Schizophrenia Bulletin Advance Access published online on September 18, 2008
Schizophrenia Bulletin, doi:10.1093/schbul/sbn127
Neurocognitive Decline in Early-Onset Schizophrenia Compared With ADHD and Normal Controls: Evidence From a 13-Year Follow-up Study
2 Division Mental Health Care, Innlandet Hospital Trust Lillehammer, Anders Sandvigsgate 17, 2629 Lillehammer, Norway
3 Center for the Study of Human Cognition, Institute of Psychology, University of Oslo, Norway
4 Asker and Bærum Hospital Trust, Institute of Psychology, University of Oslo, Norway
1 To whom correspondence should be addressed; tel: +47-40-88-90-07, fax: +47-61-27-28-10, e-mail: oei-me{at}online.no.
The issue of neurodegeneration in schizophrenia is controversial. Although most studies indicate that neurocognitive deficits are relatively stable over the course of the illness, conclusions are limited by relatively short follow-up periods and absence of age-matched control groups. Furthermore, nearly all studies deal with adult-onset schizophrenia, and few studies have considered the possible effect of age of onset. The current study represents the first attempt to compare groups of adolescents with schizophrenia, attention deficit/hyperactivity disorder (ADHD), and normal controls on a comprehensive neurocognitive test battery in a longitudinal design over 13 years. In the baseline study, adolescents with schizophrenia were examined with a broad battery of neurocognitive tests. The comparison groups consisted of adolescents with ADHD and adolescents without a psychiatric diagnosis, between 12 and 18 years of age. In the follow-up study, the schizophrenia group consisted of 15 of the initial 19 individuals, the ADHD group of 19 of the 20 individuals, and the normal comparison group of all 30 individuals. They were reevaluated with the neurocognitive test battery and clinical measures. Subjects with schizophrenia showed a significant decline or arrest in neurocognitive functioning compared with the other 2 groups, particularly in verbal memory, attention, and processing speed. The impairments may be specific to early-onset schizophrenia due to interaction between ongoing brain maturation during adolescence and disease-related mechanisms and/or secondary to neuroleptic treatment in young age and/or social isolation.
Keywords: neurocognition / early-onset schizophrenia / longitudinal