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:
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

Dr Robert Buttner LITFL Author

MBBS FACEM DDU (Emergency) CCPU. Emergency Physician in Melbourne, Australia. Co-Ultrasound Lead for Emergency Medicine at The Alfred Hospital. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor of the LITFL ECG Library.

Dr James Hayes LITFL Author Medical Educator

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

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