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Schizophrenia and Schizophrenia-Spectrum Personality Disorders in the First-Degree Relatives of Children With Schizophrenia
The UCLA Family Study
Robert F. Asarnow, PhD;
Keith H. Nuechterlein, PhD;
David Fogelson, MD;
Kenneth L. Subotnik, PhD;
Diana A. Payne, PhD;
Andrew T. Russell, MD;
Joy Asamen, PhD;
Heidi Kuppinger, PhD;
Kenneth S. Kendler, MD
Arch Gen Psychiatry. 2001;58:581-588.
Background This study tested the hypothesis that childhood-onset schizophrenia
(COS) is a variant of adult-onset schizophrenia (AOS) by determining if first-degree
relatives of COS probands have an increased risk for schizophrenia and schizotypal
and paranoid personality disorders.
Methods Relatives of COS probands (n = 148) were compared with relatives of
attention-deficit/hyperactivity disorder (ADHD) (n = 368) and community control
(n = 206) probands. Age-appropriate structured diagnostic interviews were
used to assign DSM-III-R diagnoses to probands and
their relatives. Family psychiatric history was elicited from multiple informants.
Diagnoses of relatives were made blind to information about probands' diagnoses.
Final consensus diagnoses, which integrated family history, direct interview
information, and medical records, are reported in this article.
Results There was an increased lifetime morbid risk for schizophrenia (4.95%
± 2.16%) and schizotypal personality disorder (4.20% ± 2.06%)
in the parents of COS probands compared with parents of ADHD (0.45% ±
0.45%, 0.91% ± 0.63%) and community control (0%) probands. The parents
of COS probands diagnosed as having schizophrenia had an early age of first
onset of schizophrenia. Risk for avoidant personality disorder (9.41% ±
3.17%) was increased in the parents of COS probands compared with parents
of community controls (1.67% ± 1.17%).
Conclusions The psychiatric disorders that do and do not aggregate in the parents
of COS probands are remarkably similar to the disorders that do and do not
aggregate in the parents of adults with schizophrenia in modern family studies.
These findings provide compelling support for the hypothesis of etiological
continuity between COS and AOS.
From the Neuropsychiatric
Institute and Departments of Psychiatry (Drs Asarnow, Nuechterlein,
Fogelson, Subotnik, Payne, Russell, and Kuppinger) and Psychology (Drs
Asarnow, Nuechterlein, and Asamen), University of California at Los
Angeles; Department of Psychology, Pepperdine University, Malibu, Calif
(Dr Asamen); Departments of Psychiatry and Human Genetics, Virginia
Commonwealth University, Richmond (Dr Kendler); and the Virginia
Institute of Psychiatric Genetics, Richmond (Dr Kendler).
Corresponding author: Robert F. Asarnow, PhD, Della Martin Professor
of Psychiatry and Biobehavioral Science, UCLA Department of Psychiatry, 48-240C
NPI, 760 Westwood Plaza, Los Angeles, CA 90024-1759.
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