Transient Ischemic Attack (TIA)

Samuel E. Mathis, MD and Randolph Taylor, III, MD Reviewed 06/2017
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Subject: Transient Ischemic Attack (TIA)

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BASICS

DESCRIPTION

  • A transient episode of neurologic dysfunction due to focal brain, retinal, or spinal cord ischemia without acute infarction

  • Most important predictor of stroke: 7-40% of patients with stroke report previous TIA.

  • Synonym(s): ministroke

EPIDEMIOLOGY

  • 200,000 to 500,000 new TIA cases reported each year

    • ▪ 83 cases/100,000 people/year in the United States
    • ▪ 400 to 800 cases/100,000 persons aged 50 to 59 years
  • Prevalence of TIA in general population: ~2.3%

  • Predominant age: risk increases >60 years; highest in 7th and 8th decades

  • Predominant sex: male > female (3:1)

  • Predominant race/ethnicity: African Americans > Hispanics > Caucasians. The difference in African Americans is exaggerated at younger ages.

ETIOLOGY AND PATHOPHYSIOLOGY

Temporary reduction/cessation of cerebral blood flow adversely affecting neuronal function 
  • Carotid/vertebral atherosclerotic disease

    • ▪ Artery-to-artery thromboembolism
    • ▪ Low-flow ischemia
  • Small, deep vessel disease associated with HTN

    • ▪ Lacunar infarcts
  • Cardiac diseases

    • ▪ 1-6% of patients with MI develop stroke.
  • Embolism secondary to the following:

    • ▪ Valvular (mitral valve) pathology
    • ▪ Mural hypokinesias/akinesias with thrombosis (acute anterior MI/congestive cardiomyopathies)
    • ▪ Cardiac arrhythmia (atrial fibrillation accounts for 5-20% incidence)
  • Hypercoagulable states

    • ▪ Antiphospholipid antibodies
    • ▪ Increased estrogen (e.g., oral contraceptives)
    • ▪ Pregnancy and parturition
  • Arteritis

    • ▪ Noninfectious necrotizing vasculitis
    • ▪ Drugs
    • ▪ Irradiation
    • ▪ Local trauma
  • Sympathomimetic drugs (e.g., cocaine)

  • Other causes: spontaneous and posttraumatic (e.g., chiropractic manipulation) arterial dissection

  • Fibromuscular dysplasia

Genetics

Inheritance is polygenic, with tendency to clustering of risk factors within families. 

RISK FACTORS

  • Hypertension (HTN)

  • Cardiac diseases (A-fib, MI, valvular disease)

  • Diabetes

  • Hyperlipidemia

  • Atherosclerotic disease (carotid/vertebral stenosis)

  • Cigarette smoking

  • Thrombophilias

GENERAL PREVENTION

  • Lifestyle changes: smoking cessation, diet modification, weight loss, regular aerobic exercise, and limited alcohol intake

  • Strict control of medical risk factors: diabetes (glycemic control), HTN (thiazide and/or ACE/ARB), hyperlipidemia (statins), anticoagulation when high risk of cardioembolism (e.g., atrial fibrillation, mechanical valves)

ALERT

10-20% of patients with TIA have CVA within 90 days; 25-50% of those occur within the first 48 hours.

 

Geriatric Considerations

  • Older patients have a higher mortality rate than younger patients—highest in 7th and 8th decades.

  • Atrial fibrillation is a frequent cause among the elderly.

Pediatric Considerations

  • Congenital heart disease is a common cause among pediatric patients.

  • Other causes include the following:

    • ▪ Metabolic: homocystinuria, Fabry disease
    • ▪ Central nervous system (CNS) infection
    • ▪ Clotting disorders
    • ▪ Marfan syndrome
    • ▪ Moyamoya disease
    • ▪ Sickle cell disease

Pregnancy Considerations

  • Preeclampsia, eclampsia, and HELLP

  • TTP and hemolytic uremic syndrome

  • Postpartum angiopathy

  • Cerebral venous thrombosis

  • Hypercoagulable states related to pregnancy

COMMONLY ASSOCIATED CONDITIONS

  • Atrial fibrillation

  • Uncontrolled HTN

  • Carotid stenosis

  • TIA Mimics

    • ▪ Some disease processes mimic TIA presentation
    • ▪ Seizures, migraines, metabolic disturbances, syncope
    • ▪ Gradual onset with nonspecific symptoms (headache, memory loss)

DIAGNOSIS

HISTORY

  • Obtain witness accounts with emphasis on symptom onset, progression, and recovery.

  • Carotid circulation (hemispheric): monocular visual loss, hemiplegia, hemianesthesia, neglect, aphasia, visual field defects (amaurosis fugax); less often, headaches, seizures, amnesia, confusion

  • Vertebrobasilar (brain stem/cerebellar): bilateral visual obscuration, diplopia, vertigo, ataxia, facial paresis, Horner syndrome, dysphagia, dysarthria; also headache, nausea, vomiting, and ataxia

  • Past medical history, baseline functional status

  • ABCD2 score: predicts risk of CVA within 48 hours 1[A]

    • ▪ Score of 0 to 1: 0%; 2 to 3: 1.3%; 4 to 5: 4.1%; 6 to 7: 8.1%
      • * Age >65 years: 1 point
      • * BP 140/90 mm Hg: 1 point
      • * Clinical presentation
        • ▪ Unilateral weakness: 2 points
        • ▪ Speech impaired without weakness: 1 point
      • * Duration >60 minutes: 2 points
      • * Duration 10 to 59 minutes: 1 point
      • * Diabetes: 1 point

PHYSICAL EXAM

  • Vital signs, oxygen saturation

  • Thorough neurologic and cardiac exams

DIFFERENTIAL DIAGNOSIS

  • Evolving stroke

  • Migraine (hemiplegic)

  • Focal seizure (Todd paralysis)

  • Hypoglycemia

  • Bell palsy

  • Neoplasm of brain

  • Subarachnoid hemorrhage

  • Intoxication

  • Electrolyte abnormalities

  • Head trauma

  • Central nervous system infection

  • Multiple sclerosis

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

  • Neuroimaging within 24 hours of symptom onset

  • MRI, including diffusion-weighted imaging, is the preferred brain diagnostic modality; if not available, then noncontrast head CT 2[B]

  • Noninvasive imaging of the cervicocephalic vessels should be performed routinely as part of the evaluation of suspected TIA 2[A].

  • Initial assessment of the extracranial vasculature may involve carotid US/TCD, MRA, or CTA depending on the availability and expertise and characteristics of the patient 2[B].

  • Routine blood tests (CBC, chemistry, PT/PTT, UPT, and fasting lipid panel) are reasonable in evaluation of patient with TIA 2[B].

Follow-Up Tests & Special Considerations

  • If only noninvasive testing is performed prior to CEA, it is reasonable to pursue two concordant noninvasive findings; otherwise, catheter angiography should be considered 2[B].

  • Echo is reasonable in evaluation of patients with suspected TIA especially when no other cause is noted 2[B].

  • TEE is useful in identifying PFO, aortic arch atherosclerosis, and valvular disease and is reasonable when this will alter management 2[B].

  • Prolonged cardiac monitoring is useful in patients with an unclear etiology after initial brain imaging and ECG 2[B].

  • EEG: if seizure suspected

  • Consider a sleep study due to the high prevalence of sleep apnea among TIA patients; treatment with CPAP has shown to improve patient outcomes 3[B].

TREATMENT

GENERAL MEASURES

  • TIA is a neurologic emergency. Immediate medical attention should be sought within 24 hours of symptom onset due to increased stroke risk.

  • Current evidence suggests that patients with high-risk TIAs require rapid referral and 24-hour admission (ABCD2 score ≥3 g).

  • Acute phase

    • ▪ Inpatient for high-risk individuals
    • ▪ Outpatient investigations may be considered based on patient’s stroke risk, arrangement of follow-up, and social circumstances.
  • Antiplatelet therapy to prevent recurrence or future CVA

  • Treatment/control of underlying associated conditions

MEDICATION

  • For patients with TIA, the use of antiplatelet agents rather than oral anticoagulation is recommended to reduce risk of recurrent stroke and other cardiovascular events, with the exception of cardioembolic etiologies 2[A].

  • Uncertain if switching agent in patients who have additional ischemic attacks while on antiplatelet therapy is beneficial 4[C]

First Line

  • Enteric-coated aspirin: 160 to 325 mg/day in the acute phase 5[A] followed by long-term antiplatelet therapy for noncardioembolic TIA and anticoagulation for cardioembolic etiology

  • Antiplatelet therapy

    • Aspirin 50 to 325 mg/day 4[A]
      • * Contraindications: active peptic ulcer disease and hypersensitivity to ASA or NSAIDs
      • * Precautions: may aggravate preexisting PUD; or worsen symptoms of asthma
      • * Significant possible interactions: may potentiate effects of anticoagulants and sulfonylurea analogues
    • ▪ ER dipyridamole-ASA (Aggrenox): 25/200 mg BID 4,6[B]
    • ▪ Combined therapy with dipyridamole and ASA is better than ASA alone 5,7[A].
    • ▪ More expensive than ASA alone and may have more side effects
    • Clopidogrel 75 mg/day 4[B] Can be used in patients who are allergic to ASA 4[B]
      • * Precautions: Thrombotic thrombocytopenic purpura (TTP) can occur and increases risk of bleeding when combined with aspirin.May be very slightly more effective than aspirin alone 5[B]; more expensive and more side effects than aspirin
  • Combined aspirin and clopidogrel therapy has been demonstrated to reduce the incidence of subsequent stroke by 21% without increased risk of bleeding when used for a duration of 1 month or less immediately following TIA or CVA 6[A].

  • Anticoagulation therapy

    • ▪ Direct thrombin inhibitor:
      • * Dabigatran (Pradaxa)
      • * Idarucizumab (Praxbind) reversal agent
    • ▪ Factor Xa inhibitors
      • * Apixaban (Eliquis)
      • * Rivaroxaban (Xarelto)
      • * Edoxaban (Savaysa)
        • ▪ Noninferior to warfarin in nonvalvular A-fib
        • ▪ Precautions: avoid in CKD (CrCl ≪30 mL/min)
        • ▪ Expensive but no INR needed
        • ▪ Not reversible
    • Warfarin (INR-adjusted dose) 4[A]
      • * Contraindications: intolerance/allergy, active liver disease, active bleeding, pregnancy
      • * Significant possible interactions: antibiotics, antiepileptics, antifungals, and many others
    • ▪ ASA 325 mg/day or ASA 81 mg/day and clopidogrel 75 mg/day 4[A]
      • * Patients who cannot take anticoagulation for reasons other than bleeding risk

Second Line

Ticlopidine (Ticlid): 250 mg PO BID 
  • For patients who cannot tolerate other agents

  • Contraindications: hypersensitivity, presence of hematopoietic/hemostatic disorders, conditions associated with bleeding, severe liver dysfunction

  • Precautions: neutropenia (0.8% severe), which is reversible with cessation of the drug. Monitor blood counts every 2 weeks for first 3 months. TTP can occur.

  • Significant possible interactions: Digoxin plasma levels decreased 15%; theophylline half-life increased from 8.6 to 12.2 hours.

ISSUES FOR REFERRAL

  • Neurology for ongoing workup and treatment

  • Cardiology if cardiac cause suspected

  • Vascular surgery if carotid endarterectomy appropriate

ADDITIONAL THERAPIES

  • Secondary prevention of TIA should be initiated; venous thromboembolism (VTE) prophylaxis

  • Patients with TIA or ischemic stroke should be started on a statin.

  • BP should be reduced after 24 hours. Thiazides, ACE inhibitors, and ARBs have shown to be of benefit. β-Blockers have not shown benefit in reducing recurrence or stroke.

  • Patients with DM or pre-DM should be advised to follow ADA guidelines to maintain tight glycemic control 3[A].

SURGERY/OTHER PROCEDURES

  • Consider carotid endarterectomy in patients with a high degree of carotid artery stenosis ≥70%.

  • When carotid endarterectomy is indicated for patients with TIA, surgery within 2 weeks is reasonable if there are no contraindications to early revascularization.

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Symptoms ≪72 hours and the following: 
  • ABCD2 score of >3

  • ABCD2 score of 0 to 3 and uncertainty that dx workup can be completed within 2 days as outpatient. Alternatively: If urgent imaging not available through ED or urgent neurology follow-up not available, admit ABCD2 score ≥3 with evidence of focal ischemia.

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

  • Outpatient follow-up with neuro support every 3 months for 1st year then annually

  • Close attention to recurrent or subsequent CVA

DIET

  • DASH diet or as appropriate for underlying medical problems

  • Physical activity

    • ▪ Any level of physical activity is beneficial, but at least 30 minutes of moderate-intensity physical activity daily is preferred.

PROGNOSIS

  • The risk of stroke on the ipsilateral side within 90 days and cumulative thereafter is 10-20%.

  • Frequency increases with the addition of multiple risk factors and severity of carotid stenosis.

  • Patients with larger artery occlusion or cardioembolic etiology are at increased risk of recurrence.

  • The major cause of death in the first 5 years is cardiac disease.

COMPLICATIONS

  • Stroke

  • Functional impairment

REFERENCES

Tsivgoulis  G, Stamboulis  E, Sharma  VK, et al. Multicenter external validation of the ABCD2 score in triaging TIA patients. Neurology.  2010;74(17):1351–1357.  [View Abstract]
Adams  RJ, Albers  G, Alberts  MJ, et al. Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack. Stroke.  2008;39(5):1647–1652.  [View Abstract]
Kernan  WN, Ovbiagele  B, Black  HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke.  2014;45(7):2160–2236.  [View Abstract]
Lansberg  MG, O’Donnell  MJ, Khatri  P, et al. Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest.  2012;141(2 Suppl):e601S–e636S.  [View Abstract]
Albers  GW, Amarenco  P, Easton  JD, et al. Antithrombotic and thrombolytic therapy for ischemic stroke: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th edition). Chest.  2008;133(6 Suppl):630S–669S.  [View Abstract]
Chen  S, Shen  Q, Tang  Y, et al. Efficacy and safety of adding clopidogrel to aspirin on stroke prevention among high vascular risk patients: a metaanalysis of randomized controlled trials. PLoS One.  2014;9(8):e104402.  [View Abstract]
De Schryver  EL, Algra  A, van Gijn  J. Dipyridamole for preventing stroke and other vascular events in patients with vascular disease. Cochrane Database Syst Rev.  2007;(3):CD001820.  [View Abstract]

ADDITIONAL READING

  • Simmons BB, Cirignano B, Gadegbeku AB. Transient ischemic attack: part I. diagnosis and evaluation. Am Fam Physician.  2012;86(6):521–526.

  • Simmons BB, Gadeqbeku AB, Cirignano B. Transient ischemic attack: part II. risk factor modification and treatment. Am Fam Physician.  2012;86(6):527–532.

SEE ALSO

Algorithms: Stroke; Transient Ischemic Attack; and Transient Neurologic Defects 

CODES

ICD10

  • G45.9 Transient cerebral ischemic attack, unspecified

  • G45.1 Carotid artery syndrome (hemispheric)

  • G45.0 Vertebro-basilar artery syndrome

  • G45.8 Oth transient cerebral ischemic attacks and related synd

  • G45.2 Multiple and bilateral precerebral artery syndromes

ICD9

  • 435.9 Unspecified transient cerebral ischemia

  • 435.1 Vertebral artery syndrome

  • 435.3 Vertebrobasilar artery syndrome

  • 435.8 Other specified transient cerebral ischemias

SNOMED

  • 266257000 Transient ischemic attack (disorder)

  • 230716006 Carotid territory transient ischemic attack

  • 230717002 Vertebrobasilar territory transient ischemic attack (disorder)

  • 426814001 Transient cerebral ischemia due to atrial fibrillation (disorder)

  • 88032003 Amaurosis fugax (disorder)

CLINICAL PEARLS

  • Stress smoking cessation, exercise, weight loss, limited ETOH intake, and control of HTN, hyperlipidemia, and diabetes

  • Antiplatelet therapy (e.g., aspirin, clopidogrel, or aspirin-dipyridamole) should be initiated.

  • Warfarin should be initiated in patients with atrial fibrillation or cardioembolic risk factors.

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