Early-onset psychosis — structured clinical viva

Assessment spine. Risk (suicide, aggression, vulnerability, safeguarding), multi-informant history (girl, mother, school), developmental timeline, DUP about 3 months of frank psychosis (already prognostic), MSE with examples, substance, capacity/parental consent under local statute, and medical exclusion. Baseline metabolic panel and ECG before antipsychotic.[1][5]

"Is this childhood schizophrenia?" Age 13 sits at the VEOP/COS boundary depending on exact onset definition used — be precise. Working pathway: early-onset psychosis / possible childhood-onset schizophrenia spectrum. Diagnosis may evolve with duration; avoid day-one lifelong fatalism while treating seriously. Premorbid language delay raises neurodevelopmental load but does not cancel psychosis criteria.[1]

Autism or trauma? Use discriminators: lifelong ASD pattern versus new fixed delusions and commentary hallucinations with collapse. Trauma needs chronology and PTSD phenomenology. Dual formulation allowed. Organic red flags force intensified work-up even if baseline obs are currently normal.[1]

"Strongest tablet now?" Youth and first-episode presentations respond to lower doses; high-dose polypharmacy increases harm. Name a start-low plan (e.g. aripiprazole with akathisia counselling; or another agent with TEOSS-informed side-effect discussion). Metabolic monitoring from first exposure is mandatory because first-time SGA use in youth drives cardiometabolic risk.[2][4]

School. Temporary adjustment, not automatic permanent exclusion. Written education plan, anti-stigma staff briefing, reintegration pathway — school is a treatment module.[1]

If two adequate trials fail. Escalate toward clozapine (Kumra refractory EOP evidence), not endless SGA cycling.[3]

Evidence names. TEOSS; Correll cardiometabolic youth; AACAP McClellan; NICE CYP psychosis; Marshall DUP; Kumra clozapine; family intervention evidence; EIS multi-element principles.[1][2][3][4][5]