A leading cause of morbidity and mortality.
Approximately 85% of strokes are ischaemic, caused by vascular occlusion.
A clinical emergency: timely diagnosis, triage, and intervention can improve outcome.
Care of patients in dedicated stroke units improves survival and function.
Intravenous recombinant tissue plasminogen activator is given within 4.5 hours of stroke onset.
Endovascular interventions, such as clot retrieval devices or intra-arterial thrombolysis, can be used in carefully selected patients within 6 hours of ischaemic stroke onset.
Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology. It is further subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and haemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage). Central venous sinus thrombosis is a rare form of stroke that occurs due to thrombosis of the dural venous sinuses. This monograph deals with ischaemic stroke.
Transient ischaemic attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. Patients with TIAs are at high risk for early ischaemic stroke, and their risk may be stratified by clinical scale, vessel imaging, and diffusion magnetic resonance imaging. This replaced the former definition of focal neurological impairment lasting less than 24 hours.
History and exam
- history of transient ischaemic attack (TIA)
- sudden onset of symptoms
- negative symptoms (i.e., loss of function)
- altered sensation
- sensory loss
- gaze paresis
- arrhythmias, murmurs, or pulmonary oedema
- nausea and/or vomiting
- neck or facial pain
- miosis, ptosis, and facial anhidrosis (hemilateral)
- altered level of consciousness/coma
- older age
- family history of stroke
- history of ischaemic stroke
- diabetes mellitus
- atrial fibrillation
- comorbid cardiac conditions
- carotid artery stenosis
- sickle cell disease
- people with lower levels of education
- African-American or Hispanic ancestry
- poor diet and nutrition
- physical inactivity
- alcohol abuse
- oestrogen-containing therapy
- illicit drug use
- elevated lipoprotein(a)
- hypercoagulable states
- elevated C-reactive protein
- aortic arch plaques
Assistant Professor of Internal Medicine
University of Thessaly
Hellenic Stroke Organization
Larissa University Hospital
GN is on the advisory boards for, and has received honoraria, speaker fees, and research support from: Amgen, Bayer, Boehringer-Ingelheim, BMS/Pfizer, Elpen, Galenica, Medtronic, Sanofi, and Winmedica.
Dr George Ntaios would like to gratefully acknowledge Dr Alireza Minagar, the previous contributor to this topic. AM declares that he has no competing interests.
Centre Hospitalier Universitaire Vaudois (CHUV)
JM declares that he has no competing interests.
Lecturer in Neurology
Beth Israel Deaconess Medical Center
Division of Cerebrovascular/Stroke
LRC declares that he has no competing interests.
National Clinical Director
Stroke NHS England
Professor, Stroke Medicine
Kings College London
Chair, Intercollegiate Stroke Working Party
Royal College of Physicians
TR declares that he has no competing interests.
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