What causes vertical gaze palsy in an anterior opercular (AOP) infarct?

Vertical Gaze Palsy in Midbrain Infarction

Vertical gaze palsy occurs with anterior opercular (AOP) infarcts due to interruption of vertical gaze pathways in the rostral midbrain, specifically affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and interstitial nucleus of Cajal (INC), where fibers controlling vertical eye movements decussate—creating a functionally bilateral deficit from an anatomically unilateral lesion. 1, 2

Anatomical Basis

The mechanism involves a critical anatomical principle: a single unilateral paramedian midbrain lesion can interrupt vertical gaze pathways both before and immediately after they cross the midline, producing bilateral vertical gaze dysfunction despite the stroke being on only one side. 2

Key Structures Affected

• Rostral interstitial nucleus of the MLF (riMLF): Controls vertical saccades and is essential for both upward and downward gaze 1
• Interstitial nucleus of Cajal (INC): Involved in vertical gaze holding and vestibular-mediated vertical eye movements 1
• Posterior commissure (PC): When involved, typically causes isolated upgaze palsy, though vertical gaze palsy can occur even when the PC is spared 1
• Descending fibers to inferior rectus and superior oblique subnuclei: Interruption after decussation contributes to the vertical gaze deficit 3

Clinical Patterns

Spectrum of Presentations

Unilateral midbrain infarcts can produce several distinct patterns of vertical gaze dysfunction 2:

• Isolated conjugate upgaze palsy (most common pattern) 2
• Combined upgaze and downgaze palsy (complete bidirectional vertical gaze palsy) 1, 2
• Vertical "one-and-a-half" syndrome: Conjugate upgaze palsy plus monocular depression palsy in the ipsilateral eye 3, 4
• Monocular elevation palsy 2

Associated Features

Patients may present with additional findings that help localize the lesion 4:

• Horizontal gaze abnormalities when the lesion extends to affect corticofugal and colliculofugal fibers 4
• Skew deviation with contralateral hypotropia and head tilt when rostral pons/midbrain structures are involved 5, 6
• Preserved horizontal oculocephalic movements distinguish supranuclear from nuclear/infranuclear causes 3

Temporal Course

Vertical gaze palsy from unilateral midbrain infarction may be transient, appearing in the hyperacute stage and resolving within days. 7 This occurs because:

• Initial bilateral functional impairment results from mild edema affecting both sides despite unilateral infarction 7
• Recovery can occur as early as 4 days post-onset 7
• The transient nature means this finding may be missed unless careful examination is performed immediately after stroke onset 7

Diagnostic Approach

Imaging Requirements

MRI of the brain with high-resolution T2-weighted images of the brainstem is essential to confirm midbrain lesions causing vertical gaze abnormalities. 5, 8 Specifically:

• MRI is superior to CT for detecting acute midbrain infarction 5
• T2-weighted sequences best demonstrate the paramedian thalamo-mesencephalic lesions 7
• Small field-of-view imaging of the brainstem may be needed to visualize the riMLF and INC 5

Clinical Examination

The examination must assess both vertical saccades and smooth pursuit, vestibular eye movements (oculocephalic maneuvers), and horizontal gaze to distinguish supranuclear from nuclear causes. 3, 1 Key findings include:

• Complete loss of vertical saccades, smooth pursuit, and vestibular-mediated vertical movements indicates riMLF/INC involvement 1
• Preserved horizontal gaze confirms the vertical-specific nature of the deficit 3
• Testing for skew deviation and head tilt helps identify associated posterior fossa involvement 5, 6

Management Considerations

Patients with vertical gaze palsy following stroke require urgent neurological evaluation and neuroimaging to identify the extent of midbrain involvement and guide acute stroke management. 6 Treatment priorities include:

• Addressing the underlying ischemic stroke with appropriate acute interventions 6
• Monitoring for progression, as initial transient deficits may indicate evolving infarction 7
• Referral to neuro-ophthalmology for specialized assessment and management of persistent diplopia 6

Prognosis

Many patients experience spontaneous recovery of vertical gaze function, particularly when the deficit is transient and related to perilesional edema rather than permanent tissue destruction. 7 However, persistent deficits may require:

• Prism correction for diplopia management 5
• Surgical intervention in select cases with persistent symptomatic vertical misalignment 5

Critical Clinical Pearls

The presence of vertical gaze palsy with a unilateral midbrain lesion does not indicate bilateral infarction—it reflects the unique anatomy where vertical gaze pathways decussate in the rostral midbrain, making a single strategic lesion functionally equivalent to bilateral damage. 1, 2 This distinguishes it from horizontal gaze palsies, which typically require bilateral lesions or specific pontine involvement to produce conjugate deficits.