Auditory recovery cycle dysfunction in schizophrenia: A study using event-related potentials
Schizophrenia Research Unit, Level 1, Don Everett Building, Liverpool Hospital, South Western Sydney Area Health Service, Locked Bag 7103, Liverpool, BC, NSW 1871, Australia. Psychiatry Research
(Impact Factor: 2.47).
08/2005; 136(1):17-25. DOI: 10.1016/j.psychres.2005.05.009
Previous event-related potential (ERP) studies reported evidence of impaired auditory information processing in patients with schizophrenia. The recovery cycle of the auditory N1 ERP component was measured in 17 patients with schizophrenia and 17 age- and sex-matched healthy volunteers. Subjects performed a visual distraction task while listening to 80-dB SPL, 1000-Hz tone pairs, presented with intra-pair intervals of 1, 3, 5 or 7 s, with inter-pair intervals of 9-13 s. Patients with schizophrenia had significantly reduced N1 amplitudes for S1 stimuli compared with healthy volunteers. For N1 amplitudes elicited by S2 stimuli, there was a significant group effect whilst the main effect of intra-pair interval was not significant. These results provide additional evidence of inhibitory auditory processing deficits in schizophrenia.
Available from: Vaughan Carr
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ABSTRACT: To review the first 10 years of operation of the Neuroscience Institute of Schizophrenia and Allied Disorders (NISAD), Australia's first virtual research institute.
Narrative description of the evolution of NISAD.
Since inception in 1996, NISAD has developed a wide range of activities to enhance existing efforts and develop new initiatives in schizophrenia research, initially throughout New South Wales, but increasingly on a national scale. This involved the initial development of critical research infrastructure to provide the foundation, with the subsequent focus on developing a multidisciplinary programme of schizophrenia research, across the basic to applied research spectrum. While the primary focus has been the scientific domain, NISAD has also played a leading role in increasing public awareness of schizophrenia as a disease amenable to scientific investigation.
NISAD has succeeded in building a framework to apply the latest developments in neuroscience to the study of schizophrenia and has formed a multidisciplinary network of clinicians and neuroscientists who are actively collaborating on a range of research initiatives. The 'virtual institute' structure of NISAD has proven cost-efficient and consistent with innovative thinking about research resource management.
Australian and New Zealand Journal of Psychiatry 02/2007; 41(1):78-88. DOI:10.1080/00048670601057783 · 3.41 Impact Factor
Available from: Tiffany A Greenwood
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ABSTRACT: N100 evoked potential amplitude and gating abnormalities have been widely observed in schizophrenia patients. However, previous studies have been inconclusive as to whether similar deficits are present in unaffected family members. The Consortium on the Genetics of Schizophrenia (COGS) is a multisite National Institute of Mental Health (NIMH) initiative examining neurocognitive and neurophysiological measures as endophenotypes for genetic studies of schizophrenia. We report initial results from the COGS dataset of auditory N100 amplitude and gating as candidate endophenotypes.
Evoked potential data were acquired from 142 schizophrenia probands, 373 unaffected first-degree relatives, and 221 community comparison subjects (CCS), using an auditory paired-click stimulation paradigm. Amplitude of the N100 response to each click and the click 2/click 1 ratio were dependent variables. Heritability was estimated based on kinships using Solar v.2.1.2. Group differences were examined after subjects were categorized as either "broad" or "narrow," based on the presence (broad) or absence (narrow) of nonpsychotic psychiatric comorbidity.
Heritability estimates were .40 and .29 for click1 and click2 amplitudes and .22 for the ratio. Broad and narrow patients both had impaired click 1 amplitudes. Broad relatives, but not narrow relatives, exhibited similar impairments. There were no group differences for either click 2 amplitude or the gating ratio.
N100 amplitude is a heritable measure that is abnormal in patients and a subset of relatives for whom psychiatric comorbidity may be a genetically associated phenotype. Auditory N100 gating, although heritable, is less viable as a schizophrenia endophenotype.
Biological psychiatry 09/2008; 64(12):1051-9. DOI:10.1016/j.biopsych.2008.06.018 · 10.26 Impact Factor
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ABSTRACT: Suppression of P50, N100 and P200 auditory evoked responses in a dual-click procedure is considered an index for the multistage sensory gating process. Whereas most studies use a protocol with long interstimulus intervals of 8-12 s between the stimuli pairs, there is also evidence that sensory gating occurs at much lower intervals. The aim of the study was to investigate whether a simple modified dual-click protocol with short interstimulus intervals elicts similar sensory gating ratios compared to the classic protocol.
P50, N100 and P200 amplitudes and sensory gating ratios were measured in 23 healthy subjects with 2 different dual-click protocols in 1 session: (1) a simple oddball modified with short interstimulus intervals of about 2.8 s (ISI2), and (2), the classic used with long intervals of about 8 s (ISI8).
The amplitudes of the P50, N100 and P200 responses were mostly comparable and correlated between both protocols. Mean sensory gating ratios (ISI8/ISI2) were as follows: P50, 35.4/36.4%; N40P50, 36.1/39.9%; N100, 44.4/48.4%; P200, 46.8/43.3%; N100P200, 45.3/41.8%; all differences between protocols, p > 0.1. P50 ratio scores did not show a sufficient correlation between protocols [intraclass correlation coefficient (ICC) P50, 0.13; N40P50, 0.0] compared to N100 (ICC, 0.79), P200 (ICC, 0.6) and N100P200 (ICC, 0.61).
Our results contradict the assumption that long interstimulus intervals of about 8 s are absolutely necessary to elicit a marked sensory gating phenomenon for P50, N100 and P200 auditory responses (at least when using a protocol with a simple attention task). However, because only healthy subjects were investigated, no prediction can be made for psychiatric patients, in whom neuronal processing may be different.
Neuropsychobiology 09/2008; 58(1):11-8. DOI:10.1159/000154475 · 2.26 Impact Factor
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