eMedicine Specialties > Emergency Medicine > Neurology

Transient Ischemic Attack

Author: Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Nov 17, 2009

Introduction

Background

A transient ischemic attack (TIA) is considered an acute episode of temporary neurologic dysfunction caused by a vascular occlusion. Symptoms typically last less than an hour. While the classical definition included symptoms lasting as long as 24 hours, advents in neuroimaging have suggested that many such cases represent minor strokes with resolved symptoms rather than true TIAs. Current guidelines recommend that a transient ischemic attack be defined as a transient episode of neurological dysfunction caused by focal brain, spinal-cord, or retinal ischemia, without acute infarction.1

For additional information, see Medscape's Stroke/Cerebrovascular Disease Resource Center.

Pathophysiology

Temporary reduction or cessation of cerebral blood flow in a specific neurovascular distribution can be due to low flow through a partially occluded vessel or to an acute thromboembolic event.

Frequency

United States

Between 200,000-500,000 TIAs per year are diagnosed in the United States.2,3 ED visits for TIA occur at about 1.1 visits per 1,000 US population, and TIAs are diagnosed in 0.3% of ED visits.4 TIA carries a particularly high short-term risk of stroke, and approximately 15% of diagnosed strokes are preceded by TIAs.

International

TIA occurs in about 150,000 patients per year in the United Kingdom.5 The population incidence likely mirrors that of stroke.

Mortality/Morbidity

The most important short-term risk from a TIA is that of stroke.6 The early risk of stroke following TIA is approximately 4-5% at 2 days and as high as 11% at 7 days.5,7 Additionally, despite a public education program, many patients still do not seek medical attention after experiencing TIA symptoms. Public health professionals and physicians need to do more such as promoting and participating in medical screening fairs and public outreach programs.

Race

The incidence of TIAs in blacks, at 98 cases per 100,000 population, is higher than that in whites, 81 cases per 100,000 population. Controversy exists regarding whether race influences emergent workup following TIA.8,9

Sex

The incidence of TIAs in men, at 101 cases per 100,000, is significantly higher than that in women, 70 cases per 100,000.10

Age

The incidence of TIAs appears to increase with age, from 1-3 cases per 100,000 in those younger than 35 years to up to 1500 cases per 100,000 in those older than 85.11 Fewer than 3% of all major cerebral infarcts occur in children. Pediatric strokes can often have quite different etiologies compared with adult strokes and are relatively more infrequent.

Clinical

History

A transient ischemic attack (TIA) may last only minutes and has often resolved before the patient presents to a clinician. Thus, historical questions should be addressed not just to the patient but also to family members, witnesses, and emergency medical services (EMS) personnel. Witnesses may have perceived abnormalities that the patient could not, such as changes in behavior, speech, gait, memory, and movement.

  • Significant medical history questions include the following:
    • Recent surgery (eg, carotid, cardiac)
    • Previous strokes
    • Known cardiovascular disease
    • Seizures
    • CNS infections
    • Use of illicit drugs
    • Complete medication regimen
    • Comorbidities related to metabolic disorders
  • Carefully investigate onset, duration, fluctuation, and intensity of symptoms.
  • Reviewing the patient's medical record is extremely important for identifying deficits from previous strokes, seizures, or cardiac events. The primary care physician may have great insight into previous episodes and workup.
    • Attempt to clarify when symptoms first occurred, how long they lasted, if the patient recovered completely (returned to baseline status), and if a pattern of escalating symptoms is present. For those who woke up or are found with symptoms, the time last known to be normal should be documented.
    • History of associated trauma or cardiac symptoms widens the differential diagnosis. Pertinent negative items (eg, headache, chest pain, eye pain) in the review of systems also are important.
    • Carotid or vertebral dissection can occur in association with both major and minor trauma. The patient may provide a history of blunt or torsion injury to the neck. Controversy exists regarding whether manipulation by a chiropractor or massage therapy increases the risk of arterial dissection.12
  • Elicit any risk factors for relevant underlying disease.
    • Known coagulopathy
    • History of arteritis
    • Noninfectious necrotizing vasculitis, drugs, irradiation, and local trauma are known to cause inflammatory arterial injury.
    • Thromboembolic risk factors such as carotid artery stenosis, venous or arterial thromboembolism, patent foramen ovale, atrial fibrillation, prior myocardial infarction, or left ventricular dysfunction.

Physical

The goal of the physical examination is to carefully uncover any neurologic deficits, evaluate for underlying cardiovascular risk factors, and seek any potential thrombotic or embolic source of the event.

Ideally, any neurologic deficits should be recorded with the aid of a formal and reproducible stroke scale, such as the National Institutes of Health Stroke Scale (NIHSS). A stroke scale prompts the examiner to be thorough and allows different examiners to reliably repeat the examination during subsequent phases of the evaluation. Any neurologic abnormalities should suggest the diagnosis of stroke (or ongoing neurologic event) rather than TIA.

  • Initial vital signs should include the following:
    • Temperature
    • Blood pressure
    • Heart rate and rhythm
    • Respiratory rate and pattern
    • Oxygen saturation
  • The examiner should assess the patient's overall health and appearance, making an assessment of the following:
    • Attentiveness
    • Ability to interact with the examiner
    • Language and memory skills
    • Overall hydration status
    • Development
  • Identify signs of other active comorbidities including infections (eg, sinusitis, mastoiditis, meningitis) and vasculidities. Carotid arteries can be examined for pulse upstroke, bruit, and the presence of carotid endarterectomy scars.
  • Funduscopy can identify retinal plaques, retinal pigmentation, and optic disc margins.
  • Pupil reaction to direct and consensual light exposure can be assessed.
  • In addition to performing standard auscultation, examine the chest for the presence of surgical scars or presence of a pacemaker/automatic implantable cardioverter defibrillator (AICD), or other clues that the patient may have a cardiac disorder and increased risk of a cardioembolic phenomenon.
  • Cardioembolic events are significant causes of TIAs. Identify the rhythm for irregularity or other unusual rhythms and rates, murmurs, or rubs that might suggest valvular disease, atrioseptal defects, or ventricular aneurysm (a source of mural thrombi).
  • A neurologic examination is the foundation of the TIA evaluation and should particularly focus on the neurovascular distribution suggested by the patient’s symptoms. Subsets of the neurologic examination include the following:
    • Cranial nerve testing
    • Somatic motor strength
    • Somatic sensory testing
    • Cerebellar system (be sure to see the patient walk)
  • Mental status can be assessed formally (Mini-Mental Status Examination, Quick Confusion Scale) or as part of the patient's overall response to questions and interactions with the examiner. The following signs may be present with cranial nerve dysfunction:
    • Ocular dysmotility
    • Forehead wrinkling asymmetry
    • Incomplete eyelid closure
    • Asymmetrical mouth retraction
    • Loss of the nasolabial crease
    • Swallowing difficulty
    • Lateral tongue movement
    • Weak shoulder shrugging
    • Visual field deficits
  • Somatic motor testing
    • Test muscle stretch reflexes of biceps, triceps, and brachioradialis and patellar and Achilles reflexes.
    • Inspect posture and presence of tremors. Test shoulder girdle, upper extremity, abdominal muscle, and lower extremity strength.
    • Test passive movement of major joints to look for spasticity, clonus, and rigidity.
  • The cerebellar system can be tested by assessing ocular movement, gait, and finger-to-nose and heel-to-knee movements, looking for signs of past-pointing and dystaxia, hypotonia, overshooting, gait dystaxia, and nystagmus.

Causes

The transient ischemic attack (TIA) workup is focused on emergent/urgent risk stratification. A number of potential underlying causes can be rapidly identified.

  • Atherosclerosis of carotid and vertebral arteries 
  • Embolic sources - Valvular disease, ventricular thrombus, and thrombus formation due to atrial fibrillation
  • Arterial dissection
  • Arteritis - Inflammation of the arteries occurring primarily in elderly persons, especially women
    • Noninfectious necrotizing vasculitis (primary cause)
    • Drugs
    • Irradiation
    • Local trauma
  • Sympathomimetic drugs (eg, cocaine)
  • Mass lesions (eg, tumors, subdural hematomas) - Less frequently cause transient symptoms and more often result in progressive persistent symptoms
  • TIA etiologies in children, which can be different than those in adults, include the following:
    • Congenital heart disease with cerebral thromboembolism (most common)
    • Drug abuse (eg, cocaine)
    • Clotting disorders
    • CNS infection
    • Neurofibromatosis
    • Vasculitis
    • Idiopathic progressive arteriopathy of childhood (moyamoya)
    • Fibromuscular dysplasia
    • Marfan disease
    • Tuberous sclerosis
    • Tumor

More on Transient Ischemic Attack

Overview: Transient Ischemic Attack
Differential Diagnoses & Workup: Transient Ischemic Attack
Treatment & Medication: Transient Ischemic Attack
Follow-up: Transient Ischemic Attack
References
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References

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  2. Kleindorfer D, Panagos P, Pancioli A, et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3. [Medline]. [Full Text].

  3. Johnston SC, Fayad PB, Gorelick PB, Hanley DF, Shwayder P, van Husen D. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. May 13 2003;60(9):1429-34. [Medline].

  4. Edlow JA, Kim S, Pelletier AJ, Camargo CA Jr. National study on emergency department visits for transient ischemic attack, 1992-2001. Acad Emerg Med. Jun 2006;13(6):666-72. [Medline].

  5. [Best Evidence] Giles MF, Rothwell PM. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol. Dec 2007;6(12):1063-72. [Medline].

  6. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. Dec 13 2000;284(22):2901-6. [Medline].

  7. [Best Evidence] Wu CM, McLaughlin K, Lorenzetti DL, Hill MD, Manns BJ, Ghali WA. Early risk of stroke after transient ischemic attack: a systematic review and meta-analysis. Arch Intern Med. Dec 10 2007;167(22):2417-22. [Medline].

  8. Jacobs BS, Birbeck G, Mullard AJ, et al. Quality of hospital care in African American and white patients with ischemic stroke and TIA. Neurology. Mar 28 2006;66(6):809-14. [Medline].

  9. White H, Boden-Albala B, Wang C, et al. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation. Mar 15 2005;111(10):1327-31. [Medline]. [Full Text].

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  11. Kleindorfer D, Panagos P, Pancioli A, Khoury J, Kissela B, Woo D. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3. [Medline].

  12. Cassidy JD, Boyle E, Cote P, He Y, Hogg-Johnson S, Silver FL, et al. Risk of vertebrobasilar stroke and chiropractic care: results of a population-based case-control and case-crossover study. Spine (Phila Pa 1976). Feb 15 2008;33(4 Suppl):S176-83. [Medline].

  13. [Guideline] National Institute for Health and Clinical Excellence (NICE) Stroke Guidelines. Accessed November 2009. [Full Text].

  14. Redgrave JN, Schulz UG, Briley D, Meagher T, Rothwell PM. Presence of acute ischaemic lesions on diffusion-weighted imaging is associated with clinical predictors of early risk of stroke after transient ischaemic attack. Cerebrovasc Dis. 2007;24(1):86-90. [Medline].

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  19. [Best Evidence] Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. Jan 27 2007;369(9558):283-92. [Medline].

  20. Halliday AW, Lees T, Kamugasha D, Grant R, Hoffman A, Rothwell PM. Waiting times for carotid endarterectomy in UK: observational study. BMJ. 2009;338:b1847. [Medline]. [Full Text].

  21. Gladstone DJ, Oh J, Fang J, Lindsay P, Tu JV, Silver FL. Urgency of carotid endarterectomy for secondary stroke prevention: results from the Registry of the Canadian Stroke Network. Stroke. Aug 2009;40(8):2776-82. [Medline].

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  25. Lindley RI. Patients with transient ischemic attack do not need to be admitted to hospital for urgent evaluation and treatment: against. Stroke. Apr 2006;37(4):1139-40. [Medline].

  26. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. Oct 20 2007;370(9596):1432-42. [Medline].

  27. Wu CM, Manns BJ, Hill MD, Ghali WA, Donaldson C, Buchan AM. Rapid evaluation after high-risk TIA is associated with lower stroke risk. Can J Neurol Sci. Jul 2009;36(4):450-5. [Medline].

  28. Lavallee PC, Meseguer E, Abboud H, et al. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): feasibility and effects. Lancet Neurol. Nov 2007;6(11):953-60. [Medline].

  29. Giles MF, Rothwell PM. Substantial underestimation of the need for outpatient services for TIA and minor stroke. Age Ageing. Nov 2007;36(6):676-80. [Medline].

  30. [Best Evidence] Ross MA, Compton S, Medado P, Fitzgerald M, Kilanowski P, O'Neil BJ. An emergency department diagnostic protocol for patients with transient ischemic attack: a randomized controlled trial. Ann Emerg Med. Aug 2007;50(2):109-19. [Medline].

  31. Bray JE, Coughlan K, Bladin C. Can the ABCD Score be dichotomised to identify high-risk patients with transient ischaemic attack in the emergency department?. Emerg Med J. Feb 2007;24(2):92-5. [Medline].

  32. Johnston SC, Nguyen-Huynh MN, Schwarz ME, et al. National Stroke Association guidelines for the management of transient ischemic attacks. Ann Neurol. Sep 2006;60(3):301-13. [Medline].

  33. Sheehan OC, Merwick A, Kelly LA, Hannon N, Marnane M, Kyne L. Diagnostic usefulness of the ABCD2 score to distinguish transient ischemic attack and minor ischemic stroke from noncerebrovascular events: the North Dublin TIA Study. Stroke. Nov 2009;40(11):3449-54. [Medline].

  34. [Best Evidence] Fothergill A, Christianson TJ, Brown RD Jr, Rabinstein AA. Validation and refinement of the ABCD2 score: a population-based analysis. Stroke. Aug 2009;40(8):2669-73. [Medline].

  35. [Best Evidence] Amarenco P, Labreuche J, Lavallee PC, Meseguer E, Cabrejo L, Slaoui T. Does ABCD2 score below 4 allow more time to evaluate patients with a transient ischemic attack?. Stroke. Sep 2009;40(9):3091-5. [Medline].

  36. Albers GW. A review of published TIA treatment recommendations. Neurology. Apr 27 2004;62(8 Suppl 6):S26-8. [Medline].

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Further Reading

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Keywords

transient ischemic attack, TIA, TIA symptoms, TIA causes, TIA treatment, stroke, mini stroke, ischemic stroke, carotid artery atherosclerotic disease, vertebral artery atherosclerotic disease, brain attack, hypertension, hypotension, arteritis

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Contributor Information and Disclosures

Author

Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
Joshua N Goldstein, MD, PhD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Stroke Association, Neurocritical Care Society, and Society for Academic Emergency Medicine
Disclosure: CSL Behring Consulting fee Consulting; Genentech Consulting fee Consulting

Medical Editor

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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