Cranial Nerve VI Palsy Page 1 of 4

Cranial Nerve VI Palsy

aka Abducens Nerve Paresis

Anatomy:
Nucleus of CN VI located in the caudal pontine tegmentum, sending motor neurons supplying the lateral
rectus muscle of the ipsilateral eye;
- also internuclear neurons that project (via MLF) to medial rectus subdivision of contralateral oculomotor (CN
III) nucleus (ie lesion of nucleus causes ipsilateral horizontal gaze palsy)
- fibres of CN VII (facial nerve) hook around nucleus of CN VI (facial colliculus) before exiting
- nerve fascicles exit the pons anteriorly and course through subarachnoid space where it runs a vertical
(upward) course, along ventral surface of pons (confined by adjacent AICA)
- pierces dura overlying clivus, entering into Dorello's canal, contacting tip of petrous pyramid (part of temporal
bone; adjacent to mastoid air cells)
- enters the cavernous sinus after passing through the petroclinoid (Gruber's) ligament
- runs in body of sinus (rather than lateral wall where CN III, IV, V located) along foramen lacerum (near
internal carotid artery)
- enters orbit via superior orbital fissure and shortly thereafter pierces lateral rectus muscle

History:
Usually complain of double vision (diplopia) which should be binocular (ie. abolished by covering one eye)
and purely horizontal (ie two images side-by-side)
- typically worst when looking at objects at a distance and in direction of side of palsy
- may still have diplopia in primary position (unequal balance between medial & lateral recti)

Risk factors: ask about Hx of

- trauma
- immunosuppression
- alcohol abuse
- migraines

Associated symptoms:
- headache (new or worse)
- fever
- focal weakness or numbness
- loss of hearing or taste

Examination:
1. Pupils
- look for anisocoria (associated Horner's syndrome, CN III palsy)
2. Eyelids
- is there any ptosis?
- may be seen in myasthenia gravis
3. Extra-ocular movements:
- may be subtle but should see ophthalmoplegia with failure of full abduction (iris should bury itself into
palpebral fissure in corner of eye - no white of sclera still seen when look to side)
- differentiate from conjugate gaze palsy (both eyes conjugately fail to fully gaze to on side)
4. Other cranial nerves
- to localize the lesion, identify involvement of CN VII (often brainstem)
5. Meningismus

NB: not all patients with esotropia and abduction weakness have abducens nerve palsy
- can be mimiced by number of disease states:
DDx Pseudo-Sixth
1) Myasthenia
2) Restrictive disorders (w/ signs of orbital disease - proptosis, pain, redness) esp Grave's ophthalmopathy,
trauma, tumors & orbital pseudotumor
3) Spasm of the near reflex

Localization:

1. Congenital:
a. Birth injury to nerve
b. Mobius syndrome: congenital bulbar paralysis
c. Duane's retraction syndrome - 15% bilateral, where branches of oculomotor nerve innervate the lateral

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rectus, with absence of CN VI nucleus

- see retraction of globe on attempted adduction, due to co-contraction of ad/abductors

2. Nuclear:
- lesions will damage adduction also (ie conjugate horizontal gaze palsy) since neurons project via MLF to
contralateral CN III nucleus (medial rectus)
- proximity of CN VII (its fascicles loop around) means almost always see ipsilateral LMN (peripheral) facial
palsy
- may be due to intrinsic brainstem processes incl. infarcts, trauma, inflammation (eg demyelination),
infiltrative and compression from tumors or ICH (eg cavernoma)
- may be seen in Wernicke's encephalopathy, hepatic encephalopathy, ALS

3. Brainstem (injury to nerve fascicles):

- other nearby structures that may be involved incl. sympathetic fibres (Horner's syndrome), MLF (ipsilateral
INO, combined leading to one-and-a-half syndrome with only preserved contralateral abduction) and
pyramidal tracts (contralateral hemiparesis)
- occlusion of AICA damages the pontine tegmentum with ipsilateral abduction paresis (VI), facial paresis
(VII), Horner's, facial analgesia (V) and ipsilateral peripheral deafness (VIII) with loss of taste from anterior
two-thirds of tongue (IX) - rarely complete picture
- Millard-Gubler syndrome with CN VI, VII palsies and contralateral hemiparesis, with lesion in ventral
paramedian pons
- fascicular lesions also from tumor compression (eg pontine glioma in children), inflammation, infection,
demyelination

4. Subarachnoid Space:
- compressed by nearby vessels incl. AICA, PICA, basilar (esp if dolichoectatic or aneurysm)
- nerve stretched by downward displacement of brainstem (eg herniation posterior fossa mass, elevation in
ICP)
- nerve is tethered at exit from pons and in Dorello's canal so susceptible to stretch
- false localizing value in that any mass lesion or intracranial hypertension can lead to abducen palsy, even if
problem distant from nerve location (due to mass effect and distortion)
- raised ICP commonly causes uni- or bilateral CN VI palsies
- brainstem can also sag (with CN VI palsy) in intracranial hypotension (eg. CSF leak, post dural puncture)
- trauma from blunt head injury or neurosurgical procedure (iatrogenic)
- leptomeningeal disturbance incl. meningitis (bacterial, fungal, tuberculous) & neoplastic (carcinomatosis);
usually multiple CN involved +/- bilateral CN VI palsies (see below)
- idiopathic hypertrophic pachymeningitis
- sarcoidosis
- basal tumors impinging directly on the nerve (meningioma, chordoma)
- would not see isolated VI palsy from vestibular schwannoma but can occur with trigeminal schwannoma

5. Petrous Apex:
- close proximity of nerve in Dorello's canal to petrous tip makes it susceptible to pathology in petrous
temporal bone
- Gradenigo syndrome with CN VI palsy, ipsilateral facial pain (in trigeminal distribution), facial palsy +/-
decreased hearing (due to involvement of VI nerve, gasserian ganglion & facial nerve due to localized
inflammation at tip of petrous bone from mastoiditis)
NB: abducens palsy can occur 2-3 days after pain starts and meningitis can develop
- other lesions simulating similar presentation include ICA aneurysms in intrapetrosal segment, tumors,
thrombophlebitis of transverse sinus extending into inferior petrosal sinus or after ligation of jugular vein in
radical neck dissection
NB: similar VI palsy can occur with venous thrombosis and pseudotumor-like presentation due to false-
localizing raised ICP (but without other petrous apex features)
- nerve may be injured by basal skull fracture involving petrous bone
- lesion in sphenopalantine (pterygopalantine) fossa causes loss of tearing with irritation of eye on side of
abduction paresis and trigeminal sensory neuropathy in V2 distribution
=> often from malignant lesion (esp nasopharyngeal carcinoma) extending to skull base
- Cerebellopontine angle tumor can cause VI nerve paresis with other findings incl. decreased hearing, facial
palsy, trigeminal neuropathy, ataxia, papilledema

6. Cavernous Sinus: +/- superior orbital fissure

- rarely produces isolated CN VI palsy, usually see other signs (incl. ipsilateral Horner's +/- III, IV, V1 / V2
palsy, involvement of optic nerve / chiasm, pituitary gland)
- intracavernous aneurysms (dural fistula) or sinus thrombosis
- tumors (meningioma, mets, nasopharyngeal, Burkitt's lymphoma, pituitary adenoma +/- apoplexy)

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- trauma
- granulomatous inflammation ("Tolosa-Hunt", sarcoid, TB)
- ischemia to nerve (hypertension, diabetes, giant cell arteritis, SLE, migraine)
- inflammation from herpes zoster, sphenoid sinus abscess or idiopathic pachymeningitis

7. Orbit:
- uncommon due to very short course within orbit
- proptosis is usually present and may be accompanied by conjunctival congestion and chemosis
- may see optic nerve atrophy or edema (can be normal)
- any trigeminal signs limited to V1
- may be hard to distinguish between cranial nerve paresis (III, IV, VI) and mechanical restriction of globe in
these cases
- etiologies incl. tumor (local, mets), trauma, inflammatory 'pseudotumor', cellulitis
- also from injection of anesthetic solution in preparation for mandibular surgery

8. Unknown localization:
- transient isolated palsy esp in children, ? vascular or inflammatory / post-viral
- ophthalmoplegic migraine

Work-Up of Isolated CN VI Palsy:

- most common etiology of isolated abducens lesion is post-viral in children and ischemia / infarction (eg
diabetic) in adults
- not if clinical course chronic > 3 months
- if over age 45 with Hx of hypertension or diabetes, then no need to investigate for 3 months
- reasonable to check HbA1C, fasting glucose, hemoglobin, blood pressure, ESR, ANA, VDRL if no clear
etiology found in elderly person
- imaging should be done if age < 45 years, no vascular risk factors or following minor trauma
- also if progressive ophthalmoplegia, bilateral palsies, Hx of malignancy known or if no recovery after 3
months (also if other neurological deficits)
- vascular imaging if proptosis / chemosis looking for dural carotid-cavernous fistula or cavernous sinus
thrombosis
- examine CSF (also if systemic illness, immunocompr, bilateral, other CN deficits)
- 8-30% will remain cryptogenic after work-up

Course:
- most either spontaneously improve or have underlying lesion found
- ischemic palsies almost always recover completely in 2-4 months while some recovery seen in half of
traumatic cases (but take over one year)
- if no recovery over 3-6 months then suspect underlying lesion such as tumour
- few may have chronic isolated abducens palsy of unknown cause
=> follow regularly looking for emergency of new localizing signs and ensure adequate neuroimaging and
ENT evaluation
(may be due to insidious basal tumour vs. benign process)

* Suggest patching of one eye if helpful to the patient *

- alternate patching of eyes to prevent amblyopia in children under age 8
- prisms may be useful in some to achieve binocular single vision in primary position
- strabismus surgery only considered if no improvement after 8-10 months (consists of weaknening of
ipsilateral medial rectus or some type of vertical muscle transposition)
- chemodenervation of antagonist medial rectus muscle with botulinum toxin can be tried

Bilateral Abducens Palsies:

- NOT usually due to ischemic infarction of both nerves (! - rare of rostral pontine tegmentum)
- more often a meningeal process
- includes tumours such as clivus chordoma, nasopharyngeal carcinoma, pituitary adenoma with apoplexy;
trauma also
- leptomenigeal inflammation as with carcinomatosis, fungal meningiits, TB, Lyme disease, sarcoidosis,
syphilis
- Miller-Fischer syndrome (variant of Guillain-Barre syndrome) with areflexia and ataxia also
- Infections: Lyme, Syphilis, Fungal meningitis
- Wernicke's encephalopathy
- Intracranial hypertension or hypotension
- Ecstasy use (transient reported)
- always consider myasthenia gravis

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Reference:
Kline LB, Bajandas FJ. Neuro-Ophthalmology Review Manual. 4th ed.1996.
Miller NR, Newman NJ. Walsh & Hoyt's Clinical Neuro-Ophthalmolology, 5th edition. 1999

Last update: August 2004

Reviewed by: pending

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