Cultural competence training has become increasingly common in psychiatric practice across Europe and worldwide, supported by evidence demonstrating improvements in quality of care, clinical effectiveness, and patient satisfaction. Since the publication of the original EPA guideline in 2015, the field has advanced considerably in its theoretical foundations, evidence base, and institutional support. This updated guideline addresses recent developments and challenges in research, policy, and clinical practice.

The guideline is based on a systematic meta-review of 15 systematic reviews and evidence-based guidelines on cultural competence training in psychiatric care and mental health. The evidence was synthesized to identify key concepts, educational components, implementation strategies, and current debates.

The review comprises four sections. First, it examines core elements of cultural competence training, emphasizing cultural humility, structural competence, and perspectives from the social and cultural sciences. Second, it provides practical recommendations for curriculum design, including the potential role of digital learning tools. Third, it addresses critiques of cultural competence, particularly concerns regarding essentializing and potentially racist interpretations. Finally, it explores strategies for integrating cultural competence training into existing psychiatric services, highlighting both individual and organizational factors that support implementation.

Cultural competence benefits not only migrant and ethnically diverse populations but all patients and healthcare professionals, including members of majority cultures. Successful implementation requires cultural sensitivity, critical self-reflection, and sustained commitment at individual, organizational, and system levels to achieve meaningful and lasting improvements in psychiatric care.

Recognizing atypical depression in patients with chronic pain syndromes remains a major clinical challenge in general hospital settings. Chronic pain is frequently accompanied by depressive symptoms, yet these symptoms often present in non-classical or “atypical” forms that may be overlooked or misattributed to somatic illness. Unlike typical major depression, atypical depression is characterized by mood reactivity, hypersomnia, increased appetite or weight gain, leaden paralysis, and heightened interpersonal sensitivity. In patients with chronic pain, these features may be masked by fatigue, sleep disturbances, and functional limitations related to the underlying medical condition, complicating accurate diagnosis.

In general hospitals, the focus on somatic treatment and the fragmentation of care between specialties further increase the risk of underrecognition. Patients may primarily report pain intensity, bodily discomfort, or treatment resistance, while affective symptoms remain unexpressed or are minimized. Neurobiological mechanisms shared by chronic pain and atypical depression—including dysregulation of inflammatory pathways, altered stress response systems, and changes in central pain processing—suggest a bidirectional relationship that worsens both conditions if left untreated.

Failure to identify atypical depression in this population is associated with poorer pain control, prolonged hospital stays, reduced adherence to medical treatment, and impaired functional recovery. Early recognition requires a high index of clinical suspicion, careful assessment of mood reactivity and behavioral patterns, and the use of screening tools adapted to medically ill populations. Close collaboration between internists, pain specialists, psychiatrists, and psychologists is essential.

Integrating routine mental health screening into general hospital care and promoting a biopsychosocial approach can improve diagnostic accuracy and therapeutic outcomes. Timely identification and targeted treatment of atypical depression may not only alleviate psychological distress but also enhance pain management, rehabilitation, and overall quality of life in patients with chronic pain syndromes.

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According to a biopsychosocial view of chronic pain, patients’ responses to antalgic treatments are influenced by the interventions themselves, as well as by psychological and contextual factors. This is especially relevant in the use of Spinal cord stimulation (SCS), a minimally invasive surgical technique used to treat people with chronic neuropathic pain (CNP) who have not responded to previous therapies and procedures, by modulating nerve signals.

To revise the literature on the relationship between psychological features and response to SCS in CNP, and to discuss some preliminary findings from an Italian sample of patients with CNP recruited at the University Hospital of Verona (Italy).

Selected patients from the Pain Therapy Center of the University Hospital of Verona undergo a psycho-social assessment at the Clinical Psychology unit before SCS. They were assessed on psychiatric symptoms, personality, presence of trauma, coping strategies, family/friends support, and use of alcohol or substances, with standardized questionnaires. Patients were evaluated at multiple follow-up time points.

Up-to-date literature suggests that several variables may be involved in predicting SCS outcomes, but also points to some gaps in our understanding of failed SCS. To date, 160 patients have been evaluated in our center. Overall, the sample shows elevated presence of somatization, sleep disturbances, depressive and obsessive-compulsive symptoms, together with moderate levels of catastrophizing and a personality profile characterized by health worries and cynicism, despite a high level of perceived self-efficacy and family or social support.

Collected data are presented in the context of the most recent literature, with the aim of strengthening our ability to identify patients at higher risk of SCS failure. The use of a proper pre-SCS assessment also enables the early detection of individuals who may require psychological interventions prior to or following surgery.

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Late-life depression refers to a depression occurring in older adults, defined as individuals aged 65 years and older. It is common and often mismanaged due to complex clinical profiles, polypharmacy, and limited evidence-based guidance. Existing tools poorly address psychiatric nuances in older adults. This work aims to develop French recommendations based on experts’ consensus on the use of antidepressants in unipolar late-life depression, to guide safer prescribing practices.

This tool was developed using a Delphi survey, based on a review of literature published between 2014 and 2024 and focused on “antidepressants” and “late-life depression” Experts from various fields: geriatric psychiatry, clinical pharmacy and general practice, rated items using a 9-point Likert scale. Items with a median score ≥ 7 and at least 80% agreement were validated and included in the final version of the tool.

Twenty to 23 experts per round, different from the authors of the proposed items, participated in a four-round Delphi process. The resulting tool includes 57 validated items across 10 sections and a stepped-care algorithm for treating major depression in older adults. It addresses drug choice, dosing, monitoring, comorbidities, and treatment resistance, prioritizing safe first-line options like sertraline, citalopram, and escitalopram.

A Delphi survey involving multidisciplinary experts led to a French consensus tool for prescribing antidepressants in unipolar late-life depression. It integrates clinical evidence and expert judgment to address treatment complexity, drug safety, and resistance. The tool offers practical, stepwise recommendations tailored to primary care, aiming to optimize antidepressant use, reduce iatrogenesis, and improve patient outcomes.

Chronic pain is a complex and multidimensional experience that persists beyond normal tissue healing and affects a substantial proportion of the adult population. Traditional diagnostic frameworks have been strongly based on subjective reports, limiting the understanding of the neurobiological mechanisms underlying their onset, maintenance, and cognitive-emotional impact.

This presentation aims to synthesize recent neuroimaging evidence elucidating how advances in brain imaging technologies are redefining our understanding of chronic pain, with implications for diagnosis, mechanistic models and personalized therapies.

We reviewed contemporary findings from structural and functional neuroimaging studies - primarily magnetic resonance imaging (MRI), resting-state fMRI, and advanced connectivity analyses - as well as integrative meta-analyses and systematic reviews (PubMed up to 2025).

Emerging neuroimaging research demonstrates that chronic pain is associated with widespread brain alterations in both structure and function. Key findings indicate widespread structural and functional brain alterations in chronic pain. Structurally, individuals with chronic pain show consistent reductions in grey matter volume and disruptions in white matter integrity across regions including the insula, cingulate cortex, thalamus, hippocampus, motor areas, and cerebellum, resembling patterns associated with accelerated brain ageing and neurodegeneration. Functionally, altered resting-state connectivity within salience and default mode networks has been observed, along with variable yet meaningful changes in pain-related activation. Emerging evidence from machine learning approaches and direct neural recordings suggests the presence of pain-specific brain signatures with potential as objective biomarkers. Together, these neuroimaging findings provide mechanistic insight into disrupted pain modulation, affective–sensory integration, and large-scale network dysregulation, supporting the view of chronic pain as a disorder of the central nervous system rather than solely a peripheral condition.

Brain imaging has reshaped paradigms of chronic pain by moving beyond stimulus-response models toward network-based conceptualizations that integrate sensory, emotional and cognitive components. These methods challenge traditional clinical frameworks by offering more objective markers of pain experience and suggest potential targets for neuromodulatory and personalized interventions.

chronic pain, neuroimaging, MRI, functional connectivity, biomarkers, brain networks, chronic pain mechanisms.

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Cannabinoids are increasingly discussed as adjuncts in addiction treatment, yet whether they improve clinically meaningful substance use disorder (SUD) outcomes beyond short-term symptom relief is unresolved. We determined whether cannabinoid exposure confers directional efficacy across opioid, alcohol, cocaine, tobacco, and methamphetamine use disorders, distinguishing symptomatic targets from sustained therapeutic outcomes.

PubMed and Embase (1975–2025) were searched for human studies evaluating cannabinoid exposure in relation to SUD outcomes. Two reviewers independently screened and extracted data. Risk of bias was assessed using RoB 2 for randomized controlled trials (RCTs), ROBINS-I for cohort studies, and JBI checklists for cross-sectional, case, and qualitative designs. Six prespecified endpoints (treatment retention, relapse, abstinence, craving, withdrawal severity, consumption) were mapped to each target SUD. Following Synthesis Without Meta-analysis (SWiM) guidance, structured narrative synthesis used a design-based weighting scheme (RCT 1.00 to qualitative 0.25). PROSPERO: CRD420251151193.

Ninety-seven studies (41,954 participants) contributed 195 endpoint instances: 89 Beneficial (45.6%), 80 No Significant Effect (41.0%), 12 Mixed/Partial (6.2%), and 14 Harmful/Inferior (7.2%). Short-term symptom targets accounted for most Beneficial findings (76.4%). Sustained outcomes were predominantly No Significant Effect, most pronounced in opioid use disorder. Beneficial symptom findings derived overwhelmingly from weaker study designs (craving 81.5%; withdrawal severity 85.7%; consumption 80.0%).

Cannabinoids confer short-horizon symptomatic benefits but do not demonstrate efficacy for sustained abstinence, relapse prevention, or retention, most clearly in opioid use disorder, where evidence is strongest. Findings for other disorders remain preliminary. Adequately powered adjunctive randomized trials with biochemically verified endpoints are needed.

Refugees and Migrants exposed to war, persecution and forced displacement present complex menthal health needs, frequently characaterized by trauma related disorders and social vulnerability.Systemic and network-oriented interventions have been proposed as effective strategies to address such complexity,yet empirical data on their impact on menthal health.

to describe menthal health service utilization and continuity of care among traumatized refugees receinving systemic oriented treatment within a public menthal health setting in Bologna-Italy.

this prospective observational study was conducted in a specialized outpatient service for refugees and migrants integrated into the local public menthal health system. Adult refugess or migrants with a history of traumatic exposure and clinically significant psychological distress were consecutively enrolled and followed for 12 mounths (2025). Data on sociodemographic characteristics, psychiatric diagnoses, type of interventions, outpatient contacts, emergency service use and psychiatric hospitalizations werw systematically collected.Systemic treatment approches included family and network-oriented intervetions, multidisciplinary case management and structured collaboration with social and community services.

During 2025, 147 Out of 147 patients, 103 (70%) presented with mental health issues. The cohort was predominantly male (54%), with the most frequent countries of origin being Pakistan, Tunisia, and Nigeria. A high prevalence of Post-Traumatic Stress Disorder (PTSD) was observed, frequently in comorbidity with other psychiatric disorders. Patients with PTSD received trauma-oriented psychotherapy, including EMDR, Narrative Exposure Therapy (NET), and bottom-up approaches. Notably, systemic interventions were provided to 68% of the total sample and were significantly associated with higher .

Within a public mental health framework, systemic treatment approaches appear to promote engagement and continuity of care among traumatized refugees, resulting in relatively low rates of acute service use. These findings support the implementation of integrated, network-oriented models to address the clinical and social complexity of refugee mental health, optimizing resource allocation and patient outcomes rates of continuity of care.

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Previous research has demonstrated the positive impact of early remission on disease trajectory for patients with major depressive disorder. However, there is a paucity of literature assessing the response trajectory for patients with treatment resistant depression (TRD). These analyses investigated patient outcome trajectories to Week 32, including the relationship between short- and long-term outcomes with esketamine nasal spray (ESK-NS) treatment and symptom resolution.

ESCAPE-TRD (NCT04338321), a randomized, open-label, phase IIIb study, evaluated the efficacy and safety of ESK-NS versus quetiapine extended release (QTP-XR) in patients with TRD. Rater-blinded Montgomery-Åsberg Depression Rating Scale (MADRS) total score was used to assess depressive symptoms and the trajectory of patient responses to Week 32. For ESK-NS versus QTP-XR, time to symptom resolution across MADRS items was evaluated using Kaplan–Meier analyses.

Of 676 patients, 336 and 340 were randomized to ESK-NS and QTP-XR, respectively. Most ESK-NS-treated patients achieved continuously improved outcomes to Week 32; early response was associated with better long-term outcomes. Among patients who achieved Week 4 response, 89.6% achieved remission at any point from Week 4 to 32; 78.3% of Week 8 responders achieved remission at any point from Week 8 to 32. Greater and earlier symptom resolution was observed with ESK-NS versus QTP-XR across most MADRS items.

Most ESK-NS-treated patients with TRD showed continuous improvements over time, with short-term response associated with better long-term outcomes. Long-term improvements were observed even among partial/minimal early responders, reinforcing the value of longer treatment. ESK-NS had a positive impact across the full spectrum of MADRS-assessed symptoms.

Although retrospective studies of adults found that mood and anxiety disorders may follow exposure to trauma, prospective longitudinal research on this topic in children and adolescents is still rare. The goal of this analysis was to assess the incidence of major depressive and anxiety disorders in offspring who experienced trauma or parental separation during childhood or adolescence, over almost a decade of follow-up.

As part of a family study in the community of Lausanne, we directly interviewed 461 offspring before age 18, who subsequently undertook a second diagnostic interview. The mean age of the offspring at study intake was 12.8 (s.d. 3.4) years and the mean follow-up duration was 9.3 (s.d. 4.4) years. Traumatic events were defined as having been in an accident, being a victim of crime or physical/sexual abuse or having witnessed events experienced by others. The hazard risk of psychopathology in affected versus non affected offspring was determined using time-varying shared gamma-frailty models, adjusted for intra-familial correlation.

In total, 23 offspring reported premorbid trauma and 75 reported premorbid parental separation. Analyses revealed that offspring who had experienced early trauma reported an earlier onset of anxiety disorders than offspring who had not. In contrast, offspring who had experienced early parental separation did not report more anxiety or major depressive disorders over the follow-up than those who had not experienced parental separation.

These findings underline the need for early intervention with offspring who experience early trauma to alleviate the development of future anxiety disorders.

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Bipolar disorder (BD) is frequently misdiagnosed as major depressive disorder (MDD), with diagnostic delays averaging 6–10 years leading to suboptimal treatment and poorer outcomes. Early identification of patients at risk for diagnostic conversion remains a critical clinical priority. We aimed to identify clinical predictors of BD conversion in a large population-based cohort and develop a clinically applicable prediction model.

We conducted a retrospective cohort study using electronic health records from the Catalan PADRIS-PRESTO database (2010–2019). Patients aged ≥18 years with incident MDD diagnosed in specialized mental health services (2015–2019) were followed until BD diagnosis, death, or study end. Time-varying Cox regression addressed proportional hazards violations, with competing risks analysis accounting for mortality.

Among 52,001 patients (median follow-up 4.0 years), 3,958 (7.61%) converted to BD. Psychotic features emerged as the strongest predictor (HR = 3.18, 95% CI: 2.92–3.45, E-value = 5.82), with consistent effects across follow-up. Anxiety disorders showed time-varying protection (baseline HR = 0.41, 95% CI: 0.35–0.48) that attenuated over time (interaction HR = 1.30 per period). The time-varying model achieved good discrimination (C-index = 0.745). Machine learning validation confirmed predictor importance rankings (Spearman r = 0.87).

Psychotic features during depressive episodes robustly predict BD conversion, warranting enhanced clinical monitoring. Our time-varying prediction model using routinely collected clinical data enables early risk stratification to guide diagnostic vigilance and treatment decisions.

Gaming disorder (GD) is recognized by the WHO as a behavioral addiction, yet research remains predominantly men-centric. This study explores the experiences of women gamers, their perceptions of GD, and the barriers women face in accessing care.

Semi-structured interviews were conducted with seven participants identifying as women (six cisgender women and one transgender woman) aged 21–26 years old, in France and Switzerland. Inductive reflexive thematic analysis was used to identify women’s experiences of gaming behavior, stigma, and help-seeking.

Participants reported diverse gaming behaviors, with preferences for narrative-driven games (e.g., RPG and simulations). Stigma, lack of self-awareness, limited self-recognition of problematic gaming, and broader societal misconceptions emerged as significant barriers to recognizing GD as a potential clinical issue warranting help-seeking. None had sought professional care for GD, citing gendered stereotypes and diagnostic biases as key deterrents.

The study highlights the need for women-centered diagnostic tools, clinical approaches, targeted awareness campaigns, and flexible support systems for women with GD. Future research should prioritize larger, diverse samples and intersectional approaches.

Migration is a well-established risk factor for psychotic disorders, yet the mechanisms underlying this association remain incompletely understood. Competing hypotheses have suggested either a selection effect, whereby individuals with increased vulnerability are more likely to migrate, or a causal role of migration-related exposures, including social adversity, discrimination, and environmental stressors. Distinguishing between these explanations is essential for understanding psychosis risk and identifying meaningful predictors of onset.

This presentation will discuss findings from the EU-GEI WP2 case–control study comparing first- and second-generation migrants and non-migrant groups with and without a first episode of psychosis. By accounting for underlying vulnerability while examining differences across migrant status and ancestry, the study evaluates whether migration-related risk can be explained by pre-existing susceptibility or whether environmental factors play a predominant role.

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Although a series of risk factors for mood disorders have been previously identified, research that prospectively and simultaneously tested these factors is still scarce. Using a cohort of offspring of parents with bipolar disorders (BPD) and major depressive disorders (MDD), the goal of the present paper was to simultaneously and prospectively assess the association of sociodemographic characteristics, mood and non-mood disorders in the parents and co-parents, life stressors, personality traits as well as psychopathological precursors with the incidence of (hypo)manic episodes or MDD in offspring.

We have collected clinical information on 85 probands with BPD, 74 probands with MDD, 22 probands with substance use disorders, 68 controls, 233 co-parents as well as their 451 offspring. The mean age of the offspring at study intake was 10.0 years (s.d: 4.6) and the mean duration of follow-up in offspring was 16.3 (s.d: 6.1) years.

The onset of mania/hypomania in offspring was predicted by the proband’s early onset BPD and oppositional defiant disorder, the occurrence of a major depressive or subthreshold hypomanic episode, whereas the onset of MDD was preceded by sexual abuse or witnessing of trauma to others.

Our data support differential risk factors for (hypo)mania and MDD, further suggesting the specificity of major mood disorders. The strong association between the proband’s early-onset BPD and the incidence of (hypo)mania in offspring suggests the implication of genetic or family-shared risk factors, whereas the development of MDD in offspring is likely to be more attributable to adverse environmental stressors.

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There has been growing interest in developing a clinical staging model for eating disorders (EDs). The aim of this scoping review is to investigate the extent, range, and nature of research that can inform clinical staging approaches for EDs.

This review was conducted following the Joanna Briggs Institute methodology for scoping reviews and the PRISMA extension for Scoping Reviews. A search of PubMed, PsycINFO, MEDLINE and Web of Science databases was conducted. Sixty studies were included for review, and data were extracted according to revised pre-published criteria. Studies were summarized using narrative synthesis.

Thirty-six of the included manuscripts were quantitative, 18 were qualitative, and six were conceptual/review papers. The included studies primarily focused on anorexia nervosa in white, female samples and compared only two stages of illness, equating to “early” and “longstanding” or “severe and enduring” EDs. “Middle” stages or transitions between stages were not well-defined. Stages have mostly been conceptualized using duration of illness or other behavioral or clinical parameters, with few (neuro) biological studies identified. Factors that may modify illness stage have not yet been integrated into ED staging literature.

There is growing consensus that early- and later-stage EDs have distinct characteristics and treatment requirements; however, these distinctions require clearer definition. Recommendations for future research are outlined, emphasizing integration of psychosocial and biological research, focused investigation of illness phases outside of early and longstanding phases, and evaluation of personalized, stage-based treatments. A tentative staging model for EDs is proposed.

Early adolescence marks a critical period for the onset of psychiatric symptoms, with 50% of mental disorders emerging before age 18. Recent evidence points to individuals being born preterm and/or with low birth weight (henceforth, PTB) having an increased risk of developing mental disorders in adolescence. Surprisingly, existing early detection and intervention strategies in adolescence are not tailored to PTB needs and profiles. The previous use of several disorder-specific instruments complicates unified, efficient screening.

We analyzed data on the frequency of experiencing mental health challenges from 225 adolescents aged 10-14 years (M = 12.03 years) who were born very PTB (M = 28.03 weeks, M = 999.62 g) to test the applicability of the diagnostic system for mental disorders for children and adolescents – III (DISYPS-III) to PTB adolescents.

A confirmatory factor analysis replicated the DISYPS-III’s factorial structure and internal consistency for 10- to 14-year-old PTB adolescents. Overall, PTB adolescents reported significantly more mental health challenges than the DISYPS-III community norm sample. The instrument’s transdiagnostic scales provided a better relative fit to these challenges compared to the disorder-specific scales. Results also replicated specific findings of mental health challenges from other PTB cohorts and countries, such as a higher number of comorbidities in adolescents officially diagnosed with the inattentive presentation (ADD) of ADHD.

These findings of an elevated psychological burden suggest a need for structured PTB screening of long-term mental health outcomes in adolescence that also includes 10-year-old PTB individuals, with the DISYPS-III being a suitable screening instrument.

Symptoms of depression and anxiety typically first emerge in adolescence and young adulthood, but factors that promote recovery, particularly for those exposed to social adversity, are poorly understood. We investigated whether perceived social capital was associated with clinical remission and symptomatic improvement for depression and anxiety over two years in a cohort of 1,437 young people living in the most deprived parts of Buenos Aires (Argentina), Bogota (Colombia) and Lima (Peru) in South America.

All participants, aged 15-16 and 20-24 at baseline and who met PHQ-8 or GAD-7 cut-offs for depression and anxiety at baseline, were followed for up to 24 months for evidence of clinical remission (change in symptom scores below cut-offs) or symptom improvement (continuous change in symptom scores). Remission was modelled as a repeated measure binary outcome at 6, 12 and 24 months using generalized linear mixed modelling with inverse probability weighting to handle attrition. Symptomatic improvement was modelled as a continuous outcome in separate linear mixed models for depression and anxiety. Exposures were self-reported measures of cognitive social capital (trust, reciprocity, shared values) and structural social capital (group membership, social support) at baseline using the ASCAT tool.

1,337 participants (93.0%) had at least one wave of follow-up data, with 46.3% meeting cut-offs for recovery (n=619) at one or more waves up to 24 months. In complete case analyses (n=1220, 91.2%) cognitive social capital was associated with greater odds of remission in a univariable (OR: 1.69; 95%CI: 1.04-2.78), but not full multivariable model (OR: 1.23; 95%CI: 0.83-1.75) after adjustment for confounders. Cognitive social capital was associated with symptomatic improvement in depression (Beta: -0.71; 95%CI: -1.40, -0.03) but not anxiety (Beta: -0.34; 95%CI: -1.00, 0.31) in multivariable linear models. We observed no main effects of structural social capital, but found strong evidence (p=0.0003) that high structural social capital was associated with greater odds of remaining above clinical threshold scores for depression/anxiety for adolescents (15-16 year olds) (OR: 1.78; 95%CI: 1.07-2.96), but greater odds of clinical remission for 20-24 year olds (OR: 1.83; 95%CI: 1.12-3.03).

Higher cognitive social capital predicted symptomatic improvement in depression amongst young people in Latin America. Structural social capital showed age-dependent effects on clinical remission. Together, these findings suggest that interventions that allow young people to foster meaningful community ties that facilitate trust, reciprocity, connectedness and positive support may be an effective public mental health tool for secondary prevention of depression in young people.

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Phenomenological psychopathology offers a framework for understanding mental disorders through patients’ subjective experience. While this perspective has gained renewed attention in adult psychiatry, it remains marginal in child and adolescent psychiatry, where diagnostic work is often complicated by developmental variability, evolving reflective capacities, and overlapping symptom presentations.

This presentation orients around the personalized, phenomenologically informed semi-structured interview, and discusses its relevance for early detection in young psychiatric patients.

In everyday clinical practice, early signs of severe mental illness in young patients may present in diffuse and ambiguous ways. Clinicians are faced with uncertainty about whether observed difficulties reflect e.g. transient developmental distress or emerging psychotic disorders. This diagnostic ambiguity contributes to under-recognition and delayed identification of severe mental illness, which in turn is associated with poorer outcomes and increased risk of adverse clinical and social consequences.

Current assessment practices oriented toward symptom checklists and standardized formats, risk overlooking diagnostically decisive alterations in subjective experience present in emerging severe psychopathology. In young patients, clinically central disturbances may not present as readily nameable contents (e.g., specific fears or beliefs), but as alterations in the form of experience.

From a clinical perspective, the diagnostic interview is not merely a tool for collecting symptoms, but a central clinical instrument for understanding the patient’s experience, context and suffering. A personalized, phenomenologically informed semi-structured interview allows clinicians to explore not only what the patient reports when asked, but how experiences are lived, articulated, and situated within the patient’s developmental and life context.

The aim is to show and discuss how a phenomenological approach can strengthen clinical judgment and support diagnostic decision-making in child and adolescent psychiatry.

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Schizophrenia is often a persistent mental illness characterized by cognitive deficits and altered brain network dynamics especially affecting the cortico-subcortical salience processing system. Childhood trauma has been implicated in mechanisms contributing to schizophrenia, but the role of genetic vulnerability remains unclear.

A total of 164 schizophrenia patients and 114 healthy controls were included. First, a matched subsample of 117 patients (76 with and 41 without childhood trauma), and 59 healthy controls were compared on polygenic risk scores for schizophrenia (SczPRS). SczPRS was then correlated with neurocognitive performance using a comprehensive cognitive battery (n = 147 patients) and brain-wide static and dynamic functional connectivity (sFC and dFC) using resting-state fMRI (n = 117 patients). Patients were also stratified into high-SczPRS and low-SczPRS (n = 25 each) subgroups.

Patients with childhood trauma had significantly lower SczPRS than those without. Higher Childhood Trauma Questionnaire (CTQ) scores related to lower cognitive PC score (r = −0.282, p < 0.001), but CTQ did not affect brain-wide dysconnectivity or subcortical/salience system among patients. Patients with the highest SczPRS showed lower dFC between the cingulo-opercular network and subcortical networks (F = 7.949, p = 0.007), but SczPRS did not affect cognitive performance.

Our findings reveal distinct effects of childhood trauma and polygenic risk in the neural and cognitive substrates of schizophrenia. Childhood trauma relates to poor cognitive function, while polygenic risk primarily affects salience/subcortical network dynamics. These patterns indicate that in genetically predisposed individuals who experience childhood trauma, a “double mechanistic hit” may influence the schizophrenia phenotype.

Adolescence is a developmental epoch marked by vulnerability, emergence, and existential reorientation—a time when the self is being formed as much as it is being questioned. In this contribution, I argue for a critical reappraisal of the phenomenological approach within child and adolescent psychiatry, drawing from classical sources and contemporary insights. The aim is twofold: first, to question the risks of epistemic reductionism and diagnostic imposition in adolescent psychiatry; second, to explore how phenomenology might foster non-interpretative, heterological forms of clinical engagement with the adolescent subject. I begin by revisiting Karl Jaspers’ existential philosophy and methodological framework, including his emphasis on Verstehen (understanding) and Grenzsituationen (limit situations), to show how they remain crucial for situating adolescent suffering within a broader human context, rather than confining it within symptom-based taxonomies. I then turn to the concept of heterological empathy, which foregrounds the radical alterity of the other’s experience, especially pertinent in the adolescent who may not yet possess narrative clarity or diagnostic legibility. This requires clinicians to approach their young interlocutors not through projection or interpretation, but through a receptive stance that welcomes the foreignness of their world-making. Building on this, I propose a critique of epistemic injustice in adolescent psychiatry—how young people’s self-descriptions are often discounted or filtered through adult-centric and biomedical frameworks. This contributes to both diagnostic overreach and neglect, particularly in cases where ambiguity and developmental flux are mistaken for pathology. Phenomenological psychopathology is especially well-suited to rethinking adolescence not as a problem to be managed but as a threshold structure—a phase of becoming that is both unstable and meaningful. I highlight the potential for phenomenologically-informed interventions in this age group. These include dialogical spaces that support self-articulation, embodied therapeutic practices, and intersubjective frameworks that reorient treatment from symptom eradication to existential accompaniment. In conclusion, this keynote aims to demonstrate that the application of phenomenology in adolescent psychiatry is not merely a theoretical enrichment—it is an ethical imperative. By resisting the pressures of over-diagnosis and interpretive closure, phenomenology reasserts the adolescent’s right to opacity, ambiguity, and emergence. It reconfigures the clinical relationship not as a site of knowledge extraction, but as a shared space of meaning-making where both clinician and adolescent stand as co-inhabitants of a fragile, unfolding world.

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