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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

  1. Easton, J. Donald; Johnston, S. Claiborne (11 February 2022). “Time to Retire the Concept of Transient Ischemic Attack”. JAMA. doi:10.1001/jama.2022.0300. ISSN 0098-7484. PMID 35147656 Check |pmid= value (help).

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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. 1.0 1.1 Fisher CM (2002). “Transient ischemic attacks”. N Engl J Med. 347 (21): 1642–3. doi:10.1056/NEJMp020129. PMID 12444177.
  2. 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.

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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. 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. 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).
  3. 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.
  4. 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.
  5. 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.

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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

References

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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. 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. 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. 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.

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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

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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. 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. 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. 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.
  4. 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.
  5. Gillum LA, Mamidipudi SK, Johnston SC (2000). “Ischemic stroke risk with oral contraceptives: A meta-analysis”. JAMA. 284 (1): 72–8. PMID 10872016.
  6. 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.
  7. 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

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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. 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. 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.
  3. 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).
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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.
  10. 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.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | CT | MRI | Echocardiography | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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