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Using TMS and EEG, Radhu et al. reveal reductions in long-interval cortical inhibition specific to the dorsolateral prefrontal cortex in patients with schizophrenia compared to healthy subjects and individuals with obsessive-compulsive disorder (OCD). The absence of such changes in OCD confirms that reductions in inhibition are not a generalized deficit associated with severe psychopathology.Abnormal gamma-aminobutyric acid inhibitory neurotransmission is a key pathophysiological mechanism underlying schizophrenia. Transcranial magnetic stimulation can be combined with electroencephalography to index long-interval cortical inhibition, a measure of GABAergic receptor-mediated inhibitory neurotransmission from the frontal and motor cortex. In previous studies we have reported that schizophrenia is associated with inhibitory deficits in the dorsolateral prefrontal cortex compared to healthy subjects and patients with bipolar disorder. The main objective of the current study was to replicate and extend these initial findings by evaluating long-interval cortical inhibition from the dorsolateral prefrontal cortex in patients with schizophrenia compared to patients with obsessive-compulsive disorder. A total of 111 participants were assessed: 38 patients with schizophrenia (average age: 35.71 years, 25 males, 13 females), 27 patients with obsessive-compulsive disorder (average age: 36.15 years, 11 males, 16 females) and 46 healthy subjects (average age: 33.63 years, 23 females, 23 males). Long-interval cortical inhibition was measured from the dorsolateral prefrontal cortex and motor cortex through combined transcranial magnetic stimulation and electroencephalography. In the dorsolateral prefrontal cortex, long-interval cortical inhibition was significantly reduced in patients with schizophrenia compared to healthy subjects (P = 0.004) and not significantly different between patients with obsessive-compulsive disorder and healthy subjects (P = 0.5445). Long-interval cortical inhibition deficits in the dorsolateral prefrontal cortex were also significantly greater in patients with schizophrenia compared to patients with obsessive-compulsive disorder (P = 0.0465). There were no significant differences in long-interval cortical inhibition across all three groups in the motor cortex. These results demonstrate that long-interval cortical inhibition deficits in the dorsolateral prefrontal cortex are specific to patients with schizophrenia and are not a generalized deficit that is shared by disorders of severe psychopathology. [ABSTRACT FROM AUTHOR]

Objective: Long-interval cortical inhibition (LICI) can be recorded from motor and non-motor regions of the cortex through combined transcranial magnetic stimulation (TMS) with electroencephalography (EEG). This study aimed to evaluate additional dimensions of LICI characteristics over an extended time-frequency and spatial domain. This was done by introducing two alternative measures of LICI signal amplitude: the Discrete Fourier Transform (DFT) and the Hilbert transform (HT). Both approaches estimate signal amplitude not taking into account the phase. In both cases LICI was measured as the difference between the unconditioned and conditioned activity evoked by the test pulse. Finally, we evaluated whether the topographical patterns of single and paired responses differed beyond the expected variations in amplitude. Materials and Methods: LICI was delivered as single and paired pulses to the motor cortex (MC) and dorsolateral prefrontal cortex (DLPFC) in 33 healthy subjects with TMS-EEG. Results: Significant differences (p<0.0001) between the unconditioned and conditioned evoked activity were found for both the DLPFC and MC using both methods (i.e., DFT and HT) after correcting for multiple comparisons in the time-frequency domain. The influence of inhibition was found to be significantly larger in space and time than previously considered. Single and paired conditions differ in intensity, but also in their topographic pattern (i.e., the specific spatiotemporal configuration of active sources). Conclusion: Similar results were found by both DFT and HT. The effect of inhibition across the cortex was also found to be complex and extended. In particular, it was found that LICI may be measured with high sensitivity in areas that were relatively distant from the stimulation site, which may have important practical applications. The analysis presented in this study overcomes some limitations of previous studies and could serve as a key reference for future studies examining TMS-indices of inhibition/excitation in healthy and diseased states. [ABSTRACT FROM AUTHOR]

Background Deep brain stimulation (DBS) has treatment efficacy in neurological and psychiatric disorders such as Parkinson's disease and major depression. Electroencephalography (EEG) is a versatile neurophysiological tool that can be used to better understand DBS treatment mechanisms. DBS causes artifacts in EEG recordings that preclude meaningful neurophysiological activity from being quantified during stimulation. New method In this study, we modeled the DBS stimulation artifact and illustrated a technique for removing the artifact using matched filters. The approach was validated using a synthetically generated DBS artifact superimposed on EEG data. Mean squared error (MSE) between the recovered signal and the artifact-free signal was used to quantify the effectiveness of the approach. Results The DBS artifact was characterized by a series of narrow band components at the harmonic frequencies of DBS stimulation. The filtering approach successfully removed the DBS artifact with MSE value being less than 2% of base signal power for the typical stimulation and recording setups. General guidelines on how to setup DBS EEG studies and configure the subsequent artifact removal process are described. Comparison with previous method To avoid stimulus artifacts, a number of EEG studies with DBS subjects have resorted to turning the stimulator off during recording, while other studies have used low pass filters to remove artifacts and look at frequencies well below 50 Hz. Conclusions This study establishes a method through which DBS artifact in EEG recordings can be reliably eliminated, thereby preserving a meaningful neurophysiological signal through which to better understand DBS treatment mechanisms. [ABSTRACT FROM AUTHOR]

Background: Celiac disease is associated with motor cortex hyperexcitability and neurological manifestations including cortical myoclonus. Electroencephalography abnormalities have been described, but no distinct pattern has been reported. Methods: We describe the neurophysiological characteristics of 3 patients with celiac‐associated cortical myoclonus using electroencephalography, magnetoencephalography, and transcranial magnetic stimulation. Results: Electroencephalography in all cases demonstrated lateralized low‐amplitude, electropositive beta‐frequency polyspike activity over the central head region, corresponding to motor cortex contralateral to the myoclonic limb. Jerk‐locked back‐averaging demonstrated a preceding cortical potential; magnetoencephalography source localization revealed a cortical generator in the posterior wall of the precentral gyrus for the back‐averaged potential and oscillatory abnormality. In 1 patient, cerebellar inhibition of the motor cortex was physiologically normal. Conclusions: Central head oscillatory, low‐amplitude, electropositive electroencephalography polyspike activity may be a distinct marker of celiac‐related cortical myoclonus and is consistent with celiac‐related motor cortex hyperexcitability, which may not necessarily result from cerebellar disinhibition. © 2020 International Parkinson and Movement Disorder Society [ABSTRACT FROM AUTHOR]

• Electromagnetic source imaging reveals BETS to be generated in the hippocampus. • EEG/MEG detection of BETS dependent on longitudinally extended hippocampal source. • Diphasic BETS waveform reflects back and forth propagation along hippocampal axis. Benign epileptiform transients of sleep (BETS) have a unique voltage topography and a posteriorly propagating, inferiorly rotating diphasic EEG pattern. The source generators of BETS have not been definitively identified. We aimed to clarify the cerebral localization of BETS using MEG and electromagnetic source imaging (EMSI). We analyzed BETS recorded with simultaneous MEG and EEG in four patients with epilepsy. Magnetic source imaging (MSI) and EMSI using equivalent current, single moving and rotating dipole inverse models was performed on averaged BETS potentials. MEG beamforming was performed in one case with abundant BETS. MSI and EMSI revealed hippocampal dipole source maxima in all cases, with current flow direction rotating from inferomedial to superomedial or superolateral between the first and second BETS peaks. Moving dipole analyses revealed spatiotemporal propagation along the anterior-posterior hippocampal axis and concomitant electromagnetic field rotation. Beamformer source reconstruction revealed an identical hippocampal localization. Converging evidence from different electromagnetic inverse modeling methods indicates that BETS are traveling, rotating hippocampal spikes, whose diphasic waveform is due to back and forth propagation along the anterior-posterior axis of the hippocampus. The hippocampal localization and longitudinal, rotating propagation pattern of BETS raises the possibility of a sleep-related functional role for these hippocampal spikes. [ABSTRACT FROM AUTHOR]

A patient with pilomotor seizures post anti‐LGI1 limbic encephalitis, refractory to immunotherapy and anti‐epileptic drugs, was investigated with electroencephalography and magnetoencephalography. Seizures occurred daily (14.9 ± 4.9/day), with catamenial exacerbation, inducible by hyperventilation. Anterior temporal ictal onsets were heralded (by ~15 sec) by high amplitude ipsilateral electromagnetic infraslow activity. The catamenial/ventilatory sensitivity and the infraslow activity (reflecting glial depolarization) suggested an ionic, CO2/pH‐related glioneuronal mechanism. Furosemide decreased seizure frequency by ~33%. Acetazolamide led to immediate seizure freedom, but lost efficacy with daily treatment. A cycling acetazolamide regimen (2 days on, 4 days off) plus low‐dose topiramate maintained >95% reduction (0.5 ± 0.9/day) in seizures. [ABSTRACT FROM AUTHOR]