Stroke is defined as an acute neurologic deficit lasting more than 24 hours and caused by cerebrovascular etiology. It is subdivided into ischemic stroke (caused by vascular occlusion or stenosis) and hemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal, subarachnoid, and/or intraventricular hemorrhage).
Overview
Related Diseases & Conditions
Summary
Regardless of the specific etiology, ischemic stroke occurs when blood supply in a cerebral vascular territory is critically reduced due to occlusion or critical stenosis of a cerebral artery. A minority of ischemic strokes are caused by cerebral sinus or cortical vein thrombosis. There are more than 100,000 strokes in the UK each year causing 38,000 deaths, making it a leading cause of death and disability.[1] [2] Most common symptoms are partial or total loss of strength in upper and/or lower extremities, expressive and/or receptive language dysfunction, sensory loss in upper and/or lower extremities, visual field loss, slurred speech, or difficulty with fine motor coordination and gait. Risk factors strongly associated with ischemic stroke include older age, history of transient ischemic attack or previous ischemic stroke, family history of stroke, hypertension, smoking, diabetes mellitus, atrial fibrillation, comorbid cardiac conditions, carotid artery stenosis, sickle cell disease, and dyslipidemia.[3]Summary
Narrowing of the lumen of the carotid artery. Cause of a minority of ischemic strokes. Atherosclerotic plaque in the cervical carotid artery is the most common cause. Plaque disruption and atheroembolization into the intracranial circulation is the most common mechanism for stroke. One systematic review and meta-analysis estimated the global prevalence of carotid stenosis in people ages 30 to 79 years in 2020 to be 1.5%.[4] People presenting with symptoms may include those with transient ischemic attack, stroke, and transient monocular blindness (amaurosis fugax). Strong risk factors include older age, smoking, and history of cardiovascular disease.[5] [6] [7] Summary
A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.[8] TIA should be suspected in a patient who presents with sudden-onset, focal neurologic deficit that resolves spontaneously and cannot be explained by another condition such as hypoglycemia. Until the neurologic symptoms and signs have resolved completely you cannot assume the event is a TIA, and you should proceed with investigations and management for a working diagnosis of stroke.[9] The age-adjusted annual incidence rate for TIA in the UK has been estimated at 190 cases per 100,000 population.[10] TIAs have considerable risk of early recurrent cerebral ischemic events.[11] Strong risk factors for TIA include atrial fibrillation, valvular heart disease, carotid stenosis, intracranial stenosis, congestive heart failure, hypertension, hyperlipidemia, diabetes mellitus, cigarette smoking, alcohol-use disorder, and advanced age.[12][13][14][15] [16] [17] [18] Presentation of TIA is dictated by the region of brain supplied by the obstructed vessel. Evaluation and initiation of secondary prevention should occur rapidly.Summary
Intracerebral hemorrhage (ICH) is an emergency. ICH is caused by vascular rupture with bleeding into the brain parenchyma, resulting in a primary mechanical injury to the brain tissue. The global prevalence of ICH was 18.88 million cases in 2020.[19] Suspect stroke in a patient with sudden onset of focal neurologic symptoms: unilateral weakness or paralysis in the face, arm, or leg, unilateral sensory loss, dysarthria or expressive or receptive dysphasia, vision problems (e.g., hemianopia), headache (sudden severe and unusual headache), difficulty with coordination and gait, vertigo or loss of balance, especially with the above signs.[20] Strong risk factors include hypertension, older age, family history of ICH, hemophilia, cerebral amyloid angiopathy, anticoagulation, use of illicit sympathomimetic drugs, vascular malformations, and Moyamoya syndrome.[21] [22] [23] [24] [25] [26] [27] [28]Summary
A focal abnormal dilation of the wall of an artery in the brain. Typically asymptomatic until ruptured, resulting in a subarachnoid hemorrhage. Screening with noninvasive neuroangiography is recommended for at-risk populations. Autopsy studies indicate that cerebral aneurysms are fairly common in adults, with a prevalence ranging between 1% and 5%.[29] [30] Strong risk factors include smoking, family history, female sex, age, and previous subarachnoid hemorrhage.[31]Summary
A medical emergency where there is bleeding into the subarachnoid space. The most common cause of nontraumatic subarachnoid hemorrhage is rupture of an intracranial aneurysm.[32] In the UK, more than 15,000 diagnoses were reported in 2021-2022.[33] Presents as a sudden, severe headache that peaks within 1 to 5 minutes (thunderclap headache) and lasts more than an hour; typically alongside vomiting, photophobia, and nonfocal neurologic signs. Strong risk factors include hypertension, smoking, family history, and autosomal dominant polycystic kidney disease.[34][35] [36]
Citations
1. Healthcare Quality Improvement Partnership. Is stroke care improving? the second SSNAP annual report. Dec 2015 [internet publication].[Full Text]
2. Stroke Association. Stroke statistics. 2018 [internet publication].[Full Text]
3. Boehme AK, Esenwa C, Elkind MS. Stroke risk factors, genetics, and prevention. Circ Res. 2017 Feb 3;120(3):472-95.[Abstract][Full Text]
4. Song P, Fang Z, Wang H, et al. Global and regional prevalence, burden, and risk factors for carotid atherosclerosis: a systematic review, meta-analysis, and modelling study. Lancet Glob Health. 2020 May;8(5):e721-9.[Abstract][Full Text]
5. de Weerd M, Greving JP, de Jong AW, et al. Prevalence of asymptomatic carotid artery stenosis according to age and sex: systematic review and metaregression analysis. Stroke. 2009 Apr;40(4):1105-13.[Abstract][Full Text]
6. Mathiesen EB, Joakimsen O, Bønaa KH. Prevalence of and risk factors associated with carotid artery stenosis: the Tromsø Study. Cerebrovasc Dis. 2001;12(1):44-51.[Abstract]
7. House AK, Bell R, House J, et al. Asymptomatic carotid artery stenosis associated with peripheral vascular disease: a prospective study. Cardiovasc Surg. 1999 Jan;7(1):44-9.[Abstract]
8. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009 Jun;40(6):2276-93.[Full Text]
9. National Institute for Health and Care Excellence. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management. Apr 2022 [internet publication].[Full Text]
10. Gibbs RG, Newson R, Lawrenson R, et al. Diagnosis and initial management of stroke and transient ischemic attack across UK health regions from 1992 to 1996: experience of a national primary care database. Stroke. 2001 May;32(5):1085-90.[Abstract][Full Text]
11. Amarenco P, Lavallée PC, Labreuche J, et al. One-year risk of stroke after transient ischemic attack or minor stroke. N Engl J Med. 2016 Apr 21;374(16):1533-42.[Abstract][Full Text]
12. Whisnant JP, Brown RD, Petty GW, et al. Comparisons of population-based models of risk factors for TIA and ischemic stroke. Neurology. 1999 Aug 11;53(3):532-6.[Abstract]
13. Sacco RL. Risk factors for TIA and TIA as a risk factor for stroke. Neurology. 2004 Apr 27;62(8 Suppl 6):S7-11.[Abstract]
14. Bots ML, van der Wilk EC, Koudstaal PJ, et al. Transient neurological attacks in the general population. Prevalence, risk factors, and clinical relevance. Stroke. 1997 Apr;28(4):768-73.[Abstract][Full Text]
15. Larsson SC, Wallin A, Wolk A, et al. Differing association of alcohol consumption with different stroke types: a systematic review and meta-analysis. BMC Med. 2016 Nov 24;14(1):178.[Abstract][Full Text]
16. Woo D, Gebel J, Miller R, et al. Incidence rates of first-ever ischemic stroke subtypes among blacks: a population-based study. Stroke. 1999 Dec;30(12):2517-22.[Abstract][Full Text]
17. Shinton R, Beevers G. Meta-analysis of relation between cigarette smoking and stroke. BMJ. 1989 Mar 25;298(6676):789-94.[Abstract][Full Text]
18. Hillbom M, Saloheimo P, Juvela S. Alcohol consumption, blood pressure, and the risk of stroke. Curr Hypertens Rep. 2011 Jun;13(3):208-13.[Abstract]
19. GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020 Oct 17;396(10258):1204-22.[Abstract][Full Text]
20. Government of British Columbia. Stroke and transient ischemic attack - acute and long-term management. Jun 2023 [internet publication].[Full Text]
21. Kannel WB, Wolf PA, Verter J, et al. Epidemiologic assessment of the role of blood pressure in stroke. The Framingham study. JAMA. 1970 Oct 12;214(2):301-10.[Abstract]
22. Woo D, Sauerbeck LR, Kissela BM, et al. Genetic and environmental risk factors for intracerebral hemorrhage: preliminary results of a population-based study. Stroke. 2002 May;33(5):1190-5.[Abstract]
23. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002 Jan 12;324(7329):71-86. [Erratum in: BMJ 2002 Jan 19;324(7330):141.][Abstract][Full Text]
24. Hart RG, Boop BS, Anderson DC. Oral anticoagulants and intracranial hemorrhage. Facts and hypotheses. Stroke. 1995 Aug;26(8):1471-7.[Abstract][Full Text]
25. Wojak JC, Flamm ES. Intracranial hemorrhage and cocaine use. Stroke. 1987 Jul-Aug;18(4):712-5.[Abstract]
26. Barnes B, Cawley CM, Barrow DL. Intracerebral hemorrhage secondary to vascular lesions. Neurosurg Clin N Am. 2002 Jul;13(3):289-97.[Abstract]
27. Takahashi JC, Funaki T, Houkin K, et al; JAM Trial Investigators. Significance of the hemorrhagic site for recurrent bleeding: prespecified analysis in the Japan Adult Moyamoya trial. Stroke. 2016 Jan;47(1):37-43.[Abstract][Full Text]
28. Dastur CK, Yu W. Current management of spontaneous intracerebral haemorrhage. Stroke Vasc Neurol. 2017 Mar;2(1):21-9.[Abstract][Full Text]
29. Wiebers DO, Whisnant JP, Huston J 3rd, et al. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003 Jul 12;362(9378):103-10.[Abstract]
30. Korja M, Kaprio J. Controversies in epidemiology of intracranial aneurysms and SAH. Nat Rev Neurol. 2016 Jan;12(1):50-5.[Abstract]
31. Jin D, Song C, Leng X, et al. A systematic review and meta-analysis of risk factors for unruptured intracranial aneurysm growth. Int J Surg. 2019 Sep;69:68-76.[Abstract][Full Text]
32. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006 Jan 26;354(4):387-96.
33. National Health Service Engaland. Hospital admitted patient care activity, 2021-22. Sep 2022 [internet publication].[Full Text]
34. Rinkel GJ. Intracranial aneurysm screening: indications and advice for practice. Lancet Neurol. 2005 Feb;4(2):122-8.[Abstract]
35. Etminan N, Chang HS, Hackenberg K, et al. Worldwide incidence of aneurysmal subarachnoid hemorrhage according to region, time period, blood pressure, and smoking prevalence in the population: a systematic review and meta-analysis. JAMA Neurol. 2019 May 1;76(5):588-97.[Abstract][Full Text]
36. Zuurbier CCM, Bourcier R, Constant Dit Beaufils P, et al. Number of affected relatives, age, smoking, and hypertension prediction score for intracranial aneurysms in persons with a family history for subarachnoid hemorrhage. Stroke. 2022 May;53(5):1645-50.[Abstract][Full Text]
