Detecting psychotic-spectrum disorders early in developmental years is crucial. The initial years post-symptom onset are, indeed, fundamental for effective, timely and need-based interventions. Recent decades have seen significant progress in understanding psychosis-risk syndromes, offering opportunities for early intervention to prevent or lessen the impact of psychosis. However, identifying early signs is challenging due to varied clinical presentations and a continuum of psychotic symptoms. This presentation offers an evidence-based overview of the central constructs in the field and of their prognostic salience. The overarching aim is to assist clinicians in identifying and diagnosing early psychosis and related prodromal/at risk syndromic configurations.

Here, a patient will be discussed in which adipsic hypernatremia, a rare autoimmune encephalitis, presented in combination with complex psychiatric symptoms, including psychosis and catatonia. Due to his severe condition, the patient was hospitalized on our child and adolescent psychiatry emergency unit for 8 months. His rare encephalitis (adipsic hypernatremia) is characterized by autoantibodies against the thirst center of the brain. These autoantibodies cause inflammation and apoptosis in key regions of water homeostasis, leading to lack of thirst and highly increased serum sodium. Adipsic hypernatremia is a rather recently discovered disease and in other patients the symptoms of weakness, fatigue and drowsiness have been associated with it, but no psychiatric symptomatology. Therefore, this is the first patient, in which severe and complex psychiatric symptoms presented along with adipsic hypernatremia. The patient experienced delusion, hallucinations, restlessness and pronounced depression. Further, he showed ritualized, aggressive, disinhibited and sexualized behavior, as well as self-harm and psychomotor symptoms. In this case report we render first evidence speaking for a causal link between the autoimmune adipsic hypernatremia and the psychotic disorder.

Magnetic resonance spectroscopy (MRS) studies report alterations of both glutamatergic indices and N-acetyl aspartate (NAA) not only in first episode psychosis and established schizophrenia but also in high-risk populations. However, interpretation of these findings is limited by the region-of-interest approach of current MRS techniques, restricting the measurement to delimited cerebral volumes, selected by a priori hypotheses. In that context, we developed and implemented a new technique that allows for high resolution (i.e., 5 mm isotropic) whole-brain proton MRS imaging (MRSI) to map main metabolites in all brain regions of youth at clinical high risk for psychosis (CHR-P).
An FID-MRSI sequence with a 3D phase encoding accelerated by compressed-sensing was implemented on a 3T Siemens Prisma MRI. After reconstruction, 3D MRSI data were quantified with LCModel to produce 3D metabolite maps. Concentration for total N-acetyl aspartate (tNAA), total creatinine (tCre), choline-containing compounds (Cho), myo-inositol (Ins), glutamate and glutamine (Glx) were calculated in every single voxel. CHR-P were help-seeking youth aged between 14 and 35, who presented a psychosis-risk syndrome as assessed by the Structured Interview for Psychosis-Risk Syndromes. Healthy controls (HC) matched for age and sex were recruited in the general population. Regional differences between CHR-P and HC, computed using a voxel-based / cluster-based approach will be presented for each metabolite.
In general, there is a strong need to develop new tools for the identification and stratification of CHR-P populations. This pilot study illustrates the potential of 3D MRSI to detect subtle brain alterations, in the earliest stage of psychosis.

Introduction:
Recently, not only density but also timing of sleep spindles, a major electrophysiological oscillation during Non-rapid eye movement (NREM) sleep moved into the focus of models testing the complex regulation of memory consolidation and sleep maintenance.
Specifically, noradrenergic locus coeruleus activity has been identified to be crucial for the timing and synchronous sleep spindle clustering on an infraslow time scale (10 -100 seconds). On the other hand, this clustering was then crucial for sleep-dependent memory consolidation and sleep maintenance in the healthy, adult population.
In patients with schizophrenia, impairments in key elements of this potential causal chain are prominent (i.e. altered noradrenergic activity, reduced sleep spindle density, distressing cognitive deficits and difficulties maintaining sleep). However, little is known about the timing and clustering of the sleep spindles with infraslow oscillations in this patient group.
Thus, we assess the presence and strength of sleep spindle clustering on an infraslow time scale in individuals with Early-Onset Schizophrenia (EOS) and healthy controls (HC).

Methods: Sleep electroencephalographic data of patients with EOS (N=11, 16.38 +/- 1.43 years old; 36.4% female) and age- and sex-matched healthy controls (HC; N=11, 16.50 +/- 1.69 years old; 36.4% female) are analyzed. Infraslow oscillation parameters such as area under the curve, peak frequency, and bandwidth are assessed and compared between the groups.

Results: Preliminary results indicate that sleep spindles cluster on an infraslow time scale in children and adolescents with and without schizophrenia. Compared to HC, patients with EOS show a reduction of the area under the curve and an increase in peak frequency of infraslow oscillations in specific topographical regions during NREM 2 sleep.

Discussion: Sleep spindle clustering on an infraslow time scale is detectable in children and adolescent populations. Our results further suggest that young patients with SZ may have differences in the timing of sleep spindle clustering. Next steps investigating the relationship between sleep spindle clustering, memory, and sleep maintenance in a larger sample are underway to shed further light on potential pathomechanistic links and to inform novel therapeutical approaches boosting sleep spindles.

Reward feedback, crucial for learning and decision-making, is often disrupted during the clinical high risk (CHR) stage of psychosis. While past studies have associated cognitive impairments and brain function anomalies with CHR, the impact on cognitive flexibility in response to reward feedback remains unclear. To explore this, we conducted a probabilistic reward task with 59 CHR patients and 24 healthy control (HC) subjects at the Bern Early Recognition and Intervention Center. During this task, we also monitored prefrontal neurovascular responses using functional near-infrared spectroscopy (fNIRS). Our findings revealed that CHR subjects displayed a significantly lower response to reward feedback, particularly as the task progressed. Furthermore, fNIRS data indicated that CHR subjects experienced less increase in total hemoglobin concentrations, suggesting diminished prefrontal brain activity. These results imply that CHR subjects have reduced reward sensitivity, potentially contributing to deficits in reward-based learning and cognitive flexibility.