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Fetal Hypoxia and Structural Brain Abnormalities in Schizophrenic Patients, Their Siblings, and Controls
Tyrone D. Cannon, PhD;
Theo G. M. van Erp, MA;
Isabelle M. Rosso, PhD;
Matti Huttunen, MD, PhD;
Jouko Lönnqvist, MD;
Tiia Pirkola, MA;
Oili Salonen, MD, PhD;
Leena Valanne, MD;
Veli-Pekka Poutanen, MSc;
Carl-Gustav Standertskjöld-Nordenstam, MD
Arch Gen Psychiatry. 2002;59:35-41.
Background Cortical gray matter reductions and cerebrospinal fluid (CSF) increases
are robust correlates of schizophrenia, but their relationships to obstetric
and other etiologic risk factors remain to be established.
Methods Structured diagnostic interviews, obstetric hospital records, and magnetic
resonance imaging scans of the brain were obtained for 64 schizophrenic or
schizoaffective patients (representative of all such probands in a Helsinki,
Finland, birth cohort), along with 51 of their nonpsychotic full siblings
and 54 demographically similar controls without family histories of psychosis.
Results Fetal hypoxia predicted reduced gray matter and increased CSF bilaterally
throughout the cortex in patients (gray matter effect sizes, -0.31 to -0.56;
CSF effect sizes, 0.25 to 0.47) and siblings (gray matter effect sizes, 0.33
to 0.47; CSF effect sizes, 0.17 to 0.33), most strongly in the temporal lobe.
Effect sizes were 2 to 3 times greater among cases born small for their gestational
age. Hypoxia also correlated significantly with ventricular enlargement, but
only among patients (effect size, 0.31). In contrast, fetal hypoxia was not
related to white matter among patients and siblings, nor to any tissue type
in any region among controls. The associations were independent of family
membership, overall brain volume, age, sex, substance abuse, and prenatal
infection.
Conclusions Fetal hypoxia is associated with greater structural brain abnormalities
among schizophrenic patients and their nonschizophrenic siblings than among
controls at low genetic risk for schizophrenia. This pattern of results points
to a gene-environment interaction account of the disorder's neurodevelopmental
pathogenesis.
From the Departments of Psychology (Drs Cannon and Rosso and Mr van
Erp), Psychiatry and Biobehavioral Sciences, and Human Genetics (Dr Cannon),
University of California, Los Angeles; the Department of Mental Health, National
Public Health Institute of Finland, Helsinki (Drs Huttunen and Lönnqvist
and Ms Pirkola); and the Department of Radiology, University of Helsinki (Drs
Salonen, Valanne, and Standertskjöld-Nordenstam and Mr Poutanen).
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