The prenatal hindbrain herniation through the foramen magnum is a consequence of a tethered spinal cord and prolonged prenatal CSF leakage. This transforaminal herniation may result in ‘degeneration’ of cerebellar tissue, presumably due to distortion, marked compression of cerebellar blood vessels and mechanically induced ischemia. Boltshauser et al reported this entity in three children with asymmetric involvement of the cerebellar hemispheres and sparing of the vermis. This phenomenon was called 'vanishing cerebellum in Chiari II malformation'. We demonstrate the natural history of this cerebellar disruption and its prenatal onset in two cases in which there were signs of echogenic detritus in the posterior fossa and within the lateral ventricles that disappear progressively. Case 1: Detected at 25+5w. Echogenic material partially fills the posterior fossa and replaces the cerebellum. Disappearance of the detritus and complete absence of cerebellum at 30 w. GA (T2WI). Case 2: Neurosonogram at 30 weeks depicting echogenic detritus in posterior fossa, upper cervical channel and intraventricular. Two weeks later, the fetal MRI (T2WI) shows absence of most of the cerebellum. In FFLAIR sequence hipointense intraventricular sediment is seen in posterior lateral ventricle. Both cases presented small brainstem without pontine prominence. As well as in cerebellar agenesis these findings may have a severe impact in neurocognitive development. The cases shows the natural history of vanishing cerebellum that complicate the evolution of myelomeningocele. Neurosonography and fetal MRI plays an important role in the diagnosis of these adverse events, which alters the prognosis of Chiari II malformation in the fetus. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.