Focal ischemic lesions on arterial basis may present as vascular territory distribution: middle cerebral arteries in the majority of cases (Fig. 9.1), but other main cerebral artery distribution can be affected as well. In some fetal cases, however, a clear vascular territory distribution cannot be determined (Fig. 9.2). Other times vascular watershed territories result involved the most (Figs. 9.3, 9.4, and 9.5). It is important to underline how initial focal ischemic lesions may often evolve into hemorrhagic transformation, leading to a hemorrhagic necrosis appearance (Fig. 9.6). For this reason, it is not always easy to distinguish between pure ischemic arterial lesion and focal hemorrhagic lesion, especially in subacute and chronic phase.

When the onset time of lesions is within hours or few days range before imaging, the detection of ischemic areas mainly relays on the use of DWI (Fig. 9.7); although affected by technical limitations and by motion artifacts, DWI sequence, especially when repeated, is able to highlight areas of increased signal and decrease ADC (Figs. 9.1 and 9.7). Acute lesion detection is a rare event [6], and in most of cases, MR imaging is prompted by death of one twin in monochorionic twin pregnancies or by complications during LASER treatment of placental anastomoses in monochorionic twins [7] (see chapter 10).

In most cases, focal ischemic lesions are detected in subacute or chronic phase as ultrasound hyperechogenic (subacute phase) or hypoechogenic (chronic malacia or focal atrophy) areas. In subacute phase (some days from insult onset), DWI signal could be still [8] increased, but the most important finding is represented by blurring of normal cerebral mantle layering, moderate signal increase, and mantle swelling on ultrafast T2-weighted images . In the transition period between subacute (days to 2 weeks) and chronic phase (from weeks to months), the lesion area could undergo some heterogeneous T2-weighted signal decrease and T1-weighted signal increase, due to hemorrhagic necrosis (Figs. 9.4 and 9.5).

Focal lesions evolve into chronic end-stage sequelae: focal lobe volume reduction, focal ventricle enlargement, cyst and malacyc areas formation, and nodular or linear hemosiderin deposits are all typical features of such kind of evolution (Figs. 9.5 and 9.6). End-stage sequelae may appear faster than it usually happens in adult brain focal ischemia, even in few weeks [9]. For this reason, it is very difficult to determine the age of chronic lesions only on MRI basis (Fig. 9.9). The poor capability of reparative gliosis and the high water content of fetal brain may give reason of the fast tissular liquefaction leading to malacic–cystic areas.

When focal lesions occur before 24 GW, there is the possibility that, in addition to the abovementioned sequelae, also malformations may arise (i.e., polymicrogyria, schizencephaly, heterotopias) (Fig. 9.8). In this regard, ischemia affecting neuronal pool in active proliferation, migration, and organization phase may be followed by focal development of cortical malformations, that could be considered a sort of reparative phenomenon proper of the early fetal age [10, 11]. Finally, false-negative fetal MR studies may obviously occur, especially in the evaluation of the brain of a survived or supposed normal twin in a TTTS setting (Fig. 9.9). It has to be underlined however how a focal ischemic lesion may occur at any stage of gestation and a negative fetal MR study at midgestation cannot totally predict the post-natal outcome.