Source distribution of neuromagnetic slow waves and MEG-delta activity in schizophrenic patients

Fehr, Thorsten; Kißler, Johanna; Moratti, Stephan; Wienbruch, Christian; Rockstroh, Brigitte; Elbert, Thomas

doi:10.1016/s0006-3223(01)01122-2

Cited by 74 publications

(66 citation statements)

References 35 publications

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“…The increase of in vivo gamma power after ketamine administration in hippocampus was previously reported (Hinman et al, 2007;Ma & Leung, 2007). Magnetoencephalography studies suggested a positive correlation between theta power in the temporal lobe and positive symptoms such as hallucinations (Sperling, Bleich, Maihofner, & Reulbach, 2009;Ince, Goksu, Pellizzer, Tewfik, & Stephane, 2008;Fehr et al, 2001Fehr et al, , 2003Ishii et al, 2000;Sperling, Vieth, Martus, Demling, & Barocka, 1999;Canive et al, 1998). These studies suggest an opposite change in theta power than that reported here.…”

Section: Discussion Theta and Gamma Oscillationsmentioning

confidence: 53%

Ketamine Modulates Theta and Gamma Oscillations

Lazarewicz¹,

Ehrlichman²,

Maxwell³

et al. 2010

Journal of Cognitive Neuroscience

197

163

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Ketamine, an N-methyl-D-aspartate (NMDA) receptor glutamatergic antagonist, has been studied as a model of schizophrenia when applied in subanesthetic doses. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complexmanner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complex manner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. ■ Disciplines Physical Sciences and Mathematics | Physics

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Section: Discussion Theta and Gamma Oscillationsmentioning

confidence: 53%

Ketamine Modulates Theta and Gamma Oscillations

Lazarewicz¹,

Ehrlichman²,

Maxwell³

et al. 2010

Journal of Cognitive Neuroscience

197

163

View full text Add to dashboard Cite

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“…The only significant finding was a positive correlation between beta power and psychomotor poverty. Similar studies have shown that negative symptoms are correlated with an increase in beta-and delta-band activity (Williamson 1989), whereas positive symptoms are correlated with increased theta and delta activity (Fehr 2001). Interestingly, a study of qEEG findings in lateonset schizophrenia (n = 10) showed no significant abnormality, thus raising the possibility of a biological difference in the disorder based on the age at onset (Reeves 2003).…”

Section: Psychotic Disordersmentioning

confidence: 58%

EEG in psychiatric practice: to do or not to do?

Badrakalimuthu¹,

Swamiraju²,

Waal³

2011

Adv. psychiatr. treat

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SummaryElectroencephalography (EEG) is a non-invasive investigation that can aid the diagnosis of psychiatric and neuropsychiatric disorders. A good predictor of an abnormal EEG recording is the presence of an organic factor identified during the clinical assessment. The non-invasiveness and low cost of the procedure and its ability to measure spontaneous brain activity appear to attract clinicians to utilise this investigative tool. However, studies have reported that EEGs arising from psychiatric referrals have the lowest abnormality detection rate. The focus of this article is to improve this by highlighting the current pitfalls and providing recommendations for appropriate utilisation of EEG. We describe specific EEG changes associated with major psychiatric disorders. We conclude by offering pragmatic considerations when referring a patient for EEG, emphasising the fact that the information provided to the neurophysiologist plays a crucial role in interpreting the EEG recording in a diagnostically meaningful way.

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“…In addition to neurological disease abnormal slow waves are observed in psychopathological conditions (Canive et al, 1996;Fehr et al, 2001Fehr et al, , 2003Fernandez et al, 2003;Wienbruch et al, 2003). Using a single equivalent current dipole model with band pass-filtered data in the delta (1.5-4 Hz) and theta (4-8 Hz) ranges, we Fernandez et al, 2002;Wienbruch et al, 2003) determined the origin of focal slow waves and a density function of focal generators.…”

Section: E-mail Addressmentioning

confidence: 99%

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

Wienbruch¹

2007

Journal of Neuroscience Methods

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Slow waves in the delta and theta frequency range, normal signs of deactivated networks in sleep stages, are considered 'abnormal' when prominent in the waking state and when generated in circumscribed brain areas. Structural cortical lesions, e.g. related to stroke, tumors, or scars, generate focal electric and magnetic slow wave activity in the penumbra. Focal concentrations of slow wave activity exceeding those of healthy subjects have also been found in individuals suffering from psychiatric disorders without obvious structural brain damage. Hence, identification and mapping of abnormal slow wave activity might contribute to the investigation of cortical indications of psychopathology.Here I propose a method for abnormal slow wave mapping (ASWAM), based on a 5 min resting magnetoencephalogramm (MEG) and equivalent current dipole fitting to sources in the 1-4 Hz frequency band (delta) in anatomically defined cortical regions. The method was tested in a sample of 116 healthy subjects (59 males), with the aim to provide a basis for later comparison with patient samples. As to be expected, delta dipole density was low in healthy subjects. However, its distribution differed between genders with fronto-central > posterior dipole density in male and posterior dominance in female participants, which was not significantly related to either age or headsize. Results suggest that this method allows the identification of ASWA, so that comparison against Z-scores from a larger normal control group might assist diagnostic purposes in patient groups. As specific distributions seem to reflect differences between genders, this should be considered also in the analysis of patient samples.

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Source distribution of neuromagnetic slow waves and MEG-delta activity in schizophrenic patients

Cited by 74 publications

References 35 publications

Ketamine Modulates Theta and Gamma Oscillations

Ketamine Modulates Theta and Gamma Oscillations

EEG in psychiatric practice: to do or not to do?

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

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