NotesFAQContact Us
Search Tips
Peer reviewed Peer reviewed
Direct linkDirect link
ERIC Number: EJ799385
Record Type: Journal
Publication Date: 2008-Jul
Pages: 25
Abstractor: As Provided
Reference Count: 96
ISSN: ISSN-0300-4430
The Contribution of Prenatal Stress to the Pathogenesis of Autism as a Neurobiological Developmental Disorder: A Dizygotic Twin Study
Claassen, M.; Naude, H.; Pretorius, E.; Bosman, M. C.
Early Child Development and Care, v178 n5 p487-511 Jul 2008
This paper reports on the contribution of prenatal stress to the pathogenesis of autism as a neurobiological developmental disorder in a dizygotic study. The aim was to explore whether the neurobiological impact of stress prior to week 28 of gestation might be related to the pathogenesis of autism. The following data-generating strategies were employed: a diagnostic stress inventory, the 16-Personality Factor Questionnaire, magnetic resonance imaging and blood plasma sampling. It was found that maternal stress during pregnancy may have produced elevated leucocytes and glucocorticoids during gestation, because stress affects cellular immunity due to involvement of the hipothalamic-pituary-adrenal axis. These were implicated in suboptimal placental functioning, heightened exposure of the foetus to glucocorticoids and altered neural development. The autistic subject's blood plasma pathology results showed elevated glucocorticoids and serotonin. Significant cortisol and serotonin differences were noted in the blood plasma pathology results of the autistic subject and the control. Hyperserotonemia and elevated glucocorticoids were therefore implicated in altered programmed neural development, as suggested by the autistic subject's magnetic resonance images. Differences in head circumference were also noted. It was concluded that prenatal maternal stress might have significantly contributed to the pathogenesis of autism. (Contains 4 tables.)
Routledge. Available from: Taylor & Francis, Ltd. 325 Chestnut Street Suite 800, Philadelphia, PA 19106. Tel: 800-354-1420; Fax: 215-625-2940; Web site:
Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A