Transient Ischaemic Attack (TIA)

Notes

Overview

Transient ischemic attack is defined as transient neurologic symptoms without evidence of acute infarction. It is a common and important risk factor for future stroke. TIAs are produced by temporary ischemia to a vascular territory, usually caused by thrombosis or embolism and less commonly by vasculitis, hematologic disorders such as sickle cell disease or vasospasm.

The stroke risk after a TIA is around 10% at 2 weeks, with half of these events occurring within 48 hours. This emphasises the need for rapid clinical assessment and investigations in patients with TIA.

Definition

Stroke: Acute onset of a focal neurologic deficit due to a cerebral infarction or hemorrhage.
Transient Ischaemic Attack (TIA): TIA is a transient episode of neurological dysfunction caused by focal brain or retinal ischaemia, without infarction. When there is evidence of brain infarction, the episode is considered to be a mild stroke (if symptoms are minor or disappear).
Amaurosis Fugax: Transient monocular blindness that often is described as a gray shade being pulled down over the eye caused by ischemia to the retinal artery.

Anatomy and Physiology

Cerebral Anatomy and Blood supply

Anatomy – Cerebral anatomy and blood supply (Circle of Willis)

Sensory Pathways

Motor Pathways

Motor Pathway

Risk Factors

Hypertension
Smoker
Large waist-to-hip ratio
High alcohol intake
Diabetes mellitus
Unhealthy diet
Psychosocial stress
Regular physical activity

The highest- risk patients for stroke are those with previous ischemic events such as TIA.

Clinical Manifestation

The focal neurologic symptoms produced by ischemia depend on the area of the cerebral circulation involved

Common Presentation (Sudden onset)

Memory loss
Headache
Blurred vission
Unilateral paresis
Transient monoocular blindness
Diplopia

Cranial Nerve Examination

Diplopia
Hemianopia
Monocular blindness
Disconjugate gaze
Facial drooping
Lateral tongue movement
Dysphagia
Vestibular dysfunction

Cerebellar Examination

Nystagmus
Past-pointing
Dystaxia
Ataxia

Many patients with suspected TIA turn out to have a different diagnosis (eg migraine, hypoglycaemia, seizure).

The ABCD (Age, Blood pressure, Clinical presentation, Diabetes mellitus, Duration of symptoms) score should be determined during the initial evaluation and can help assess the immediate risk of repeat ischemia and stroke.

Differential Diagnosis

CONDITION	CLINICAL MANIFESTATION
Brain tumor	Severe unilateral headache with nausea and vomiting
Central nervous system infection (e.g., meningitis, encephalitis)	Fever, headache, confusion, neck stiffness, nausea, vomiting, photophobia, change in mental status
Falls/trauma	Headache, confusion, bruising
Hypoglycemia	Confusion, weakness, diaphoresis
Migraines	Severe headaches with or without photophobia, younger age
Multiple sclerosis	Diplopia, limb weakness, paresthesia, urinary retention, optic neuritis
Seizure	Confusion with or without loss of consciousness, urinary incontinence, tongue biting, tonic-clonic movements
Subarachnoid hemorrhage	Severe headache with sudden onset and photophobia
Vertigo (central or peripheral)	Generalized dizziness and diaphoresis with or without hearing loss

TIA is more likely with sudden onset, unilateral paresis, speech disturbance, or transient monocular blindness.

Investigations

TIA and Stroke is a medical emergency!

Imaging

CT or MRI
ECG
Carotid imaging within 24 hours

Urgent brain imaging is required. Computerised tomography (CT) can help to exclude a stroke mimic and to differentiate haemorrhagic to ichaemic stroke.

Laboratory investigation

FBC
EUC
Blood glucose
LFT
Lipid studies
Cardiac markers?

Other (for differentials)

Rapid plasma reagin testing
Cerebrospinal fluid analysis
Urine drug screening
Coagulation profile

All patients with suspected TIA should get FBC, EUC erythrocyte sedimentation rate (ESR), lipid profile, glucose level, ECG and brain (CT/MRI) and carotid imaging.

Pathophysiology

Treatment

INDICATION FOR CT/MRI

Patient on anticoagulants or with abnormal coagulation

Plan to give thrombolysis or immediate anticoagulants

Deteriorating conscious level or rapidly progressing deficits

Suspected cerebellar haematoma, to exclude hydrocephalus

Medical Management

Urgent brain CT or MRI (within 24hours)
Antiplatelet – Aspirin (within 24-48 hours) if CT/MRI scans excludes haemorrhage
- The first dose should be at least 150 to 300 mg
- Dosage thereafter can be reduced (e.g. 100 mg daily)
Long-term antiplatelet therapy: aspirin +/- dipyridamole or clopidogrel should be prescribed to all people with ischaemic stroke or TIA

Anticogulant is preferred for cardioembolic events (Ischaemic heart disease) if CT/MRI scans excludes haemorrhage.

Aggressive risk factor modification Interventions following a stroke or TIA are aimed at preventing future episodes

Treat hypertension
Smoking cessation
Lose weight if obese
Increase physical activity
Treat Diabetes mellitus
Treat dyslipidaemia with statin
Hormone Replacement Therapy should be stopped
Carotid endarterectomy or stenting

In patients found to have a high-grade ipsilateral carotid stenosis, carotid endarterectomy should be performed urgently. The benefit of surgery is greatest within 2 weeks of the TIA or mild stroke as this is the period of greatest risk of recurrent stroke.

Dont Forget Primary Survey when someone presents to ED

Airway

Is the patient able to protect his/her airway?
Can the patient swallow without evidence of aspiration?
Perform a swallow screen and keep patient nil by mouth if swallowing unsafe

Breathing

Is the patient breathing adequately?
Check oxygen saturation and give supplementary oxygen if oxygen saturation < 95%

Circulation

Are peripheral perfusion, pulse and blood pressure adequate?
Treat with fluid replacement, anti-arrhythmics and inotropic drugs as appropriate

Hydration

Is the patient dehydrated or unable to swallow?
Give fluids parenterally or by nasogastric tube if swallow is unsafe

Nutrition

Assess nutritional status
Consider nutritional supplements
If dysphagia persists for a day or two, start feeding via a nasogastric tube

Medication

If the patient is dysphagic, consider alternative routes for essential medications

Blood pressure

Unless there is heart failure or renal failure, evidence of hypertensive encephalopathy or aortic dissection, do not lower the blood pressure in the first week since it will often return towards the patient’s normal level within the first few days
Early blood pressure reduction may decrease cerebral perfusion and increase infarction to offset potential benefits. Trials of early blood pressure lowering are ongoing

Blood glucose

Is the blood glucose ≥11.1 mmol/l
Hyperglycaemia may increase infarct volume, therefore use insulin (via infusion or glucose/potassium/insulin (GKI)) to normalise levels but monitor closely to avoid hypoglycaemia

Temperature

Is the patient febrile?
Raised brain temperature may increase infarct volume
Investigate and treat any cause but give antipyretics early

Pressure areas

These should be formally assessed and measures taken to reduce the risk
Treat infection, maintain nutrition, provide a pressure-relieving mattress and turn immobile patients regularly

Incontinence

Ensure the patient is not constipated or in urinary retention
Avoid urinary catheterisation unless the patient is in acute urinary retention or incontinence is threatening pressure areas

Complication and Prognosis

Complications

Stroke
Myocardial infarction
Depression
Anxiety
Unable to drive

Prognosis By definition, a patient with a TIA has no residual symptoms from the primary event.The highest- risk patients for stroke are those with previous ischemic events such as TIA, >10% of TIA patients seen in the emergency department will have a stroke within 3 months.

References

AAFP – Transient Ischemic Attack: Part I. Diagnosis and Evaluation – 2012
AAFP – Transient Ischemic Attack: Part II. Risk Factor Modification and Treatment – 2012
Best Practice
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