The pathogenesis of experimental periventricular cerebral necrosis and its possible relation to the periventricular leucomalacia of birth trauma

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Abstract
Obliteration of the basilar artery followed by constriction or closure of one or both common carotid arteries in mature cats experimentally produced periventricular cerebral necrosis. The multiple, patchy and well-defined lesions were characterized by disintegration of myelin, marked softening and breakdown of tissue and an intense macrophage reaction with no increase of astrocytes at the periphery. The cerebral gray matter was almost completely preserved. These observations and their similarity to lesions seen in the brains of infants and children following anoxia and cerebral palsy strongly suggest the implication of an hemodynamic factor. Comparative and developmental anatomy studies of the cerebral vascular system indicate that the periventricular white matter is selectively vulnerable to hemodynamic derangements primarily for two reasons. First, the deep cerebral white matter receives its main blood supply from a system of primitive arteriovenous units which are essentially terminal vessels and second, there exists in this zone a functional and anatomical separation of such arteries which are derived from the three major cerebral arteries. The gray matter is preserved in the immature and relatively smooth brains because the ample, poorly differentiated leptomeningeal anastomotic channels are capable of transporting and shunting large quantities of blood.