Abnormalities of Inhibitory Neuronal Mechanisms in the Motor Cortex of Patients with Schizophrenia

Bajbouj, Malek; Gallinat, Juergen; Niehaus, L.; Ue, Lang; Röricht, Simone; Bu, Meyer

doi:10.1055/s-2004-815529

Cited by 48 publications

(5 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Different studies pointed towards a reduced SICI in medicated chronic schizophrenia patients [20,37,38] and FE-SZ patients [11], whereas other studies failed to show this difference [18,19]. CSP in medicated patients was found to be shortened [20] or prolonged [19,21,39,40] compared to HC. The situation for ADHD is more clearly laid out.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2013

View full text Add to dashboard Cite

Background: First-episode schizophrenia (FE-SZ) and attention deficit hyperactivity disorder (ADHD) are both neuropsychiatric disorders associated with an impaired dopaminergic transmission. Though displaying different clinical phenotypes, a common pathophysiological pathway is discussed controversially. Several studies using transcranial magnetic stimulation (TMS) revealed abnormalities in human motor cortex excitability in both schizophrenia and ADHD patients. Studies on cortical excitability comparing these two diseases directly are lacking. Method: In this study, a total of 94 subjects were analyzed. Twenty-five FE-SZ patients were directly compared with 28 ADHD patients and 41 healthy controls (HC). We investigated cortical excitability (inhibitory and facilitatory networks) with single- and paired-pulse TMS to the left and right motor cortex. Results: Compared to HC, FE-SZ/ADHD patients displayed an impaired cortical inhibition over the left hemisphere. Apart from an enhanced intracortical facilitation, FE-SZ patients did not differ compared to ADHD patients in the main outcome measures. Both patient groups presented a dysfunctional hemispheric pattern of cortical inhibition and facilitation in comparison with HC. Conclusion: The results of this study indicate a pattern of cortical disinhibition and abnormal hemispheric balance of intracortical excitability networks in two different psychiatric diseases. These effects might be associated with an imbalance in GABAergic and dopaminergic transmission and might provide evidence for a common pathophysiological pathway of both diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2013

View full text Add to dashboard Cite

show abstract

“…TS: stimulation intensity to elicit 1 mV MEP. ISI: 3 ms; 10 ms MagPro R30 Right FDI Bajbouj et al 42 16 (4) 16 (4) 31.3 (10.5) 33.6 (10.2) SCH** CSP 80% of maximum stimulator intensity 2 x Magstim 200. figure-of-eight coil Right FDI Bridgman et al 43 11 (4) 13 (3) 38.5 (9) 35.5 (10.5) SCH + SAD* SICI.…”

Section: Methodsmentioning

confidence: 99%

Excitation/inhibition imbalance in schizophrenia: a meta-analysis of inhibitory and excitatory TMS-EMG paradigms

Lányi,

Koleszár,

Schulze Wenning

et al. 2024

Schizophr

View full text Add to dashboard Cite

Cortical excitation-inhibition (E/I) imbalance is a potential model for the pathophysiology of schizophrenia. Previous research using transcranial magnetic stimulation (TMS) and electromyography (EMG) has suggested inhibitory deficits in schizophrenia. In this meta-analysis we assessed the reliability and clinical potential of TMS-EMG paradigms in schizophrenia following the methodological recommendations of the PRISMA guideline and the Cochrane Handbook. The search was conducted in three databases in November 2022. Included articles reported Short-Interval Intracortical Inhibition (SICI), Intracortical Facilitation (ICF), Long-Interval Intracortical Inhibition (LICI) and Cortical Silent Period (CSP) in patients with schizophrenia and healthy controls. Meta-analyses were conducted using a random-effects model. Subgroup analysis and meta-regressions were used to assess heterogeneity. Results of 36 studies revealed a robust inhibitory deficit in schizophrenia with a significant decrease in SICI (Cohen’s d: 0.62). A trend-level association was found between SICI and antipsychotic medication. Our findings support the E/I imbalance hypothesis in schizophrenia and suggest that SICI may be a potential pathophysiological characteristic of the disorder.

show abstract

“…A study explored important aspects of the pathophysiological mechanisms using the paired-pulse method, in which ( n = 30 schizophrenic patients) served as subjects and half were untreated [ 49 ]. However, a decrease is noted in cortical inhibition, only significant in the untreated patients compared to controls and no difference in the facilitation [ 49 , 50 ]. In the treated patients, an inclination to reduced inhibition is perceived compared to the untreated schizophrenia patients [ 27 , 33 ].…”

Section: Methodsmentioning

confidence: 99%

“…The application of TMS can assist in studying the transcallosal connection between primary motor cortices (M1) in both human hemispheres, which include transcallosal inhibition (TCI) and facilitation (TCF) with onset latency, typically (30-40 ms). Moreover, the latency and duration of the TCI are known as the transcortical conduction time (transcallosal conduction time, TCT) [ 50 ]. The resulting phenomenon is called a cortical silent period (CSP) or a contralateral silent period.…”

Section: Methodsmentioning

confidence: 99%

Assessment of Cortical Plasticity in Schizophrenia by Transcranial Magnetic Stimulation

et al. 2021

View full text Add to dashboard Cite

Neural plasticity refers to the capability of the brain to modify its structure and/or function and organization in response to a changing environment. Evidence shows that disruption of neuronal plasticity and altered functional connectivity between distinct brain networks contribute significantly to the pathophysiological mechanisms of schizophrenia. Transcranial magnetic stimulation has emerged as a noninvasive brain stimulation tool that can be utilized to investigate cortical excitability with the aim of probing neural plasticity mechanisms. In particular, in pathological disorders, such as schizophrenia, cortical dysfunction, such as an aberrant excitatory-inhibitory balance in cortical networks, altered cortical connectivity, and impairment of critical period timing are very important to be studied using different TMS paradigms. Studying such neurophysiological characteristics and plastic changes would help in elucidating different aspects of the pathophysiological mechanisms underlying schizophrenia. This review attempts to summarize the findings of available TMS studies with diagnostic and characterization aims, but not with therapeutic purposes, in schizophrenia. Findings provide further evidence of aberrant excitatory-inhibitory balance in cortical networks, mediated by neurotransmitter pathways such as the glutamate and GABA systems. Future studies with combining techniques, for instance, TMS with brain imaging or molecular genetic typing, would shed light on the characteristics and predictors of schizophrenia.

show abstract

Abnormalities of Inhibitory Neuronal Mechanisms in the Motor Cortex of Patients with Schizophrenia

Abstract: The prolonged TI suggests an abnormal activation of interhemispheric connections between the motor cortices and may be related to previously reported pathology of the corpus callosum in schizophrenic patients.

Cited by 48 publications

References 46 publications

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

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

Excitation/inhibition imbalance in schizophrenia: a meta-analysis of inhibitory and excitatory TMS-EMG paradigms

Assessment of Cortical Plasticity in Schizophrenia by Transcranial Magnetic Stimulation

Contact Info

Product

Resources

About