Histopathology of Intracerebral Hemorrhage

Introduction

Intracerebral hemorrhage (ICH) is a subtype that is responsible for 10–15% of all strokes with significant morbidity and mortality. An ICH can be primary or secondary . A primary ICH results when a vulnerable small or large blood vessel ruptures without an identifiable reason for structural weakness and blood leaks out under pressure causing considerable damage to surrounding structures. A secondary ICH occurs when an underlying identifiable cause results in parenchymal hemorrhage. The causes include aneurysm, arteriovenous malformation, hemorrhagic transformation of arterial or venous ischemic stroke, trauma, coagulopathy, and hemorrhage from an underlying primary or secondary parenchymal neoplastic lesion. Whatever the cause, based on whether the hemorrhage is from an arterial or a venous pressure head there are consequences of neuronal injury of varying degree.

In the past 20 years there has been considerable technological advancements in improved minimally invasive techniques for the treatment of specific neurovascular disease, however, the mortality rates from ICH at 1 month has remained static at approximately 40% . Treatment of the insult that the brain parenchyma undergoes as a result of a hemorrhage is still by current standards of treatment for ICH largely supportive. These supportive measures include intracranial pressure control, brain edema treatment, and hemodynamic stability maintenance. Unfortunately these treatment strategies, not surprisingly, have not been able to reduce mortality or improve neurological outcome. The human population continues to age around the world and hence it can be extrapolated that the incidence of ICH will continue to increase. Thus it is crucial to improve our understanding of the underlying mechanisms of brain injury to be able to identify more effective therapeutic targets to improve neurological outcome from an ICH. For the purposes of this chapter we will present a detailed analysis of the existing understanding of the mechanisms of injury from ICH, cellular level correlates of severity of neuronal injury, and early and late brain injury.

Histopathological Changes