γ-band electroencephalographic oscillations in a patient with somatic hallucinations

Baldeweg, Torsten; Spence, Sean A.; Hirsch, Steven R.; Gruzelier, John

doi:10.1016/s0140-6736(05)79575-1

Cited by 174 publications

(92 citation statements)

References 5 publications

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“…Intriguingly, a positive correlation between auditory hallucinations and signal power or phase locking, particularly in the left hemisphere (Mulert et al, 2011(Mulert et al, , 2012Spencer et al, 2009;Ying et al, 2013), has been observed (Mulert et al, 2011(Mulert et al, , 2012Spencer et al, 2009;Ying et al, 2013) in the presence of concurrent increases in spontaneous or induced gamma power (Baldeweg et al, 1998;Hirano et al, 2015;Spencer, 2011). Thus, there appears to be a positive or negative modulation of the gamma oscillatory signal including the 40 Hz ASSR in schizophrenia.…”

Section: Introductionmentioning

confidence: 98%

40 Hz Auditory Steady-State Response Is a Pharmacodynamic Biomarker for Cortical NMDA Receptors

Sivarao

Chen

Senapati

et al. 2016

Neuropsychopharmacol

113

106

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Schizophrenia patients exhibit dysfunctional gamma oscillations in response to simple auditory stimuli or more complex cognitive tasks, a phenomenon explained by reduced NMDA transmission within inhibitory/excitatory cortical networks. Indeed, a simple steady-state auditory click stimulation paradigm at gamma frequency (~40 Hz) has been reproducibly shown to reduce entrainment as measured by electroencephalography (EEG) in patients. However, some investigators have reported increased phase locking factor (PLF) and power in response to 40 Hz auditory stimulus in patients. Interestingly, preclinical literature also reflects this contradiction. We investigated whether a graded deficiency in NMDA transmission can account for such disparate findings by administering subanesthetic ketamine (1-30 mg/kg, i.v.) or vehicle to conscious rats (n = 12) and testing their EEG entrainment to 40 Hz click stimuli at various time points (~7-62 min after treatment). In separate cohorts, we examined in vivo NMDA channel occupancy and tissue exposure to contextualize ketamine effects. We report a robust inverse relationship between PLF and NMDA occupancy 7 min after dosing. Moreover, ketamine could produce inhibition or disinhibition of the 40 Hz response in a temporally dynamic manner. These results provide for the first time empirical data to understand how cortical NMDA transmission deficit may lead to opposite modulation of the auditory steady-state response (ASSR). Importantly, our findings posit that 40 Hz ASSR is a pharmacodynamic biomarker for cortical NMDA function that is also robustly translatable. Besides schizophrenia, such a functional biomarker may be of value to neuropsychiatric disorders like bipolar and autism spectrum where 40 Hz ASSR deficits have been documented.

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Section: Introductionmentioning

confidence: 98%

40 Hz Auditory Steady-State Response Is a Pharmacodynamic Biomarker for Cortical NMDA Receptors

Sivarao

Chen

Senapati

et al. 2016

Neuropsychopharmacol

113

106

View full text Add to dashboard Cite

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“…The few studies that have examined the relationship between schizophrenic symptom profile and oscillatory activity in the gamma range have tended to find positive symptoms, such as reality distortion (Gordon et al 2001) or hallucinatory activity (Baldeweg et al 1998) associated with increased gamma activity, and negative symptoms, such as psychomotor poverty, associated with decreased gamma (Gordon et al 2001;Lee et al 2003). Moreover, some studies have shown generalized abnormal increases in beta activity (Kissler et al 2000) and beta synchrony (Nagase et al 1992;Wada et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Modeling Gaba Alterations in Schizophrenia: A Link Between Impaired Inhibition and Altered Gamma and Beta Range Auditory Entrainment

Vierling-Claassen¹,

Siekmeier²,

Stufflebeam³

2008

Schizophrenia Research

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Vierling-Claassen D, Siekmeier P, Stufflebeam S, Kopell N. Modeling GABA alterations in schizophrenia: a link between impaired inhibition and altered gamma and beta range auditory entrainment. J Neurophysiol 99: 2656 -2671, 2008. First published February 20, 2008 doi:10.1152/jn.00870.2007. The disorganized symptoms of schizophrenia, including severely disordered thought patterns, may be indicative of a problem with the construction and maintenance of cell assemblies during sensory processing and attention. The gamma and beta frequency bands (15-70 Hz) are believed relevant to such processing. This paper addresses the results of an experimental examination of the cortical response of 12 schizophrenia patients and 12 control subjects when presented with auditory click-train stimuli in the gamma/beta frequency band during measurement using magnetoencephalography (MEG), as well as earlier work by Kwon et al. These data indicate that control subjects show an increased 40-Hz response to both 20-and 40-Hz stimulation as compared with patients, whereas schizophrenic subjects show a preference for 20-Hz response to the same driving frequencies. In this work, two computational models of the auditory cortex are constructed based on postmortem studies that indicate cortical interneurons in schizophrenic subjects have decreased GAT-1 (a GABA transporter) and GAD 67 (1 of 2 enzymes responsible for GABA synthesis). The models transition from control to schizophrenic frequency response when an extended inhibitory decay time is introduced; this change captures a possible effect of these GABA alterations. Modeling gamma/beta range auditory entrainment in schizophrenia provides insight into how biophysical mechanisms can impact cognitive function. In addition, the study of dynamics that underlie auditory entrainment in schizophrenia may contribute to the understanding of how gamma and beta rhythms impact cognition in general.

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“…Since sensory and cognitive-related GFO are altered in schizophrenia, one may predict that baseline GFO could somehow modulate them (Hakami et al, 2009). Increased baseline GFO have been recorded in patients during psychotic episodes, including somatic and visual hallucinations (Baldeweg et al, 1998;Becker et al, 2009;Behrendt, 2003;Ffytche, 2008;Spencer et al, 2004), and in early psychosis (Bartha et al, 1997;Theberge et al, 2002). Increases in the amount of baseline GFO are a significant source of excessive network noise in the brain (Baldeweg et al, 1998; Gandal et al, 2011;Hakami et al, 2009;Rolls et al, 2008).…”

mentioning

confidence: 99%

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

Kulikova

Tolmacheva

Anderson

et al. 2012

Eur J of Neuroscience

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Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing Sofya P Kulikova (1,2)*, Elena A Tolmacheva (1,2)**, Paul Anderson (1,2,3), Julien Gaudias (1,2)***, Brendan E Adams (1,2)****, Thomas Zheng (1,2,3), and Didier Pinault (1,2)(1) INSERM U666, physiopathologie et psychopathologie cognitive de la schizophrénie, Strasbourg, France. Abstract:Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in cortex-related networks. However, the underlying anatomo-functional mechanisms remain elusive. Clinical and experimental evidence suggest that these deficits result from a hyporegulation of glutamate N-Methyl d-Aspartate receptors (NMDAr). Here we modeled these deficits in rats with ketamine, a non-competitive NMDAr antagonist and a translational psychotomimetic substance at subanesthetic doses. We tested the hypothesis that ketamine-induced sensory deficits involve an impairment of the ability of the thalamocortical (TC) system to discriminate the relevant information from the baseline activity. Furthermore we wanted to assess whether ketamine disrupts synaptic plasticity in TC systems. We conducted multisite network recordings in the rat somatosensory TC system, natural stimulation of the vibrissae and high-frequency electrical stimulation (HFS) of the thalamus.A single systemic injection of ketamine increased the amount of baseline GFO, reduced the amplitude of the sensory-evoked TC response and decreased the power of the sensoryevoked GFO. Furthermore, cortical application of ketamine elicited local and distant increases in baseline GFO. The ketamine effects were transient. Unexpectedly, HFS of the TC pathway had opposite actions. In conclusion, ketamine and thalamic HFS have opposite effects on the ability of the somatosensory TC system to discriminate the sensory-evoked response from the baseline GFO during information processing. Investigating the link between the state and function of the TC system may conceptually be a key strategy to design innovative therapies against neuropsychiatric disorders. 3The anatomofunctional mechanisms of sensory and cognitive deficits in schizophrenia are unknown. These deficits are commonly associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in corticocortical and thalamocortical (TC) circuits (Bokde et al., 2009;Clinton and Meador-Woodruff, 2004;de Haan W. et al., 2009;Friston, 2002;Herrmann and Demiralp, 2005;Light et al., 2006;Lisman, 2011;Meyer-Lindenberg, 2010;Pinault, 2011;Spencer et al., 2003;Uhlhaas and Singer, 2006). At least four types of GFO should be considered: 1) Spontaneously-occurring (baseline) GFO, which are dominant during desynchronized state of the electroencephalogram (Jasper, 1936;Sheer, 1975); 2) Sensory-evoked GFO, which are phase-locked to the stimulus onset (Pantev et al., 1991;Spencer et al., 2008b); 3) Steadystate GFO during r...

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γ-band electroencephalographic oscillations in a patient with somatic hallucinations

Cited by 174 publications

References 5 publications

40 Hz Auditory Steady-State Response Is a Pharmacodynamic Biomarker for Cortical NMDA Receptors

40 Hz Auditory Steady-State Response Is a Pharmacodynamic Biomarker for Cortical NMDA Receptors

Modeling Gaba Alterations in Schizophrenia: A Link Between Impaired Inhibition and Altered Gamma and Beta Range Auditory Entrainment

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

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