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(Stroke. 2006;37:301.)
© 2006 American Heart Association, Inc.

Advances in Stroke 2005

Advances in Intracerebral Hemorrhage Management

From the Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland (S.J.); and the Department of Neurology, Boston University Medical Center, Boston, MA (C.S.K.).

Correspondence to Carlos Kase, Boston University School of Medicine, 80 E Concord St, Boston, MA. E-mail cskase@bu.edu

Key Words: intracerebral hemorrhage

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Recent advances in the evaluation and management of intracerebral hemorrhage (ICH) include: the identification of molecular markers that correlate with events in its early course, complications, and outcome; the impact of previous treatment with antiplatelet or anticoagulant agents on the outcome after ICH; the analysis of the results of the large international STICH (Surgical Trial in Intracerebral Hemorrhage) study; and the publication of the results of the recombinant activated Factor VII trial in ICH.

Molecular Markers of ICH Complications, Course, and Outcome

Recent research interest in ICH has attempted to produce a better understanding of the events that occur early in its course, including hematoma growth, development of perihematoma edema, and the resultant tissue injury, factors that can cause early neurological deterioration and can have impact on its long-term outcome.^1–3 These interrelated processes are accompanied by a cascade of events that correlate with elevation of certain molecular markers in serum.

The process of perihematoma edema formation starts early after ICH onset, generally within 3 hours,⁴ and it increases gradually in severity for at least 72 hours.⁵ Several mechanisms in sequence contribute to the formation of edema, including: a first phase of clot retraction with extrusion of serum; a second phase (for the first 2 days) of activation of the coagulation cascade with production of thrombin; and a final phase (after 3 days from onset) of red blood cell lysis with hemoglobin-induced neuronal damage.⁵ The central role of thrombin in promoting perihematoma edema has been documented in both experimental⁶ and human⁷ ICH, with evidence of reduced edema formation after . . . [Full Text of this Article]

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