Because the fetal brain is a dynamic structure, it is important for radiologists to familiarize themselves with the normal appearance of it at different gestational ages in order to be better able to identify and characterize abnormalities with fetal MRI. Changes in fetal brain maturation proceed through different stages in a predictable fashion: by gestational weeks (GW) 12–23, the brain demonstrates a smooth surface except for the interhemispheric fissure. Sulci appear with this order: Sylvian and interhemispheric (GW 10–15); calcarine, parieto-occipital, and cingulate (GW 16–19); central and superior temporal (GW 20–23); precentral, postcentral, and superior frontal (GW 24–27); inferior frontal and inferior temporal (GW 28–31); insular, parietal, superior occipital, secondary frontal, secondary parietal, and secondary temporal (GW 32–35); and inferior occipital, tertiary frontal, and tertiary parietal (GW 36–39) (Fig. 11.5) [13]. Sulcation in the whole cerebral cortex is seen from GW 30 on, whereas infolding of the cortex and opercular formation will not be seen before GW 33. The developing nervous system has a multilayered appearance; till GW 28, from the surface to the depth, four layers could be recognized: the cortical plate, the subplate, and the intermediate and the ventricular zone that contains the germinal matrix. Afterwards, such distinction will fade away till the only distinction between white and gray matter (Fig. 11.6).

The germinal matrix appears as a band of T2 hypointensity/T1 hyperintensity, for the high density of cells and microvessels, surrounding the ventricles in early gestation until the third trimester, when it gradually regresses to be present only in the caudo-thalamic groove at term. The cortical plate is seen as a band of T2 hypointensity/T1 hyperintensity at the periphery of the brain. The intervening parenchyma is of higher signal intensity on T2-weighted images but contains two visible layers as well, usually discernable between GW 20 and 28 [14].

By GW 23, cerebral ventricles appear relatively large, corresponding to the normal fetal hydrocephalus, gradually becoming smaller thereafter. The atria of the lateral ventricles remain relatively stable in size from GW 15 to 35, and the size should be less than 10 mm at the level of the atria when measured in an axial plane both by ultrasound and MRI. The cavum septi pellucidi is situated between the two lateral ventricles. It is a transient structure that remains visible till the end of pregnancy, and it has the same signal characteristics of the ventricles. Sonographic measurements of the third ventricle in the axial plane have revealed an upper limit of normal ranging from 1.0–1.2 mm by GW 12 to 3.5–3.6 mm at term, although no MR correlation has yet been performed. The cisterna magna may be difficult to visualize in the third trimester with ultrasound because of attenuation from the calvarium at the skull base; however, this is well visualized with MRI throughout the second and third trimesters. The subarachnoid space overlying the cortical convexities is slightly dilated at all gestational ages, most markedly by GW 21–26. The corpus callosum develops between GW 8 and 20. With MR, it is normally visible by GW 20 as a subtle T2 hypointensity. It forms in an orderly progression from genu to splenium, with the rostrum being formed last. The cerebellum, as the cerebral hemispheres, has a progressive development of the sulci. The first fissure that appears is the posterolateral one, by GW 12–13, and it divides the corpus cerebelli from the flocculonodular lobe. The development of the primary fissure that divides the anterior from the posterior lobe follows by GW 14–15, and subsequently, the prepyramidal, preculminate, and precentral fissures are seen by GW 15–16, and the horizontal fissure by GW 21. The foliation of the vermis starts in GW 14, and between 24 and 37 GW, the number of foliae in each lobule accounts for 50 % of the amount in adults. By GW 17, the primary fissure of the vermis should be visible, as should a normal fastigial point with an acute angle. The prepyramidal fissure is visible by GW 21, the preculminate fissure by GW 21–22, and the secondary fissure by GW 24. By GW 27, all vermian lobules and fissures are visible. The craniocaudal length of the vermis reaches that of the cerebellar hemispheres by GW 18–19. The vermis extends caudally to cover the roof of the fourth ventricle, completely covering it by GW 22–24.

The pons and the mesencefalus begin to differentiate themselves by GW 8. They appear hyperintense in T2-weighted images and hypointense in T1-weighted images in their ventral portion, but they become more and more hypointense in T2 and hyperintense in T1 in their dorsal portion, because of the progressive myelination of the ascending tract. The medulla oblongata contains ascending myelinated sensitive tracts, hypointense in T2-weighted images, and pyramidal tracts, whose myelination will begin in the postnatal period, which appear hyperintense in T2-weighted images [15].

The first role of fetal MRI is to explore the fetal brain anatomy to ensure that every structure is correctly developing and to make measurements on the fetal brain to ascertain that its development corresponds to the gestational age (Fig. 11.7). The obtained measurements could be compared with brain normal linear biometric values extrapolated by literature (Tables) [16, 17].

Ventriculomegaly (VM) represents the most frequent encephalic anomaly seen at fetal magnetic resonance imaging (MRI), with an incidence varying between 0.5 and 2 per 1,000 births per year. The frequency of associated malformations, both cerebral and extracerebral, varies between 41 and 78 % [18]. The causes of VM are as follows:

Lateral ventricles are characterized by an anterior portion (frontal horn) and a posterior portion (atrium and occipital horn). In normal conditions, the ventricular cavity at the atrium is almost completely occupied by plexus choroid glomus. When a ventricle enlarges itself, the fluid accumulates between the choroid plexus and the medial wall, giving an image of dangling plexus. Ventricular measurement can be conducted on coronal images, placing calipers at the atrial level on the axis which is perpendicular to the ventricular one or on axial images and placing calipers at the luminal margins of ventricular atria, perpendicular to the long axis of the ventricle, at the level of the glomus of the choroid plexus. The measure is stable during the second and third trimester, with a medium diameter of 6–8 mm, and it is normal till a limit value of 10 mm.

VM can be both monolateral and bilateral; s can be both monolateral and bilateral, symmetric or asymmetric, and it is diagnosed when the atrial diameter (AD) of one or both ventricles is ≥10 mm (corresponding to 4 standard deviations (SD) above the mean) from 14 weeks of gestational age to term (Fig. 11.8). It is classified into three degrees of severity depending on the width of dilatation [19]:

The factors that most affect the prognosis of a fetus with VM are width of dilatation (mild, moderate, severe), presence of associated anomalies (structural, chromosomal), and an underlying etiological factor (i.e., infections, alloimmune thrombocytopenia) [20]. More than 60 % of cases of severe VM are associated with structural anomalies (Fig. 11.8). Prognosis for severe VM associated with other malformations is unfavorable, with a 2-year survival rate not exceeding 16 %. Prognosis of isolated severe VM is slightly better, with a 33 % survival rate at 2 years and normal neurological and physical development in 10–62.5 % of cases, depending on the study [21]. Moderate VM is associated with other anomalies in 10–50 % of the cases, whereas mild VM is associated in a very low percentage of cases. Prognosis is conditioned by the existing concomitant anomalies. Regarding the prognosis of isolated forms, a delay in neurological development can be found in 25 % of cases of moderate and in up to 7 % of cases of mild VM [22].

Another factor influencing the prognosis of isolated VM, either moderate or mild, is the evolution of dilatation over time. VM progression occurs in 16 % of cases, whereas stabilization is reported in 43 % of cases, and an in utero normalization occurs in 41 % of cases. Progression is associated with a 22 % rate of chromosomal anomalies and with a negative prognosis in 44 % of cases in comparison with 1 and 7 %, respectively, of the forms that do not progress (stabilization or regression) [23].