The role of obstetric complications in the development of schizophrenia / Isabelle M. Rosso.

Format:

Book

Manuscript

Microformat

Thesis/Dissertation

Author/Creator:

Rosso, Isabelle M.

Contributor:

Cannon, Tyrone, advisor.

University of Pennsylvania.

Language:

English

Subjects (All):

Penn dissertations--Psychology.

Psychology--Penn dissertations.

Local Subjects:

Penn dissertations--Psychology.

Psychology--Penn dissertations.

Physical Description:

viii, 81 pages ; 29 cm

Production:

2000.

Summary:

The neurodevelopmental hypothesis of schizophrenia proposes that adverse events during fetal brain development relate to a form of schizophrenia with an earlier age at onset, more severe negative symptoms, and greater neuroanatomical deficits. While obstetric complications are robust correlates of schizophrenia, controversy remains concerning the nature of the neurally-disruptive mechanism(s) involved, their relationship with genetic risk factors, and their contribution to clinical and neuropathological features of the disorder. This study used a prospective cohort design to examine whether complications associated with fetal hypoxia, prenatal infection, and fetal underdevelopment predict risk for adult schizophrenia with an early onset, whether these obstetric influences depend on, covary with, or are independent of genetic risk, and whether they predict severity of negative symptoms and volumetric brain abnormalities. Structured diagnostic interviews, obstetric records, and magnetic resonance scans of the brain were obtained on 70 probands with schizophrenia or schizoaffective disorder, ascertained so as to be representative of all such probands in a Helsinki birth cohort, along with 52 of their non-psychotic siblings and 54 demographically-similar controls without a family history of psychosis. Hypoxia-associated complications significantly increased odds of early-onset schizophrenia, but not later-onset schizophrenia or unaffected sibling status, after accounting for the non-significant effects of prenatal infection and fetal underdevelopment. After controlling for putative secondary sources of negative symptoms, a history of fetal hypoxia but not infection or underdevelopment predicted significantly higher negative symptom scores. Obstetric history was not related to positive symptom scores. Among patients and their siblings, fetal hypoxia was associated with reduced gray matter and increased sulcal cerebrospinal fluid bilaterally throughout the cortex, most prominently in the temporal lobe. These associations were accentuated among cases born underdeveloped. Hypoxia was also correlated with ventricular enlargement, but only among patients. In contrast, fetal hypoxia was not significantly related to white matter, nor to any tissue type in any region in the controls. Together, these findings support a role for obstetric complications in the neurodevelopmental pathogenesis of schizophrenia. They also indicate that hypoxia may be a primary obstetric mechanism in schizophrenia, acting in interaction with genetic risk in influencing disease liability.

Notes:

Adviser: Tyrone Cannon.

Thesis (Ph.D. in Psychology) -- University of Pennsylvania, 2000.

Includes bibliographical references.

Local Notes:

University Microfilms order no: 9989648.

OCLC:

244971402