In this study we describe a new pattern of cerebral damage that may affect both preterm and at-term neonates with a history of neonatal distress or seizures in the first week of life. The main feature of this pattern is the involvement of deep medullary veins (DMV), small vessels that drain deep white matter.
In our patients, congested and thrombotic DMV appear on T1-, T2-, and susceptibility-weighted images as linear lesions, radially oriented in the periventricular white matter, with signs of perivenular infarction. Notably, with respect to classic paratrigonal periventricular leukomalacia of the preterm newborn, DMV-related damage seems particularly conspicuous in the frontal white matter regions.
The main unsolved issue about DMV lesions concerns their etiology. Our first aim is to acquire more data that could shed light on the etiology of this condition we believe could be the common endpoint sustained due to different causes.
In our published cohort we excluded patients with venous sinus thrombosis, and we hypothesized that central venous hypertension and congestion may play a role in the pathophysiology of DMV engorgement. However, this hypothesis is currently supported only by very scarce data such as work from our group, also published in the AJNR, on 5 fetuses showing a similar brain pattern; all these fetuses had in common heart failure and central venous hypertension due to congenital or acquired causes.
Recently, in the neonatal imaging literature, some reports showed a similar pattern of damage in newborns with viral encephalitis, in particular those with Parechovirus and Rotavirus infections. In such cases the inflammatory process would particularly involve the perivenular white matter.