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Delayed intraventricular hemorrhage is common and worsens outcomes in intracerebral hemorrhage. Neurology 2013; 80:1295. 161. Dastur CK, Yu W. Current management of spontaneous intracerebral haemorrhage. Stroke Vasc Neurol 2017; 2:21. 162. Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke 2022; 53:e282. 163. Loggini A, Mansour A, El Ammar F, et al. Inversion of T Waves on Admission is Associated with Mortality in Spontaneous Intracerebral Hemorrhage. J Stroke Cerebrovasc Dis 2021; 30:105776. 164. Wittstock M, Meyer K, Klinke J, et al. Effects of insular involvement on functional outcome after intracerebral hemorrhage. Acta Neurol Scand 2021; 144:559. 165. Tung GA, Julius BD, Rogg JM. MRI of intracerebral hematoma: value of vasogenic edema ratio for predicting the cause. Neuroradiology 2003; 45:357. 166. Oleinik A, Romero JM, Schwab K, et al. CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy. Stroke 2009; 40:2393. Topic 1133 Version 39.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 34/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate GRAPHICS Typical locations of intracerebral hemorrhage Typical locations of hypertensive ICH are putamen (A), thalamus (B), subcortical white matter (C), pons (D) and cerebellum (E). Thalamic and subcortical hemorrhages often extend into ventricles (B and C). Cerebral amyloid angiopathy, drug abuse, or vascular anomaly often causes lobar hemorrhage (F). ICH: intracerebral hemorrhage. Reproduced with permission from: Dastur CK, Yu W. Current management of spontaneous intracerebral haemorrhage. Stroke Vasc Neurol 2017; 2(1):21-29. Copyright 2017 BMJ Publishing Group Ltd. Graphic 118071 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 35/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Distinctive distribution of cerebral microbleeds (A-C) CMBs on T2*-weighted gradient echo MRI sequences suggestive of deep penetrating (hypertensive) vasculopathy. CMBs predominate in bilateral thalami (A), brainstem (B), and dentate nucleus of cerebellum (C). (D-F) CMBs on T2*-weighted gradient echo MRI sequences suggestive of cerebral amyloid angiopathy. CMBs predominate in cerebral hemispheres (D, E). Associated findings include lobar hemorrhage (D; arrow and thick arrow) and superficial siderosis (F; circles). CMB: cerebral microbleeds; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 36/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Graphic 132282 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 37/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Lobar hemorrhage in cerebral amyloid angiopathy Acute superficial lobar hemorrhage in the left frontal lobe seen on computed tomography scan in a patient with cerebral amyloid angiopathy (A). Flair magnetic resonance image performed one week later shows the high signal intensity of subacute hemorrhage with surrounding edema extending into the subcortical white matter (B). Hemorrhage (now low signal intensity consistent with hemosiderin) and edema are mostly resolved on a three-month follow-up study (C). Courtesy of Eric D Schwartz, MD. Graphic 50480 Version 4.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 38/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate MRI of brain arteriovenous malformation T2-weighted MRI of the brain demonstrates multiple flow voids in the right hemisphere, suggestive of a large arteriovenous malformation. MRI: magnetic resonance imaging. From: Flemming KD, Lanzino G. Management of Unruptured Intracranial Aneurysms and Cerebrovascular Malformations. Continuum (Minneap Minn) 2017; 23:181. DOI: 10.1212/CON.0000000000000418. Copyright 2017 American Academy of Neurology. Reproduced with permission from Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited. Graphic 53992 Version 6.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 39/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Cerebellar hematoma due to ruptured AVM (A) Noncontrast head CT showing acute right cerebellar ICH with smaller adjacent focus of hemorrhage (black arrow). (B) Subsequent FLAIR sequence on brain MRI after decompressive craniectomy showing flow void (white arrow) adjacent to ICH (white dashed arrow). (C) Digital subtraction angiogram subsequently identified an AVM with a nidus (white arrowhead), feeding artery (white thick arrow), and draining vein (white short arrow). CT: computed tomography; ICH: intracerebral hemorrhage; FLAIR: fluid-attenuated inversion recovery; MRI: magnetic resonance imaging; AVM: arteriovenous malformation. Courtesy of Glenn A Tung, MD, FACR. Graphic 132273 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 40/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Intracerebral hemorrhage due to cerebral sinus thrombosis Noncontrast head CT showing left frontal ICH (arrow) and vasogenic edema (arrowhead) (A). Mid-sagittal plane on CT angiography (B) and MRV (C) showing filling defect (thick arrows) in superior sagittal sinus (B). Subsequent brain MRI with FLAIR (D) and T2* gradient recall echo (E) imaging showing larger ICH (arrows) and associated edema (arrowheads). ICH: intracerebral hemorrhage; CT: computed tomography; MRV: magnetic resonance venography; MRI: magnetic resonance imaging; FLAIR: fluid-attenuated inversion recovery. Courtesy of Glenn A Tung, MD, FACR. Graphic 132274 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 41/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Hemorrhagic transformation of ischemic infarction Noncontrast head CT (A) shows heterogeneous hyperdensity within hypodense region involving right frontal and insular lobes. On subsequent MRI of the brain, FLAIR (B), T2* gradient recall echo (C), and DWI (D) sequences show hypointense ICH (thin arrows) and hyperintensities consistent with acute infarction in the distribution of the right middle cerebral artery (thick arrows). CT: computed tomography; MRI: magnetic resonance imaging; FLAIR: fluid-attenuated inversion recovery; DWI: diffusion-weighted imaging; ICH: intracerebral hemorrhage. Courtesy of Glenn A Tung, MD, FACR. Graphic 132275 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 42/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Brain lesions in reversible cerebral vasoconstriction syndrome Representative brain images from patients with RCVS are shown to highlight different lesion patterns. The numbers in parenthesis show the percentages of the lesion patterns; totals exceed 100% due to lesion combinations. (A) No acute parenchymal lesion (24%). Normal axial DWI, GRE, and FLAIR images are shown. The hyperintense dot sign is present on FLAIR (far right, arrow). (B) Border zone/watershed infarcts (25%). On the far left, DWI shows typical symmetric, posterior infarcts that spare the cortical ribbon. In https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 43/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate the middle and on the far right, DWI shows widespread watershed infarcts. (C) Vasogenic edema (28%). Subcortical crescent-shaped T2- hyperintense lesions consistent with the posterior reversible encephalopathy syndrome are seen on FLAIR. (D) Hemorrhagic lesions (42%). The two images on the left (axial GRE) show simultaneous lobar and deep intraparenchymal hemorrhages. The two images on the right show convexal subarachnoid hemorrhages on CT and axial GRE. (E) Lesion combinations (28%). The two images on the left show bilateral watershed infarcts on DWI and the two images on the right show lobar as well as convexal subarachnoid hemorrhages on axial FLAIR and CT, all in the same patient. RCVS: reversible cerebral vasoconstriction syndrome; DWI: diffusion- weighted images; GRE: gradient-echo; FLAIR: fluid-attenuated inversion recovery; CT: computed tomography. From: Singhal AB, Topcuoglu MA, Fok JW, et al. Reversible cerebral vasoconstriction syndromes and primary angiitis of the central nervous system: clinical, imaging, and angiographic comparison. Ann Neurol 2016; 79:882. http://onlinelibrary.wiley.com/wol1/doi/10.1002/ana.24652/abstract. Copyright 2016 American Neurological Association. Reproduced with permission of John Wiley & Sons Inc. This image has been provided by or is owned by Wiley. Further permission is needed before it can be downloaded to PowerPoint, printed, shared or emailed. Please contact Wiley's permissions department either via email: permissions@wiley.com or use the RightsLink service by clicking on the 'Request Permission' link accompanying this article on Wiley Online Library (http://onlinelibrary.wiley.com). Graphic 109962 Version 2.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 44/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Excessive perihematomal edema in a patient with hemorrhagic lung metastasis Noncontrast head CT showing left frontal ICH surrounded by excessive volume of hypodense vasogenic edema (A, B). MRI performed one day later shows hyperintense vasogenic edema on T2*-weighted gradient echo image (C). Pre- (D) and post-contrast (E) T1-weighted MRI images demonstrate enhancement (arrows) consistent with underlying tumor. CT: computed tomography; ICH: intracerebral hemorrhage; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. Graphic 132284 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 45/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Intracerebral hemorrhage due to mycotic aneurysm Noncontrast head CT (A) showing small right parietal ICH (circle). CT angiogram in axial (B) and coronal (C) planes showing small mycotic aneurysm (arrow) adjacent to ICH (circle). CT: computed tomography; ICH: intracerebral hemorrhage. Courtesy of Glenn A Tung, MD, FACR. Graphic 132276 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 46/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate 12-year-old with moyamoya syndrome secondary to neurofibromatosis type 1 Magnetic resonance angiogram shows occlusion of left supraclinoid internal carotid artery (circles) and lentic collateral vessels (arrow). Courtesy of Glenn A Tung, MD, FACR. Graphic 129107 Version 3.0