What is the primary management approach for a patient with bilateral thalamic infarct presenting with vertical gaze palsy?

Management of Vertical Gaze Palsy in Bilateral Thalamic Infarct

The primary management approach for vertical gaze palsy in bilateral thalamic infarct is urgent neurological evaluation with neuroimaging to confirm the extent of midbrain-thalamic involvement, followed by acute stroke management and supportive care with prism correction for persistent diplopia. 1

Acute Phase Management

Immediate Neurological Assessment

• Perform urgent MRI brain imaging with high-resolution T2-weighted sequences of the brainstem to confirm bilateral thalamic infarction and assess for associated midbrain involvement 1, 2
• Complete neurological evaluation is essential as vertical gaze palsy from thalamic infarcts indicates involvement of paramedian territory and potential rostral midbrain tegmentum damage 3
• Assess both vertical saccades and smooth pursuit, vestibular eye movements, and horizontal gaze to distinguish supranuclear from nuclear causes 1
• Test for skew deviation (which occurs in approximately 45% of thalamic infarct cases with neuro-ophthalmologic manifestations) and head tilt to identify associated posterior fossa involvement 3

Acute Stroke Protocol

• Apply standard acute ischemic stroke management including consideration of thrombolysis if within appropriate time window and no contraindications exist 4
• Maintain cerebral perfusion pressure >60 mmHg through volume replacement and/or catecholamines if necessary 4
• Implement general intensive care measures including strict blood glucose control, treatment of hyperthermia, and early enteral nutrition 4
• Initiate anticoagulation or antiplatelet therapy based on stroke etiology (embolic vs thrombotic) 5

Symptomatic Management of Vertical Gaze Palsy

Diplopia Management

• For patients with symptomatic vertical diplopia, prism correction may be necessary for persistent deficits 1
• Small vertical deviations can be managed with prism glasses, though lateral incomitance may limit successful implementation 4
• Monitor patients closely as most oculomotor abnormalities from thalamic infarction resolve spontaneously within a few months 3

Prognostic Indicators

• Critical warning signs for permanent deficit include: no improvement within 3 months, combined upgaze and downgaze palsy, and involvement of the paramedian tegmentum of the rostral midbrain 3
• Approximately 18% of patients with oculomotor abnormalities from thalamic infarction develop permanent deficits 3
• Bilateral thalamic infarcts affecting paramedian territory (84.8% of cases with neuro-ophthalmologic features) carry higher risk of persistent vertical gaze abnormalities 3

Rehabilitation Phase

Functional Rehabilitation

• Initiate early rehabilitation already in the intensive care unit once the patient is stable 4
• Successful functional and vocational rehabilitation of vertical diplopia from central lesions is possible, though requires specialized neuro-ophthalmologic input 6
• Progressive mobilization should begin after resolution of acute phase and absence of signs of significant intracranial hypertension 4

Common Pitfalls to Avoid

• Do not assume benign etiology: Vertical gaze palsy is a specific indicator of central pathology requiring immediate investigation, even if the remainder of the neurological examination appears normal 2
• Do not delay imaging: High-resolution brainstem imaging is essential as standard CT may miss small thalamic-mesencephalic infarcts 1, 7
• Do not overlook vascular anatomy: Bilateral thalamic infarcts often result from occlusion of a single unpaired perforating artery (artery of Percheron) arising from one posterior cerebral artery 7
• Do not prematurely declare permanent deficit: Most vertical gaze abnormalities improve within 3 months; permanent deficits should only be considered if no improvement occurs after this timeframe 3