, as MMN can be detected even in animals such as the mouse, it might provide a useful biomarker for assessing the effects of the drugs developed to fight the cognitive and functional impairments in schizophrenia patients.

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Section: Mmn In Separating First-episode and Chronic Patientsmentioning

confidence: 76%

Section: Mmn Amplitude Reduction In Schizophreniamentioning

confidence: 84%

Central auditory dysfunction in schizophrenia as revealed by the mismatch negativity (MMN) and its magnetic equivalent MMNm: a review

Näätänen

Kähkönen

2008

Int. J. Neuropsychopharm.

Self Cite

215

137

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“…Whereas antipsychotics have not been shown to affect the neurophysiological components investigated in the present study, less is known about the effects of mood stabilizers and antidepressants. [49][50][51][52][53] …”

Section: Limitationsmentioning

confidence: 99%

Neurophysiological biomarkers support bipolar-spectrum disorders within psychosis cluster

Kaur

Battisti

Lagopoulos

et al. 2012

J Psychiatry Neurosci

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IntroductionA current topic of controversy in psychiatry is whether or not bipolar-spectrum disorders should be considered as part of the psychosis cluster in the upcoming DSM-V. Currently, bipolarspectrum disorders are classified as mood disorders in line with the Kraeplinian dichotomy; however, recent literature suggests that there may be more overlap in the underlying neurobiology in these major psychiatric illnesses than once thought.1 It is not unusual for patients with similar pheno typic presentation and common symptomatology to receive a diagnosis of either a bipolar-spectrum or a schizophrenia-spectrum disorder, particularly in the early stages of illness. Thus, investigation of the underlying neurobiology of these 2 major psychi atric groups is crucial to our understanding of their pathophysiological overlap. Shared genetic vulnerabilities in individuals with bipolar disorder and schizophrenia have been documented and describe how some symptoms overlap and how some are unique. [2][3][4][5] In support of the shared genetic basis of these disorders, there is evidence that first-degree relatives of probands with bipolar disorder or schizophrenia are at increased risk for either disorder, irrespective of the phenotype present in their relative. Background: Mismatch negativity (MMN) and P3a are event-related potentials that index deviance detection and the orienting response, respectively. We have previously shown that the MMN/P3a complex is impaired in patients with schizophrenia and affective spectrum psychoses, which suggests that it may index a common pathophysiology and argues against the purported specificity in schizo phrenia. Further research is warranted to determine whether patients with bipolar-spectrum disorders show similar impairments in these biomarkers. Methods: We assessed patients aged 15-30 years with early schizophrenia-spectrum disorders (schizophrenia, schizoaffective disorder, schizophreniform disorder), early bipolar-spectrum disorders (bipolar I or II, with and without psychotic features) and healthy, matched controls. We acquired MMN/P3a amplitudes during a 2-tone, auditory paradigm with 8% duration deviants. Clinical, psychosocial and neuro psychological assessments were also undertaken. Results: We included 20 patients with schizophrenia-spectrum disorders, 20 with bipolar-spectrum disorders and 20 controls in our study. Both patient groups showed significantly reduced frontocentral MMN and central P3a amplitudes. The schizophrenia-spectrum group had additional impairments in left temporal MMN and frontal P3a. Both patient groups performed worse than controls across psychosocial and clinical measures; however, only the schizophrenia-spectrum group performed significantly worse than controls for cognitive measures. Correlational analyses between patient groups revealed associations between frontocentral or left temporal MMN and psychiatric symptomatology or quality of life measures. Limitations: Limitations to our study include the modest sample size and the lack of control with r...

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“…MMN amplitude reduction in schizophrenia is well-documented (Naatanen & Kahkonen, 2009; Nagai et al, 2013a; Umbricht & Krljes, 2005), including in chronic (Brockhaus-Dumke et al, 2005; Catts et al, 1995; Jahshan et al, 2012; Javitt, Doneshka, Zylberman, Ritter, & Vaughan, 1993; Javitt, Grochowski, Shelley, & Ritter, 1998; Javitt, Shelley, Silipo, & Lieberman, 2000b; Kiang, Braff, Sprock, & Light, 2009; Light & Braff, 2005; Magno et al, 2008; Michie et al, 2000; Oades et al, 2006; Oknina et al, 2005; Rasser et al, 2011; Salisbury, Shenton, Griggs, Bonner-Jackson, & McCarley, 2002; Shelley et al, 1991; Umbricht, Bates, Lieberman, Kane, & Javitt, 2006), recent onset (Atkinson, Michie, & Schall, 2012; Jahshan et al, 2012; Javitt et al, 2000b; Kaur et al, 2011, 2012b, 2013, Perez et al, 2014; Todd et al, 2008; Umbricht et al, 2006), and some (Bodatsch et al, 2011; Brockhaus-Dumke et al, 2005; Catts et al, 1995) but not all (Devrim-Ucok, Keskin-Ergen, & Ucok, 2008; Kirino & Inoue, 1999; Korostenskaja et al, 2005) unmedicated patients. The status of MMN in first episode schizophrenia is more controversial, with some studies reporting reduced frequency-deviant MMN (Oknina et al, 2005) or duration-deviant MMN (Bodatsch et al, 2011; Hermens et al, 2010; Kaur et al, 2011; Nagai et al, 2013b; Oades et al, 2006), at least in patients lacking any college education (Umbricht et al, 2006), but other studies reporting normal duration-deviant MMN (Magno et al, 2008) or frequency-deviant MMN (Bodatsch et al, 2011; Devrim-Ucok et al, 2008; Magno et al, 2008; Nagai et al, 2013b; Salisbury et al, 2002; Valkonen-Korhonen et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Equivalent mismatch negativity deficits across deviant types in early illness schizophrenia-spectrum patients

Hay

Roach

Srihari

et al. 2015

Biological Psychology

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Neurophysiological abnormalities in auditory deviance processing, as reflected by the mismatch negativity (MMN), have been observed across the course of schizophrenia. Studies in early schizophrenia patients have typically shown varying degrees of MMN amplitude reduction for different deviant types, suggesting that different auditory deviants are uniquely processed and may be differentially affected by duration of illness. To explore this further, we examined the MMN response to 4 auditory deviants (duration, frequency, duration + frequency “double deviant”, and intensity) in 24 schizophrenia-spectrum patients early in the illness (ESZ) and 21 healthy controls. ESZ showed significantly reduced MMN relative to healthy controls for all deviant types (p < 0.05), with no significant interaction with deviant type. No correlations with clinical symptoms were present (all ps > 0.05). These findings support the conclusion that neurophysiological mechanisms underlying processing of auditory deviants are compromised early in illness, and these deficiencies are not specific to the type of deviant presented.

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Effects of olanzapine on auditory P300 and mismatch negativity (MMN) in schizophrenia spectrum disorders

Cited by 66 publications

References 37 publications

Central auditory dysfunction in schizophrenia as revealed by the mismatch negativity (MMN) and its magnetic equivalent MMNm: a review

Central auditory dysfunction in schizophrenia as revealed by the mismatch negativity (MMN) and its magnetic equivalent MMNm: a review

Neurophysiological biomarkers support bipolar-spectrum disorders within psychosis cluster

Equivalent mismatch negativity deficits across deviant types in early illness schizophrenia-spectrum patients

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