• Sudden weakness or numbness, often on the left side of the body
• Slurred speech
• Facial weakness
• Double vision, abnormal eye movements, dizziness, imbalance
• Difficulty swallowing
• In severe cases, reduced consciousness or breathing problems

Right pontine infarct: treatment plan

1. Immediate assessment and stabilization

• Establish time last known well, NIHSS, glucose, oxygen saturation, temperature, ECG.
• ABCs, IV access, cardiac monitoring, frequent neurological observations.
• NPO until bedside swallow screening. If abnormal, speech and language assessment and appropriate enteral-feeding plan.
• Non-contrast CT head urgently to exclude hemorrhage, then MRI brain with DWI/ADC to confirm and define the pontine infarct.
• CT angiography or MR angiography from aortic arch to vertex to look for vertebral or basilar artery stenosis/occlusion or vertebral dissection. A normal early CT does not exclude a posterior-fossa infarct.

2. Reperfusion treatment if acute

• If disabling ischemic-stroke symptoms and within the appropriate window, assess urgently for IV thrombolysis with alteplase or tenecteplase, after exclusion criteria are reviewed.
• If CTA/MRA shows basilar artery occlusion, arrange immediate neurointerventional assessment for mechanical thrombectomy. Current AHA/ASA guidance recommends EVT within 24 hours in selected patients with basilar occlusion, NIHSS at least 10, mild established ischemic damage, and good pre-stroke function. See the 2026 AHA/ASA guideline.

3. Acute medical care

• Avoid hypoxia, hypotension, fever, and hypoglycemia.
• Manage BP according to whether thrombolysis/thrombectomy is being considered. Do not rapidly lower BP without a specific indication.
• DVT prevention: intermittent pneumatic compression; pharmacologic prophylaxis if safe.
• Manage aspiration risk, bladder retention, pressure injury risk, and early mobilization.
• Treat seizures only if present. Routine anticonvulsant prophylaxis is not standard.

4. Antithrombotic treatment

• Non-cardioembolic infarct: antiplatelet therapy, commonly aspirin.
• Minor non-cardioembolic stroke/high-risk TIA: short course dual antiplatelet therapy, usually aspirin plus clopidogrel, may be considered when bleeding risk is acceptable and guided by the stroke team.
• Atrial fibrillation or another cardioembolic source: oral anticoagulation is usually indicated, but timing depends on infarct size, neurological status, hemorrhagic transformation risk, and repeat imaging. Do not combine long-term anticoagulation with antiplatelets unless there is another clear indication.

5. Etiologic work-up and secondary prevention

• ECG/telemetry, echocardiography, and prolonged rhythm monitoring when appropriate to find atrial fibrillation or another embolic source.
• HbA1c, fasting lipid profile, CBC, renal function, electrolytes, coagulation profile.
• Evaluate for hypertension, diabetes, dyslipidemia, smoking, obstructive sleep apnea, and obesity.
• High-intensity statin unless contraindicated.
• Long-term BP, diabetes, lipid, diet, exercise, and smoking-cessation plan.
• PT, OT, speech/swallow therapy, and rehabilitation plan from early admission.

Differential diagnosis

A. Vascular causes most important to distinguish

1. Pontine hemorrhage
   CT head distinguishes this urgently. May cause coma, pinpoint pupils, quadriplegia, abnormal breathing.
2. Basilar artery thrombosis/occlusion
   May cause fluctuating deficits, dysarthria, diplopia, quadriparesis, reduced consciousness, or locked-in syndrome. Requires CTA/MRA urgently.
3. Vertebral artery dissection
   Especially with neck trauma/manipulation, sudden neck or occipital pain, younger age, or posterior circulation symptoms.
4. Other posterior-circulation ischemia
   Cerebellar infarct, medullary infarct, midbrain infarct, AICA/PICA territory syndromes.

B. Important stroke mimics

1. Hypoglycemia or severe hyperglycemia
   Check capillary glucose immediately.
2. Seizure with postictal (Todd) weakness
3. Vestibular neuritis or peripheral vertigo
   Usually causes vertigo but not clear focal long-tract signs, severe dysarthria, diplopia, limb weakness, or crossed sensory findings. A central HINTS examination by an experienced clinician may help in continuous acute vestibular syndrome.
4. Demyelination, such as multiple sclerosis
   Often subacute, may have prior episodes, and MRI pattern differs.
5. Brainstem tumor, metastasis, abscess, or inflammatory lesion
   More often progressive rather than abrupt, though hemorrhage into a lesion can be sudden.
6. Osmotic demyelination syndrome
   Consider after overly rapid correction of chronic hyponatremia. May cause dysarthria, dysphagia, quadriparesis, or altered consciousness.
7. Toxic-metabolic disorders
   Drug/sedative intoxication, Wernicke encephalopathy, electrolyte disturbances, encephalopathy.
8. Migraine with brainstem aura or functional neurological disorder
   Diagnoses of exclusion only after urgent vascular causes are assessed.

Clinical localization clue