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Updated: Jan 30, 2026

Minimally Invasive Endoscopic Intracerebral Hemorrhage Evacuation
Published on: October 15, 2021
Hematoma location and morphology of anticoagulation-associated intracerebral hemorrhage
David J Seiffge1, Sami Curtze1, Nelly Dequatre-Ponchelle1
1From the Stroke Research Group (D.J.S., D.W.), UCL Queen Square Institute of Neurology, University College London and the National Hospital for Neurology and Neurosurgery, Queen Square, London, UK; Stroke Centre and Neurology (D.J.S.), University Hospital and University Basel, Switzerland; Department of Neurology (S.C., T.T.), Helsinki University Hospital, Finland; Degenerative & Vascular Cognitive Disorders, Department of Neurology (N.D.-P., C.C.), INSERM U1171, CHU Lille, University of Lille, France; Department of Clinical and Experimental Sciences, Neurology Clinic (A.P.), University of Brescia, Italy; Department of Clinical Neuroscience/Neurology (T.T.), Institute of Neurosciences and Physiology, Sahlgrenska Academy at University of Gothenburg; and Department of Neurology (T.T.), Sahlgrenska University Hospital, Gothenburg, Sweden.
Objective:
To study hematoma location and morphology of intracerebral hemorrhage (ICH) associated with oral anticoagulants (OAC) and delineate causes and mechanism.
Methods:
We performed a systematic literature research and meta-analysis of studies comparing neuroimaging findings in patients with OAC-ICH compared to those with ICH not associated with OAC (non-OAC ICH). We calculated pooled risk ratios (RRs) for ICH location using the Mantel-Haenszel random-effects method and corresponding 95% confidence intervals (95% CI).
Results:
We identified 8 studies including 6,259 patients (OAC-ICH n = 1,107, pooled OAC-ICH population 17.7%). There was some evidence for deep ICH location (defined as ICH in the thalamus, basal ganglia, internal capsule, or brainstem) being less frequent in patients with OAC-ICH (OAC-ICH: 450 of 1,102/40.8% vs non-OAC ICH: 2,656 of 4,819/55.1%; RR 0.94, 95% CI 0.88-1.00, p = 0.05, I = 0%) while cerebellar ICH location was significantly more common in OAC-ICH (OAC-ICH: 111 of 1,069/10.4% vs non-OAC ICH: 326 of 4,787/6.8%; RR 1.45, 95% CI 1.12-1.89, p = 0.005, I = 21%) compared to non-OAC ICH. There was no statistically significant relationship to OAC use for lobar (OAC-ICH: 423 of 1,107/38.2% vs non-OAC ICH: 1,884 of 5,152/36.6%; RR 1.02, 95% CI 0.89-1.17, p = 0.75, I = 53%, p for heterogeneity = 0.04) or brainstem ICH (OAC-ICH: 36 of 546/6.6% vs non-OAC ICH: 172 of 2,626/6.5%; RR 1.04, 95% CI 0.58-1.87, p = 0.89, I = 59%, p for heterogeneity = 0.04). The risk for intraventricular extension (OAC-ICH: 436 of 840/51.9% vs non-OAC ICH: 1,429 of 3,508/40.7%; RR 1.26, 95% CI 1.16-1.36, p < 0.001, I = 0%) was significantly increased in patients with OAC-ICH. We found few data on ICH morphology in OAC-ICH vs non-OAC ICH.
Conclusion:
The overrepresentation of cerebellar ICH location and intraventricular extension in OAC-ICH might have mechanistic relevance for the underlying arteriopathy, pathophysiology, or bleeding pattern of OAC-ICH, and should be investigated further.
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