The auditory steady-state response (ASSR)

O’Donnell, Brian F.; Vohs, Jenifer L.; Krishnan, Giri P.; Rass, Olga; Hetrick, William P.; Morzorati, Sandra L.

doi:10.1016/b978-0-7020-5307-8.00006-5

Cited by 150 publications

(65 citation statements)

References 59 publications

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“…This is an important finding, given the increasing use of the ASSR as a biomarker in investigations of neuropsychiatric disorders (O’Donnell et al, 2013; Sivarao et al, 2016; Thune et al, 2016). Consistent with our previous findings with EEG data (McFadden et al, 2014), we found the ASSR to be reliable across two sessions, spaced approximately one week apart.…”

Section: Discussionmentioning

confidence: 76%

“…40 Hz amplitude-modulated stimuli (e.g., amplitude-modulated tones, white noise, or click trains) can be used to entrain the ASSR, which peaks around 40 Hz in humans (Azzena et al, 1995; Hari et al, 1989) and can be measured using electroencephalography (EEG) or magnetoencephalography (MEG). ASSR abnormalities have been observed in autism spectrum disorders (Wilson et al, 2007), schizophrenia (Brenner et al 2003; Hayrynen et al, 2016; Kwon et al, 1999; Light et al, 2006; O’Donnell et al, 2013; Roach et al, 2013; Spencer et al, 2008; Thune et al, 2016), and bipolar disorder (Isomura et al, 2016; Maharajh et al, 2007; O’Donnell et al, 2004; Oda et al, 2012; Rass et al, 2010). Heritability of these abnormalities has been suggested, as they have also been identified in first-degree relatives of individuals with autism (Rojas et al, 2011) and schizophrenia (Hong et al, 2004; Rass et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Much evidence suggests that ASSR abnormalities reflect dysfunctional gamma-aminobutyric acid (GABA) neurotransmission, leading to inefficiencies in brain inhibitory function (Brenner et al, 2009; Kwon et al, 1999; Lewis et al, 2005; O’Donnell et al, 2013; Vohs et al, 2010). However, there is also evidence suggesting that the ASSR involves glutamatergic dysfunction (Brenner et al, 2009; Kwon et al, 1999; Leishman et al, 2015; O’Donnell et al, 2013; Plourde et al, 1997; Sivarao et al, 2013; Sivarao, 2015; Sivarao et al, 2016; Vohs et al, 2012), particularly supported by emerging evidence that the 40 Hz ASSR may be more sensitive to N -methyl-D-aspartate (NMDA) receptor antagonism than to GABA-A receptor antagonism (Sullivan et al, 2015). With this growing body of evidence, the ASSR demonstrates strong potential as a biomarker in clinical studies of neuropsychiatric disorders (O’Donnell et al, 2013; Sivarao, 2015; Thune et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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MEG and EEG demonstrate similar test-retest reliability of the 40 Hz auditory steady-state response

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Hild

Steinmetz

et al. 2017

International Journal of Psychophysiology

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The auditory steady-state response (ASSR) is increasingly being used as a biomarker in neuropsychiatric disorders, but research investigating the test-retest reliability of this measure is needed. We previously reported ASSR reliability, measured by electroencephalography (EEG), to 40 Hz amplitude-modulated white noise and click train stimuli. The purpose of the current study was to (a) assess the reliability of the MEG-measured ASSR to 40 Hz amplitude-modulated white noise and click train stimuli, and (b) compare test-retest reliability between MEG and EEG measures of ASSR, which has not previously been investigated. Additionally, impact of stimulus parameter choice on reliability was assessed, by comparing responses to white noise and click train stimuli. Test-retest reliability, across sessions approximately one week apart, was assessed in 17 healthy adults. On each study day, participants completed two passive listening tasks (white noise and click train stimuli) during separate MEG and EEG recordings. Between-session correlations for evoked power and inter-trial phase coherence (ITPC) were assessed following source-space projection. Overall, the MEG-measured ASSR was significantly correlated between sessions (p < 0.05, FDR corrected), suggesting acceptable test-retest reliability. Results suggest greater response reproducibility for ITPC compared to evoked responses and for click train compared to white noise stimuli, although further study is warranted. No significant differences in reliability were observed between MEG and EEG measures, suggesting they are similarly reliable. This work supports use of the ASSR as a biomarker in clinical interventions with repeated measures.

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Section: Discussionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MEG and EEG demonstrate similar test-retest reliability of the 40 Hz auditory steady-state response

Legget

Hild

Steinmetz

et al. 2017

International Journal of Psychophysiology

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“…Periodic auditory stimulation entrains the electro-encephalogram (EEG) to a specific phase and frequency, often referred to as the auditory steady-state response (ASSR). In both human and animal models, the ASSR has been used to assess the functional integrity of neural circuits that support synchronization (Picton et al, 2003; Brenner et al, 2009; O'Donnell et al, 2013). In schizophrenia, reduced ASSR power (magnitude) and phase locking (phase consistency across trials), particularly at 40 Hz, are observed in EEG (Kwon et al, 1999; Brenner et al, 2003; Light et al, 2006; Spencer et al, 2008, 2009; Vierling-Claassen et al, 2008; Krishnan et al, 2009) as well as in magneto-encephalogram (MEG) (Teale et al, 2008; Maharajh et al, 2010; Tsuchimoto et al, 2011) studies.…”

Section: Introductionmentioning

confidence: 99%

Brain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model

Nakao

Nakazawa

2014

Front. Neurosci.

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In schizophrenia, evoked 40-Hz auditory steady-state responses (ASSRs) are impaired, which reflects the sensory deficits in this disorder, and baseline spontaneous oscillatory activity also appears to be abnormal. It has been debated whether the evoked ASSR impairments are due to the possible increase in baseline power. GABAergic interneuron-specific NMDA receptor (NMDAR) hypofunction mutant mice mimic some behavioral and pathophysiological aspects of schizophrenia. To determine the presence and extent of sensory deficits in these mutant mice, we recorded spontaneous local field potential (LFP) activity and its click-train evoked ASSRs from primary auditory cortex of awake, head-restrained mice. Baseline spontaneous LFP power in the pre-stimulus period before application of the first click trains was augmented at a wide range of frequencies. However, when repetitive ASSR stimuli were presented every 20 s, averaged spontaneous LFP power amplitudes during the inter-ASSR stimulus intervals in the mutant mice became indistinguishable from the levels of control mice. Nonetheless, the evoked 40-Hz ASSR power and their phase locking to click trains were robustly impaired in the mutants, although the evoked 20-Hz ASSRs were also somewhat diminished. These results suggested that NMDAR hypofunction in cortical GABAergic neurons confers two brain state-dependent LFP abnormalities in the auditory cortex; (1) a broadband increase in spontaneous LFP power in the absence of external inputs, and (2) a robust deficit in the evoked ASSR power and its phase-locking despite of normal baseline LFP power magnitude during the repetitive auditory stimuli. The “paradoxically” high spontaneous LFP activity of the primary auditory cortex in the absence of external stimuli may possibly contribute to the emergence of schizophrenia-related aberrant auditory perception.

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“…[Clementz et al, 1998; Schulze et al, 2008; Perez et al, 2013] Twin studies have demonstrated that these ERPs are heritable [Hall et al, 2006; Hall et al, 2011a] and are genetically correlated with liability to SCZ or psychotic BIP. [Bramon et al, 2005; Hall et al, 2009b] Taken together, these findings suggest that ERP impairments are endophenotypes for psychosis [Turetsky et al, 2007; O’Donnell et al, 2013]. …”

Section: Introductionmentioning

confidence: 95%

Genomewide association analyses of electrophysiological endophenotypes for schizophrenia and psychotic bipolar disorders: A preliminary report

Hall

Chen

Cohen

et al. 2015

American J of Med Genetics Pt B

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Several event-related potentials (ERP), including P3, sensory gating (P50), and gamma oscillation, are robustly impaired in patients with schizophrenia (SCZ) and bipolar disorder (BIP). Although these ERPs are known to be heritable, little is known about the specific genetic loci involved and the degree to which they overlap with loci influencing mood and psychotic disorders. In the present study, we conducted GWAS to a) identify common variants associated with ERP endophenotypes, and b) construct polygenic risk scores (PRS) to examine overlap between genetic components of ERPs and mood and psychotic disorders. The sample consisted of 271 patients with SCZ or psychotic BIP diagnosis and 128 controls for whom ERP and genomewide data were available. GWAS were conducted using the full sample. PRS, derived from the Psychiatric Genomics Consortium (PGC) analyses of SCZ, BIP, and major depressive disorder were applied to each ERP phenotype. We identified a region on chromosome 14 that was significantly associated with sensory gating (peak SNP rs10132223, P = 1.27 × 10−9). This locus has not been previously associated with psychotic illness in PGC-GWAS. In the PRS analyses, patients with a higher load of SCZ risk alleles had reduced gamma response whereas patients with a higher load of BIP risk alleles had smaller P3 amplitude. We observed a genomewide significant locus on chromosome 14 for P50. This locus may influence P50 but not psychotic illness. Among patients with psychotic illness, PRS results indicated genetic overlap between SCZ loci and gamma oscillation and between BIP loci and P3 amplitude.

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The auditory steady-state response (ASSR)

Cited by 150 publications

References 59 publications

MEG and EEG demonstrate similar test-retest reliability of the 40 Hz auditory steady-state response

MEG and EEG demonstrate similar test-retest reliability of the 40 Hz auditory steady-state response

Brain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model

Genomewide association analyses of electrophysiological endophenotypes for schizophrenia and psychotic bipolar disorders: A preliminary report

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