Compared with neonates born at term, those born much before term are at heightened risk of a number of brain abnormalities seen on sonography (US).1,2
Among these is the presence of a hyperechoic lesion in the white matter adjacent to a large intraventricular hemorrhage (IVH), sometimes referred to as “grade IV IVH.” The article that described the most widely used IVH classification applied the term “grade IV IVH” to a lesion that was interpreted as the result of an extension of the hemorrhage from the ventricle into the adjacent white matter.3
Although this is possible, some authors consider it so unlikely that they have suggested eliminating the term “grade IV IVH.”4–6
Among other terms proposed for the association of IVH and adjacent periventricular increased echogenicity are “intraventricular hemorrhage with periventricular echodense lesions,”7
“periventricular intraparenchymal echodensities,”8
and “hemorrhagic leucomalacia.”2
Perhaps the main advantage of these descriptive terms is that they do not imply a mechanism of injury.
Another term proposed for this combination of imaging findings is “periventricular hemorrhagic infarction” (PVHI). A recent publication provided 4 references for the following definition of PVHI: “an echodense lesion in the periventricular white matter which is unilateral or, if bilateral, obviously asymmetric, and associated with a germinal matrix-intraventricular hemorrhage lesion which is usually ipsilateral or larger on the ipsilateral side.”9
The hyperechoic lesion adjacent to a ventricle containing a large amount of blood tends not to go around the ventricle, and therefore, is not truly periventricular. Rather it tends to be located near the lateral corner of the ventricle, suggesting that paraventricular would be a more appropriate descriptive term. The argument that the paraventricular hyperechoic lesions that accompany large IVH are due to infarction has been made elsewhere.10
A recent review of the pathogenesis of cerebral white matter injury of prematurity includes the following statement, “Although other pathologies occur in premature infants—for example, severe intraventricular hemorrhage, periventricular hemorrhagic infarction, hydrocephalus, cerebellar disease—cerebral white matter injury seems to be the predominant lesion.”11
This implies that cerebral white matter injury is distinct from the lesion some call PVHI. Perhaps the pathogenesis of the hyperechoic white matter lesion adjacent to a large IVH does not differ appreciably from what is generically labeled “white matter damage.”
If the presumed mechanism leading to infarction is compression of veins by a distended ventricle, then one should expect a blood-distended ventricle. Sometimes, however, moderate-sized hyperechoic lesions are seen in the white matter adjacent to lateral ventricles that contain some blood, but not enough to result in any distention. This leads to the question of whether these white matter lesions have an etiology other than venous infarction.