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February 2016

Deconstructing the Psychosis Risk Syndrome: Moving the Field of Prevention Forward

Author Affiliations
  • 1Division of Psychiatry Research, The Zucker Hillside Hospital, North Shore–Long Island Jewish Health System, Glen Oaks, New York
  • 2Center for Psychiatric Neuroscience, The Feinstein Institute for Medical Research, North Shore–Long Island Jewish Health System, Manhasset, New York
  • 3Department of Psychiatry, Hofstra North Shore–Long Island Jewish School of Medicine, Hempstead, New York
  • 4Department of Molecular Medicine, Hofstra North Shore–Long Island Jewish School of Medicine, Hempstead, New York
JAMA Psychiatry. 2016;73(2):105-106. doi:10.1001/jamapsychiatry.2015.2454

The movement toward prevention of psychosis was launched in the mid-1990s1 with the introduction of a set of criteria for identifying individuals at risk for future illness. Referred to as the prodromal phase of illness, it was theorized that by identifying youngsters (primarily adolescents and young adults) several years before onset, preemptive intervention could block the emergence of florid psychosis. Three subgroups were included in the definition of clinical high risk (CHR), also called ultrahigh risk (UHR), based to a large extent on the clinical observation: (1) presence of attenuated positive symptoms (APS) considered an early, subtle form of the hallmark symptoms of psychosis; (2) presence of positive symptoms at full psychotic intensity for brief, limited time points, referred to as brief intermittent psychotic symptoms (BIPS) or brief limited intermittent psychotic episode (BLIPS); and (3) a trait/state combination of genetic risk or schizotypal personality disorder accompanied by functional decline, labeled genetic risk and decline (GRD). These 3 subgroups have remained relatively unchanged since their introduction, and their criteria have dominated prodromal research.2 They are typically merged into a single CHR research entity, with no distinction made and with no understanding of the extent to which variability in conversion rates across studies is due to differences in subgroup composition. Furthermore, the CHR research entity is based on the implicit assumption that the 3 subgroups are comparable although there is no evidence available to indicate that APS, BIPS, and GRD represent similar progressions of the disease, and, in fact, they appear to be quite separate and (sometimes very) different risk syndromes.

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