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Hintergrund: In Basel haben wir verschiedene Studien zur Verbesserung der Methodik zur Fruherkennung von Psychosen (FePsy) durchgefuhrt. Methodik: Vom 01.03.2000 bis 29.02.2004 wurden 234 Individuen mithilfe des Basler Screening Instruments fur Psychosen (BSIP) gescreent. Bei 10 6 Patienten konnte ein Risikostatus fur Psychosen diagnostiziert werden, 53 davon konnten bis zu 7 Jahre (Mittel 5. 4 Jahre) nachuntersucht werden. Die weiteren Untersuchungen erfolgten u.a. mit einem spezifisch entwickelten Anamnese - Instrument, verschiedenen Skalen zur Psychopathologie, Untersuchungen der Neuropsychologie u n d Feinmotorik , klinische m und quantitative m EEG, MRI des Gehirns, Labor. Ergebnisse: Allein auf der Basis des BSIP konnte eine relativ zuverlassige Vorher sage getroffen werden: 21 (39.6 % ) der als „ Risikopatienten “Identifizierten entwickelten innerhalb der Beobachtungszeit tatsachlich eine Psychose. Post hoc konnte durch spezifischere Gewichtung der Psychopathologie und Einbezug neuropsychologischer Untersuchungen die Vorhersagegenauigkeit auf 81 % gesteigert werden. Die anderen oben genannten Verfahren konnen offensichtlich zur weiteren Verbesserung der Pradiktion beitragen. Schlussfolgerungen: Die Risikoabklarung fur Psychose sollte stufenweise und unter Einbezug verschiedener Untersuchungsebenen erfolgen. Background: We have conducted various studies in Basel with the aim of improving the methods for the early detection of psychosis (Fruherkennung von Psychosen, FePsy).Methods: From 1.3.2000 to 29.2.2004 234 individuals were screened using the Basel Screening Instrument for Psychosis (BSIP). 106 patients were identified as at risk for psychosis; out of these 53 remained in follow-up for up to 7 years (mean 5.4 years). The assessments were done with a specifically developed instrument for history taking, various scales for the psychopathology, assessments of neuropsychology and fine motor functioning, clinical and quantitative EEG, MRI of the brain, laboratory etc.Results: Based on the BSIP alone, a relatively reliable prediction was possible: 21 (39.6 %) of the individuals identified as at risk developed psychosis within the follow-up time. Post-hoc prediction could be improved to 81 % by weighting psychopathology and including neuropsychology. Including the other domains obviously allows further improvements of prediction.Conclusions: The risk for psychosis should be assessed in a stepwise procedure. In a first step, a clinically oriented screening should be conducted. If an at-risk status is found, further assessments in various domains should be done in a specialised centre.

It is unclear yet whether cannabis use is a moderating or causal factor contributing to grey matter alterations in schizophrenia and the development of psychotic symptoms. We therefore systematically reviewed structural brain imaging and post mortem studies addressing the effects of cannabis use on brain structure in psychosis. Studies with schizophrenia (SCZ) and first episode psychosis (FEP) patients as well as individuals at genetic (GHR) or clinical high risk for psychosis (ARMS) were included. We identified 15 structural magnetic resonance imaging (MRI) (12 cross sectional / 3 longitudinal) and 4 post mortem studies. The total number of subjects encompassed 601 schizophrenia or first episode psychosis patients, 255 individuals at clinical or genetic high risk for psychosis and 397 healthy controls. We found evidence for consistent brain structural abnormalities in cannabinoid 1 (CB1) receptor enhanced brain areas as the cingulate and prefrontal cortices and the cerebellum. As these effects have not consistently been reported in studies examining non-psychotic and healthy samples, psychosis patients and subjects at risk for psychosis might be particularly vulnerable to brain volume loss due to cannabis exposure