There is severe bilateral ventriculomegaly. The overlying parenchyma is severely thinned and stretched due to ventricular enlargement and, as a result, assessment of lamination of the hemispheres (an important landmark of normality at this GA) is impossible. The degree of opercularisation (Sylvian fissure deepening and closure) expected at this GA is not seen, again relating to gross ventricular dilatation. However, opercularisation failure is also characteristic of primary disorders of sulcation, such as lissencephalies and tubulinopathies, which may also be associated with ventriculomegaly.
None of the other primary hemispheric fissures (calcarine, parietooccipital, central) that should be visible in a normal fetus The expected high T2 signal is not visualised in the cerebral acqueduct. However, caution needs to be exercised with regard to interpreting this as being indicative of aqueduct stenosis in the fetus as the small size of the aqueduct and motion can obscure the linear T2 hyper intensity in the aqueduct seen more easily at later gestation.
Note that the ganglionic eminences are NOT enlarged - this is an important distinguishing feature of this condition compared with other causes of ventriculomegaly plus brainstem kink i.e. dystroglycanopathy and tubulinopathy.
There is also subtle cerebellar vermian dysplasia (the vermis is foliated but was <10th centile for GA in height and AP diameter and is not semicircular in outline as is normally the case). Transverse cerebellar diameter was <3rd centile.
There is a ventral kink at the pontomesencephalic junction.
Adduction of the thumb is noted. Being able to capture this on MR is probably an indication of the high proportion of time that the thumb spends in this position in the fetus!