Transcranial magnetic stimulation (TMS) is a non-invasive and painless neuroelectrophysiological examination technology. TMS-motor evoked potential (TMS-MEP) is widely used to assess motor cortex excitability and conduction of descending corticobulbar tract and corticospinal tract. Recently, deeper understanding on principles of magnetic stimulation and diversification of stimulation coil and pattern has greatly expanded the application of TMS in clinical diagnosis. Moreover, MEP operation procedures are becoming more scientific and standardized. This paper reviews the progress of conventional diagnostic TMS pattern, several special stimulation patterns and the combined application of TMS, electroencephalograpy (EEG) and fMRI. DOI: 10.3969/j.issn.1672-6731.2017.04.011
Abstract Background and hypothesis Substantive inquiry into the predictive power of eye movement (EM) features for clinical high-risk (CHR) conversion and their longitudinal trajectories is currently sparse. This study aimed to investigate the efficiency of machine learning predictive models relying on EM indices and examine the longitudinal alterations of these indices across the temporal continuum. Study design EM assessments (fixation stability, free-viewing, and smooth pursuit tasks) were performed on 140 CHR and 98 healthy control participants at baseline, followed by a 1-year longitudinal observational study. We adopted Cox regression analysis and constructed random forest prediction models. We also employed linear mixed-effects models (LMMs) to analyze longitudinal changes of indices while stratifying by group and time. Study results Of the 123 CHR participants who underwent a 1-year clinical follow-up, 25 progressed to full-blown psychosis, while 98 remained non-converters. Compared with the non-converters, the converters exhibited prolonged fixation durations, decreased saccade amplitudes during the free-viewing task; larger saccades, and reduced velocity gain during the smooth pursuit task. Furthermore, based on 4 baseline EM measures, a random forest model classified converters and non-converters with an accuracy of 0.776 (95% CI: 0.633, 0.882). Finally, LMMs demonstrated no significant longitudinal alterations in the aforementioned indices among converters after 1 year. Conclusions Aberrant EMs may precede psychosis onset and remain stable after 1 year, and applying eye-tracking technology combined with a modeling approach could potentially aid in predicting CHRs evolution into overt psychosis.
Abnormal mismatch negativity (MMN), thought to be a putative marker of glutamatergic function, has been reported in non-Asian, first episode schizophrenia and clinical high-risk for psychosis (CHR) individuals as indicative of impairments in pre-attentive processes. However, reports of abnormal MMN in Asian populations are sparse, as well as its relationships to glutamate and γ–aminobutyric acid (GABA) levels in medial prefrontal cortex. The present longitudinal study explored MMN differences between CHR subjects who will and who will not remit, and its relationships with prefrontal glutamate and GABA levels. All subjects participated in the ShangHai At-Risk for Psychosis (SHARP) program. CHR subjects met the criteria defined by the Chinese version of the Structural Interview for Prodromal Syndromes (SIPS). From the SHARP sample, 76 CHR subjects (41 male, age 18.63 ± 5.02 years) and 53 HC (31 male, age 17.72 ± 3.18 years) completed both MMN test and proton magnetic resonance spectroscopy (1H MRS) scans using a MEGA-PRESS sequence at their initial visit. CHR subjects were divided into remitted (37) and non-remitted (34) individuals based on their clinical symptoms and functional scores at a one-year follow up. Duration MMN amplitude was measured at electrodes F1/2, Fz, FC1/2, FCz, C1/2 and Cz. Concentrations of glutamate+glutamine (Glx) and GABA in the medial prefrontal cortex (mPFC) were quantified using the LCModel software (version 6.3-0I). Repeated measures analysis of variance (ANOVA) with group (remitted CHR, non-remitted CHR and HC) as the between-group factor and electrodes (Fz, FCz and Cz) as the within-group factor were performed for the midline sites, and the ANOVA using F1/2, FC1/2 and C1/C2 with laterality (left and right hemisphere) as an additional within-group factor was performed for the lateral sites. Correlations of the dMMN amplitude (averaged over the 9 electrodes) and Glx and GABA concentrations were assessed by Pearson correlation tests for each group. There was a significant main effect of group (F(2,121)=3.14, p<0.05) for the midline fronto-central dMMN amplitude. Post-hoc tests showed that non-remitted CHR subjects had lower baseline dMMN amplitude (-4.75 ± 0.37μv) than HC (-5.92 ± 0.30μv, p<0.05), whereas dMMN in remitted CHR (-5.22 ± 0.36μv, p=0.41) was comparable to dMMN in HC. The main effect of group was marginally significant at lateral sites (F(2,121)=2.83, p=0.06). DMMN amplitude in non-remitted CHR (-4.67 ± 0.37μv) tended to be lower than those in HC (-5.76 ± 0.29μv, p<0.1), while remitted CHR had dMMN amplitude (-5.11 ± 0.35μv, p=0.47) comparable to HC. There was no significant main effect of laterality or interaction of group × laterality. In non-remitted CHR subjects, dMMN amplitude was significantly correlated with Glx level (r=-0.47, p<0.01) and with GABA level (r=-0.38, p<0.05) in the mPFC. However, the correlation of dMMN amplitude with Glx or GABA levels was not significant among either HC or remitted CHR. In line with previous studies, reduced dMMN amplitude distinguished between remitted and non-remitted CHR subjects, with remitted CHR not different from HCs. Our finding further supports the idea that reduced dMMN amplitude could be a candidate biomarker for predicting outcome in CHR. More importantly, we linked the reduced dMMN amplitude in non-remitted CHR to their Glx and GABA levels in mPFC, the region identified as one of dMMN sources (responsible for attention switching) thus supporting the idea that NMDA-mediated disruptions may play a key role in predicting psychosis and functional outcome.
Objective: We aimed to examined whether the electrophysiological signatures of error monitoring are associated with clinical insight among outpatients with attenuated psychosis syndrome (APS) and first-episode psychosis (FEP).Methods: Event-related potentials, including the error-related negativity (ERN), error positivity (Pe), and correct response negativity (CRN), were recorded during FEP patients (n = 32), APS individuals (n = 58), and healthy controls (HC, n = 49) performed a modified flanker task. Clinical insight was measured using the Schedule of Assessment of Insight and included awareness of insight, relabeling of specific symptoms, and treatment compliance.Results: Compared with HC, FEP patients showed smaller ERN (p < 0.001) and Pe (p = 0.011) amplitudes and APS individuals showed a smaller ERN amplitude (p = 0.009). ERN negatively correlated with each dimension of clinical insight (p < 0.05) in the total outpatient sample. For APS individuals, ERN correlated with awareness of insight (r = -0.255, p = 0.054), treatment compliance (r = -0.281, p = 0.033), and overall clinical insight (r = -0.294, p = 0.025); Pe correlated marginally with awareness of insight (r = 0.257, p = 0.051), treatment compliance (r = 0.257, p = 0.051), and overall clinical insight (r = 0.248, p = 0.060). For FEP patients, ERN correlated marginally with relabeling of specific symptoms (r = -0.336, p = 0.060). No positive results were found for CRN.Conclusion: Error-monitoring deficits probably contributes to impaired insight in the early stages of psychosis, before and after the onset of the first episode.
Abstract Objective Cataplexy is a complicated and dynamic process in narcolepsy type 1 ( NT 1) patients. This study aimed to clarify the distinct stages during a cataplectic attack and identify the changes of the primary motor cortex ( PMC ) excitability during these stages. Methods Thirty‐five patients with NT 1 and 29 healthy controls were recruited to this study. Cataplectic stages were distinguished from a cataplectic attack by video‐polysomnogram monitoring. Transcranial magnetic stimulation motor‐evoked potential ( TMS ‐ MEP ) was performed to measure the excitability of PMC during quiet wakefulness, laughter without cataplexy, and each cataplectic stage. Results Based on the video and electromyogram observations, a typical cataplectic attack ( CA ) process is divided into four stages: triggering ( CA 1), resisting ( CA 2), atonic ( CA 3), and recovering stages ( CA 4). Compared with healthy controls, NT 1 patients showed significantly decreased intracortical facilitation during quiet wakefulness. During the laughter stage, both patients and controls showed increased MEP amplitude compared with quiet wakefulness. The MEP amplitude significantly increased even higher in CA 1 and 2, and then dramatically decreased in CA 3 accompanied with prolonged MEP latency compared with the laughter stage and quiet wakefulness. The MEP amplitude and latency gradually recovered during CA 4. Interpretation This study identifies four stages during cataplectic attack and reveals the existence of a resisting stage that might change the process of cataplexy. The fluctuation of MEP amplitude and MEP latency shows a potential participation of PMC and motor control pathway during cataplexy, and the increased MEP amplitude during CA 1 and 2 strongly implies a compensatory mechanism in motor control that may resist or avoid cataplectic attack.
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