Is vertical diplopia caused by cranial nerve (CN) 3 dysfunction?

Vertical Diplopia and Cranial Nerve III

Yes, cranial nerve III (oculomotor nerve) dysfunction commonly causes vertical diplopia, along with other characteristic findings including ptosis, pupillary abnormalities, and impaired eye movements in multiple directions. 1

Why CN III Causes Vertical Diplopia

CN III innervates multiple extraocular muscles that control vertical eye movements, including the superior rectus (elevation), inferior rectus (depression), and inferior oblique (elevation and extorsion). 1 When CN III is damaged, the unopposed action of muscles innervated by other cranial nerves—particularly the lateral rectus (CN VI) and superior oblique (CN IV)—results in the characteristic "down and out" position of the affected eye, producing vertical misalignment and diplopia. 2

Key Clinical Features of CN III Palsy

Ptosis is a hallmark finding that helps distinguish CN III palsy from other causes of vertical diplopia. 2 The levator palpebrae superioris muscle, which elevates the upper eyelid, is specifically innervated by the superior division of CN III. 2 Complete ptosis may actually mask diplopia symptoms until the lid is manually elevated. 1

Pupil Involvement: A Critical Distinction

• Pupil-sparing CN III palsy (intact pupillary function with extraocular muscle weakness) typically suggests microvascular ischemia in patients with diabetes, hypertension, or hyperlipidemia. 1

• Pupil-involving CN III palsy (dilated, poorly reactive pupil) is a medical emergency requiring urgent neuroimaging with MRA or CTA to rule out posterior communicating artery aneurysm. 1

Important caveat: Even with pupil-sparing presentation, if there is partial extraocular muscle involvement or incomplete ptosis, you cannot assume microvascular etiology—a compressive lesion may present this way, and neuroimaging is recommended. 1

Other Causes of Vertical Diplopia to Consider

Superior Oblique Palsy (CN IV)

Superior oblique palsy is one of the most common causes of vertical strabismus in adults, with an annual incidence of 6.3 cases per 100,000 people. 1 Patients present with hypertropia that worsens in opposite lateral gaze and with head tilt to the same side (Parks-Bielschowsky three-step test). 1 Unlike CN III palsy, there is no ptosis. 2

Skew Deviation

Skew deviation is a vertical misalignment of prenuclear (brainstem) origin that can mimic CN III or CN IV palsy. 1, 3 Critical distinguishing feature: Skew deviation is more likely to improve with supine positioning compared to true cranial nerve palsies. 4 It is always accompanied by other neuro-ophthalmologic abnormalities and warrants neuroimaging for brainstem pathology including stroke, demyelination, tumor, or hemorrhage. 1, 3

Diagnostic Approach

When evaluating vertical diplopia:

1. Assess for ptosis: Present in CN III palsy, absent in CN IV palsy and skew deviation. 2

2. Check pupillary function: Pupil involvement in CN III palsy requires urgent vascular imaging. 1

3. Perform Parks-Bielschowsky three-step test: Helps identify superior oblique palsy. 1

4. Test supine vs. upright positioning: Improvement when supine suggests skew deviation over cranial nerve palsy. 4

5. Neuroimaging: MRI brain with contrast and dedicated cranial nerve sequences is preferred for non-traumatic presentations; include MRA or CTA when aneurysm is suspected. 1

Common Pitfalls

• Do not diagnose "partial CN III palsy" prematurely—consider skew deviation, thyroid eye disease, myasthenia gravis, and orbital pathology. 5

• Do not assume pupil-sparing means benign etiology if there is incomplete muscle involvement or ptosis. 1

• Do not confuse CN III palsy with CN VI palsy: CN VI causes horizontal diplopia only, with esotropia and no ptosis. 2