Mechanisms of brain injury after intracerebral haemorrhage

Lancet Neurol. 2006 Jan;5(1):53-63. doi: 10.1016/S1474-4422(05)70283-0.


The past decade has resulted in a rapid increase in knowledge of mechanisms underlying brain injury induced by intracerebral haemorrhage (ICH). Animal studies have suggested roles for clot-derived factors and the initial physical trauma and mass effect as a result of haemorrhage. The coagulation cascade (especially thrombin), haemoglobin breakdown products, and inflammation all play a part in ICH-induced injury and could provide new therapeutic targets. Human imaging has shown that many ICH continue to expand after the initial ictus. Rebleeding soon after the initial haemorrhage is common and forms the basis of a current clinical trial using factor VIIa to prevent rebleeding. However, questions about mechanisms of injuries remain. There are conflicting data on the role of ischaemia in ICH and there is uncertainty over the role of clot removal in ICH therapy. The next decade should bring further information about the underlying mechanisms of ICH-induced brain injury and new therapeutic interventions for this severe form of stroke. This review addresses our current understanding of the mechanisms underlying ICH-induced brain injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Age Factors
  • Animals
  • Blood Coagulation / physiology
  • Brain Edema / etiology
  • Brain Edema / pathology
  • Brain Injuries / etiology*
  • Brain Injuries / genetics
  • Brain Injuries / pathology
  • Brain Injuries / therapy
  • Cerebral Hemorrhage / complications*
  • Cerebral Hemorrhage / genetics
  • Cerebral Hemorrhage / therapy
  • Cerebrovascular Circulation / physiology
  • Humans
  • Iron / metabolism
  • Sex Factors
  • Time Factors


  • Iron