There is delay of cerebral sulcation for gestational age. There is underdeveloped Sylvian operculisation. The parieto-occipital and calcarine sulci are not seen and would be expected at this stage, particularly in as there is no evidence of ventricular enlargement to account for their absence. In addition, the normal zonal anatomy of the cerebral hemispheres is difficult to identify and this does not appear to be due to motion degradation.
Frontooccipital cerebral hemispheric measurement is below the lower limit of the normal range.
The corpus callosum is present. No abnormality of the cerebellum, brainstem or orbits. No evidence of intraventricular haemorrhage.
Importantly, there is a normal appearance of the ganglionic eminences, which would typiically be enlarged in conditions producing lissencephaly, such as LIS1 gene mutation, dystroglycanopathies, tubulinopathies and mutations of the RELN and ARX genes.
MRI followup was recommended at this stage, to determine whether there was a persistent lag of sulcal development.