At a glance
What it is
A transient ischaemic attack (TIA) is a temporary episode of focal neurological deficit caused by reduced blood flow to the brain or retina, resolving completely within 24 hours (usually within minutes) and leaving no permanent infarction on diffusion-weighted MRI. The mechanism mirrors that of ischaemic stroke: arterial thromboembolism from atherosclerotic plaques (carotid, vertebral, or intracranial arteries) or cardiac embolism (atrial fibrillation being the most important source). TIA is a warning — without treatment, the short-term risk of full stroke is 10–15% within the first 48 hours. The ABCD2 score stratifies early stroke risk.
Symptoms
Sudden onset of any of: unilateral weakness, numbness, or paralysis of the face, arm, or leg; slurred or garbled speech or difficulty understanding others (dysphasia); transient monocular visual loss (amaurosis fugax — a curtain coming down over one eye, from retinal ischaemia); diplopia; vertigo or loss of balance. Episodes typically last 2–15 minutes. Multiple TIAs may occur and may involve the same or different territory. A TIA can only be diagnosed in retrospect — during the episode itself, it is indistinguishable from a stroke in evolution and must be treated as such.
Approach
TIA is a medical emergency requiring same-day specialist evaluation (brain imaging, ECG, carotid ultrasound, blood tests including lipids, glucose, and full blood count). Immediate dual antiplatelet therapy (aspirin + clopidogrel for 21 days, then single antiplatelet) dramatically reduces early stroke risk. Anticoagulation for AF-related TIA. Statin therapy. Carotid endarterectomy or stenting within 2 weeks for significant ipsilateral carotid stenosis (> 50–70%). Blood pressure and diabetes optimisation. Lifestyle modification (smoking cessation, exercise, diet). Secondary prevention with long-term antiplatelet or anticoagulant therapy is continued indefinitely.
What a transient ischaemic attack is
A TIA is a transient episode of brain or retinal ischaemia — blood flow is temporarily insufficient to meet the metabolic demands of the affected neural tissue. The tissue is threatened but does not infarct (die). When flow is restored, the deficit resolves. If the block persists long enough to cause infarction, it is a stroke.
**Why TIA demands urgent treatment**
The early stroke risk after TIA is highest in the first 48 hours. Without treatment, approximately 10–15% of patients will have a stroke within 2 days. With immediate evaluation and secondary prevention, this risk can be reduced by 80%. TIA is therefore one of the most important preventable causes of disabling stroke.
**Causes**
*Large artery atherosclerosis* — the most common cause. Cholesterol-laden plaques in the carotid arteries, vertebral arteries, or intracranial vessels rupture and generate emboli that temporarily occlude downstream arteries. Significant carotid stenosis (> 50–70%) is surgically correctable and reduces stroke risk substantially.
*Cardioembolic* — clots formed in the heart travel to the brain. Atrial fibrillation (AF) is the most important source; others include prosthetic heart valves, recent myocardial infarction, dilated cardiomyopathy, and patent foramen ovale. AF-related TIA requires anticoagulation, not antiplatelet therapy.
*Small vessel disease* — lipohyalinosis of penetrating arteries causes lacunar TIAs; risk factors are hypertension and diabetes.
**ABCD2 score — stratifying early stroke risk**
| Factor | Points | |---|---| | Age ≥ 60 | 1 | | Blood pressure ≥ 140/90 on presentation | 1 | | Clinical features: unilateral weakness (2), speech disturbance only (1) | 0–2 | | Duration: ≥ 60 min (2), 10–59 min (1) | 0–2 | | Diabetes | 1 |
Score 4–7 = high risk (8% 2-day stroke risk). All TIA patients warrant urgent same-day evaluation regardless of score, since the ABCD2 score alone does not reliably distinguish low from high risk.
**Secondary prevention**
The components of secondary prevention after TIA are: - *Antiplatelet therapy*: aspirin + clopidogrel for 21 days after non-cardioembolic TIA (POINT and CHANCE trial protocols), then single antiplatelet indefinitely - *Anticoagulation*: for AF or other cardioembolic sources - *Statin*: high-intensity statin (atorvastatin 40–80 mg/day) to reduce atherosclerosis progression - *Antihypertensives*: blood pressure < 130/80 mmHg - *Carotid revascularisation*: endarterectomy or stenting for symptomatic stenosis > 50–70% within 2 weeks - *Lifestyle*: smoking cessation, Mediterranean diet, regular moderate exercise, moderate alcohol restriction
Treatment options at Alimran Medical Center
Injection therapies
- Botox® injections
- Prolotherapy
- Ozone injection
- Trigger point injections
Advanced therapies
Physiotherapy
- Electrical stimulation
- Short and long wave therapy
- Laser therapy
- Ultrasound therapy
- Balance rehabilitation and cardiovascular exercise
Book a consultation
The secretary schedules first appointments during clinic hours; please have prior imaging, operative notes and a current medication list available at the time of the call.
This page provides general information about transient ischaemic attack (tia) and is not a substitute for individual medical assessment. If your symptoms are severe or worsening, contact a clinician promptly.