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Background Better protection can be provided during neurosurgery due to the establishment of somatosensory-evoked potential (SEP) and motor-evoked potential (MEP) monitoring technologies. However, some studies have showed that inhaled halogenated anesthetics have a significant impact on neurophysiological monitoring. Methods A total of 40 consecutive patients undergoing neurosurgery were randomly assigned to two groups receiving inhaled anesthetics, either desflurane or sevoflurane. Multiples levels (concentrations of 0.3, 0.6 and 0.9) of anesthetics were administered at minimum alveolar concentration (MAC), and then the latencies and amplitudes of SEPs and MEPs were recorded. Results SEP and MEP signals were well preserved in patients who underwent neurosurgery under general anesthesia supplemented with desflurane or sevoflurane at concentrations of 0.3, 0.6 and 0.9 MAC. In each desflurane or sevoflurane group, the amplitudes of SEPs and MEPs decreased and the latencies of SEPs were prolonged significantly as the MAC increased ( P  < 0.05). The SEP latencies of both the upper and lower limbs in the desflurane group were significantly longer, and the SEP amplitudes were significantly lower than those in the sevoflurane group ( P  < 0.05). The MEP amplitudes in the desflurane group were significantly lower than those in the sevoflurane group ( P  < 0.05), only the amplitudes of the upper limbs at 0.3 MAC did not vary significantly. Conclusions SEPs and MEPs were inhibited in a dose-dependent manner by both desflurane and sevoflurane. At the same MAC concentration, desflurane appeared to have a stronger inhibitory effect than sevoflurane. All patients studied had normal neurological examination findings, hence, these results may not be applicable to patients with preexisting deficits. Trial registration The study registered on the Chinese Clinical Trial Registry ( www.chictr.org.cn ), Clinical Trials identifier ChiCTR2100045504 (18/04/2021).

The effects of caffeine are mediated through its non-selective antagonistic effects on adenosine A1 and A2A adenosine receptors resulting in increased neuronal activity but also vasoconstriction in the brain. Caffeine, therefore, can modify BOLD FMRI signal responses through both its neural and its vascular effects depending on receptor distributions in different brain regions. In this study we aim to distinguish neural and vascular influences of a single dose of caffeine in measurements of task-related brain activity using simultaneous EEG–FMRI. We chose to compare low-level visual and motor (paced finger tapping) tasks with a cognitive (auditory oddball) task, with the expectation that caffeine would differentially affect brain responses in relation to these tasks. To avoid the influence of chronic caffeine intake, we examined the effect of 250mg of oral caffeine on 14 non and infrequent caffeine consumers in a double-blind placebo-controlled cross-over study. Our results show that the task-related BOLD signal change in visual and primary motor cortex was significantly reduced by caffeine, while the amplitude and latency of visual evoked potentials over occipital cortex remained unaltered. However, during the auditory oddball task (target versus non-target stimuli) caffeine significantly increased the BOLD signal in frontal cortex. Correspondingly, there was also a significant effect of caffeine in reducing the target evoked response potential (P300) latency in the oddball task and this was associated with a positive potential over frontal cortex. Behavioural data showed that caffeine also improved performance in the oddball task with a significantly reduced number of missed responses. Our results are consistent with earlier studies demonstrating altered flow-metabolism coupling after caffeine administration in the context of our observation of a generalised caffeine-induced reduction in cerebral blood flow demonstrated by arterial spin labelling (19% reduction over grey matter). We were able to identify vascular effects and hence altered neurovascular coupling through the alteration of low-level task FMRI responses in the face of a preserved visual evoked potential. However, our data also suggest a cognitive effect of caffeine through its positive effect on the frontal BOLD signal consistent with the shortening of oddball EEG response latency. The combined use of EEG–FMRI is a promising methodology for investigating alterations in brain function in drug and disease studies where neurovascular coupling may be altered on a regional basis. ► Caffeine reduced task related BOLD responses in visual and motor cortex. ► However, amplitude and latency of visual evoked potentials remained unaltered. ► Performance and frontal BOLD response in an auditory oddball task were enhanced. ► Correspondingly, caffeine reduced the latency of target-evoked potentials. ► EEG–FMRI can separate vascular and neural influences of caffeine in low consumers.

This study aimed to compare the effects of ciprofol and propofol on motor evoked potentials (MEPs) and somatosensory evoked potentials (SEPs) in elderly patients undergoing spinal surgery. This trial enrolled 60 elderly patients scheduled for elective spinal surgery with intraoperative neurophysiological monitoring (IONM) and assigned them to Group C (receiving ciprofol) or Group P (receiving propofol) using random allocation. Primary outcome measures focused on MEPs and SEPs amplitudes of lower extremities at T6. The secondary outcomes encompassed neurophysiological measures (MEPs and SEPs latencies at T6, as well as their amplitudes and latencies at T5), hemodynamic parameters of heart rate (HR), mean arterial pressure (MAP), and bispectral index (BIS) values at T1-T6, along with the incidence of hypotension, bradycardia, requirements for vasoactive medications. Neurophysiological recordings at T6 showed significantly higher amplitudes in Group C across all measured parameters during inter-group comparison. For MEPs, Group C demonstrated greater amplitudes in lower extremities (1378 μV, IQR 1256-1605 vs 1121 μV, IQR 1077-1307; <0.001). Similarly, SEPs were significantly elevated in Group C for lower extremities (1.34 μV, IQR 0.9-1.63 vs 1.11 μV, IQR 0.82-1.16; =0.013). However, no inter-group differences existed in MEPs or SEPs latency. From T3 to T6, Group C exhibited higher MAP values than in Group P(all <0.05); and no intergroup difference in BIS values was observed at T5-T6 (T5: 47.4 ± 4.0 vs 49.1 ± 4.7, = 0.145; T6: 46.4 ± 3.5 vs 46.2 ± 4.0, =0.892). Group C had a reduced need for vasoactive medications (13% vs 50%, = 0.002), less hypotension incidence (17% vs 40%, = 0.045). Ciprofol outperforms propofol in hemodynamic stability for the elderly undergoing spinal surgery, with less suppression of the amplitudes of MEPs and SEPs, and no prolongation of latency, thereby potentially improving the quality of IONM. ChiCTR2400091429.

PurposeThis study was designed to evaluate the effect of preoperative pregabalin on intraoperative neurophysiological monitoring in adolescents undergoing surgery for spinal deformities.MethodsThirty-one adolescents undergoing posterior spinal fusion were randomized to receive preoperatively either pregabalin 2 mg/kg twice daily or placebo. The ability to make reliable intraoperative neurophysiological measurements, transcranial motor (MEPs) and sensory evoked potentials (SSEP) was evaluated.ResultsTwo patients (pregabalin group) did not fulfil the inclusion criteria and one patient’s (placebo group) spinal monitoring was technically incomplete and these were excluded from the final data. In the rest, spinal cord monitoring was successful. Anaesthesia prolonged the latency of MEPs and increased the threshold current of MEP. The current required to elicit MEPs did not differ between the study groups. There were no statistically significant differences between the study groups regarding the latency of bilateral SSEP (N32 and P37) and MEP latencies at any time point.ConclusionsPreoperative pregabalin does not interfere spinal cord monitoring in adolescents undergoing posterior spinal fusion.Level of evidenceI.

Background We hypothesized that the addition of dexmedetomidine in a clinically relevant dose to propofol-remifentanil anesthesia regimen does not exert an adverse effect on motor-evoked potentials (MEP) and somatosensory-evoked potentials (SSEP) in adult patients undergoing thoracic spinal cord tumor resection. Methods Seventy-one adult patients were randomized into three groups. Propofol group ( n  = 25): propofol-remifentanil regimenand the dosage was adjusted to maintain the bispectral index (BIS) between 40 and 50. DP adjusted group ( n  = 23): Dexmedetomidine (0.5 μg/kg loading dose infused over 10 min followed by a constant infusion of 0.5 μg/kg/h) was added to the propofol-remifentanil regimen and propofol was adjusted to maintain BIS between 40 and 50. DP unadjusted group ( n  = 23): Dexmedetomidine (administer as DP adjusted group) was added to the propofol-remifentanil regimen and propofol was not adjusted. All patients received MEP, SSEP and BIS monitoring. Results There were no significant changes in the amplitude and latency of MEP and SSEP among different groups ( P  > 0.05). The estimated propofol plasma concentration in DP adjusted group (2.7 ± 0.3 μg/ml) was significantly lower than in propofol group (3.1 ± 0.2 μg/ml) and DP unadjusted group (3.1 ± 0.2 μg/ml) ( P  = 0.000). BIS in DP unadjusted group (35 ± 5) was significantly lower than in propofol group (44 ± 3) ( P  = 0.000). Conclusions The addition of dexmedetomidine to propofol-remifentanil regimen does not exert an adverse effect on MEP and SSEP monitoring in adult patients undergoing thoracic spinal cord tumor resection. Trial registration The study was registered with the Chinese Clinical Trial Registry on January 31st, 2014. The reference number was ChiCTR-TRC-14004229.

Hyperarousal symptoms in generalized anxiety disorder (GAD) are often incongruent with the observed physiological state, suggesting that abnormal processing of interoceptive signals is a characteristic feature of the disorder. To examine the neural mechanisms underlying interoceptive dysfunction in GAD, we evaluated whether adrenergic modulation of cardiovascular signaling differentially affects the heartbeat-evoked potential (HEP), an electrophysiological marker of cardiac interoception, during concurrent electroencephalogram and functional magnetic resonance imaging (EEG-fMRI) scanning. Intravenous infusions of the peripheral adrenergic agonist isoproterenol (0.5 and 2.0 micrograms, μg) were administered in a randomized, double-blinded and placebo-controlled fashion to dynamically perturb the cardiovascular system while recording the associated EEG-fMRI responses. During the 0.5 μg isoproterenol infusion, the GAD group (n = 24) exhibited significantly larger changes in HEP amplitude in an opposite direction than the healthy comparison (HC) group (n = 24). In addition, the GAD group showed significantly larger absolute HEP amplitudes than the HC group during saline infusions, when cardiovascular tone did not increase. No significant group differences in HEP amplitude were identified during the 2.0 μg isoproterenol infusion. Using analyzable blood oxygenation level-dependent fMRI data from participants with concurrent EEG-fMRI data (21 GAD and 21 HC), we found that the aforementioned HEP effects were uncorrelated with fMRI signals in the insula, ventromedial prefrontal cortex, dorsal anterior cingulate cortex, amygdala, and somatosensory cortex, brain regions implicated in cardiac signal processing in prior fMRI studies. These findings provide additional evidence of dysfunctional cardiac interoception in GAD and identify neural processes at the electrophysiological level that may be independent from blood oxygen level-dependent responses during peripheral adrenergic stimulation.

Multiple sclerosis is a degenerative inflammatory disease of the CNS characterised by immune-mediated destruction of myelin and progressive neuroaxonal loss. Myelin in the CNS is a specialised extension of the oligodendrocyte plasma membrane and clemastine fumarate can stimulate differentiation of oligodendrocyte precursor cells in vitro, in animal models, and in human cells. We aimed to analyse the efficacy and safety of clemastine fumarate as a treatment for patients with multiple sclerosis. We did this single-centre, 150-day, double-blind, randomised, placebo-controlled, crossover trial (ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neuropathy on stable immunomodulatory therapy. Patients who fulfilled international panel criteria for diagnosis with disease duration of less than 15 years were eligible. Patients were randomly assigned (1:1) via block randomisation using a random number generator to receive either clemastine fumarate (5·36 mg orally twice daily) for 90 days followed by placebo for 60 days (group 1), or placebo for 90 days followed by clemastine fumarate (5·36 mg orally twice daily) for 60 days (group 2). The primary outcome was shortening of P100 latency delay on full-field, pattern-reversal, visual-evoked potentials. We analysed by intention to treat. The trial is registered with ClinicalTrials.gov, number NCT02040298. Between Jan 1, 2014, and April 11, 2015, we randomly assigned 50 patients to group 1 (n=25) or group 2 (n=25). All patients completed the study. The primary efficacy endpoint was met with clemastine fumarate treatment, which reduced the latency delay by 1·7 ms/eye (95% CI 0·5–2·9; p=0·0048) when analysing the trial as a crossover. Clemastine fumarate treatment was associated with fatigue, but no serious adverse events were reported. To our knowledge, this is the first randomised controlled trial to document efficacy of a remyelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis. Our findings suggest that myelin repair can be achieved even following prolonged damage. University of California, San Francisco and the Rachleff Family.

Background and Objective: The objective of this study was to examine the effects of natalizumab on functional parameters assessed by evoked potentials (visual [VEP], somatosensory [SEP] and motor evoked potentials [MEP]) in a cohort study in relapsing–remitting multiple sclerosis patients. Methods: EP data of 44 patients examined 12 months prior to natalizumab treatment, at the timepoint of treatment initiation and 1 year later were compared. Sum scores (VEP, MEP, SEP) were evaluated and correlated with the Expanded Disability Status Scale. Results: Improvement of the VEP sum score was found in 33% of natalizumab-treated patients but only in 9% of the same patients prior to treatment (p = 0.041). A comparable situation was found for SEP (improvement: 32% versus 5%; worsening: 11% versus 37%; p = 0.027). For MEP no significant differences were seen (improvement: 10% versus 18%; worsening: 5% versus 29%; p = 0.60). EP recordings (VEP = SEP > MEP) have the capacity to demonstrate treatment effects of natalizumab on a functional level. Conclusions: Natalizumab therapy increases the percentage of patients showing stable or even ameliorated electrophysiological parameters in the investigated functional systems.

While the deleterious effects of acute ethyl alcohol intoxication on executive control are well-established, the underlying spatiotemporal brain mechanisms remain largely unresolved. In addition, since the effects of alcohol are noticeable to participants, isolating the effects of the substance from those related to expectations represents a major challenge. We addressed these issues using a double-blind, randomized, parallel, placebo-controlled experimental design comparing the behavioral and electrical neuroimaging acute effects of 0.6 vs 0.02 ​g/kg alcohol intake recorded in 65 healthy adults during an inhibitory control Go/NoGo task. Topographic ERP analyses of covariance with self-reported dose expectations allowed to dissociate their neurophysiological effects from those of the substance. While alcohol intoxication increased response time variability and post-error slowing, bayesian analyses indicated that it did not modify commission error rates. Functionally, alcohol induced topographic ERP modulations over the periods of the stimulus-locked N2 and P3 components, arising from pre-supplementary motor and anterior cingulate areas. In contrast, alcohol decreased the strength of the response-locked anterior cingulate error-related component but not its topography. This pattern indicates that alcohol had a locally specific influence within the executive control network, but disrupted performance monitoring processes via global strength-based mechanisms. We further revealed that alcohol-related expectations induced temporally specific functional modulations of the early N2 stimulus-locked medio-lateral prefrontal activity, a processing phase preceding those influenced by the actual alcohol intake. Our collective findings thus not only reveal the mechanisms underlying alcohol-induced impairments in impulse control and error processing, but also dissociate substance- from expectations- related functional effects. •ERPs were recorded during a Go/NoGo task after 0.6 ​g/kg acute alcohol intoxication.•Alcohol induced topographic ERP modulations of the preSMA/ACC N2 and P3 components.•Alcohol induced global field power ERP modulations of the ACC ERN component.•Alcohol-related expectations modulated early mediolateral PFC N2 component.•Spatiotemporal dissociation of the effect of alcohol from those of the related expectations.

Background Recurrent observations have indicated the presence of deficits in mismatch negativity (MMN) among schizophrenia. There is evidence suggesting a correlation between increased dopaminergic activity and reduced MMN amplitude, but there is no consensus on whether antipsychotic medications can improve MMN deficit in schizophrenia. Methods We conducted clinical assessments, cognitive function tests, and EEG data collection and analysis on 31 drug-naïve patients with schizophrenia. Comprehensive evaluation tools such as PANSS and MCCB. MMN amplitude was analyzed by event-related potential (ERP) approaches, evoked theta power was analyzed by event-related spectral perturbation (ERSP) approaches. Results Our findings indicate that antipsychotic treatment significantly improved clinical symptoms, as evidenced by reductions in PANSS positive, negative, general symptoms, and total scores (all p  < 0.001). Cognitive function improvements were observed in language learning, working memory, and overall MCCB scores ( p  < 0.05), although other cognitive domains showed no significant changes. However, no significant improvements were noted in MMN amplitude and evoke theta power after four weeks of antipsychotic treatment ( p  > 0.05). Conclusion These results suggest that while antipsychotic medications effectively alleviate clinical symptoms, their impact on MMN amplitude and evoke theta power deficit is limited in the short term. Moreover, the amelioration of cognitive impairment in individuals with schizophrenia is not readily discernible, and it cannot be discounted that the enhancement observed in language acquisition and working memory may be attributed to a learning effect. These findings underscore the complexity of the neurobiological mechanisms involved and highlight the need for further research to optimize individualized treatment strategies for schizophrenia. Trial Registration ChiCTR2000038961, October 10, 2020.