WEBINO Syndrome: Usual Clinical Manifestations
WEBINO (Wall-Eyed Bilateral Internuclear Ophthalmoplegia) syndrome presents with three cardinal features: bilateral adduction deficits, abduction nystagmus in both eyes, and large-angle exotropia in primary gaze position. 1, 2, 3
Core Ocular Motor Findings
The defining ocular manifestations include:
- Bilateral adduction impairment on horizontal gaze, meaning both eyes fail to move inward toward the nose when attempting lateral gaze 2, 4, 5
- Nystagmus of the abducting eye bilaterally—when each eye attempts to look outward, it develops rhythmic jerking movements 2, 4, 5
- Severe exotropia in primary gaze—the eyes are deviated outward (wall-eyed appearance) when looking straight ahead, which is the distinguishing feature from standard bilateral INO 1, 2, 3
- Deficiency or absence of convergence—inability to turn both eyes inward together 4
- Preserved vertical gaze—up and down eye movements remain intact 5
Anatomical Localization
The syndrome results from:
- Bilateral lesions of the medial longitudinal fasciculus (MLF) in the paramedian pontine or mesencephalic tegmentum 2, 3, 5
- Imbalance of the paramedian pontine reticular formation (PPRF) on both sides, which contributes to the exotropia 5
- Lesions may involve the pretectal area in some cases 2
Associated Neurological Features
Patients commonly present with additional findings:
- Sudden onset diplopia—the most common presenting complaint 2, 4, 3
- Gait ataxia—particularly when lesions extend beyond the MLF 2
- Spastic tetraparesis—in cases of demyelinating disease 5
- Cranial nerve palsies—including bilateral facial nerve involvement in MS cases 5
- Pseudobulbar palsy—in progressive demyelinating disease 5
Common Etiologies
The underlying causes vary by age and risk factors:
- Ischemic stroke—particularly in older patients with vascular risk factors, affecting the mesencephalic or pontine tegmentum 2, 3
- Multiple sclerosis—especially in younger patients with demyelinating lesions, can cause persistent WEBINO even in progressive stages 5
- Myasthenia gravis—a rare but important treatable cause that can mimic structural WEBINO 4
- Iatrogenic causes—including immunosuppressive medications like tacrolimus in transplant recipients 2
Critical Diagnostic Pitfall
The key distinguishing feature from simple bilateral INO is the large-angle exotropia in primary position—without this wall-eyed appearance, the diagnosis is bilateral INO rather than WEBINO syndrome. 1, 3 This exotropia results from the combination of bilateral MLF damage plus PPRF imbalance, creating unopposed lateral rectus tone. 5
Clinical Course Considerations
- Acute onset is typical with vascular etiologies, developing suddenly over minutes to hours 2, 3
- Persistent symptoms can occur with demyelinating disease, lasting months despite treatment 5
- Complete remission is possible with treatable causes like myasthenia gravis when appropriately managed with anticholinesterase therapy 4
- Partial improvement may occur with corticosteroid pulse therapy in demyelinating cases 5
The recognition of WEBINO requires identifying all three core features together—bilateral adduction deficits, bilateral abduction nystagmus, and primary gaze exotropia—as this constellation points to specific bilateral MLF pathology requiring urgent neuroimaging and etiologic workup. 2, 3