π§ Note: Anatomical diagrams of the pons are often displayed inverted compared to radiological (CT/MRI) orientation β except as shown below.
This distinction is important when correlating anatomy with clinical findings or interpreting imaging.
π Introduction
- π©Έ Pontine strokes are most often lacunar infarcts due to occlusion of small penetrating arteries from the basilar trunk.
- π Common risk factors include age, hypertension, diabetes, and atherosclerosis.
- β οΈ Bilateral lesions are uncommon but can occur with basilar artery occlusion β potentially devastating with βlocked-inβ presentation.
𧬠Aetiology
- π― Usually small-vessel occlusion of penetrating branches of the basilar artery β unilateral pontine infarcts.
- π« Basilar occlusion at the origins of perforators β possible bilateral pontine infarction.
- π Shared risk factors with other small-vessel strokes: hypertension, diabetes, ageing, and lipohyalinosis.
- π« Large-vessel infarcts (basilar atherothrombosis, embolism) β wider territory infarction Β± coma.
- π§ Oedema near 4th ventricle may obstruct CSF flow β acute hydrocephalus requiring ventricular drainage.
π§© Clinical Features
- β‘ Contralateral hemiparesis or hemisensory loss β corticospinal and medial lemniscus involvement.
- π« No cortical signs (e.g., aphasia, neglect, hemianopia) β helps differentiate from cortical stroke.
- π Ipsilateral facial palsy (LMN type) β facial nucleus or fascicle lesion.
- π Diplopia or lateral gaze palsy β due to abducens (VI) nerve involvement.
- π Locked-in syndrome: Quadriplegia + anarthria but preserved consciousness and vertical eye movement.
- π Vertigo, nystagmus, ataxia β if cerebellar peduncles affected.
- π₯ Pyrexia & autonomic instability β involvement of reticular or hypothalamic pathways.
- π£οΈ Dysarthriaβclumsy hand syndrome or pure motor stroke presentations (lacunar syndromes).
- π Fluctuating symptoms β βpontine warning syndromeβ, similar to capsular warning episodes.
πΌοΈ Anatomical & Imaging Examples
π Pontine infarcts typically respect the midline and may extend posteriorly toward the cerebellum.
π§ͺ Investigations
- π©Έ Routine bloods: FBC, U&E, LFTs, glucose, lipid profile.
- π§ CT Β± CTA: To confirm acute stroke, rule out haemorrhage, and assess basilar patency.
- π§² MRI brain: More sensitive for small infarcts β DWI highlights acute ischaemia early.
- π MRA / CTA: Evaluate for vertebrobasilar stenosis or occlusion.
π©Ί Management
- π Reperfusion therapy: IV thrombolysis (within window) or thrombectomy for basilar occlusion β improves survival in selected patients.
- π₯ Stroke Unit care: Multidisciplinary monitoring, oxygenation, and early rehab initiation.
- π Antiplatelet: Aspirin 300 mg Β± Clopidogrel after imaging confirms ischaemia.
- βοΈ Risk factor control: Optimize BP, glucose, and address AF or dyslipidaemia.
- π§ Statins: Start high-intensity statin (e.g., atorvastatin 80 mg) for secondary prevention.
- π£οΈ Rehabilitation: Physiotherapy, occupational therapy, and speech therapy for motor/speech recovery and swallow safety.
π‘ Teaching tip:
Pontine strokes are often clinically silent or subtle initially but may deteriorate rapidly.
Always assess eye movements, facial symmetry, and bulbar function in any suspected brainstem event.
Locked-in syndrome is the hallmark of extensive bilateral pontine infarction β preserved awareness but paralysis below the eyes.