Evidence-Based Medicine

Transient Ischemic Attack (TIA)

Transient Ischemic Attack (TIA)

Background

  • A transient ischemic attack (TIA) is defined as a brief episode of neurologic dysfunction caused by focal cerebral ischemia not associated with permanent cerebral infarction. The current distinction between TIA and ischemic stroke is based on the presence (for stroke) or absence (for TIA) of evidence of infarction, but recent views suggest that TIA may be better thought of as minor ischemic stroke.
  • TIAs may be caused by atheroemboli from carotid or vertebral artery stenosis, cardiogenic emboli in patients with valvular stenosis or arrhythmias such as atrial fibrillation, paradoxical emboli through intracardiac defects, aortic arch emboli, and in patients with hypercoagulable, prothrombotic, or hyperviscous states such as sickle cell disease, thrombocytosis, or leukemia.
  • Risk factors for TIA include:
    • metabolic conditions such as metabolic syndrome, diabetes mellitus type 2, and chronic kidney disease
    • modifiable risk factors such as obesity, smoking, hyperlipidemia, heavy alcohol use, and substance abuse
    • cardiovascular conditions such as hypertension, atrial fibrillation, carotid stenosis, or history of prior myocardial infarction, nonischemic cardiomyopathies, TIA, or stroke
    • hormone replacement therapy and oral contraceptives
  • Most TIAs resolve within 1-2 hours but there is a risk of subsequent stroke, particularly within a few days of the TIA, and the duration of symptoms does not predict this risk.
  • A TIA should be regarded as a medical emergency as part of the spectrum of Acute Cerebrovascular Syndrome.

Evaluation

  • Patients with a suspected TIA should be evaluated as soon as possible after the event (Strong recommendation).
  • Diagnostic evaluation focuses on:
    • Differentiating TIA from stroke and non-ischemic mimics.
    • Determining etiology to inform management, particularly secondary prevention strategies.
    • Determining short-term risk of subsequent stroke to inform management including appropriate disposition or patient, timeliness of subsequent testing, follow-up visits, and specialty referral.
  • A careful history is important to evaluate for TIA and differentiate it from non-ischemic mimics since most patients will not report symptoms at time of evaluation but must describe symptoms from their recollection.
    • Ask about loss of normal neurologic function ("negative symptoms") as most patients with TIA will report these and their presence increases suspicion of ischemia. Examples include motor weakness, decreased or altered speech, diminished vision, and decreased sensation (anesthesia).
    • Addition of abnormal symptoms ("positive symptoms") may be seen in some patients with TIA but should raise suspicion of non-ischemic mimics. Examples include involuntary movements, increased speech volume or incomprehensible speech, visual sensations such as light flashes or visual aura (scintillating scotoma), abnormal sensation (dysesthesia), and pain.
    • Neurologic symptoms consistent with cerebral ischemia from the anterior circulation may include:
      • motor or sensory dysfunction of the contralateral face and/or contralateral extremities
      • ipsilateral vision loss or homonymous hemianopia
      • speech disturbances such as aphasia or dysarthria
    • Neurologic symptoms consistent with a posterior circulation event (vertebrobasilar circulation) may include:
      • nausea and vomiting
      • dizziness
      • motor or sensory dysfunction of the ipsilateral face and/or contralateral extremities (crossed pattern)
      • visual loss in 1 or both homonymous visual fields including cortical blindness and Anton syndrome (lack of awareness of blindness)
      • brainstem and cerebellar findings such as ataxia, vertigo, diplopia, dysphagia, and dysarthria
  • Use validated tools such as Face Arm Speech Test (FAST) or Recognition of Stroke in the Emergency Room (ROSIER) scale to quickly screen for ongoing focal neurologic deficits.
  • A careful neurologic exam is important to assess for ongoing subtle abnormalities including mental status, cranial nerves, strength, sensations, vision, language (fluency and articulation), gait, and coordination.
  • In patients referred for a suspected TIA or minor stroke, the most frequent noncerebrovascular diagnoses include migraine, syncope, seizure, psychiatric conditions, vertigo, and peripheral nerve conditions.
  • Exclude hypoglycemia as the cause of symptoms.
  • Initial blood tests for the evaluation of patients with a suspected TIA may include (Weak recommendation):
    • complete blood count with platelet count evaluating for inflammation, thrombocytosis, and myelodysplastic disease
    • chemistry panel to assess for electrolyte imbalances and kidney dysfunction
    • prothrombin time (INR) and activated partial thromboplastin time (aPTT) to assess for coagulopathy
    • fasting lipid panel to assess for risk of atherosclerotic vascular disease
    • fasting glucose and consider obtaining a HbA1c if diabetes is suspected
    • serial cardiac biomarkers (troponin) if acute coronary syndrome suspected
  • Consider a hypercoagulable workup in younger patients with a TIA, especially in those without vascular risk factors, cervical dissection, or underlying identifiable causes.
  • Perform neuroimaging as soon as possible, preferably within 24 hours of symptom onset (Strong recommendation).
    • Magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) is preferred modality.
    • Noncontrast computed tomography (CT) is poorly sensitive for stroke and TIA but is an acceptable alternative if MRI not available or feasible.
  • Conduct noninvasive vascular imaging of the cervical and intracranial vessels with ultrasound, computed tomographic angiography, or magnetic resonance angiography as soon as possible to help determine etiology and risk of stroke, and to inform management (Strong recommendation).
  • An electrocardiogram (ECG) should be obtained to assess for atrial fibrillation, ventricular hypertrophy, or signs of cardiac ischemia (Strong recommendation).
  • Consider prolonged cardiac monitoring (inpatient telemetry or Holter monitoring) in patients with an etiology not identified after initial neuroimaging and ECG. Holter monitoring for 2-3 days may be reasonable initially but, if no findings and cardioembolic etiology still suspected, monitoring for up to 30 days is recommended to assess for paroxysmal atrial fibrillation.
  • Consider transthoracic and, depending on the clinical circumstance, a transesophageal echocardiogram to assess for valvular or cardiogenic sources of emboli (Weak recommendation). This is particularly important if known cardiac disease or embolic pattern on MRI.
  • An evaluation conducted rapidly after TIA that is thorough and focused on determining TIA etiology allows for earlier implementation of targeted management strategies to reduce the risk of subsequent stroke.

Acute Management

  • Consider diagnosis of stroke rather than TIA if patient does not return to baseline. See Stroke (Acute Management) for details.
  • Early initiation of individualized secondary prevention strategies can reduce the risk of subsequent stroke and should be tailored to the suspected underlying etiology.
  • For acute management of TIA, offer aspirin (unless contraindicated) to be started immediately.
  • Assess the patient for risk of subsequent stroke as soon as possible to assist in determining management.
    • Results of MRI, vascular imaging, blood tests, echocardiogram, and electrocardiography may contribute to assessing risk factors and subsequent treatment.
    • TIA patients with significant carotid stenosis and those with transient symptoms with infarction are at a higher risk of both short- and long-term subsequent stroke than in patients with other etiologies.
    • Risk stratification tools such as the ABCD3-I score can help inform management but should not be used by themselves to determine risk.
  • Determine the appropriate care setting depending on the timing and nature of symptoms and the risk of stroke.
    • If presenting within 48 hours of the suspected TIA, the patient is considered to be:
      • at the HIGHEST RISK for stroke if the symptoms include transient, fluctuating, and/or persistent unilateral weakness, or speech disturbance, and should be immediately sent to the Emergency Department (ED) with the capacity for advanced stroke care
      • at a HIGH RISK for stroke if there are transient, fluctuating, or persistent symptoms without motor weakness or speech disturbance, and should be sent for a same-day assessment at closest stroke prevention clinic or to an ED with the capacity for advanced stroke care
    • Also consider hospitalization if
      • presenting within 72 hours of TIA and (Weak recommendation):
        • it is unclear if outpatient workup can be completed within 2 days
        • other evidence indicates event caused by focal ischemia
      • there is otherwise suspicion of high risk of subsequent stroke or need for specialized care, especially if
        • stuttering or crescendo TIA events
        • known cardioembolism failing outpatient treatment
        • cardiac decompensation
    • Patients presenting within 2-14 days after the suspected TIA are considered to be at INCREASED RISK for stroke and should have a comprehensive assessment by a healthcare professional with stroke expertise as soon as possible and:
      • no more than 24 hours after first contact if the symptoms include transient, fluctuating, and/or persistent unilateral weakness, or speech disturbance
      • no more than 14 days after first contact If there are transient, fluctuating, or persistent symptoms without motor weakness or speech disturbance
    • Patients considered to be at a LOWER RISK for stroke include those:
      • presenting more than 14 days after the suspected TIA who should be assessed by a neurologist or stroke specialist as soon as possible (no more than 30 days after onset of the symptoms)
      • with atypical sensory symptoms (such as patchy numbness and/or tingling) who may be assessed by a stroke specialist as needed

Prevention of Stroke After TIA

  • There is a risk of stroke following the TIA, particularly within the first few days. A thorough evaluation conducted rapidly after TIA allows for earlier implementation of risk prevention strategies.
  • Management strategies to reduce the risk typically include antiplatelet or anticoagulation therapies, depending on the etiology and comorbidities, and other therapies as appropriate.
  • Antiplatelet agents should be used rather than anticoagulation for patients with noncardioembolic TIA (Strong recommendation).
    • Options for most patients include aspirin 81-325 mg/day, clopidogrel 75 mg/day, or aspirin/dipyridamole 25 mg/200 mg daily.
    • For high-risk TIA (ABCD2 ≥ 4), consider dual antiplatelet therapy (DAPT) with combination aspirin plus clopidogrel for 10-21 days, with single antiplatelet thereafter
    • see Antithrombotic Therapy for Secondary Prevention of Stroke or TIA for a complete discussion of strategies.
  • For patients with atrial fibrillation
    • Use oral anticoagulation regimens (Strong recommendation). Options include warfarin, apixaban, rivaroxaban, and dabigatran.
    • Optimal timing for starting anticoagulation unclear but consider 4-14 days after TIA.
  • For patients with carotid artery stenosis:
    • Perform carotid endarterectomy (CEA) for patients with a perioperative morbidity and mortality risk estimated to be < 6% who have had a TIA or nondisabling ischemic stroke within the last 6 months and have either:
      • ipsilateral severe (70%-99%) stenosis documented by noninvasive imaging (Strong recommendation)
      • ipsilateral moderate (50%-69%) stenosis documented by catheter-based imaging (Strong recommendation)
    • Consider carotid artery stenting (CAS) as an alternative to CEA for symptomatic patients with an average or low risk of complications associated with endovascular intervention plus stenosis > 70% by noninvasive imaging or > 50% by catheter angiography (Weak recommendation).
    • See Carotid Artery Stenosis Repair for a complete discussion of strategies.
  • Additional risk factor reduction through statin therapy, blood pressure reduction, smoking cessation, and avoidance of heavy alcohol use should be implemented to prevent stroke in patients who have had a TIA (Strong recommendation). Consider advising moderate physical activity (Weak recommendation). See Secondary Prevention of Stroke or Transient Ischemic Attack for a complete discussion of strategies.

Published: 25-06-2023 Updeted: 25-06-2023

References

  1. Duca A, Jagoda A. Transient Ischemic Attacks: Advances in Diagnosis and Management in the Emergency Department. Emerg Med Clin North Am. 2016 Nov;34(4):811-835
  2. Coutts SB. Diagnosis and Management of Transient Ischemic Attack. Continuum (Minneap Minn). 2017 Feb;23(1, Cerebrovascular Disease):82-92
  3. Easton JD, Saver JL, Albers GW, et al. 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. 2009 Jun;40(6):2276-93
  4. Casaubon LK, Boulanger JM, Blacquiere D, et al; Heart and Stroke Foundation of Canada Canadian Stroke Best Practices Advisory Committee. Canadian Stroke Best Practice Recommendations (CSBPR): Hyperacute stroke care guidelines, update 2015. Int J Stroke 2015 Aug;10(6):924-40

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