th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topics (see "Patient education: Hemorrhagic stroke (The Basics)" and "Patient education: Stroke (The Basics)") Beyond the Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond the Basics)") https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 13/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate SUMMARY Classification Stroke is classified into two major types (see 'Definitions' above): Brain ischemia due to thrombosis, embolism, or systemic hypoperfusion Brain hemorrhage due to intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH) Ischemia - There are three main subtypes of brain ischemia ( table 1): Thrombosis generally refers to local in situ obstruction of an artery. The obstruction may be due to disease of the arterial wall, such as atherosclerosis, arteriosclerosis, dissection, or fibromuscular dysplasia; there may or may not be superimposed thrombosis. Thrombotic strokes can be divided into either large or small vessel disease. These two subtypes of thrombosis are worth distinguishing since the causes, outcomes, and treatments are different. (See 'Thrombosis' above.) Embolism refers to particles of debris originating elsewhere that block arterial access to a particular brain region. The source of embolism is most often from the heart or from an artery (artery-to-artery embolism). (See 'Embolism' above.) Systemic hypoperfusion is a more general circulatory problem, manifesting itself in the brain and perhaps other organs. (See 'Systemic hypoperfusion' above.) Blood disorders are an uncommon primary cause of stroke. However, increased blood coagulability can result in thrombus formation and subsequent cerebral embolism in the presence of an endothelial lesion located in the heart, aorta, or large arteries that supply the brain. (See 'Blood disorders' above.) Ischemic stroke classification The TOAST classification scheme for ischemic stroke ( table 3) is widely used and has good interobserver agreement. The SSS-TOAST system divides each of the original TOAST subtypes into three subcategories as "evident," "probable," or "possible" based upon the weight of diagnostic. The Causative Classification System (CCS) ( table 4) is an automated version of the SSS-TOAST. (See 'Classification systems for ischemic stroke' above.) Brain hemorrhage There are two main subtypes of brain hemorrhage: ICH refers to bleeding directly into the brain parenchyma. Accumulation of blood occurs over minutes or hours. The most common causes of ICH are hypertension, trauma, https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 14/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate bleeding diatheses, amyloid angiopathy, illicit drug use (mostly amphetamines and cocaine), and vascular malformations. Less frequent causes include bleeding into tumors, aneurysmal rupture, and vasculitis. (See 'Intracerebral hemorrhage' above.) SAH refers to bleeding into the cerebrospinal fluid within the subarachnoid space that surrounds the brain. The two major causes of SAH are rupture of arterial aneurysms that lie at the base of the brain and bleeding from vascular malformations that lie near the pial surface. Bleeding diatheses, trauma, amyloid angiopathy, and illicit drug use are less common. Rupture of an aneurysm releases blood directly into the cerebrospinal fluid (CSF) under arterial pressure. The blood spreads quickly within the CSF, rapidly increasing intracranial pressure. Death or deep coma ensues if the bleeding continues. (See 'Subarachnoid hemorrhage' above.) Epidemiology Globally, ischemia accounts for 62 percent, intracerebral hemorrhage 28 percent, and subarachnoid hemorrhage 10 percent of all incident strokes, reflecting a higher incidence of hemorrhagic stroke in low- and middle-income countries. In the United States, the proportion of all strokes due to ischemia, intracerebral hemorrhage, and subarachnoid hemorrhage is 87, 10, and 3 percent, respectively. (See 'Epidemiology' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Caplan LR. Intracranial branch atheromatous disease: a neglected, understudied, and underused concept. Neurology 1989; 39:1246. 2. Caplan LR. Basic pathology, anatomy, and pathophysiology of stroke. In: Caplan's Stroke: A Clinical Approach, 4th ed, Saunders Elsevier, Philadelphia 2009. p.22. 3. Brain embolism, Caplan LR, Manning W (Eds), Informa Healthcare, New York 2006. 4. Caplan LR. Brain embolism, revisited. Neurology 1993; 43:1281. 5. Caplan LR. Brain embolism. In: Clinical Neurocardiology, Caplan LR, Hurst JW, Chimowitz M (Eds), Marcel Dekker, New York 1999. p.35. 6. Ay H, Furie KL, Singhal A, et al. An evidence-based causative classification system for acute ischemic stroke. Ann Neurol 2005; 58:688. 7. Doufekias E, Segal AZ, Kizer JR. Cardiogenic and aortogenic brain embolism. J Am Coll Cardiol 2008; 51:1049. https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 15/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate 8. Roach GW, Kanchuger M, Mangano CM, et al. Adverse cerebral outcomes after coronary bypass surgery. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators. N Engl J Med 1996; 335:1857. 9. Kamel H, Bartz TM, Elkind MSV, et al. Atrial Cardiopathy and the Risk of Ischemic Stroke in the CHS (Cardiovascular Health Study). Stroke 2018; 49:980. 10. Flemming KD, Brown RD Jr, Petty GW, et al. Evaluation and management of transient ischemic attack and minor cerebral infarction. Mayo Clin Proc 2004; 79:1071. 11. Meissner I, Khandheria BK, Sheps SG, et al. Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander? A prospective population-based transesophageal echocardiography study. J Am Coll Cardiol 2004; 44:1018. 12. Petty GW, Khandheria BK, Meissner I, et al. Population-based study of the relationship between atherosclerotic aortic debris and cerebrovascular ischemic events. Mayo Clin Proc 2006; 81:609. 13. Russo C, Jin Z, Rundek T, et al. Atherosclerotic disease of the proximal aorta and the risk of vascular events in a population-based cohort: the Aortic Plaques and Risk of Ischemic Stroke (APRIS) study. Stroke 2009; 40:2313. 14. Amarenco P, Duyckaerts C, Tzourio C, et al. The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 1992; 326:221. 15. Amarenco P, Cohen A, Tzourio C, et al. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 1994; 331:1474. 16. Cohen A, Tzourio C, Bertrand B, et al. Aortic plaque morphology and vascular events: a follow-up study in patients with ischemic stroke. FAPS Investigators. French Study of Aortic Plaques in Stroke. Circulation 1997; 96:3838. 17. Di Tullio MR, Russo C, Jin Z, et al. Aortic arch plaques and risk of recurrent stroke and death. Circulation 2009; 119:2376. 18. Caplan LR. The aorta as a donor source of brain embolism. In: Brain embolism, Caplan, LR, Manning, WJ (Eds), Informa Healthcare, New York 2006. p.187. 19. Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993; 24:35. 20. Ay H, Benner T, Arsava EM, et al. A computerized algorithm for etiologic classification of ischemic stroke: the Causative Classification of Stroke System. Stroke 2007; 38:2979. 21. Arsava EM, Ballabio E, Benner T, et al. The Causative Classification of Stroke system: an international reliability and optimization study. Neurology 2010; 75:1277. https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 16/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate 22. McArdle PF, Kittner SJ, Ay H, et al. Agreement between TOAST and CCS ischemic stroke classification: the NINDS SiGN study. Neurology 2014; 83:1653. 23. Caplan LR. Intracerebral haemorrhage. Lancet 1992; 339:656. 24. Kase CS, Caplan LR. Intracerebral Hemorrhage, Butterworth-Heinemann, Boston 1996. 25. Gorelick PB, Hier DB, Caplan LR, Langenberg P. Headache in acute cerebrovascular disease. Neurology 1986; 36:1445. 26. Linn FH, Wijdicks EF, van der Graaf Y, et al. Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage. Lancet 1994; 344:590. 27. Krishnamurthi RV, Feigin VL, Forouzanfar MH, et al. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health 2013; 1:e259. 28. GBD 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet Neurol 2021; 20:795. 29. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report From the American Heart Association. Circulation 2022; 145:e153. 30. GBD 2016 Lifetime Risk of Stroke Collaborators, Feigin VL, Nguyen G, et al. Global, Regional, and Country-Specific Lifetime Risks of Stroke, 1990 and 2016. N Engl J Med 2018; 379:2429. 31. GBD 2016 Neurology Collaborators. Global, regional, and national burden of neurological disorders, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol 2019; 18:459. 32. Wang W, Jiang B, Sun H, et al. Prevalence, Incidence, and Mortality of Stroke in China: Results from a Nationwide Population-Based Survey of 480 687 Adults. Circulation 2017; 135:759. 33. Koton S, Schneider AL, Rosamond WD, et al. Stroke incidence and mortality trends in US communities, 1987 to 2011. JAMA 2014; 312:259. 34. Vangen-L nne AM, Wilsgaard T, Johnsen SH, et al. Declining Incidence of Ischemic Stroke: What Is the Impact of Changing Risk Factors? The Troms Study 1995 to 2012. Stroke 2017; 48:544. 35. Madsen TE, Khoury JC, Leppert M, et al. Temporal Trends in Stroke Incidence Over Time by Sex and Age in the GCNKSS. Stroke 2020; 51:1070. 36. Feigin VL, Forouzanfar MH, Krishnamurthi R, et al. Global and regional burden of stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet 2014; 383:245. https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 17/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate 37. GBD 2016 Stroke Collaborators. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol 2019; 18:439. 38. Lanska DJ. Geographic distribution of stroke mortality in the United States: 1939-1941 to 1979-1981. Neurology 1993; 43:1839. 39. Casper ML, Wing S, Anda RF, et al. The shifting stroke belt. Changes in the geographic pattern of stroke mortality in the United States, 1962 to 1988. Stroke 1995; 26:755. 40. Centers for Disease Control and Prevention (CDC). Disparities in deaths from stroke among persons aged <75 years United States, 2002. MMWR Morb Mortal Wkly Rep 2005; 54:477. 41. Rich DQ, Gaziano JM, Kurth T. Geographic patterns in overall and specific cardiovascular disease incidence in apparently healthy men in the United States. Stroke 2007; 38:2221. 42. Glymour MM, Kosheleva A, Boden-Albala B. Birth and adult residence in the Stroke Belt independently predict stroke mortality. Neurology 2009; 73:1858. 43. White H, Boden-Albala B, Wang C, et al. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation 2005; 111:1327. 44. Schneider AT, Kissela B, Woo D, et al. Ischemic stroke subtypes: a population-based study of incidence rates among blacks and whites. Stroke 2004; 35:1552. 45. Morgenstern LB, Smith MA, Lisabeth LD, et al. Excess stroke in Mexican Americans compared with non-Hispanic Whites: the Brain Attack Surveillance in Corpus Christi Project. Am J Epidemiol 2004; 160:376. Topic 1089 Version 33.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 18/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate GRAPHICS Pathophysiologic ischemic stroke classification Large vessel atherothrombotic stroke More common Bifurcation of the common carotid artery Siphon portion of the common carotid artery Middle cerebral artery stem Intracranial vertebral arteries proximal to middle basilar artery Origin of the vertebral arteries Less common Origin of the common carotid artery Posterior cerebral artery stem Origin of the major branches of the basilar-vertebral arteries Origin of the branches of the anterior, middle, and posterior cerebral arteries Small vessel (lacunar) stroke Mechanism Lipohyalinotic occlusion Less frequently proximal atherothrombotic occlusion Least likely embolic occlusion Most common locations Penetrating branches of the anterior, middle, and posterior cerebral and basilar arteries Cardioaortic embolic stroke Cardiac sources definite - antithrombotic therapy generally used Left atrial thrombus Left ventricular thrombus Atrial fibrillation and paroxysmal atrial fibrillation Sustained atrial flutter Recent myocardial infarction (within one month) Rheumatic mitral or aortic valve disease Bioprosthetic and mechanical heart valve https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 19/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Chronic myocardial infarction with ejection fraction <28 percent Symptomatic heart failure with ejection fraction <30 percent Dilated cardiomyopathy Cardiac sources definite - anticoagulation hazardous Bacterial endocarditis (exception nonbacterial) Atrial myxoma Cardiac sources possible Mitral annular calcification Patent foramen ovale Atrial septal aneurysm Atrial septal aneurysm with patent foramen ovale Left ventricular aneurysm without thrombus Isolated left atrial spontaneous echo contrast ("smoke") without mitral stenosis or atrial fibrillation Mitral valve strands Ascending aortic atheromatous disease (>4 mm) True unknown source embolic stroke Other Dissection Moyamoya Binswanger's disease Primary thrombosis Cerebral mass Graphic 55099 Version 4.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 20/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Anatomy of the cerebral arterial circulation Frontal view of the carotid arteries, vertebral arteries, and intracranial vessels and their communication with each other via the circle of Willis. Reproduced with permission from: U acker R. Atlas Of Vascular Anatomy: An Angiographic Approach, Second Edition. Philadelphia: Lippincott Williams & Wilkins, 2006. Copyright 2006 Lippincott Williams & Wilkins. Graphic 51410 Version 6.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 21/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Major cerebral vascular territories Representation of the territories of the major cerebral vessels shown in a coronal section of the brain. Reproduced with permission from Kistler, JP, et al, Cerebrovascular Diseases. Harrison's Principles of Internal Medicine, 13th ed, McGraw-Hill, New York 1994. Copyright 1994 McGraw-Hill Companies, Inc. Graphic 65199 Version 2.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 22/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Stuttering time course of thrombotic stroke The course of weakness of the right limb in a patient with a thrombotic stroke reveals fluctuating symptoms, varying between normal and abnormal, progressing in a stepwise or stuttering fashion with some periods of improvement. Graphic 64107 Version 2.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 23/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Time course of lacunar infarction Penetrating artery occlusions usually cause symptoms that develop over a short period of time, hours or at most a few days, compared to large artery-related brain ischemia which can evolve over a longer period. A stuttering course may ensue, as with large artery thrombosis. This patient had a pure motor hemiparesis. Graphic 52246 Version 1.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 24/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Time course of embolic stroke Embolic stroke occurs suddenly, with symptoms maximal at onset. This patient had multiple embolic events with different clinical symptoms (initially weakness, followed by paresthesias). Graphic 73261 Version 1.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 25/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Cardioaortic sources of cerebral embolism Sources with high primary risk for ischemic stroke Sources with low or uncertain primary risk for ischemic stroke Atrial fibrillation Cardiac sources of embolism: Paroxysmal atrial fibrillation Mitral annular calcification Left atrial thrombus Patent foramen ovale Left ventricular thrombus Atrial septal aneurysm Sick sinus syndrome Atrial septal aneurysm and patent foramen ovale Atrial flutter Left ventricular aneurysm without thrombus Recent myocardial infarction (within one month prior to stroke) Left atrial spontaneous echo contrast ("smoke") Mitral stenosis or rheumatic valve disease Congestive heart failure with ejection fraction <30% Mechanical heart valves Bioprosthetic heart valves Chronic myocardial infarction together with low ejection fraction (<28%) Apical akinesia Dilated cardiomyopathy (prior established Wall motion abnormalities (hypokinesia, diagnosis or left ventricular dilatation with an akinesia, dyskinesia) other than apical akinesia ejection fraction of <40% or fractional shortening of <25%) Nonbacterial thrombotic endocarditis Hypertrophic cardiomyopathy Infective endocarditis Left ventricular hypertrophy Papillary fibroelastoma Left ventricular hypertrabeculation/non- compaction Left atrial myxoma Recent aortic valve replacement or coronary artery bypass graft surgery Presence of left ventricular assist device Paroxysmal supraventricular tachycardia Aortic sources of embolism: Complex atheroma in the ascending aorta or proximal arch (protruding with >4 mm thickness, or mobile debris, or plaque ulceration) The high- and low-risk cardioaortic sources in this table are separated using an arbitrary 2% annual https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 26/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate or one-time primary stroke risk threshold. Data from: 1. Ay H, Benner T, Arsava EM, et al. A computerized algorithm for etiologic classi cation of ischemic stroke: the Causative Classi cation of Stroke System. Stroke 2007; 38:2979. 2. Ay H, Furie KL, Singhal A, et al. An evidence-based causative classi cation system for acute ischemic stroke. Ann Neurol 2005; 58:688. 3. Arsava EM, Ballabio E, Benner T, et al. The Causative Classi cation of Stroke system: an international reliability and optimization study. Neurology 2010; 75:1277. 4. Kamel H, Elkind MS, Bhave PD, et al. Paroxysmal supraventricular tachycardia and the risk of ischemic stroke. Stroke 2013; 44:1550. 5. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant 2017; 36:1080. Reproduced and modi ed with permission from: Ay H, Furie KL, Singhal A, et al. An evidence-based causative classi cation system for acute ischemic stroke. Ann Neurol 2005; 58:688. Copyright 2005 American Neurological Association. Graphic 60843 Version 11.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 27/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate TOAST classification of subtypes of acute ischemic stroke Large-artery atherosclerosis Cardioembolism Small-vessel occlusion Stroke of other determined etiology Stroke of undetermined etiology Two or more causes identified Negative evaluation Incomplete evaluation Graphic 62571 Version 1.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 28/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Causative Classification System (CCS) of ischemic stroke etiology Stroke Level of Criteria mechanism confidence 1. Either occlusive or stenotic ( 50 percent diameter reduction or <50 percent diameter reduction with plaque ulceration or Large artery Evident atherosclerosis thrombosis) vascular disease judged to be caused by atherosclerosis in the clinically relevant extracranial or intracranial arteries, and 2. The absence of acute infarction in vascular territories other than the stenotic or occluded artery 1. History of 1 transient monocular blindness (TMB), TIA, or stroke from the territory of index artery affected by atherosclerosis within the last month, or Probable 2. Evidence of near-occlusive stenosis or nonchronic complete occlusion judged to be caused by atherosclerosis in the clinically relevant extracranial or intracranial arteries (except for the vertebral arteries), or 3. The presence of ipsilateral and unilateral internal watershed infarctions or multiple, temporally separate, infarctions exclusively within the territory of the affected artery Possible 1. The presence of an atherosclerotic plaque protruding into the lumen and causing mild stenosis (<50 percent) in the absence of any detectable plaque ulceration or thrombosis in a clinically relevant extracranial or intracranial artery and history of 2 TMB, TIA, or stroke from the territory of index artery affected by atherosclerosis, at least one event within the last month, or 2. Evidence for evident large artery atherosclerosis in the absence of complete diagnostic investigation for other mechanisms https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 29/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Cardio-aortic embolism Evident The presence of a high-risk cardiac source of cerebral embolism Probable 1. Evidence of systemic embolism, or 2. The presence of multiple acute infarctions that have occurred closely related in time within both right and left anterior or both anterior and posterior circulations in the absence of occlusion or near-occlusive stenosis of all relevant vessels. Other diseases that can cause multifocal ischemic brain injury such as vasculitides, vasculopathies, and hemostatic or hemodynamic disturbances must not be present. Possible 1. The presence of a cardiac condition with low or uncertain primary risk of cerebral embolism, or 2. Evidence for evident cardio-aortic embolism in the absence of complete diagnostic investigation for other mechanisms Small artery Evident Imaging evidence of a single and clinically relevant acute infarction occlusion <20 mm in greatest diameter within the territory of basal or brainstem penetrating arteries in the absence of any other pathology in the parent artery at the site of the origin of the penetrating artery (focal atheroma, parent vessel dissection, vasculitis, vasospasm, etc) Probable 1. The presence of stereotypic lacunar transient ischemic attacks within the past week, or 2. The presence of a classical lacunar syndrome Possible 1. Presenting with a classical lacunar syndrome in the absence of imaging that is sensitive enough to detect small infarctions, or 2. Evidence for evident small artery occlusion in the absence of complete diagnostic investigation for other mechanisms Other causes Evident The presence of a specific disease process that involves clinically appropriate brain arteries Probable A specific disease process that has occurred in clear and close temporal or spatial relationship to the onset of brain infarction such as arterial dissection, cardiac or arterial surgery, and cardiovascular interventions Possible Evidence for an evident other cause in the absence of complete diagnostic investigation for mechanisms listed above https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 30/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Undetermined Unknown (no Cryptogenic embolism: causes evident, probable, or 1. Angiographic evidence of abrupt cut-off consistent with a blood clot within otherwise angiographically normal looking intracranial arteries, or possible criteria for 2. Imaging evidence of complete recanalization of previously the causes occluded artery, or above) 3. The presence of multiple acute infarctions that have occurred closely related in time without detectable abnormality in the relevant vessels Other cryptogenic: Those not fulfilling the criteria for cryptogenic embolism Incomplete evaluation: The absence of diagnostic tests that, under the examiner's judgment, would have been essential to uncover the underlying etiology Unclassified The presence of >1 evident mechanism in which there is either probable evidence for each, or no probable evidence to be able to establish a single cause Reproduced with permission from: Ay H, Benner T, Arsava EM. A computerized algorithm for etiologic classi cation of ischemic stroke: the Causative Classi cation of Stroke System. Stroke 2007; 38:2979. Graphic 57732 Version 4.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 31/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Time course of neurologic changes in intracerebral hemorrhage Schematic representation of rapid downhill course in terms of unusual behavior (solid line), hemimotor function (dotted line), and consciousness (dash-dotted line) in a patient with intracerebral (intraparenchymal) hemorrhage. Graphic 61491 Version 3.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 32/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Headache and vomiting in stroke subtypes The frequency of sentinel headache, onset headache, and vomiting in three subtypes of stroke: subarachnoid hemorrhage, intraparenchymal (intracerebral) hemorrhage, and ischemic stroke. Onset headache was present in virtually all patients with SAH and about one-half of those with IPH; all of these symptoms were infrequent in patients with IS. SAH: subarachnoid hemorrhage; IPH: intraparenchymal (intracerebral) hemorrhage; IS: ischemic stroke. Data from: Gorelick PB, Hier DB, Caplan LR, Langenberg P. Headache in acute cerebrovascular disease. Neurology 1986; 36:1445. Graphic 60831 Version 4.0 https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 33/34 7/6/23, 12:16 PM Stroke: Etiology, classification, and epidemiology - UpToDate Contributor Disclosures Louis R Caplan, MD No relevant financial relationship(s) with ineligible companies to disclose. Scott E Kasner, MD Grant/Research/Clinical Trial Support: Bayer [Stroke]; Bristol Meyers Squibb [Stroke]; Medtronic [Stroke]; WL Gore and Associates [Stroke]. Consultant/Advisory Boards: Abbvie [Stroke]; AstraZeneca [Stroke]; BMS [Stroke]; Diamedica [Stroke]; Medtronic [Stroke]. All of the relevant financial relationships listed have been mitigated. John F Dashe, MD, PhD No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/stroke-etiology-classification-and-epidemiology/print 34/34