Intracerebral haemorrhage pathophysiology: time is brain

Abstract

Intracerebral haemorrhage is associated with high mortality and morbidity. Cerebral small vessel disease, either due to hypertensive small vessel disease or to amyloid angiopathy, is the common substrate for primary spontaneous intracerebral haemorrhage.

The current understanding of brain injury induced by intracerebral haemorrhage is based on both clinical and experimental studies. The initial injury immediately after its onset is from the direct mechanical force of the expanding hematoma, resulting in cytotoxic edema and cellular necrosis. After this, the degrading hematoma releases its breakdown products, which lead to the activation of oxygen free radicals, matrix metalloproteinases, complement proteins and inflammatory markers, thus determining an increase of the BBB permeability, the recruitment of inflammatory cells, apoptosis, and ultimately the exacerbation of cerebral edema and neuronal death.

Evidence suggests that early and aggressive medical management and specialist care can improve the overall outcome in patients with intracerebral haemorrhage. The growing insight into the molecular pathophysiological mechanisms may contribute to the development of neuroprotective strategies.