Transient Ischaemic Attack

Transient ischaemic attack (TIA) is a neurological emergency.

Traditionally, it was defined as a focal neurological dysfunction due to vascular disturbance, resolving within 24 hours. However, this 24-hour cut-off was arbitrary. Most TIAs last less than an hour, often under 10 minutes.

Modern definition (“tissue-based”) of TIA:

  1. Complete clinical resolution of symptoms.
  2. No ischaemic lesion on diffusion-weighted MRI.

Patients with transient symptoms and imaging evidence of infarction are now considered to have had a minor ischaemic stroke.

Importantly, TIA and minor stroke are managed similarly.

Neuroimaging begins with CT and CT angiography; definitive imaging is MRI with diffusion-weighted imaging (DWI).

Prompt diagnosis and treatment significantly reduce stroke risk (up to 80% reduction). Stroke risk without treatment is up to 20% at 3 months, highest within the first 48 hours.

History

Charles Miller Fisher (1913-2012) was the first to describe transient ischaemic attacks (TIA) as stroke precursors in 1952

Pathophysiology

Causes of vascular occlusive disease:

  • Thrombosis: large or small vessel atherosclerosis
  • Emboli:
    • Atherosclerotic arteries
    • Cardiac sources: AF, infarction, valvular disease, cardiomyopathy
  • Vascular dissection: carotid, vertebral, type A dissection
  • Hypercoagulable states: dehydration, infection, malignancy, prothrombotic disorders
  • Inflammatory causes: vasculitis (autoimmune/connective tissue disease)
Clinical assessment

TIAs are typically <1 hour in duration. Symptoms >1 hour likely indicate minor stroke.

If symptoms are ongoing or fluctuating, treat as stroke.

Key history:
  • Time and duration of symptoms
  • Symptom pattern (anterior vs posterior circulation)
  • Number of episodes
  • Medications (e.g. anticoagulants)
  • Vascular risk factors (diabetes, HTN, smoking, lipids, FHx)
Anterior circulation features:
  • Limb/facial weakness
  • Dysphasia
  • Monocular visual loss (amaurosis fugax)
Posterior circulation features:
  • Vertigo, diplopia, vomiting
  • Visual disturbances (nystagmus, ophthalmoplegia)
Examination:
  • Vital signs, GCS, BSL
  • Neurological exam
  • Cardiac signs (AF, murmurs)
Likelihood of TIA:

Definite:

  • Focal symptoms <1 hr
  • Limb/facial motor or sensory deficits
  • Visual field loss, aphasia

Possible:

  • Ataxia, diplopia, dysphasia, vertigo

Unlikely:

  • Amnesia, confusion, hallucinations, isolated facial numbness
Risk assessment

High-risk features:

  • AF
  • Amaurosis fugax
  • Crescendo symptoms (≥2 recent)
  • TIA while on antiplatelet/anticoagulation
  • High-grade carotid stenosis
  • ABCD2 score ≥ 4
  • Minor stroke (DWI lesion)
Differential diagnoses

Common mimics:

  • Migraine aura
  • Hypotension
  • Seizure (e.g. Todd’s paresis)
  • Peripheral vertigo
  • MS, metabolic (e.g. hypoglycaemia), psychogenic

Less common:

  • Intracerebral/SAB haemorrhage
  • Tumour
  • PRES
Investigations
Bloods:
  • FBC, U&Es, CRP/ESR, BSL
  • Lipids (can defer if non-fasted)
  • INR if anticoagulated
  • Others as indicated (e.g. procoagulant screen)
ECG:
  • AF, old MI, LVH
Imaging:

CT/CTA:

  • First-line in ED
  • Excludes bleed, mass lesion
  • Full 4-vessel CTA from aortic arch to vertex

MRI/MRA:

  • Gold-standard
  • Differentiates infarct from chronic changes
  • More sensitive for carotid flow than Doppler

Carotid US:

  • Alternative if CTA contraindicated

Echo (TTE/TOE):

  • Consider if cardiac source suspected, especially in young patients
Management
Antiplatelet therapy

High-risk TIA / minor stroke:

  • Dual therapy for 3 weeks:
    • Aspirin 300 mg stat, then 75 mg daily
    • Clopidogrel 300 mg stat, then 75 mg daily
    • OR Ticagrelor 180 mg stat, then 90 mg bd
  • Then single agent for at least 3 months

Second-line:

  • Consider Ticagrelor if Clopidogrel ineffective

Third-line:

  • Dipyridamole + aspirin (Asasantin SR)

Low-risk TIA (ABCD2 <4):

  • Single agent (aspirin, clopidogrel, or ticagrelor)
Anticoagulation

For AF or embolic source:

  • DOACs preferred unless contraindicated
  • Warfarin if valvular AF, mechanical valve, or severe renal impairment

Consider heparin/enoxaparin if:

  • Crescendo TIAs with carotid stenosis pending surgery
  • Cardiac thrombus or myxoma (discuss with stroke team)
Carotid surgery
  • Consider for symptomatic ≥ 50% stenosis (ipsilateral)
Risk factor management
  • BP: <140/90 mmHg (<130/80 mmHg if diabetic/lacunar stroke)
  • Statins (regardless of baseline LDL if atherosclerotic TIA)
  • Glycaemic control, weight loss, exercise
  • Smoking cessation
  • Sleep apnoea screening
Disposition
  • TIA clinic follow-up for discharged high-risk patients
  • Assess by stroke specialist within 24 hours
  • Admit to Short Stay Unit or similar
  • Urgent surgical referral if dissection or carotid stenosis

References

Publications

Fellowship Notes

MBBS DDU (Emergency) CCPU. Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Co-creator of the LITFL ECG Library. Twitter: @rob_buttner

Dr James Hayes LITFL author

Educator, magister, munus exemplar, dicata in agro subitis medicina et discrimine cura | FFS |

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