EXPERIMENTAL STUDIES 780 | VOLUME 65 | NUMBER 4 | OCTOBER 2009 www.neurosurgery-online.com Ivan Marinkovic, M.D. Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland; and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Daniel Strbian, M.D., Ph.D. Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland; and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Eric Pedrono, M.Sc. Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Olga Y. Vekovischeva, Ph.D. Department of Pharmacology, Institute of Biomedicine, University of Helsinki, Helsinki, Finland Shashank Shekhar, M.D. Department of Neurology, Helsinki University Central Hospital, and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Aysan Durukan, M.D. Department of Neurology, Helsinki University Central Hospital, and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Esa R. Korpi, M.D., Ph.D. Institute of Biomedicine, Pharmacology, University of Helsinki, Helsinki, Finland Usama Abo-Ramadan, Ph.D. Department of Neurology, Helsinki University Central Hospital, and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Turgut Tatlisumak, M.D., Ph.D. Department of Neurology, Helsinki University Central Hospital, and Experimental MRI Laboratory, Biomedicum Helsinki, Helsinki, Finland Reprint requests: Daniel Strbian, M.D., Ph.D., Department of Neurology, Helsinki University Central Hospital, Haartmaninkatu 4, PL 340, 00290 Helsinki, Finland. Email: daniel.strbian@hus.fi Received, November 24, 2008. Accepted, April 24, 2009. Copyright © 2009 by the Congress of Neurological Surgeons I n Western countries, intracerebral hemor- rhage (ICH) accounts for 10% to 15% of all strokes, and the percentage in Asian and black populations is even higher (20%–30%) (20). ICH is associated with high mortality, with 60% to 70% of the patients surviving through the first month but only 40% to 50% through the first year (12, 20), many of them with severe disabilities. Poor outcome results both from early and delayed changes after ICH. After the hemorrhagic event, direct tissue destruction and dissection of blood occurs, fol- lowed by edema formation. These changes are complicated by the mass effect of the growing hematoma (in 40% of patients within 20 h) (1), leading to increased intracranial pressure (ICP) and to disruption and displacement of brain structures. A role for mast cells has recently emerged in mediating edema and hematoma growth under experimental conditions (18). Delayed damage is mediated by toxins associ- ated with blood breakdown products, throm- bin, and inflammation (5, 21). Furthermore, necrosis, apoptosis (7), excitotoxicity (15), and disruption of the blood-brain barrier (14) all contribute to brain damage. The counterpart to emergency thrombolysis treatment of acute ischemic stroke is hemostatic therapy with the aim of cessation of hematoma growth. Thus far, ε-aminocaproic acid, aprotinin, and tranexamic acid have been tested, albeit unsuccessfully (8, 13). Recently, recombinant activated factor VII has reduced growth of hematoma volume but without improvement in survival or functional outcome (9), and surgical evacuation of ICH has not been beneficial (11). ABBREVIATIONS: ICH, intracerebral hemorrhage; ICP, intracranial pressuree; TUNEL, terminal de- oxynucleotidyl transferase dUTP nick-end labeling Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.neurosurgery-online.com). DECOMPRESSIVE CRANIECTOMY FOR INTRACEREBRAL HEMORRHAGE OBJECTIVE: Intracerebral hemorrhage (ICH) has a high mortality rate and leaves most survivors disabled. The dismal outcome is mostly due to the mass effect of hematoma plus edema. Major clinical trials show no benefit from surgical or medical treatment. Decompressive craniectomy has, however, proven beneficial for large ischemic brain infarction with massive swelling. We hypothesized that craniectomy can improve ICH outcome as well. METHODS: We used the model of autologous blood injection into the basal ganglia in rats. After induction of ICH and then magnetic resonance imaging, animals were ran- domly allocated to groups representing no craniectomy (n = 10) or to craniectomy at 1, 6, or 24 hours. A fifth group without ICH underwent craniectomy only. Neurological and behavioral outcomes were assessed on days 1, 3, and 7 after ICH induction. Furthermore, terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells were counted. RESULTS: After 7 days, compared with the ICH + no craniectomy group, all craniectomy groups had strikingly lower mortality (P  0.01), much better neurological outcome (P  0.001), and more favorable behavioral outcome. A trend occurred in the ICH + no craniectomy group toward more robust apoptosis. CONCLUSION: Decompressive craniectomy performed up to 24 hours improved out- come after experimental ICH, with earlier intervention of greater benefit. KEY WORDS: Decompressive craniectomy, Intracerebral hemorrhage, Magnetic resonance imaging, Mortality, Rat Neurosurgery 65:780–786, 2009 DOI: 10.1227/01.NEU.0000351775.30702.A9 www.neurosurgery-online.com