Our diagnosis was hence fetal stroke: probably ischemic stroke with secondary hemorrhagic transformation.
(Hemorrhagic stroke could also be a possibility although the absence of mass effect and central lucency without hemorrhagic signal make this hypothesis less likely. Besides, in most pediatric and fetal clastic lesions, hemorrhage and ischemia are associated.)
We performed a second fetal brain MRI at 32WG (not shown), which showed the same findings as the postnatal neonatal brain MRI displayed.
The evolution of the images is typical of a clastic lesion: after resorption of the ischemic tissue and hematoma, there was now a focal porencephaly with hemosiderin tattooing on its margins.
(Conversely, persistence of the same MRI findings would have indicated a hypercellular brain tumor, which could have been a differential diagnosis.)
The child was delivered normally at 38WG. Neonatal clinical examination was normal. Neurological development will be under close watch for the next few years.
We screened both child and mother for infectious causes (CMV, toxoplasmosis, syphilis, CMV, hepatitis B, rubeola, Parvovirus B19), for alloimmune thrombocytopenia and for autoimmune diseases: the extensive screening did not pick up any risk factor.
Fetal stroke has been associated with postnatal epilepsy, intellectual disability, and cerebral palsy. The entity is caused by antenatal ischemic, thrombotic, or hemorrhagic injury. Although roughly half of the cases are idiopathic, the most common maternal conditions associated with fetal stroke are alloimmune thrombocytopenia and trauma. Fetal and pediatrics stroke display different patterns from those expected in adult patients: lenticulostriate territory is often involved.
For more information, refer to the references below.