Traumatic basal ganglia hemorrhage: clinicopathologic features and outcome

Abstract

Traumatic basal ganglia hemorrhage (TBGH) is probably secondary to rupture of lenticulostriate or anterior choroidal arteries. We evaluated 6 consecutive cases of this entity to define its clinical and pathologic dimensions. Relative frequency of TBGH was 3% (3 left, 3 right) in this acute rehabilitation population. Lesion size and associated pathology varied. Contralateral hemiparesis, present in all, recovered to varying extents, apparently related to lesion location (posterior limb, internal capsule, or midperiventricular white matter), not size. Prolonged muteness occurred in 4 of 6; these 4 patients also had severe diffuse axonal injury. Clinical findings corresponded with previously recognized subcortical hemisphere profiles. All achieved a moderate disability or good recovery rating on the Glasgow Outcome Scale. Rather than any features of the TBGH itself, duration of coma and/or associated temporal herniation predicted slower recovery and worse outcome. In conclusion, TBGH is a rare entity compatible with a favorable recovery, especially when occurring in isolation. The hemorrhage itself determines clinical signs related to particular subcortical structures involved and the side of the lesion. Overall cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.