This study aimed to compare the peripheral-to-central auditory systems of people with coronavirus disease 2019 to a well-matched control group and examine the long-term effects of coronavirus disease 2019 on the auditory system.

Participants who were outpatients of coronavirus disease 2019 (n = 30) were compared with a well-matched control group (n = 30). Behavioural and electrophysiological tests were performed, and tests were repeated at six months in the coronavirus disease 2019 group.

Statistically significant differences were observed in the right ear at 10 kHz (p = 0.007) and 12.5 kHz (p = 0.028), and in the left ear at 10 kHz (p = 0.040) and 12.5 kHz (p = 0.040) between groups. The groups had no difference regarding the other audiological test results (p > 0.05).

Extended high-frequency thresholds were affected in the coronavirus disease 2019 patients. No other findings indicated that the peripheral-to-central auditory system was affected. The effect on extended high-frequency thresholds appeared permanent, but no clinically significant new, late-onset auditory system effects were observed.

This study aimed to determine the precautions that can be taken to increase the reliability of the vestibular evoked myogenic potentials test without being affected by the asymmetry of the sternocleidomastoid muscle and the issues that should be considered in the interpretation of vestibular evoked myogenic potential results if these precautions are not taken.

Individuals with sternocleidomastoid muscle activity of less than 30 μV in cervical vestibular evoked myogenic potential testing and an asymmetry ratio of more than 0.35 were excluded. In our study, individuals were divided into different groups according to sternocleidomastoid muscle asymetry.

A total of 53 individuals were included in the study. Intergroup comparisons were made to determine the effect of electromyogram scaling and filter use on amplitude asymmetry ratio according to sternocleidomastoid muscle asymmetry.

Keeping the sternocleidomastoid muscle asymmetry not exceeding 10 μV maximises the reliability of cervical vestibular evoked myogenic potentials. As a result of our study, it can be concluded that in clinical applications the asymmetry should not exceed 20 μV.

A major pathophysiological hypothesis of schizophrenia states an increased activity of glutamatergic neurons leading to an imbalance of neural excitation and inhibition (E/I-imbalance). One potential molecular mechanism of E/I-imbalance is a dysfunction of voltage-gated sodium channels, which are crucial for the generation of action potentials, the fundamental event of neuronal excitation. Indeed, patients with schizophrenia exhibit an increased burden of rare exonic variants of sodium channel genes, but the literature describing their electrophysiological effect is scarce.

The aim of this project is to assess the functional impact of three mutations of the Sodium Voltage-Gated Channel Alpha Subunit 2 (SCN2A) gene / NaV1.2 channel which were identified in four patients with schizophrenia, using a heterologous expression system.

Three variants of the human SCN2A gene (R850P, V1282F and S1656P) were created using site-directed mutagenesis. HEK293T cells transfected with either the mutant or wild type constructs are being investigated by voltage-clamp technique, applying activation, steady-state fast inactivation, use dependency and ramp protocols.

All three mutated constructs were successfully created. Preliminary recordings from the V1282F mutant indicate a shift of both the activation and steady-state fast inactivation to the hyperpolarized direction.

In a subgroup of patients, E/I imbalance may be a consequence of Nav1.2 mutations leading to increased excitability of glutamatergic neurons. By integrating insights from different mutations we aim to identify traits of a potentially shared disease pathway which may provide a basis for the development of novel therapeutics.

No significant relationships.

Autism Spectrum Disorder and Social Anxiety Disorder are mental illnesses characterized by a dysfunction in social behavior (SB); a phenomenon largely mediated by the medial prefrontal cortex (mPFC). Clinical studies have demonstrated that lysergic acid diethylamide (LSD), a partial agonist of the 5-HT2A receptor, can promote SB. However, its mechanism of action on SB is unknown.

To assess the effects of repeated LSD administration on social behavior in mice and to identify which mPFC receptors mediate LSD’s behavioral effects.

Eight-week-old C57BL/6J male mice received vehicle or repeated LSD (30 μg/kg/day i.p. for 7 days) as well the selective 5-HT2A receptor antagonist MDL, or the AMPA receptor antagonist NBQX. Twenty-four hours following the last injection, mice underwent the Direct Social Interaction Test and the Three-Chamber Test (TCT) to assess sociability and preference for social novelty. in vivo electrophysiological recordings were performed in mice treated with vehicle or LSD using multi-barrelled electrodes for microiontophoretic ejections of the selective 5-HT2A receptor agonist DOI or the selective AMPA receptor agonist quisqualate on mPFC pyramidal neurons.

Repeated treatment with low doses of LSD increased the interaction time in the DSI as well as sociability and social novelty indices in the TCT. These pro-social effects were blocked by the intra-PFC administration of both 5-HT2A and AMPA antagonists. LSD also potentiated, in a current-dependent manner, the excitatory response of mPFC neurons to 5-HT2Aand AMPA agonists.

Repeated, low doses of LSD increases social behavior via a mechanism of action that is mediated by 5-HT2A and AMPA in the mPFC.

The electrical current distribution of a cochlear implant electrode within the cochlea is essential for post-operative hearing performance. The slim straight electrode is designed to enable the placement of contacts in a lateral or medial direction to the modiolus. The electrophysiological effect of this different contact direction is so far unknown. The aim of this study was to determine the influence of intracochlear laterally or medially directed electrode contacts on electrophysiological behaviour.

A slim straight electrode was inserted into the cochleae of five patients, and the neural response threshold was measured in a laterally and medially directed contact position. The cochleae in five temporal bone specimens were de-capped allowing an insertional observation of the contact position (lateral versus medial) of the electrode.

There was no difference in neural response threshold between a lateral and a medial position of the contacts. Temporal bone study indicated no intracochlear torsion of the electrode.

Our study provides evidence that the intracochlear position of slim straight electrode contacts does not affect the neural response threshold.

A wealth of clinical studies have identified objective biomarkers, which separate schizophrenia patients from healthy controls on a group level, but current diagnostic systems solely include clinical symptoms. In this study, we investigate if machine learning algorithms on multimodal data can serve as a framework for clinical translation.

Forty-six antipsychotic-naïve, first-episode schizophrenia patients and 58 controls underwent neurocognitive tests, electrophysiology, and magnetic resonance imaging (MRI). Patients underwent clinical assessments before and after 6 weeks of antipsychotic monotherapy with amisulpride. Nine configurations of different supervised machine learning algorithms were applied to first estimate the unimodal diagnostic accuracy, and next to estimate the multimodal diagnostic accuracy. Finally, we explored the predictability of symptom remission.

Cognitive data significantly classified patients from controls (accuracies = 60–69%; p values = 0.0001–0.009). Accuracies of electrophysiology, structural MRI, and diffusion tensor imaging did not exceed chance level. Multimodal analyses with cognition plus any combination of one or more of the remaining three modalities did not outperform cognition alone. None of the modalities predicted symptom remission.

In this multivariate and multimodal study in antipsychotic-naïve patients, only cognition significantly discriminated patients from controls, and no modality appeared to predict short-term symptom remission. Overall, these findings add to the increasing call for cognition to be included in the definition of schizophrenia. To bring about the full potential of machine learning algorithms in first-episode, antipsychotic-naïve schizophrenia patients, careful a priori variable selection based on independent data as well as inclusion of other modalities may be required.

Attention deficits have been frequently reported in schizophrenia. It has been suggested that treatment with second-generation antipsychotics can ameliorate these deficits. In this study, the influence of 6 months treatment with quetiapine, a compound with less affinity for dopamine D2 receptors than for serotonergic 5-HT2A receptors, on electrophysiological parameters of attention was investigated in a group of antipsychotic-naïve, first-episode schizophrenia patients compared with a group of age- and gender-matched healthy controls.

A total of 34 first-episode, antipsychotic-naïve patients with schizophrenia and an equal number of healthy controls were tested in a selective attention and a typical mismatch negativity (MMN) paradigm at baseline and after 6 months. The patients were treated with quetiapine according to their clinical needs during the period between baseline and follow-up, whereas controls received no treatment.

Patients showed lower MMN and P200 amplitude than healthy controls in the selective attention paradigm at baseline, while this was not the case for MMN of the typical MMN paradigm. Interestingly, after 6 months treatment, this MMN deficit was only ameliorated in patients treated with above median dosages of quetiapine. Patients had lower P3B amplitude, yet showed similar levels of processing negativity and N100 amplitude compared with healthy controls, both at baseline and follow-up.

The results indicate that deficits in MMN, P200 and P3B amplitude are present at early stages of schizophrenia, although depending on the paradigm used. Furthermore, the results indicate that 6 months quetiapine treatment ameliorates MMN but not P3B deficits, and only in those subjects on higher dosages.

Deficient mismatch negativity (MMN) has been proposed as a candidate biomarker in schizophrenia and may therefore be potentially useful in early identification and intervention in early onset psychosis. In this study we explored whether deficits in the automatic orienting and reorienting responses, measured as MMN and P3a amplitude, are present in young adolescents with first-episode psychosis (FEP) and whether findings are specific to psychosis compared to young adolescents with attention deficit hyperactivity disorder (ADHD).

MMN and P3a amplitude were assessed in young adolescents (age 12–17 years) with either FEP (N = 27) or ADHD (N = 28) and age- and gender-matched healthy controls (N = 43). The MMN paradigm consisted of a four-tone auditory oddball task with deviant stimuli based on frequency, duration and their combination.

Significantly less MMN was found in patients with psychosis compared to healthy controls in response to frequency and duration deviants. MMN amplitudes in the group of patients with ADHD were not significantly different from patients with psychosis or healthy controls. No significant group differences were found on P3a amplitude.

Young adolescents with FEP showed impaired MMN compared to healthy controls while intermediate and overlapping levels of MMN were observed in adolescents with ADHD. The findings suggest that young FEP patients already exhibit pre-attentive deficits that are characteristic of schizophrenia albeit expressed on a continuum shared with other neuropsychiatric disorders.