Time-critical presentations
Stroke and TIA — emergency pathway
Overview and approach
Stroke causes sudden neurological deficit; TIA is transient focal dysfunction and still requires urgent evaluation.
- Australian and New Zealand Living Clinical Guidelines for Stroke Management (Stroke Foundation) cover pre-hospital care, assessment, reperfusion, antithrombotics and secondary prevention, with an emergency department summary1.
- Stroke is a clinical diagnosis: an abrupt focal deficit with a vascular cause. Imaging supports it and separates the roughly 85% that are ischaemic from the 15% that are haemorrhagic3.
- Why minutes matter: neurons store no glycogen, so symptoms start within seconds. With no flow at all, tissue dies within about 4-10 minutes. Around the dead core is the penumbra, which is not working but can still recover; saving it is the aim of reperfusion3.
- How cells die: energy failure stops the ion pumps, neurons depolarise, calcium floods in, glutamate is released and over-excites neighbours, and free radicals damage membranes. Fever and high glucose make the injury worse3.
- Main causes of ischaemic stroke: cardioembolism (AF, mural thrombus after MI, valve disease, endocarditis, paradoxical embolus), artery-to-artery embolism or thrombosis (carotid bifurcation, aortic arch), small-vessel (lacunar) disease (about 20%), and arterial dissection, a common cause under 603.
- TIA: most last under an hour. Despite full recovery, 15-50% show an infarct on imaging. Stroke risk is about 10-15% over 3 months, with most strokes in the first 2 days3.
Assessment and clinical features
ABCDE, glucose, exact last-known-well time, anticoagulants, baseline function and focal assessment; include posterior circulation symptoms.
- Vascular syndromes:
- ACA infarct: dysarthria, aphasia, contralateral weakness (leg and shoulder worse than arm, hand and face), minimal sensory change, left limb apraxia, urinary incontinence.
- MCA infarct: contralateral hemiparesis and hemisensory loss, hemianopia, aphasia if dominant hemisphere (expressive anterior, receptive posterior, global if extensive), neglect if non-dominant.
- PCA infarct: contralateral homonymous hemianopia (occipital), hemisensory loss and burning hemi-body pain (thalamic); unilateral sensory loss plus hemianopia without paralysis suggests PCA territory; bilateral can reduce visual-motor coordination.
- Cerebellar infarct: non-specific nausea, vomiting, dizziness, unsteadiness, headache; look for incoordination, ataxia, horizontal nystagmus; altered consciousness or coma may occur.
- Stroke mimics: seizure (including ongoing focal seizures), tumour, migraine aura and metabolic encephalopathy. Infection or metabolic upset can also bring back an old stroke deficit that then clears3.
- Migraine aura vs stroke: aura symptoms spread slowly across a limb over minutes rather than seconds, cross vascular territories and may have scintillating visual symptoms. Aura can occur without headache, even in people over 65 with no migraine history3.
- Many patients do not call for help themselves because stroke is usually painless and they may not recognise their own deficit (anosognosia)3.
- Clinical features cannot reliably separate bleeding from ischaemia. A lower conscious level, higher BP and worsening after onset favour haemorrhage; a deficit that is maximal at onset or improving favours ischaemia3.
- Amaurosis fugax: brief loss of vision in one eye, often described as a shade coming down or up. It warns of internal carotid disease in about a quarter of symptomatic cases3.
- Lateral medullary (Wallenberg) syndrome: vertigo, nystagmus, vomiting, ipsilateral facial numbness with contralateral loss of pain and temperature in the body, ipsilateral Horner's, hoarseness, difficulty swallowing and ipsilateral limb ataxia. Usually vertebral or PICA occlusion. Signs on opposite sides of face and body point to the brainstem3.
- Basilar occlusion: signs on both sides (weakness of all four limbs, bulbar palsy, cranial nerve and cerebellar signs) and reduced consciousness3.
The classic lacunar syndromes3.
| Syndrome | Usual site |
|---|---|
| Pure motor (face, arm and leg) | Posterior limb of internal capsule or pons |
| Pure sensory | Thalamus |
| Ataxic hemiparesis | Pons or internal capsule |
| Dysarthria with a clumsy hand | Pons or genu of internal capsule |
Differentials and investigations
Activate stroke pathway with urgent brain/vascular imaging, ECG and blood tests. Exclude haemorrhage before antithrombotic decisions.
- A lacunar presentation can still come from a carotid or cardiac embolus, so keep looking for an embolic source3.
- A tight carotid stenosis may give a high-pitched bruit that fades and can disappear as the artery nears occlusion, so a quiet neck does not exclude it3.
Management and follow-up
Specialists assess reperfusion eligibility using current living guidelines. Manage swallowing safety, physiology, rehabilitation and cause-based secondary prevention.
- Reperfusion: tenecteplase or alteplase within 4.5 hours after CT excludes haemorrhage; aspirin is not given in the first 24 hours after thrombolysis2.
Red flags and clinical pearls
Do not give aspirin before haemorrhage is excluded or assume resolved symptoms are benign. Reperfusion selection is time- and imaging-dependent.
- Cerebellar infarct: swelling in the posterior fossa can compress the brainstem and cause sudden respiratory arrest, sometimes with few warning signs3.
- Neck or head pain in the hours to days before a stroke in a younger patient suggests carotid or vertebral dissection3.
- Small-vessel TIAs can recur several times a day ("stuttering lacunes") before a completed stroke3.
References
- Stroke Foundation: Living Clinical Guidelines for Stroke Management (InformMe)
- Living Guidelines Chapter 3: Acute medical and surgical management
- Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 370, Cerebrovascular diseases.
Last updated from Sen’s notes on 22 October 2026.