Intracerebral Hemorrhage as a Surgical Challenge-Where Should We Focus?

Intracerebral hemorrhage (ICH) 1) lacerates the brain parenchyma and disrupts white matter tracts; 2) causes mass effect and disturbs the function of neighboring white matter tracts or cortical regions; and 3) releases molecules that induce inflammation and oxidative stress, which creates a tissue microenvironment that predisposes to death of neurons. Because of the aforementioned deleterious effects of ICH, it would seem logical that removal of ICH would reduce the degree of secondary parenchymal damage caused by mass effect and toxicity of clot breakdown products. However, the neurologic impairment left by the ICH is not only related to the mass effect but also to the disruption of white matter tracts or destruction of cortical regions, basal ganglia, thalamus, cerebellum, or brainstem during the acute bleeding. Moreover, it is unknown to what extent the inflammation and oxidative stress triggered by the presence of blood in the parenchyma affects the degree of neuronal damage and outcome of the patient despite evacuation of the blood clot. Experiments in animal models suggest that pharmaceutical or other biologic therapy against the toxic effects of clot-derived iron may improve the outcome of patients with ICH. This suggests that the major improvements in the management and outcome of patients with ICH may come from research focused on the biology of ICH-induced brain injury.