Bilateral Pontine Infarction due to Basilar Artery Thrombosis

Bilateral pontine infarction is a catastrophic posterior-circulation stroke pattern most often caused by thrombosis or embolic occlusion of the basilar artery. The pons is a “high-density” structure: tiny lesions can interrupt long tracts (corticospinal, corticobulbar, spinothalamic), cranial nerve nuclei, and the reticular activating system, so presentations range from mild dysarthria to coma or locked-in syndrome. Clinically, the key is to recognise a brainstem syndrome early, obtain urgent vascular imaging (CTA/MRA), and activate reperfusion pathways because basilar occlusion has a very poor natural history without recanalisation.

🧭 Why the Pons is Vulnerable: Vascular Anatomy

The basilar artery forms from the vertebral arteries at the pontomedullary junction and runs along the ventral pons to bifurcate into the posterior cerebral arteries. It supplies the pons through multiple small branches with limited collateral “forgiveness,” so occlusion can produce bilateral infarction. Bilateral pontine infarction classically reflects compromise of the paramedian perforators that supply the medial pons on both sides, but larger basilar clots can also compromise circumferential branches and cerebellar arteries (AICA/SCA), producing mixed pontine–cerebellar infarcts.

• Paramedian pontine perforators: small penetrating arteries from the basilar trunk supplying the medial basis pontis and tegmentum; bilateral involvement can interrupt corticospinal/corticobulbar tracts and medial tegmental structures.
• Short circumferential branches: supply lateral pons; involvement adds facial weakness, abducens involvement, sensory deficits, and ataxia depending on level.
• Long circumferential branches (including contributions from AICA/SCA territories): can add cerebellar signs (vertigo, nystagmus, dysmetria) and hearing symptoms if AICA territory is involved.

🧬 Pathophysiology: From Basilar Thrombosis to Bilateral Pontine Infarcts

Basilar occlusion may be embolic (e.g., cardioembolism) or thrombotic on an atherosclerotic plaque (often with underlying intracranial atherosclerotic disease). The pons is vulnerable because its perforators are end-arteries; when flow drops, oxygen delivery fails, ATP-dependent pumps collapse, and neurons depolarise, triggering glutamate excitotoxicity, intracellular calcium influx, cytotoxic oedema, and ultimately infarction. Clinically, this translates into rapidly evolving deficits: a patient may fluctuate for hours with transient brainstem ischaemic symptoms (“herald” TIAs) before sudden deterioration when the basilar occludes completely or collateral flow fails.

• Embolic BAO: abrupt onset, severe deficit, often less prodrome; source may be AF, mural thrombus, valvular disease.
• Thrombotic BAO: may have stuttering/stepwise course, vertebrobasilar TIAs, and risk factors for intracranial atherosclerosis.
• Penumbra concept applies: a time-sensitive zone of hypoperfused but salvageable tissue may exist; reperfusion therapies aim to restore flow before irreversible injury.

Pontine anatomy - upside down compared to Imaging

🚨 Clinical Presentation: Red Flags for Brainstem Stroke

Basilar thrombosis can present deceptively. Early symptoms may be “non-specific” (vertigo, nausea, imbalance, visual blurring) and mistaken for peripheral vestibular disease, migraine, intoxication, or functional symptoms. The clue is usually a mismatch: severe gait unsteadiness, focal cranial nerve signs, or evolving consciousness change. Bilateral pontine involvement often produces bilateral long-tract signs plus cranial nerve findings, with deterioration that can be sudden.

• Early/“herald” symptoms: transient vertigo, diplopia, dysarthria, drop attacks, transient weakness/numbness, visual disturbance.
• Cranial nerve signs: diplopia (VI palsy), facial weakness (VII), dysphagia/dysarthria, abnormal pupils or gaze palsies depending on level.
• Long-tract signs: bilateral weakness, hyperreflexia, extensor plantars; sensory loss can be bilateral or crossed depending on tract involvement.
• Consciousness/respiration: reduced consciousness suggests involvement of reticular activating system or widespread brainstem dysfunction; respiratory pattern changes can be a late ominous sign.
• Locked-in syndrome: quadriplegia and anarthria with preserved awareness; classically preserved vertical eye movements and blinking (if midbrain pathways spared).

🧠 Bedside Pattern Recognition: “Bilateral Pons” Syndromic Thinking

When both sides of the ventral pons are affected, corticospinal and corticobulbar disruption dominates: bilateral weakness, dysarthria, and pseudobulbar features can occur. If tegmental structures are involved, you add gaze palsies, altered consciousness, and sensory tract involvement. The key bedside habit is to actively look for central signs in “dizzy” patients: direction-changing nystagmus, skew deviation, abnormal head impulse test (often normal in central causes), new limb ataxia, or cranial nerve palsy.

• Medial (paramedian) involvement: dense weakness, dysarthria, internuclear pathways/gaze issues depending on level.
• Lateral involvement: facial weakness, gaze palsy, sensory loss, ataxia, vestibular symptoms.
• Mixed pontine–cerebellar features: vertigo and ataxia plus cranial nerve/long-tract signs should raise BAO suspicion urgently.

🩻 Imaging Strategy in Suspected Basilar Occlusion

Non-contrast CT can be normal early in posterior circulation stroke, so do not let a “normal CT head” falsely reassure you if the clinical story screams brainstem. The critical test is vascular imaging (CTA head/neck or MRA) to confirm basilar occlusion and define anatomy for thrombectomy planning. MRI (especially DWI) is highly sensitive for acute infarction and can help with prognosis and selection, but should not delay reperfusion decisions if CTA confirms treatable occlusion and the patient is within a suitable time window.

• CT head (NCCT): rules out haemorrhage; early posterior fossa ischaemia can be subtle.
• CTA head/neck: rapid confirmation of BAO; assesses vertebral disease and clot location/length.
• MRI DWI: detects pontine infarcts early; helps delineate core vs potentially salvageable tissue (where locally used).
• Perfusion imaging: sometimes used in extended windows to estimate salvageable tissue, depending on local protocols.

⏱️ Hyperacute Management (UK-style pathway)

Treat suspected basilar thrombosis as a time-critical emergency equivalent to anterior large-vessel occlusion. Stabilise airway and breathing early because reduced consciousness, bulbar dysfunction, and aspiration risk are common; involve critical care early if there is any threat to airway protection. Run parallel processes: rapid neurological assessment, glucose check, urgent CT/CTA, and immediate discussion with the nearest thrombectomy-capable neuroscience centre. Even if onset time is unclear, posterior circulation strokes may have treatable windows, and many networks will consider thrombectomy based on imaging and clinical severity.

• Immediate priorities: ABCDE, oxygenation/ventilation, treat hypoglycaemia, manage seizures, aspiration precautions.
• Blood pressure: avoid precipitous drops; manage according to thrombolysis/thrombectomy protocols if reperfusion planned.
• Antiplatelets/anticoagulants: do not give empiric anticoagulation “for BAO” before imaging; timing depends on reperfusion therapy and haemorrhage risk.
• Early senior escalation: stroke consultant + interventional neuroradiology discussion as soon as BAO is suspected.

💉 Intravenous Thrombolysis (IVT)

If the patient is eligible and within the licensed/accepted time window, IV thrombolysis should be given promptly after haemorrhage is excluded, even if thrombectomy is being pursued (“bridging therapy”), unless contraindications exist. In BAO, IVT alone may recanalise smaller clots but is less reliable for large clot burdens; nevertheless, early IVT can improve early reperfusion chances and should not be delayed by transfer logistics. Practical UK point: give IVT where you are (if a thrombolysis site) and transfer urgently for EVT when indicated.

• When to consider: disabling posterior-circulation deficit with imaging excluding haemorrhage and no contraindications.
• Bridge to EVT: IVT plus EVT is commonly favoured when both are suitable and timely.

🧲 Endovascular Thrombectomy (EVT) for Basilar Artery Occlusion

Randomised evidence for basilar thrombectomy matured substantially in recent years, supporting EVT in appropriately selected patients, including some beyond the traditional 6-hour window. Trials such as ATTENTION (within 12 hours) and BAOCHE (6–24 hours) demonstrated improved functional outcomes compared with best medical therapy in selected BAO patients, albeit with procedural risks and higher rates of intracranial haemorrhage in some analyses. Modern European guidance provides structured recommendations for BAO management, including the role of combined IVT+EVT when eligible, and technical considerations for the endovascular approach.

• Core principle: confirm BAO on CTA/MRA, then treat eligible patients with EVT as quickly as possible.
• Time windows: many centres consider EVT up to 24 hours in selected BAO patients, guided by severity and imaging (local criteria apply).
• Selection factors: neurological severity, pre-stroke function, infarct core burden on imaging, presence of salvageable tissue, comorbidity and procedural feasibility.
• Technique notes: aspiration vs stent-retriever strategies vary; rescue angioplasty/stenting may be considered if severe underlying basilar stenosis prevents durable recanalisation.

🫁 Critical Care and Complications in Bilateral Pontine Infarction

Bilateral pontine infarction often requires high-dependency or intensive care because bulbar dysfunction and reduced consciousness predispose to aspiration, respiratory failure, and pneumonia. Brainstem strokes can also produce autonomic instability, impaired cough, secretion retention, and difficulty weaning ventilation. Neurologically, watch for early malignant progression (expanding infarction and oedema in the posterior fossa), and for complications of immobility such as DVT/PE, pressure injury, and severe spasticity.

• Airway protection: early swallow screening; low threshold for NG feeding; consider intubation if airway reflexes are impaired.
• Aspiration pneumonia: common; prevent with positioning, secretion management, and early MDT swallowing input.
• Dysautonomia: BP and HR instability can occur; manage in monitored setting.
• Communication in locked-in: establish reliable eye-coded communication early; involve SLT and neurorehab teams.

🧾 Aetiology Work-up (After the Hyperacute Phase)

Once stabilised, the work-up targets the embolic vs atherosclerotic mechanism because secondary prevention differs. Cardioembolism is common (especially AF), but intracranial vertebrobasilar atherosclerosis is also an important cause of BAO. Assess heart rhythm and structure, large artery disease in vertebral and basilar segments, and less common causes (dissection, vasculitis, prothrombotic states) guided by age and context.

• ECG and prolonged rhythm monitoring: detect AF/paroxysmal AF.
• Echocardiography: structural sources (LV thrombus, valvular disease) where indicated.
• Vascular imaging: vertebral origin stenosis, basilar stenosis, tandem lesions.
• Bloods: lipids, HbA1c, inflammatory markers if vasculitis suspected; targeted thrombophilia testing if appropriate.

🛡️ Secondary Prevention (UK Context)

Secondary prevention after BAO mirrors other ischaemic strokes but mechanism matters: anticoagulation for AF-related stroke, antiplatelet therapy for non-cardioembolic mechanisms, and aggressive vascular risk factor control for intracranial atherosclerosis. High-intensity statin therapy, BP optimisation, smoking cessation, diabetes management, and lifestyle interventions are core. If EVT involved stenting/angioplasty, antithrombotic regimens follow neurointerventional protocols and haemorrhage risk assessment.

• AF/cardioembolic: anticoagulation when safe (timing depends on infarct size and haemorrhage risk).
• Non-cardioembolic: antiplatelet therapy; dual antiplatelets may be used short-term in selected minor stroke/TIA contexts per local policy.
• Risk factors: statin, BP control, smoking cessation, exercise/weight, diabetes optimisation.
• Rehab: early neurorehab referral; focus on swallowing, communication, mobility, spasticity, mood and cognition.

📈 Prognosis and Rehabilitation

Without recanalisation, basilar occlusion carries high mortality and severe disability risk; successful reperfusion is the major modifiable determinant of outcome. Even with bilateral pontine infarction, meaningful recovery is possible in selected patients, especially when consciousness is preserved and early complications are prevented. Prognosis depends on infarct burden (especially dorsal tegmental involvement), time to reperfusion, collateral flow, age, and premorbid function. Rehabilitation should be intensive and multidisciplinary: swallowing and nutrition, respiratory physiotherapy, communication strategies (particularly for locked-in), prevention of contractures, and long-term psychological support for patients and families.

• Major outcome driver: degree and speed of recanalisation.
• Complication prevention: aspiration, infection, DVT/PE, pressure injury, depression/delirium.
• Locked-in: early assistive communication and neurorehab planning are crucial; avoid diagnostic nihilism.

🔍 Differential Diagnosis (Don’t-Miss Mimics)

Not every “collapsed, dizzy, dysarthric” patient has BAO, but BAO is the one you cannot afford to miss. Consider pontine haemorrhage (CT usually diagnostic), metabolic/toxic states, Wernicke’s encephalopathy, demyelination, brainstem encephalitis, Guillain–Barré (can mimic locked-in with areflexia), myasthenia crisis, and severe peripheral vestibular syndromes. The discriminator is focal brainstem signs plus a central oculomotor pattern, and the definitive discriminator is CTA/MRA showing basilar patency or occlusion.

• Pontine haemorrhage: abrupt coma, pinpoint pupils; CT shows bleed.
• GBS: progressive weakness, areflexia; sensation often preserved; no focal cranial nerve pattern like BAO.
• Myasthenia crisis: fatigable weakness, ptosis, bulbar symptoms; normal imaging and reflexes usually preserved.
• Wernicke: confusion, ataxia, ophthalmoplegia; treat immediately with IV thiamine.