Brainstem Infarction

Brainstem infarction is ischaemic stroke of the medulla, pons or midbrain, usually from occlusion of the vertebral, basilar or paramedian perforating arteries. It produces cranial nerve, long tract and cerebellar signs and can be fatal when the reticular formation or respiratory centres are involved.

Brainstem infarcts account for about 10% of ischaemic strokes. Pontine lacunes from small vessel disease are the commonest, and large artery disease and embolism cause the more severe syndromes.

Syndromes. Lateral medullary (Wallenberg), medial medullary, medial and lateral pontine, locked in, Weber, Claude, Benedikt and top of the basilar syndromes, depending on the territory.

Prognosis. Mortality is high with basilar occlusion and bilateral pontine infarction. Isolated lateral medullary and small pontine infarcts have a good outlook, but dysphagia and vertigo may persist.

Pathophysiology.

Occlusion of paramedian and circumferential perforators causes infarction of tegmentum and basis, with crossed cranial nerve and long tract signs. Branch atheroma at the origin of perforators and parent vessel disease cause most pontine strokes.

Early neurological worsening is common because perforator territories have little collateral supply.

• Lateral medullary syndrome: ipsilateral facial pain and temperature loss, Horner syndrome, limb ataxia, dysphagia and hoarseness, and contralateral body pain and temperature loss, with vertigo and vomiting.
• Medial pontine infarct: contralateral hemiparesis, dysarthria, and ataxia; bilateral lesions cause quadriparesis and locked in syndrome.
• Midbrain infarct: third nerve palsy with contralateral hemiparesis (Weber), tremor and ataxia, or vertical gaze palsy.
• Diplopia, internuclear ophthalmoplegia, facial weakness, dysarthria, dysphagia and respiratory irregularity.

Red flags.

• Falling consciousness, abnormal respiration or gaze palsy.
• Progressive deficit in the first days.
• Severe dysphagia with aspiration risk.

• MRI with diffusion weighted imaging is the test of choice; CT often misses brainstem infarcts, and early MRI can be falsely negative, so repeat after 24 to 48 hours when suspicion remains.
• CT angiography or MR angiography of the vertebral and basilar arteries; high resolution vessel wall imaging for dissection.
• Bedside HINTS examination in acute vertigo with nystagmus: normal head impulse, direction changing nystagmus or skew deviation point to a central cause.
• 12 lead ECG, rhythm monitoring, echocardiography and blood tests (glucose, lipids, full blood count).
• Bedside swallow screen and formal assessment.

Differential diagnosis. Brainstem haemorrhage, demyelination, brainstem encephalitis, Wernicke encephalopathy, tumour, central pontine myelinolysis, Guillain-Barré syndrome (Bickerstaff variant), myasthenia gravis and vestibular neuritis.

• Airway and respiratory support, swallowing assessment and nasogastric feeding when dysphagia is present, and early rehabilitation.
• Alteplase 0.9 mg/kg intravenously (maximum 90 mg), 10% as a bolus over 1 minute and the rest as an infusion over 60 minutes, within 4.5 hours of onset or last known well. Monitor neurological observations and blood pressure every 15 minutes for 2 hours, every 30 minutes for the next 6 hours, then hourly to 24 hours; keep blood pressure under 185/110 mmHg before and under 180/105 mmHg after treatment; repeat imaging at 24 hours or with deterioration. Contraindicated with previous intracranial haemorrhage, INR over 1.7, platelets under 100 x 10^9/L, glucose under 2.7 mmol/L, anticoagulant use within 48 hours or major surgery within 14 days; no renal adjustment.
• Tenecteplase 0.25 mg/kg intravenously as a single bolus over 5 to 10 seconds (maximum 25 mg), within 4.5 hours, with the same monitoring and contraindications as alteplase; no renal adjustment.
• Basilar occlusion: urgent thrombectomy assessment; it is considered with a severe deficit (NIHSS of 10 or more) within 12 hours of onset.
• Aspirin 300 mg orally once as a loading dose (300 mg rectally if swallowing is impaired), starting 24 hours after thrombolysis, then 75 mg orally once daily with food. Maximum 300 mg daily. Monitor bleeding, dyspepsia and full blood count. Avoid in active peptic ulcer, bleeding disorders, aspirin sensitive asthma and in children under 16 years; use caution when eGFR is under 10.
• Minor stroke or high risk TIA: add clopidogrel 300 mg orally once as a loading dose, then 75 mg orally once daily with aspirin for 21 days, then clopidogrel alone. Maximum 75 mg daily after loading. Monitor bleeding and full blood count. Avoid in active bleeding; use caution in severe hepatic impairment; reduced effect in CYP2C19 poor metabolisers; avoid omeprazole and esomeprazole; avoid in pregnancy unless clearly needed.
• Atorvastatin 80 mg orally once daily, long term. Maximum 80 mg daily. Monitor lipids at 4 to 12 weeks and ALT at baseline and if symptoms occur. No dose change in renal impairment; avoid in active liver disease; limit to 20 mg daily with clarithromycin; contraindicated in pregnancy and breastfeeding. Aim for LDL cholesterol under 1.8 mmol/L.
• Blood pressure under 130/80 mmHg long term; diabetes and smoking control; anticoagulation when a cardioembolic source is found.
• Vertebral dissection: antithrombotic therapy for 3 to 6 months.

Monitoring. Neurological observations and swallow checks in the first days; repeat imaging for deterioration; review at 3 months.

Referral and escalation. Stroke unit or intensive care when consciousness or breathing is affected; thrombectomy centre for basilar occlusion; speech and language therapy and rehabilitation.

Special groups. Older adults: high aspiration risk, so early swallowing assessment and nutrition. Young adults: look for dissection and cardiac or haematological causes.