A Similar but Distinctive Pattern of Impaired Cortical Excitability in First-Episode Schizophrenia and ADHD

Hasan, Alkomiet; Schneider, Marc; Schneider‐Axmann, Thomas; Ruge, Diane; Retz, Wolfgang; Rösler, Michael; Falkai, Peter; Wobrock, Thomas

doi:10.1159/000343912

Cited by 14 publications

(16 citation statements)

References 107 publications

(93 reference statements)

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“…This is worthy of further investigation, as the results of the western blots, which were conducted separately for tissue from each hemisphere, indicated a selective left-sided effect. This may be relevant to schizophrenia as a number of studies 59 have suggested that alterations in hemispheric asymmetry, including in one example, selective reductions in inhibition in the left hemisphere, 60 may be important in the disorder.…”

Section: Discussionmentioning

confidence: 99%

Association of aberrant neural synchrony and altered GAD67 expression following exposure to maternal immune activation, a risk factor for schizophrenia

et al. 2014

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A failure of integrative processes within the brain, mediated via altered GABAergic inhibition, may underlie several features of schizophrenia. The present study examined, therefore, whether maternal immune activation (MIA), a risk factor for schizophrenia, altered inhibitory markers in the hippocampus and medial prefrontal cortex (mPFC), while also altering electroencephalogram (EEG) coherence between these regions. Pregnant rats were treated with saline or polyinosinic:polycytidylic acid mid-gestation. EEG depth recordings were made from the dorsal and ventral hippocampus and mPFC of male adult offspring. Glutamic decarboxylase (GAD67) levels were separately assayed in these regions using western blot. GAD67 expression was also assessed within parvalbumin-positive cells in the dorsal and ventral hippocampus using immunofluorescence alongside stereological analysis of parvalbumin-positive cell numbers. EEG coherence was reduced between the dorsal hippocampus and mPFC, but not the ventral hippocampus and mPFC, in MIA animals. Western blot and immunofluorescence analyses revealed that GAD67 expression within parvalbumin-positive cells was also reduced in the dorsal hippocampus relative to ventral hippocampus in MIA animals when compared with controls. This reduction was observed in the absence of parvalbumin-positive neuronal loss. Overall, MIA produced a selective reduction in EEG coherence between the dorsal hippocampus and mPFC that was paralleled by a similarly specific reduction in GAD67 within parvalbumin-positive cells of the dorsal hippocampus. These results suggest a link between altered inhibitory mechanisms and synchrony and, therefore point to potential mechanisms via which a disruption in neurodevelopmental processes might lead to pathophysiology associated with schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Association of aberrant neural synchrony and altered GAD67 expression following exposure to maternal immune activation, a risk factor for schizophrenia

et al. 2014

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“…A meta-analysis including ppTMS studies from 1990 to 2012 found no changes of ICF, but decreased short-interval intracortical inhibition, in schizophrenia (41). By contrast, later research with small sample sizes revealed significant increases of ICF in first-episode schizophrenia compared with healthy control subjects (42). In addition, I-wave facilitation was found to be increased in patients with schizophrenia (43).…”

Section: Introductionmentioning

confidence: 89%

Glutamatergic Dysfunction and Glutamatergic Compounds for Major Psychiatric Disorders: Evidence From Clinical Neuroimaging Studies

Li¹,

Yang²,

Lin³

2019

Front. Psychiatry

118

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Excessive glutamate release has been linked to stress and many neurodegenerative diseases. Evidence indicates abnormalities of glutamatergic neurotransmission or glutamatergic dysfunction as playing an important role in the development of many major psychiatric disorders (e.g., schizophrenia, bipolar disorder, and major depressive disorder). Recently, ketamine, an N-methyl-d-aspartate antagonist, has been demonstrated to have promisingly rapid antidepressant efficacy for treatment-resistant depression. Many compounds that target the glutamate system have also become available that possess potential in the treatment of major psychiatric disorders. In this review, we update evidence from recent human studies that directly or indirectly measured glutamatergic neurotransmission and function in major psychiatric disorders using modalities such as magnetic resonance spectroscopy, positron emission tomography/single-photon emission computed tomography, and paired-pulse transcranial magnetic stimulation. The newer generation of antidepressants that target the glutamatergic system developed in human clinical studies is also reviewed.

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“…SICI was not correlated with illness duration in patients with schizophrenia, 45,60 although those who had a relatively short duration of illness (e.g., less than 3 years) or treatment (i.e., not longer than 6 weeks continuously) also showed reduced SICI in the motor cortex compared to healthy controls. 46,60,174 Therefore, the decrease in SICI in schizophrenia may have been independent of illness and treatment duration.…”

Section: J Psychiatry Neurosci 2021;46(6)mentioning

confidence: 99%

“…43 TMS and other noninvasive stimulation techniques are used to elicit plastic changes in synaptic organization, interfering with the function of specific cortical areas by inducing long-term potentiation or long-term depression. [44][45][46][47] For example, transcranial direct current stimulation (tDCS) is a neuromodulation technique that induces changes in cortical excitability by applying a small current over the scalp. This technique modu lates the activity of spontaneous neurons by tonic depolarization (anodal tDCS) or hyperpolarization (cathodal tDCS) of their membrane, inducing long-lasting changes in neuronal firing rates.…”

Section: Introductionmentioning

confidence: 99%

A systematic review of TMS and neurophysiological biometrics in patients with schizophrenia

Hou

Santoro

Biondi

et al. 2021

jpn

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Background: Transcranial magnetic stimulation can be combined with electromyography (TMS-EMG) and electroencephalography (TMS-EEG) to evaluate the excitatory and inhibitory functions of the cerebral cortex in a standardized manner. It has been postulated that schizophrenia is a disorder of functional neural connectivity underpinned by a relative imbalance of excitation and inhibition. The aim of this review was to provide a comprehensive overview of TMS-EMG and TMS-EEG research in schizophrenia, focused on excitation or inhibition, connectivity, motor cortical plasticity and the effect of antipsychotic medications, symptom severity and illness duration on TMS-EMG and TMS-EEG indices. Methods: We searched PsycINFO, Embase and Medline, from database inception to April 2020, for studies that included TMS outcomes in patients with schizophrenia. We used the following combination of search terms: transcranial magnetic stimulation OR tms AND interneurons OR glutamic acid OR gamma aminobutyric acid OR neural inhibition OR pyramidal neurons OR excita* OR inhibit* OR GABA* OR glutam* OR E-I balance OR excitation-inhibition balance AND schizoaffective disorder* OR Schizophrenia OR schizophreni*. Results: TMS-EMG and TMS-EEG measurements revealed deficits in excitation or inhibition, functional connectivity and motor cortical plasticity in patients with schizophrenia. Increased duration of the cortical silent period (a TMS-EMG marker of γ-aminobutyric acid B receptor activity) with clozapine was a relatively consistent finding. Limitations: Most of the studies used patients with chronic schizophrenia and medicated patients, employed cross-sectional group comparisons and had small sample sizes. Conclusion: TMS-EMG and TMS-EEG offer an opportunity to develop a novel and improved understanding of the physiologic processes that underlie schizophrenia and to assess the therapeutic effect of antipsychotic medications. In the future, these techniques may also help predict disease progression and further our understanding of the excitatory/inhibitory balance and its implications for mechanisms that underlie treatment-resistant schizophrenia.

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A Similar but Distinctive Pattern of Impaired Cortical Excitability in First-Episode Schizophrenia and ADHD

Cited by 14 publications

References 107 publications

Association of aberrant neural synchrony and altered GAD67 expression following exposure to maternal immune activation, a risk factor for schizophrenia

Association of aberrant neural synchrony and altered GAD67 expression following exposure to maternal immune activation, a risk factor for schizophrenia

Glutamatergic Dysfunction and Glutamatergic Compounds for Major Psychiatric Disorders: Evidence From Clinical Neuroimaging Studies

A systematic review of TMS and neurophysiological biometrics in patients with schizophrenia

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