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Neurocognitive Impairments in Nonpsychotic Parents of Children With Schizophrenia and Attention-Deficit/Hyperactivity Disorder
The University of California, Los Angeles Family Study
Robert F. Asarnow, PhD;
Keith H. Nuechterlein, PhD;
Kenneth L. Subotnik, PhD;
David L. Fogelson, MD;
Richard D. Torquato, MA;
Diana L. Payne, PhD;
Joy Asamen, PhD;
Jim Mintz, PhD;
Donald Guthrie, PhD
Arch Gen Psychiatry. 2002;59:1053-1060.
Background We tested the hypotheses that certain neurocognitive impairments index genetic liability to schizophrenia and that childhood-onset schizophrenia (COS) is a variant of adult-onset schizophrenia (AOS) by determining whether parents of COS probands show the types of neurocognitive impairments found in relatives of AOS probands.
Methods Parents of COS probands (n = 79) were compared with parents of attention-deficit/hyperactivity disorder (ADHD; n = 190) and community control (CC; n = 115) probands on 3 neurocognitive tasks shown in previous research to detect impairments in patients with AOS and ADHD and in the relatives of patients with AOS. Parents with a diagnosis of psychosis were excluded from the study.
Results On the Degraded Stimulus–Continuous Performance Test and the Trail-Making Test B–Adolescent Version, the parents of COS probands performed significantly worse than the parents of CC and ADHD probands, who did not differ significantly from each other. On the Span of Apprehension, we found no significant group differences. Using rigorous cutoffs, a combination of scores on the 3 neurocognitive tests identified 16 (20%) of the mothers and fathers of COS probands compared with 0% of the mothers and fathers of CC probands. There was diagnostic specificity of the neurocognitive impairments. A combination of neurocognitive scores identified 6 (12%) of the mothers of COS probands vs 0% of the mothers of ADHD probands. A cutoff that identified 2 (2%) of the fathers of ADHD probands classified 5 (17%) of the fathers of COS probands. We found no significant differences in neurocognitive functions between the parents of ADHD and CC probands.
Conclusions The aggregation of neurocognitive impairments in the parents of COS probands provides further evidence of etiologic continuity between COS and AOS. A substantial subgroup of parents of COS probands had a worse neurocognitive performance than that of any of the parents of ADHD and CC probands. Receiver operating characteristic curves showed that when rigorous cutoffs define neurocognitive impairments, the combination of scores on certain neurocognitive tasks produced a level of diagnostic accuracy in the parents of COS probands that is sufficient for use in genetic linkage studies.
From the Neuropsychiatric Institute and the Department of Psychiatry and Biobehavioral Sciences (Drs Asarnow, Nuechterlein, Subotnik, Fogelson, Payne, Asamen, Mintz, and Guthrie and Mr Torquato), the Department of Psychology (Drs Asarnow and Nuechterlein), the Mental Retardation Research Center (Drs Asarnow and Guthrie), and the Department of Biostatistics (Dr Guthrie), University of California, Los Angeles; and the Graduate School of Education and Psychology, Pepperdine University, Malibu, Calif (Dr Asamen).
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