In a European longitudinal, general population study, Hanssen et al47 assessed the diagnostic value of subclinical psychotic experiences by quantifying how many individuals with a lifetime subclinical psychotic experience also had a lifetime diagnosis of affective or nonaffective
psychotic disorder. They found that the diagnostic value for any subclinical psychotic experience was 8%.47 The same authors assessed the 2-year predictive value of new onset subclinical psychotic experiences Inhibitors,research,lifescience,medical on later new onset of affective or nonaffective psychotic disorder and found that this also was 8% – as this was calculated over 2 years the 1-year predictive value would be 4%. This latter finding was somewhat
surprising, as the predictive value of 4% is much higher than the expected 1% described above. The reason for the discrepancy was that affective and nonaffective psychotic disorder Inhibitors,research,lifescience,medical in this general population sample were combined into a single category with a higher rate than the traditional 0.01% to 0.02% schizophrenia incidence. In addition, the high incidence of psychotic disorder in general population studies, as opposed to find more treatment samples, is well known35,41 and can Inhibitors,research,lifescience,medical be taken to prove that case definition on the basis of treatment introduces a degree of treatment bias, also known as Inhibitors,research,lifescience,medical Berkson bias, in psychiatric incidence studies.48 Given predictive and diagnostic values of 4% to 8 %, how effective would prodromal intervention be if a treatment with a 50% success rate existed? Let us very optimistically assume that, given the 4% predictive value described above, a treatment Inhibitors,research,lifescience,medical existed that could be applied in the prodromal phase and would abort transition to full-blown psychotic disorder in 50% of treated cases. If we wished to apply this treatment on the basis of a screening program for subclinical psychotic experiences in the general population, how many people who screened positive would
need to be treated to prevent one case of psychotic disorder? This can be calculated quite simply as 0.04 (the predictive value) x 0.5 (the treatment success rate) =0.02 or, in other words, for every 100 Mannose-binding protein-associated serine protease cases who screened positive for subclinical psychosis and received treatment, 2 transitions would be prevented. In other words, the number needed to treat49 would be 50 and, more importantly, the number needed to inconvenience would be 49, ie, 49 individuals would needlessly receive treatment. Clearly, such figures indicate that early intervention in the general population is not feasible, at least not on the basis of the subclinical psychosis screening criterion.