Traumatic intraventricular hemorrhage: report of twenty-six cases and consideration of the pathogenic mechanism

Abstract

A series of 26 patients suffering traumatic intraventricular hemorrhage (IVH) after closed head injury is reviewed, and the pathogenic mechanism of the traumatic IVH is discussed considering the site of origin of the IVH. Computed tomographic detection of the origin of the IVH was possible in 15 patients (Group 1): 6 had frontal or temporal contusional intracerebral hemorrhage spreading into the ventricle (Subgroup A), 5 had the original hemorrhage in the caudate nucleus (Subgroup B), and 4 originally bled in the thalamus (Subgroup C). The origin of the IVH was not determined in 11 patients (Group 2): 6 had concomitant hemorrhage around the brain stem (Subgroup D), and 5 had small IVH with or without small intracerebral hemorrhage (Subgroup E). The site of impact was not uniform in Subgroup A, whereas the other four subgroups usually had frontal or occipital impact. In Subgroup A, the IVH was discovered more than several hours after trauma. In the other four subgroups, however, the IVH was detected in as short a time as 0.5 to 1.5 hours after trauma. In Subgroups B and C, the impact along the long axis of the skull and the early occurrence of hemorrhage in the basal ganglia suggest that shear injury between the perforating vessels and the basal ganglia may be the responsible mechanism. The several other possible mechanisms in Subgroups D and E are reviewed and discussed in relation to diffuse brain injury.