. 2021 Dec 21;46(6):E675–E701. doi: 10.1503/jpn.210006

Table 4.

Overview of results from TMS-EEG studies

Stimulation site	Main findings		Hypothesis
Stimulation site	Frequency domain	Time domain	Hypothesis
Left primary motor cortex	Three studies demonstrated no significant difference in the degree of LICI-induced inhibition of oscillatory activity in the primary motor cortex⁹⁹,¹⁰⁵ or frontal region¹⁰⁶ between medicated (or medicated chronic) patients and healthy controls. As well, medicated patients¹⁰⁵ and patients with a first episode of psychosis⁹¹ did not show a significant difference from healthy controls after single-pulse stimulation of the left primary motor cortex	Median nerve stimulation (i.e., short-latency afferent inhibition) induced a larger increase of the P180 amplitude in medicated patients relative to healthy controls in the left primary motor cortex⁹⁷	Impaired cortical inhibition and excitation (mediated by e.g., GABAergic and glutamatergic neurotransmission, respectively) in the frontal lobes of patients would lead to impairment in the generation and modulation of TMS-EEG activity in both the frequency and time domains. As well, dysregulation of the central cholinergic system in patients with schizophrenia would affect the modulation of the N100 component by the SAI paradigm, a marker of cholinergic activity⁹⁷
Premotor cortex	One study showed significantly decreased ERSP and intertrial coherence values in the γ range in medicated patients within the first 100 ms post-TMS in a frontocentral region that included premotor and sensorimotor areas.⁸³ Another study showed reduced ERSP in the β/γ range and slowed natural frequency at the stimulation site in medicated patients with chronic schizophrenia, patients with bipolar disorder and patients with major depressive disorder compared to healthy controls¹⁰⁷	No studies
Left dlPFC	Relative to healthy controls, chronic (or medicated chronic) patients with schizophrenia exhibited reduced LICI of γoscillations in 2 studies¹⁰⁵,¹⁰⁶ and of oscillations in all frequency bands in 1 study,⁹⁹ measured by area under the curve¹⁰⁵ or ERSP⁹⁹ in the dlPFC or by ERSP in a frontal region.¹⁰⁶ Two of these studies also showed reduced LICI of γ oscillations in the dlPFC compared to patients with bipolar disorder,¹⁰⁵ and of θ, α and β oscillations compared to patients with obsessive–compulsive disorder.⁹⁹ One study demonstrated less SICI-induced inhibition of evoked δ power, and less SICI-induced inhibition and ICF-induced facilitation of ERSP in the dlPFC of medicated patients with chronic schizophrenia relative to healthy controls¹⁰⁸	SICI and ICF induced significantly greater changes in the amplitude of TMS-evoked EEG potentials in the left dlPFC in healthy controls compared to medicated patients with chronic schizophrenia.¹⁰⁸ SAI increased the N100 amplitude in healthy controls but not in medicated patients in the dlPFC.⁹⁷ Because modulation of N100 amplitude is a robust primary marker for SAI, the authors suggested that SAI is reduced in the dlPFC in patients with schizophrenia⁹⁷

dlPFC = dorsolateral prefrontal cortex; EEG = electroencephalography; ERSP = event-related spectral perturbation; GABA = γ-aminobutyric acid; ICF = intracortical facilitation; LICI = long-interval intracortical inhibition; N100 = negative deflection at around 100 ms; P180 = positive deflection at around 180 ms; SAI = short-latency afferent inhibition; SICI = short-interval intracortical inhibition; TMS = transcranial magnetic stimulation.