Reduced prepulse inhibition in adolescents at risk for psychosis: a 2-year follow-up study

Reduced prepulse inhibition in adolescents at risk for psychosis: a 2-year follow-up study

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J Psychiatry Neurosci 2011;36(2):127-34

Tim Ziermans, PhD; Patricia Schothorst, MD, PhD; Maurice Magnée, PhD; Herman van Engeland, MD, PhD; Chantal Kemner, PhD

Ziermans (at the time of writing), Schothorst, Magnée, van Engeland, Kemner, — Department of Child and Adolescent Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht; Kemner — Department of Developmental Psychology, Faculty of Social Sciences, Utrecht University, Utrecht, the Netherlands

Abstract

Background: Reduced prepulse inhibition (PPI) of the auditory startle reflex is a hallmark feature of attention-processing deficits in patients with schizophrenia and other psychotic disorders. Recent evidence suggests that these deficits may also be present before the onset of psychosis in individuals at ultra-high risk (UHR) and become progressively worse as psychosis develops. We conducted a longitudinal follow-up study to observe the development of PPI over time in UHR adolescents and healthy controls.

Methods: Two-year follow-up data of PPI measures were compared between UHR adolescents and a matched control group of typically developing individuals.

Results: We included 42 UHR adolescents and 32 matched controls in our study. Compared with controls, UHR individuals showed reduced PPI at both assessments. Clinical improvement in UHR individuals was associated with an increase in PPI parameters.

Limitations: A developmental increase in startle magnitude partially confined the interpretation of the association between clinical status and PPI. Furthermore, post hoc analyses for UHR individuals who became psychotic between assessments had limited power owing to a low transition rate (14%).

Conclusion: Deficits in PPI are present before the onset of psychosis and represent a stable vulnerability marker over time in UHR individuals. The magnitude of this marker may partially depend on the severity of clinical symptoms.


Submitted Apr. 5, 2010; Revised June 17, 23, 2010; Accepted June 24, 2010.

Acknowledgments: The authors thank Mirjam Simons-Sprong, Petra Klaassen, Anneke Schouten, Nieke Kobussen and Emmie van Schaffelaar for their contributions in collecting the data for this study.

Competing interests: Drs. Ziermans, Schothorst, Magnée and van Engeland’s work was supported in part by a ZonMw grant (the Netherlands organisation for health research and development, project 2630.0001) to their institution. Dr. Kemner’s work was supported in part by NWO-VIDI and NCU grants from the Dutch Science Foundation to his institutions.

Contributors: Drs. Ziermans, Schothorst, van Engeland and Kemner designed the study. Dr. Ziermans acquired the data, which Drs. Ziermans, Magnée and Kemner analyzed. Drs. Ziermans and Kemner wrote the article. All authors critically reviewed the article and approved its publication.

DOI: 10.1503/jpn.100063

Correspondence to: Dr. T. Ziermans, Department of Neuroscience, Karonlinska Institutet, Retzius Väg 8, 17 177 Stockholm, Sweden; tim.ziermans@ki.se