Developing psychosis and its risk states through the lens of schizotypy

Abstract

Starting from the early descriptions of Kraepelin and Bleuler, the construct of schizotypy was developed from observations of aberrations in nonpsychotic family members of schizophrenia patients. In contemporary diagnostic manuals, the positive symptoms of schizotypal personality disorder were included in the ultra high-risk (UHR) criteria 20 years ago, and nowadays are broadly employed in clinical early detection of psychosis. The schizotypy construct, now dissociated from strict familial risk, also informed research on the liability to develop any psychotic disorder, and in particular schizophrenia-spectrum disorders, even outside clinical settings. Against the historical background of schizotypy it is surprising that evidence from longitudinal studies linking schizotypy, UHR, and conversion to psychosis has only recently emerged; and it still remains unclear how schizotypy may be positioned in high-risk research. Following a comprehensive literature search, we review 18 prospective studies on 15 samples examining the evidence for a link between trait schizotypy and conversion to psychosis in 4 different types of samples: general population, clinical risk samples according to UHR and/or basic symptom criteria, genetic (familial) risk, and clinical samples at-risk for a nonpsychotic schizophrenia-spectrum diagnosis. These prospective studies underline the value of schizotypy in high-risk research, but also point to the lack of evidence needed to better define the position of the construct of schizotypy within a developmental psychopathology perspective of emerging psychosis and schizophrenia-spectrum disorders.

Keywords: adolescence; basic symptoms; development; prodrome; schizophrenia.

© The Author 2014. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Figures

Fig. 1.

Model of the assumed relationship and interactions between dimensions of schizotypy, clinical expressions of schizotypy, symptomatic CHR criteria, and overt psychosis. In line with Rado’s and Meehl’s description, this dimensional model assumes a distribution of schizotypal characteristics in the general population from absence via clinically significant expressions in terms of schizotypal (personality) disorder (SPD) to the most extreme, ie, psychotic expression, with increasing severity of schizotypy being associated with higher levels of distress and/or functional impairment. Attenuated psychotic symptoms (APS) might appear at as a clinical manifestation or as an exacerbation of the underlying schizotypy, in particular of features of the cognitive-perceptual and, though to a lesser degree, the disorganization dimension. The occurrence of APS might be triggered by aberrations in information processing at neurobiological level that are perceived and expressed as basic symptoms, in particular of cognitive-perceptive basic symptoms and cognitive disturbances. Neurobiological aberrations have been consistently described in multitude for patients with psychosis, while physiological correlates of schizotypy in terms of a trait or biomarker are yet to be discovered.