Transient ischemic attack
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]
Synonyms and keywords: TIA; mini stroke
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
A transient ischemic attack is caused by the temporary disturbance of blood supply to a restricted area of the brain, resulting in brief neurologic dysfunction that usually persists for less than 24 hours.
Discontinuation of the use of the term transient ischemic attack has been proposed[1].
Causes
The most common cause of a TIA is an embolus (a small blood clot) that occludes an artery in the brain. This most frequently arises from an atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart due to atrial fibrillation. Other reasons include excessive narrowing of large vessels due to an atherosclerotic plaque and increased blood viscosity due to some blood diseases. TIA is related with other medical conditions like hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.
Diagnosis
History and Symptoms
Symptoms vary widely from person to person depending on the area of the brain involved. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax), difficulty speaking (dysarthria), weakness on one side of the body (hemiparesis), numbness usually on one side of the body, and loss of consciousness. If there are neurological symptoms persisting for more than 24 hours, it is classified as a cerebrovascular accident (stroke).
Electrocardiogram
An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain.
CT
TIAs do not show brain changes on CT scans. (Most strokes do show changes on such tests).
MRI
TIAs do not show brain changes on MRI scans. (Most strokes do show changes on such tests).
Echocardiography
An echocardiogram is useful in detecting thrombus within the heart chambers. Such patients benefit from anticoagulation.
Ultrasound
If the TIA affects an area supplied by the carotid artery, an ultrasound (TCD) scan may demonstrate carotid stenosis.
Treatment
Surgery
For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended.
Primary Prevention
Prevention of TIAs includes controlling risk factors, such as high blood pressure, diabetes, heart disease, and other associated disorders. Smoking should be stopped.
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
The concept of TIA was first discussed in 1950 by Charles Miller Fischer based on the observation that transient ischemic stroke in patients may lead to stroke in the same arterial territory in the future. He also proposed that treatment and prevention of transient ishemic attack may help prevent the patient from full blown stroke in the future. [1]
Historical perspective
The concept of TIA was first discussed in 1950 by Charles Miller Fischer based on the observation that transient ischemic stroke in patients may lead to stroke in the same arterial territory in the future. He also proposed that treatment and prevention of transient ishemic attack may help prevent the patient from full blown stroke in the future. [1][2]
References
- ↑ 1.0 1.1 Fisher CM (2002). “Transient ischemic attacks”. N Engl J Med. 347 (21): 1642–3. doi:10.1056/NEJMp020129. PMID 12444177.
- ↑ FISHER M, ADAMS RD (1951). “Observations on brain embolism with special reference to the mechanism of hemorrhagic infarction”. J Neuropathol Exp Neurol. 10 (1): 92–4. PMID 14804137.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
The pathophysiologic mechanism of transient ischemic stroke may include temporary blockage of cerebral large or small blood vessel due to atherothrombotic or embolic cause followed by complete resolution of symptoms within few hours of onset. There may be mild tissue ischemia and hypoxia responsible for transitory symptomatology of patient. The specific clinical presentation of the patient correlates with the area of brain affected due to ischemia[1][2]
Definition of Transient ischemic attack
According to American stroke association, transient ischemic stroke is defined as a transient episode of neurological dysfunction caused by a focal brain, spinal cord, or retinal ischaemia, without acute infarction.[1]
Pathophysiology
The pathophysiologic mechanism of transient ischemic stroke may include temporary blockage of large or small cerebral blood vessel due to atherothrombotic or embolic cause followed by complete resolution of symptoms within few hours of onset. There may be mild tissue ischemia and hypoxia responsible for transitory symptomatology of patient. The specific clinical presentation of the patient correlates with the area of brain affected due to ischemia[1][2]

Genetic association
There may be genetic predisposition in patients suffering from transient ischemic stroke.[3][4][5]
References
- ↑ 1.0 1.1 1.2 Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E; et al. (2009). “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. 40 (6): 2276–93. doi:10.1161/STROKEAHA.108.192218. PMID 19423857.
- ↑ 2.0 2.1 Caronna JJ (1976). “Transient ischemic attacks: Pathophysiology and medical management”. Postgrad Med. 59 (3): 106–11. PMID 1264882 : 1264882 Check
|pmid=value (help). - ↑ Chinnery PF, Elliott HR, Syed A, Rothwell PM, Oxford Vascular Study (2010). “Mitochondrial DNA haplogroups and risk of transient ischaemic attack and ischaemic stroke: a genetic association study”. Lancet Neurol. 9 (5): 498–503. doi:10.1016/S1474-4422(10)70083-1. PMC 2855429. PMID 20362514.
- ↑ Flossmann E, Rothwell PM (2005). “Family history of stroke in patients with transient ischemic attack in relation to hypertension and other intermediate phenotypes”. Stroke. 36 (4): 830–5. doi:10.1161/01.STR.0000158920.67013.53. PMID 15746455.
- ↑ Francis J, Raghunathan S, Khanna P (2007). “The role of genetics in stroke”. Postgrad Med J. 83 (983): 590–5. doi:10.1136/pgmj.2007.060319. PMC 2600010. PMID 17823225.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The most common cause of a TIA is an embolus (a small blood clot) that occludes an artery in the brain. This most frequently arises from an atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart due to atrial fibrillation. Other reasons include excessive narrowing of large vessels due to an atherosclerotic plaque and increased blood viscosity due to some blood diseases. TIA is related with other medical conditions like hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.
Causes
The etiology of TIA may be divided in to following based on the pathophysiology involved:
Atherosclerotic or large artery TIA
- Caused by atherosclerosis of internal carotid artery at origin or intracranially
- Also called low flow TIA
- Lasts few minutes to hours
- May cause recurrent TIAs producing stereotyped symptoms based on the branches of vessel involved
Embolic TIA
- Caused by an embolic source from artery or heart
- Common causes of embolism include atrial fibrillation and ventricular thrombus
- Usually lasts hours
Lacunar or small vessel TIA
- Involves small penetrating intracerebral vessels
- Usually caused by atheroscerotic narrowing of small blood vessels or lipohyalanosis
- May invlove internal capsule, basal ganglia or thalamus
Dissection
- Commonly cause symptoms due to cerebral ischemia or embolism
- Interruption of blood flow at the petrous portion of internal carotid artery or at the level of C1-C2 of vertebral artery as it enters foramen transversarium
- Symptoms may last from minutes to hours to days.
- May be detected by neurovascular imaging
Causes by Organ System
| Cardiovascular | No underlying causes |
| Chemical/Poisoning | No underlying causes |
| Dental | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Certolizumab pegol, iloperidone, interferon gamma, oprelvekin, sorafenib |
| Ear Nose Throat | No underlying causes |
| Endocrine | No underlying causes |
| Environmental | No underlying causes |
| Gastroenterologic | No underlying causes |
| Genetic | No underlying causes |
| Hematologic | No underlying causes |
| Iatrogenic | No underlying causes |
| Infectious Disease | No underlying causes |
| Musculoskeletal/Orthopedic | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional/Metabolic | No underlying causes |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | No underlying causes |
| Ophthalmologic | No underlying causes |
| Overdose/Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | No underlying causes |
| Renal/Electrolyte | No underlying causes |
| Rheumatology/Immunology/Allergy | No underlying causes |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | No underlying causes |
Causes in Alphabetical Order
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References
Differentiating Transient Ischemic Attack from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: , Aysha Anwar, M.B.B.S[2]
Overview
The differential diagnosis of TIA may include seizures, hypoglycemia, electrolyte disturbances, migraine, renal, hepatic or pulmonary encephalopathy, syncope , subdural hematoma, ischemic stroke, brain tumour, conversion disorder, multiple sclerosis, compressive myelopathy of spinal cord, vestibular disorders, cerebral amyloid angiopathy, nerve root compression, orthostatic hypertension, hypertensive encephalopathy [1][2][3]
Differential diagnosis
The differential diagnosis of TIA may include:[1][2][3]
- Hypoglycemia
- Electrolyte disturbances
- Migraine
- Renal, hepatic or pulmonary encephalopathy
- Syncope
- Subdural hematoma
- Ischemic stroke
- Brain tumour
- conversion disorder
- Multiple sclerosis
- Compressive myelopathy of spinal cord
- Vestibular disorders
- Cerebral amyloid angiopathy
- Nerve root compression
- Orthostatic hypertension
- Hypertensive encephalopathy
- Seizures
- Transient neurological attack
References
- ↑ 1.0 1.1 García-Moncó JC, Marrodán A, Foncea Beti N, Gómez Beldarrain M (2002). “[Stroke and transient ischemic attack-mimicking conditions: a prospective analysis of risk factors and clinical profiles at a general hospital]”. Neurologia. 17 (7): 355–60. PMID 12236954.
- ↑ 2.0 2.1 Nadarajan V, Perry RJ, Johnson J, Werring DJ (2014). “Transient ischaemic attacks: mimics and chameleons”. Pract Neurol. 14 (1): 23–31. doi:10.1136/practneurol-2013-000782. PMC 3913122. PMID 24453269.
- ↑ 3.0 3.1 Scheidt CE, Baumann K, Katzev M, Reinhard M, Rauer S, Wirsching M; et al. (2014). “Differentiating cerebral ischemia from functional neurological symptom disorder: a psychosomatic perspective”. BMC Psychiatry. 14: 158. doi:10.1186/1471-244X-14-158. PMC 4046041. PMID 24885264.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
The estimated incidence of TIA may range from 200,000 to 500,000 per year. The estimated prevalence of TIA approximates to about 5 million people which correlates to population prevalence of 2.3%. [1][2][3]
Epidemiology
There may be certain limitations to assess the accurate incidence and prevalence data on transient ischemic stroke due to different criterias used for TIA in different epidemiological studies. Also, there may be underestimation of transient focal neurological symptoms by public and health care system. However, the estimated incidence and the prevalence of TIA in USA in year the 1999 is as follows:[1][2][3]
- The estimated incidence of TIA may range from 200,000 to 500,000 per year.[1][2][3]
- The estimated prevalence of TIA approximates to about 5 million people which correlates to population prevalence of 2.3%.[1][2][3]
Demographics
Age
The incidence of TIA increases remarkably with age irrespective of gender and race.[1]
Gender
The incidence of TIA is more common in males.[1]
Race
The incidence of TIA is high among African American race in older age group. However, the incidence of TIA is reported to be high in Mexican Americans compared with non-Hispanic whites at younger ages.[1]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E; et al. (2009). “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. 40 (6): 2276–93. doi:10.1161/STROKEAHA.108.192218. PMID 19423857.
- ↑ 2.0 2.1 2.2 2.3 Schuknecht HF (1987). “Temporal bone collections in Europeand the United States. Observations on a productive laboratory, pathologic findings of clinical relevance, and recommendations”. Ann Otol Rhinol Laryngol Suppl. 130: 1–19. PMID 3109304.
- ↑ 3.0 3.1 3.2 3.3 Johnston SC, Fayad PB, Gorelick PB, Hanley DF, Shwayder P, van Husen D; et al. (2003). “Prevalence and knowledge of transient ischemic attack among US adults”. Neurology. 60 (9): 1429–34. PMID 12743226.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
The risk factors of transient ischemic attack may include modifiable and non modifiable risk factors such as age, sex, race, coronary artery disease, atrial fibrillation, hypercoaguable state, hypertension, diabetes mellitus, cigarette smoking and alcohal consumption.[1][2][3]
Risk Factors
The risk factors of transient ischemic attack may include modifiable and non modifiable risk factors:[1][2][3][4][5][6][7]
| Modifiable risk factors | Non modifiable risk factors |
|---|---|
| Hypertension | Age >55 years |
| Diabetes mellitus | Family history of TIA or ischemic stroke |
| Atrial fibrillation | African American and hispanic race |
| Coronary heart disease | Male gender |
| Cigarette smoking | Genetic disorders |
| Alcohal consumption | Previous history of stroke or TIA |
| Hyperhomocysteinemia | |
| Obesity | |
| Hyperlipidemia | |
| Hypothyroidism | |
| Oral contraceptive use | |
| Sedentary life style | |
| Hypercoagulable disorders |
References
- ↑ 1.0 1.1 Khare S (2016). “Risk factors of transient ischemic attack: An overview”. J Midlife Health. 7 (1): 2–7. doi:10.4103/0976-7800.179166. PMC 4832890. PMID 27134474.
- ↑ 2.0 2.1 Flossmann E, Rothwell PM (2006). “Family history of stroke does not predict risk of stroke after transient ischemic attack”. Stroke. 37 (2): 544–6. doi:10.1161/01.STR.0000198879.11072.f2. PMID 16385089.
- ↑ 3.0 3.1 Kelly PJ, Shih VE, Kistler JP, Barron M, Lee H, Mandell R; et al. (2003). “Low vitamin B6 but not homocyst(e)ine is associated with increased risk of stroke and transient ischemic attack in the era of folic acid grain fortification”. Stroke. 34 (6): e51–4. doi:10.1161/01.STR.0000071109.23410.AB. PMID 12738890.
- ↑ Berry JD, Dyer A, Cai X, Garside DB, Ning H, Thomas A; et al. (2012). “Lifetime risks of cardiovascular disease”. N Engl J Med. 366 (4): 321–9. doi:10.1056/NEJMoa1012848. PMC 3336876. PMID 22276822.
- ↑ Gillum LA, Mamidipudi SK, Johnston SC (2000). “Ischemic stroke risk with oral contraceptives: A meta-analysis”. JAMA. 284 (1): 72–8. PMID 10872016.
- ↑ Breuer J, Pacou M, Gauthier A, Brown MM (2014). “Herpes zoster as a risk factor for stroke and TIA: a retrospective cohort study in the UK”. Neurology. 82 (3): 206–12. doi:10.1212/WNL.0000000000000038. PMC 3902756. PMID 24384645.
- ↑ Turnbull F, Blood Pressure Lowering Treatment Trialists’ Collaboration (2003). “Effects of different blood-pressure-lowering regimens on major cardiovascular events: results of prospectively-designed overviews of randomised trials”. Lancet. 362 (9395): 1527–35. PMID 14615107. Review in: ACP J Club. 2004 May-Jun;140(3):72
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
If left untreated, the symptoms of transient ischemic attack may subside with in few hours. However, there is increased risk of stroke in these patients in future. The risk is highest in the next within hours and subsequently decreases after days, weeks to months.[1]The prognosis of TIA depends on the possibilty of developing ischemic stroke in the future. There is 11 percent increased risk of ischemic stroke in patients having TIA for next seven days and 25-29% in next five years.[2] This is especially true in patients with TIA due to small-vessel disease (SVD) etiology with motor weakness (capsular warning syndrome).[2]
Natural History
If left untreated, the symptoms of transient ischemic attack may subside with in few hours. However, there is increased risk of stroke in these patients in future. The risk is highest in the next within hours and subsequently decreases after days, weeks to months.[1]
Complications
Complications of TIA include:[3][4][5][6][7]
- Ischemic stroke
- Hemorrhagic stroke
- Dementia
- Recurrent TIA
- Anxiety
Prognosis
The prognosis of TIA depends on the possibilty of developing ischemic stroke in the future. There is 11 percent increased risk of ischemic stroke in patients having TIA for next seven days and 25-29% in next five years.[2] This is especially true in patients with TIA due to small-vessel disease (SVD) etiology with motor weakness (capsular warning syndrome).[2]
The ABCD2 score
The ABCD2 score can predict likelihood of subsequent stroke.[8][9][10]
The score is calculated as:
Age
- ≥ 60 years = 1 point
- Blood pressure at presentation ≥ 140/90 mm Hg = 1 point
Clinical features
- Unilateral weakness = 2 points
- Speech disturbance without weakness = 1 point
Duration of attack
- ≥ 60 minutes = 2 points
- 10–59 minutes = 1 point
- Diabetes = 1 point
Interpretation of score, the risk for stroke:
Score 0-3 (low)
- 2 day risk = 1.0%
- 7 day risk = 1.2%
Score 4-5 (moderate)
- 2 day risk = 4.1%
- 7 day risk = 5.9%
Score 6–7 (high)
- 2 day risk = 8.1%
- 7 day risk = 11.7%
References
- ↑ 1.0 1.1 Sorensen AG, Ay H (2011). “Transient ischemic attack: definition, diagnosis, and risk stratification”. Neuroimaging Clin N Am. 21 (2): 303–13, x. doi:10.1016/j.nic.2011.01.013. PMC 3109304. PMID 21640301.
- ↑ 2.0 2.1 2.2 2.3 Paul NL, Simoni M, Chandratheva A, Rothwell PM (2012). “Population-based study of capsular warning syndrome and prognosis after early recurrent TIA”. Neurology. 79 (13): 1356–62. doi:10.1212/WNL.0b013e31826c1af8. PMC 3448742. PMID 22972645.
- ↑ Amarenco P, Lavallée PC, Labreuche J, Albers GW, Bornstein NM, Canhão P; et al. (2016). “One-Year Risk of Stroke after Transient Ischemic Attack or Minor Stroke”. N Engl J Med. 374 (16): 1533–42. doi:10.1056/NEJMoa1412981. PMID 27096581 : 27096581 Check
|pmid=value (help). - ↑ Schuknecht HF (1987). “Temporal bone collections in Europe and the United States. Observations on a productive laboratory, pathologic findings of clinical relevance, and recommendations”. Ann Otol Rhinol Laryngol Suppl. 130: 1–19. PMID 3109304.
- ↑ Jacquin A, Aboa-Eboulé C, Rouaud O, Osseby GV, Binquet C, Durier J; et al. (2012). “Prior transient ischemic attack and dementia after subsequent ischemic stroke”. Alzheimer Dis Assoc Disord. 26 (4): 307–13. doi:10.1097/WAD.0b013e3182420b2c. PMID 22193354.
- ↑ Broomfield NM, Quinn TJ, Abdul-Rahim AH, Walters MR, Evans JJ (2014). “Depression and anxiety symptoms post-stroke/TIA: prevalence and associations in cross-sectional data from a regional stroke registry”. BMC Neurol. 14: 198. doi:10.1186/s12883-014-0198-8. PMC 4189556. PMID 25269762.
- ↑ Coutts SB, Hill MD, Campos CR, Choi YB, Subramaniam S, Kosior JC; et al. (2008). “Recurrent events in transient ischemic attack and minor stroke: what events are happening and to which patients?”. Stroke. 39 (9): 2461–6. doi:10.1161/STROKEAHA.107.513234. PMID 18617658.
- ↑ Johnston SC, Rothwell PM, Nguyen-Huynh MN; et al. (2007). “Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack”. Lancet. 369 (9558): 283–92. doi:10.1016/S0140-6736(07)60150-0. PMID 17258668.
- ↑ Rothwell PM, Giles MF, Flossmann E; et al. (2005). “A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack”. Lancet. 366 (9479): 29–36. doi:10.1016/S0140-6736(05)66702-5. PMID 15993230.
- ↑ Cutting S, Regan E, Lee VH, Prabhakaran S (2016). “High ABCD2 Scores and In-Hospital Interventions following Transient Ischemic Attack”. Cerebrovasc Dis Extra. 6 (3): 76–83. doi:10.1159/000450692. PMC 5091225. PMID 27721312.
Diagnosis
Diagnosis
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Treatment
Treatment
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