Brief description.

This case refers to a female newborn infant born at 41 weeks of gestational age from spontaneous delivery, with meconium stained amniotic fluid and one tight umbilical cord loop at the neck. She developed partial focal seizures involving the right upper limb shortly after birth. A MRI brain performed within 24 hours from birth showed extensive left temporal-fronto-parietal ischemic stroke due to segmental reduction at the origin of one of the trifurcation branches of the left middle cerebral (see the arrow in the attached file), with normal flow signal of the remaining arterial vessels of the skull base and normal flow of the main venous sinuses.

A follow-up brain MRIperformed two months later shows a flimsy aspect of the A1 segment of the right anterior cerebral artery (see the arrow in the attached file), which was not evident at the previous angiographic sequence. The A2 tract of the right anterior brain is currently supplied by the controlateral carotid circulation via the anterior communicating artery. No further reductions in the flow of the remaining arterial vessels in the volume examined; in particular, the segmental vascular stenosis detected in the previous brain MRI examination of one of the trifurcation branches of the left middle cerebral is no longer evident.

Tests performed (protein C, S, ATIII assay and activity;V Leiden genetics, MTHFR and factor II G20210A mutation) were all negative. The child is currently in good health and has adequate neurological development and she is sizures free since the introduction of phenobarbital.

As this is the first time I see such an evolution after a previous neonatal ischemic stroke in a follow-up brain MRI, I would like to know if anyone thinks they can explain it with a postnatal regression (hypoplasia) of the A1 vascular section, perhaps as a consequence of a circulatory adjustment because of the previous ischemic stroke, or I have to suspect a vasculitis (even in a healthy baby).

Thanks in advance for the help you want to give us