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To review the prenatal characteristics and postnatal outcomes of Early-onset and Late-onset cerebral ventriculomegaly (VM). Single-center retrospective study 2013–2017; VM cases grouped into Early-onset VM (EVM; Diagnosis at/before 24 weeks) and Late-onset VM (LVM; Beyond 24 weeks). LVM cases had normal ventricle width measurement at mid-trimester scan. Infection serology, cytogenetics, MRI, sonographic follow-up, perinatal and neurodevelopmental outcomes were analyzed. During the 5-year period, 64,662 women underwent an anomaly screening scan and 302 fetuses were identified with ventriculomegaly; 183 (60.6%) classified as early-onset and 119 (39.4%) LVM. The mean ventricular width was significantly higher in LVM cohort (14.1 mm vs 11.6 mm;  p  &lt; .01). EVM cases were more often associated with structural anomalies ( p  &lt; .05). Possible etiologies for EVM were aneuploidy and cerebral malformations like Absent Corpus Callosum, spina bifida, Dandy–Walker malformation, etc., whereas LVM followed aqueductal stenosis, hemorrhage, porencephaly, cerebral tumors, etc. Pregnancy outcomes were available for 251 cases. The pregnancy resulted in more live births in LVM group (87.4% vs 65.6%,  p  = &lt; .01). Multivariate regression analysis demonstrated additional malformations ( p  &lt; .0001, OR11.5 [95%CI: 4–35.2]), progression of VM ( p  = .004, OR 10.2 [95% CI: 2.1–52.3]) and severity of VM (OR 5.3 [95%CI: 0.8–37.7]) were significant predictors of Neurodevelopmental Impairment (NDI). Late gestation at diagnosis was more often associated with NDI ( p  = .063, OR2.4 [95%CI: 0.9–6.2]), although statistically insignificant. EVM has a significantly different sonographic spectrum and outcomes compared to LVM. EVM is milder and associated with an increased risk of aneuploidy and structural malformations. LVM often occurs secondary to acquired brain lesions.

Sonographic spectrum and postnatal outcomes of early-onset versus late-onset fetal cerebral ventriculomegaly