Fig. 5.

Congenital structural anomalies and disrupted development. (i) In utero CMV infection leading large bilateral sub-occipital cysts (A), extensive polymicrogyria (some examples are given—B—depicted on 64mT as thickened cortex with shallow sulci), patchy WM T2 hyperintensities (C), ventriculomegaly (D), and bilateral subependymal cysts (E). (ii) Cerebellopontine Hypoplasia with severe ventriculomegaly (D) and malpositioned choroid plexi (F), leading to enlargement of a midline crossing inter-hemispheric cyst (G). The left cerebral hemisphere is smaller than the right, there is extensive polymicrogyria (examples given—B), hypoplastic cerebellar hemispheres and vermis (H), hypoplastic pons and brainstem (I), dilated quadrigeminal cistern (J), thin stretched corpus callosum (K), small deep grey matter structures with wide thalamic adhesion (L) and absence of myelin which is abnormal for this infant’s gestational maturity (M). White matter striations are seen on 3T T2w imaging (N)—some correlative findings are present on 64mT imaging, but these are ill-defined, presenting mainly as generalised high T2 white matter at ULF. Choroid plexi are markedly less distinct, but remain identifiable, on 64mT imaging. GA: gestational age; PMA: post-menstrual age; Low Res: low resolution.