The ganglionic eminence (GE) is a transitory structure of the ventral telencephalon localized in human fetal brain along the lateral walls of the frontal (and to a less extent the temporal) horns of the lateral ventricles. Pathology shows that GE, being part of the germinal matrix pool, persists longer than other proliferative areas and only by term it has nearly completely disappeared. GE increases progressively in volume with gestational age (GA), reaching its peak at about 18-22 weeks and then almost disappearing around the 30^th week [1-4].

GE is of paramount importance in developing neuroscience human studies, because of the recent evidence of GE as substantial contributor to GABA-ergic interneuron precursors heading to the cortex via the tangential migration pathway. Interest is boosted also by pathology evidence of decreased number of GABA-ergic interneurons in schizophrenia, autism and in some severe epileptic encephalopathies (the so called “inteneuronopathies”), as the one related to ARX gene [5, 6].

However, GE prenatal imaging characterization in normal and abnormal conditions is poor.

Following a 3500 cases fetal MR data base search, we are able to present the in-vivo MR normal features of GE across gestation, together with abnormalities of GE and their possible cerebral abnormal associations. Two senior pediatric neuroradiolgists assessed those cases, which had been reported presenting anomalies in GE region. A total of 18 fetuses were assessed. MR studies had been performed at 1.5 Tesla by mean of multiplanar ss-FSE T2-weighted and FSE T1-weighted sections.

The in-vivo MR imaging features of normal GE, as a germinal matrix pool extending around the lateral walls of the frontal (and to a less extent the temporal) horns of the lateral ventricles, are presented. How GE volume and shape change between 19 and 30 week of gestation is depicted; pictorial assay of available histological or in-vitro MR imaging GE examples from the literature are reported for comparison.

We present GE malformative (not clastic) anomalies divided into main groups: 1) bilateral symmetric well limited cavitations as inverted open C shape separating the GE from parenchyma; 2) GE volume increase associated or not with the above mentioned cavitation. About half of cases carrying such anomalies are associated with severe micro-lissencephaly (figure 1), while the others present with minor to moderate brain anomalies (mild corpus callosum dysgenesis, mild cerebellar vermis hypoplasia, borderline ventriculomegaly) (figure 2 and 3). When available, histology samples reveal a higher neuroblast density in GE volume increase with respect to controls.

As group apart are considered those cases with surely clastic GE lesions, featuring unequivocally haemorrhagic changes on T1-weighted images.

GE cavitations can be considered a sign of halted brain development, since they may be associated with severe cerebral derangement as in micro-lissencephaly cases. GE volume increase with cell crowding is a sign of abnormal brain development as well, even if present in less severe cerebral derangement.

It can be hypothesized that GABA–ergic neuroblasts accumulate within an abnormal GE, because impeded from reaching their final cortical destination. If isolated GE anomalies may exist should be investigated by further imaging research.