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.