Objective The justification for magnetic resonance imaging (MRI) in isolated mild ventriculomegaly remains controversial. This study was undertaken to evaluate the contribution of third-trimester MRI in isolated 10-to 12-mm fetal ventriculomegaly.Design Observational prospective cohort study.Setting Universitary prenatal reference centre.Population From February 2000 to May 2005, we prospectively collected data concerning fetuses referred to us for cerebral MRI following detection of ventriculomegaly by ultrasound scan (n = 310).Methods Among these, we identified and analysed those cases in which ventriculomegaly was isolated and did not exceed 12 mm in ultrasound examinations prior to MRI scan (n = 185).Main outcome measure Cases in which MRI provided additional information that was likely to have an impact on prenatal management were detailed.Results During the study period, 310 MRI were performed because of fetal ventriculomegaly. Hundred and eighty-five were suspected to be isolated 10-to 12-mm ventriculomegalies in ultrasound scan and formed our database. MRI confirmed the 10-to 12-mm isolated fetal ventriculomegaly in 106 cases (57.3%) and found other abnormalities in 5 (4.7%) of these 106 cases. MRI found ventricular measurement to be less than 10 mm in 43 cases (23.3%) and more than 12 mm in 36 cases (19.4%). Among these 36 fetuses with ventricle size more than 12 mm, 6 (16.7%) had other abnormalities, whereas MRI did not find other abnormalities in the 43 cases with ventricle size below 10 mm.Conclusion Before advantages of MRI to ultrasound examination can be demonstrated, it seems reasonable that MRI should remain an investigational tool, restricted to selected clinical situations in which the results are expected to modify case management. Where ultrasound scan suspects isolated ventriculomegaly of 10 to 12 mm, our data suggest that when the finding is confirmed with MRI this could be expected in around 5% of cases. Therefore, the policy of routine MRI in such cases should depend on prenatal centres' priorities.

Autism is a neurodevelopmental disorder with a strong genetic component, probably involving several genes. Genome screens have provided evidence of linkage to chromosome 2q31-q33, which includes the SLC25A12 gene. Association between autism and single-nucleotide polymorphisms in SLC25A12 has been reported in various studies. SLC25A12 encodes the mitochondrial aspartate/glutamate carrier functionally important in neurons with highmetabolic activity. Neuropathological findings and functional abnormalities in autism have been reported for Brodmann's area (BA) 46 and the cerebellum. We found that SLC25A12 was expressed more strongly in the post-mortem brain tissues of autistic subjects than in those of controls, in the BA46 prefrontal cortex but not in cerebellar granule cells. SLC25A12 expression was not modified in brain subregions of bipolar and schizophrenic patients. SLC25A12 was expressed in developing human neuronal tissues, including neocortical regions containing excitatory neurons and neocortical progenitors and the ganglionic eminences that generate neocortical inhibitory interneurons. At mid-gestation, when gyri and sulci start to develop, SLC25A12 molecular gradients were identified in the lateral prefrontal and ventral temporal cortex. These fetal structures generate regions with abnormal activity in autism, including the dorsolateral prefrontal cortex (BA46), the pars opercularis of the inferior frontal cortex and the fusiform gyrus. SLC25A12 overexpression or silencing in mouse embryonic cortical neurons also modified dendrite length and the mobility of dendritic mitochondria. Our findings suggest that SLC25A12 overexpression may be involved in the pathophysiology of autism, modifying neuronal networks in specific subregions, such as the dorsolateral prefrontal cortex and fusiform gyrus, at both pre-and postnatal stages.