Source distribution of neuromagnetic slow-wave activity in schizophrenic patients—effects of activation

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

doi:10.1016/s0920-9964(02)00213-x

Cited by 63 publications

(48 citation statements)

References 27 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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“…MEG studies have replicated the well-known pattern of fronto-temporal low-frequency activity observed in EEC, and have also demonstrated abnormal sensory gating and basic cognitive processing (Canive et al, 1996;Kissler et al, 2000;Fehr et al, 2003;Wienbruch et al, 2003;Edgar et al, 2005;Lopez-Ibor et al, 2008;Naatanen and Kahkonen, 2009). A further step in this research is non-linear dynamics analysis (NDA).…”

Section: Introductionmentioning

confidence: 80%

Lempel–Ziv complexity in schizophrenia: A MEG study

Fernández

López‐Ibor

Turrero

et al. 2011

Clinical Neurophysiology

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SchizophreniaLempel-Ziv complexity Magnetoencephalography Neurodevelopmental Neurodegenerative• Schizophrenic patients show higher complexity values as compared to controls.• Schizophrenic patients showed a tendency to reduced complexity values as a function of age while controls showed the opposite tendency.• The tendency observed in schizophrenic patients parallels the tendency observed in Alzheimer disease patients. ABSTRACTObjective: The neurodevelopmental-neurodegenerative debate is a basic issue in the field of the neuropathological basis of schizophrenia (SCH). Neurophysiological techniques have been scarcely involved in such debate, but nonlinear analysis methods may contribute to it. Methods: Fifteen patients (age range 23-42 years) matching DSM IV-TR criteria for SCH, and 15 sex-and age-matched control subjects (age range 23-42 years) underwent a resting-state magnetoencephalographic evaluation and Lempel-Ziv complexity (LZC) scores were calculated. Results: Regression analyses indicated that LZC values were strongly dependent on age. Complexity scores increased as a function of age in controls, while SCH patients exhibited a progressive reduction of LZC values. A logistic model including LZC scores, age and the interaction of both variables allowed the classification of patients and controls with high sensitivity and specificity. Conclusions: Results demonstrated that SCH patients failed to follow the "normal" process of complexity increase as a function of age. In addition, SCH patients exhibited a significant reduction of complexity scores as a function of age, thus paralleling the pattern observed in neurodegenerative diseases. Significance: Our results support the notion of a progressive defect in SCH, which does not contradict the existence of a basic neurodevelopmental alteration.

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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-wave activity in schizophrenic patients—effects of activation

Cited by 63 publications

References 27 publications

Ketamine Modulates Theta and Gamma Oscillations

Ketamine Modulates Theta and Gamma Oscillations

Lempel–Ziv complexity in schizophrenia: A MEG study

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

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