Immediate plan: stroke-unit / neurologist management

1. Urgent reassessment and monitoring
   • Admit or continue in a monitored stroke unit.
   • Serial NIHSS, consciousness, pupils, extraocular movements, limb power, dysphagia screen, glucose, oxygen saturation, temperature, and cardiac rhythm monitoring.
   • Keep NPO until a formal swallow screen. Dysarthria can coexist with unsafe swallowing and aspiration risk.
   • Urgently escalate if reduced consciousness, worsening diplopia/gaze deficit, new weakness, vomiting/headache, or respiratory compromise. Posterior circulation strokes may deteriorate despite a small initial lesion.
2. Confirm vascular anatomy and mechanism
   • Review DWI/ADC MRI and obtain/review CTA or MRA of head and neck, specifically vertebral arteries, basilar artery, posterior cerebral arteries, and perforator disease.
   • A small pontine lesion is often small-vessel disease, but vertebrobasilar atherosclerosis, dissection, cardioembolism, and basilar occlusion must be excluded. Small-vessel disease is the most common cause of paramedian pontine infarction, though large-vessel vertebrobasilar disease and cardiac embolism occur. Localization in Clinical Neurology, 8e, p. 937.
   • ECG, telemetry, echocardiography as indicated, lipid profile, HbA1c, CBC, electrolytes/renal function, coagulation testing, and vascular risk review.
3. Reperfusion decision depends on exact time last known well
   • If within 4.5 hours and deficit is disabling, assess immediately for IV thrombolysis eligibility. Diplopia/gaze palsy and dysarthria may be disabling even if the NIHSS is numerically low.
   • Current AHA/ASA guidance supports either tenecteplase 0.25 mg/kg IV bolus, maximum 25 mg, or alteplase 0.9 mg/kg, maximum 90 mg, for eligible patients in the standard window. This must be prescribed by the stroke team after excluding hemorrhage and contraindications. See the 2026 AHA/ASA pharmacotherapy summary.
   • If CTA/MRA shows basilar or other treatable large-vessel occlusion, discuss urgent mechanical thrombectomy with a neurointerventional stroke center. Do not assume that a “small pontine infarct” rules out a dangerous evolving posterior-circulation occlusion.
   • If onset is unknown or outside the usual window, advanced CT/MR perfusion and stroke-specialist assessment may identify selected patients for reperfusion treatment.
4. Antithrombotic treatment
   • If thrombolysis is not given and imaging excludes hemorrhage: start antiplatelet therapy promptly per local protocol, commonly aspirin.
   • If thrombolysis is given: do not give antiplatelet or anticoagulant for the first 24 hours; repeat brain imaging is generally obtained before starting it.
   • Short-course dual antiplatelet therapy may be appropriate for selected minor non-cardioembolic strokes, but should be individualized. It is not an automatic choice when symptoms are disabling, infarction is more than trivial, bleeding risk is elevated, or a cardioembolic source is found.
   • Anticoagulation is for a demonstrated indication such as atrial fibrillation, with timing decided by infarct size, hemorrhagic-transformation risk, and the stroke team. It is not routine acute treatment for a perforator pontine infarct.
5. Supportive and preventive management
   • Avoid hypotension, dehydration, fever, hypoxia, and hypo/hyperglycemia.
   • Blood pressure targets depend on whether thrombolysis/thrombectomy is being considered. Do not lower BP aggressively without a stroke-team target, because cerebral perfusion can worsen.
   • High-intensity statin unless contraindicated, with long-term LDL lowering tailored to vascular cause.
   • DVT prevention, early mobilization when safe, physiotherapy, speech and swallow therapy, occupational therapy.
   • Eye patching or temporary occlusion of one lens can reduce disabling diplopia initially. Formal neuro-ophthalmology/orthoptic review and prisms can be considered later if diplopia persists.

Interpreting the gaze finding

• Right horizontal conjugate gaze palsy: both eyes cannot look to the right. This fits a right abducens nucleus or PPRF lesion in the pons.
• Right internuclear ophthalmoplegia: impaired adduction of the right eye on left gaze, often with abducting nystagmus of the left eye. This suggests right MLF involvement.
• One-and-a-half syndrome: right gaze palsy plus impaired right-eye adduction on left gaze, caused by a lesion involving the right PPRF/abducens region and MLF.
• “Double vision in the left eye” needs clarification. Stroke-related diplopia is usually binocular and resolves when either eye is covered. True monocular diplopia persisting with the opposite eye covered is more often ocular, such as corneal, lens, or refractive pathology, and does not by itself localize to the pons.

Expected outcome

• Dysarthria and imbalance often improve over days to weeks with rehabilitation.
• Eye movement deficits and diplopia may improve over weeks to months, but can remain partially persistent.
• The first 24-72 hours require observation for neurological progression.
• Long-term outcome depends more on stroke mechanism, vessel imaging, dysphagia, motor deficits, and control of hypertension, diabetes, smoking, lipids, and atrial fibrillation than on the MRI lesion size alone.

High-risk monitoring changes

• New drowsiness, confusion, agitation, inability to stay awake
• Falling GCS or reduced responsiveness
• Coma

• Worsening or new gaze palsy, especially loss of horizontal eye movements
• New pupillary asymmetry, fixed/sluggish pupils, or abnormal light responses
• New ptosis, facial weakness, dysphagia, weak cough, dysphonia, or inability to handle secretions
• New bilateral facial or bulbar weakness

• New hemiparesis, especially progression from unilateral weakness to bilateral weakness
• Rapidly worsening arm/leg power
• New quadriparesis or quadriplegia
• New extensor plantar responses bilaterally

• Patient appears unresponsive or cannot speak/move limbs but may remain conscious.
• Ask them to look up/down or blink to command. Vertical eye movements and eyelid opening may be preserved even when horizontal eye movements, speech, and limb movement are lost.

• New irregular, shallow, or labored breathing
• Falling oxygen saturation without another explanation
• Apnea or need for escalating airway support
• Marked BP lability, unexplained bradycardia/tachycardia, or temperature dysregulation

• Repeated brief episodes of worsening dysarthria, diplopia, weakness, ataxia, vertigo, vomiting, or dysphagia
• Symptoms that worsen with low blood pressure, dehydration, or position change

Practical bedside monitoring

• Frequent neurological observations, including GCS/level of consciousness, pupils, eye movements, speech, facial symmetry, limb power, dysphagia/secretions, and NIHSS.
• Record whether diplopia is binocular and the direction in which gaze is limited.
• Continuous pulse oximetry and cardiac telemetry.
• Have a low threshold for neurocritical-care transfer if deficits fluctuate, consciousness declines, or airway protection becomes uncertain.