What is the appropriate management for acute double vision?

Management of Acute Double Vision

Acute double vision requires immediate risk stratification to identify life-threatening causes, with same-day urgent neuroimaging (MRI brain and orbits with contrast) mandated for red flags including pupil involvement, severe headache, associated neurologic deficits, bilateral sixth nerve involvement, or progressive symptoms. 1, 2

Immediate Risk Assessment

The first critical step is distinguishing binocular from monocular diplopia by having the patient cover each eye separately—binocular diplopia (resolves when either eye is covered) indicates ocular misalignment and neurologic causes, while monocular diplopia (persists with opposite eye covered) suggests ocular pathology requiring ophthalmologic management. 3, 4

Red Flags Requiring Emergency Evaluation

Patients with any of the following must be sent immediately to an emergency department affiliated with a certified stroke center: 5

• Pupil-involving third nerve palsy (requires urgent evaluation to exclude aneurysm or compressive lesion) 1, 2
• Severe headache with temporal tenderness or jaw claudication (suspect giant cell arteritis—initiate high-dose corticosteroids immediately to prevent vision loss in the fellow eye) 5, 6
• Multiple cranial nerve palsies (suggests extensive brainstem involvement) 1
• Associated posterior circulation symptoms including vertigo, ataxia, or dysarthria (suggests brainstem stroke) 1, 6
• Bilateral sixth nerve involvement (raises concern for increased intracranial pressure or meningeal process) 1, 2
• Progressive symptoms or failure to respond to treatment 1

Diagnostic Imaging Strategy

MRI brain and orbits with contrast is the examination of choice for evaluating acute diplopia, providing superior detection of brainstem lesions, demyelinating plaques, and posterior circulation pathology compared to CT. 1, 2 CT should only be used when concern exists for ferrous-metallic foreign body, orbital fracture is suspected, or immediate imaging is needed and MRI is not rapidly available—but if CT is initially negative and clinical suspicion remains high, proceed to MRI as CT scans can miss posterior fossa pathology. 6, 2

Essential Clinical Examination

Perform a detailed sensorimotor examination including: 2

• Cover-uncover testing to detect ocular misalignment
• Assessment of versions, ductions, saccades, pursuit, and vergence
• Pupillary examination (pupil-sparing versus pupil-involving third nerve palsy has vastly different implications) 2
• Testing for internuclear ophthalmoplegia (INO) pattern (impaired adduction with contralateral abduction nystagmus—most common in multiple sclerosis) 1
• Forced duction and forced generation testing to distinguish mechanical restriction from paresis 2

Common Etiologies by Pattern

Sixth Nerve Palsy (Most Common Cranial Neuropathy)

Presents with horizontal diplopia worse at distance and in lateral gaze toward the affected side. 5, 1 The majority of acute sixth nerve palsies in adults are vasculopathic (associated with diabetes and hypertension), with most resolving within 6 months and about one-third within 8 weeks. 5 However, if no recovery is apparent by 6 months, approximately 40% demonstrate serious underlying pathology warranting further evaluation. 5, 2

Internuclear Ophthalmoplegia

In patients with multiple sclerosis presenting with new onset diplopia, INO from a demyelinating lesion in the medial longitudinal fasciculus is the most likely cause. 1 Failure to identify the INO pattern may delay MS diagnosis. 1

Skew Deviation

Lesions in the rostral pons and midbrain result in contralateral hypotropia and head tilt, whereas abnormalities in the vestibular periphery, medulla, and more caudal pons result in ipsilateral hypotropia and head tilt. 5 Vertical diplopia from skew deviation is more likely to improve with supine positioning than that caused by trochlear nerve palsies. 4

Management Algorithm

For Acute Presentation with Red Flags:

1. Send immediately to emergency department affiliated with certified stroke center with a note indicating "Ocular TIA" or "Ocular Stroke"—call ahead to warn them "a stroke patient is on the way." 5
2. Initiate high-dose corticosteroids immediately if giant cell arteritis is suspected (based on age >50, temporal tenderness, jaw claudication, elevated ESR/CRP) to prevent vision loss. 5, 6
3. Obtain urgent MRI brain and orbits with contrast 1, 2
4. Refer to neurology or neuro-ophthalmology for comprehensive evaluation 1, 2

For Stable Diplopia Without Red Flags:

1. Fresnel or ground-in prisms provide temporary relief while awaiting recovery 2
2. Eye patching eliminates diplopia but removes binocular vision 1, 2
3. Monitor for 6 months before considering definitive interventions 5, 2
4. Botulinum toxin or strabismus surgery may be considered for persistent cases after 6 months if no recovery occurs 1, 6, 2

For Patients with Multiple Sclerosis:

High-dose corticosteroids for acute MS relapses causing diplopia (though be aware of potential adverse effects including central serous retinopathy), with referral to neurology for MS disease-modifying therapy optimization. 1

Critical Pitfalls to Avoid

• Do not assume vasculopathic sixth nerve palsy without considering other etiologies—in MS patients, demyelinating etiology requires different management. 1
• Do not rely on CT imaging for brainstem pathology—MRI is essential for detecting demyelinating lesions and posterior circulation strokes. 1, 6
• Do not assume BPPV when double vision is present with dizziness—BPPV does not cause diplopia, and coexisting diplopia suggests central pathology requiring immediate neuroimaging. 6
• Do not delay evaluation in elderly patients—consider sagging eye syndrome presenting as divergence insufficiency esotropia with mild ptosis and deep superior lid sulcus defect. 2
• Do not perform further testing yourself before referring patients with acute retinal arterial ischemia—immediate referral to stroke center takes priority. 5