Neurosurgery in Hemorrhagic Stroke

Abstract

Spontaneous or nontraumatic intracerebral hemorrhage (ICH) accounts for 10–12 % of all strokes and has an incidence of 10–30/100,000/year in the general population. The case fatality during the course of ICH is up to 59 % after 1 year and 82 % after 10 years, mainly due to the heterogeneous pathogenesis of ICH or the resulting medical, systemic complications of ICH. Primary ICH accounts for 80–85 % of all ICHs and is commonly caused by arterial hypertension or cerebral amyloid angiopathy. In line with other acute brain injuries, such as traumatic brain injury or aneurysmal subarachnoid hemorrhage, the chronological sequence of pathophysiological events during the course of spontaneous ICH can be divided into early and delayed. The pathogenesis of delayed brain injury during the course of ICH is assumed to be derived from direct cytotoxic effects of blood iron, thrombin, and other blood breakdown products as well as free radicals and inflammation. Additionally, the local mass effect due to the hematoma mass is assumed to cause compression of the vasculature in the brain tissue surrounding the hematoma. Impairment of perihematomal perfusion is assumed to be a main contributor to secondary brain injury and ultimately poor neurological outcome following ICH. The rationale for hematoma evacuation is the reduction of secondary brain injury, thus the improvement of outcome, as compared to the natural course of ICH. However, despite novel data from large prospective, randomized clinical trials, the appropriate treatment of ICH, i.e., surgical, or conservative management remains unclear. The currently available data suggests that the indication for surgical treatment and even the appropriate surgical modality should account for various factors, such as hematoma location (deep seated vs. superficial) and hematoma volume, patient age, comorbidities, as well as estimated neurological outcome based on hematoma location and initial neurological status.