eMedicine Specialties > Ophthalmology > Extraocular Muscles

Abducens Nerve Palsy

Author: Michael P Ehrenhaus, MD, Director, Department of Cornea, External Disease & Refractive Surgery, Assistant Professor, Department of Ophthalmology, State University of New York Downstate Medical Center
Coauthor(s): Mohammedyusuf E Hajee, MD, Clinical Instructor, Staff Physician, Department of Ophthalmology, Director, Blood Flow Laboratory, State University of New York-Downstate Medical Center; Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Contributor Information and Disclosures

Updated: May 21, 2009

Introduction

Background

Cranial nerve VI, also known as the abducens nerve, innervates the ipsilateral lateral rectus (LR), which functions to abduct the ipsilateral eye. It has the longest subarachnoid course of all the cranial nerves; therefore, its syndromes are similar to those of the fourth nerve because of their long intracranial courses. The sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth ventricle and just lateral to the medial longitudinal fasciculus (MLF). About 40% of its neurons project into the ipsilateral MLF only to cross over to the contralateral side and ascend to innervate that contralateral medial rectus subnucleus to participate in contralateral eye adduction.1,2,3

Patients usually present with binocular horizontal diplopia (double vision producing a side-by-side image with both eyes open) and esotropia in primary gaze. The deviation, as would be expected, is noted to be greater when the patient fixates with the paretic eye at distance. Patients also may present with a head-turn to maintain binocularity and binocular fusion and to minimize diplopia.

It is rare to find true congenital sixth nerve palsy. A typical workup of a sixth nerve palsy involves excluding paresis of other cranial nerves (including VII and VIII), checking ocular muscle motility, and evaluating pupillary responsiveness. Checking deep tendon reflexes (DTRs) and motor function to exclude corticospinal tract involvement also is important. MRI is indicated for any brainstem findings to exclude pontine glioma in children (most have papilledema and nystagmus without other cranial nerve involvement) and in adults who show no improvement.

In young adults, a lumbar puncture (LP) for cerebrospinal fluid (CSF) analysis is completed to exclude meningitis in patients who have no history of diabetes or hypertension and who have a head CT scan negative for other pathology. Elderly patients should have blood testing for an erythrocyte sedimentation rate (ESR) and/or a C-reactive protein to screen for giant cell arteritis (also known as temporal arteritis or cranial arteritis). Poor or no resolution should prompt a full neurologic evaluation and a consideration of other possible diagnoses (eg, congenital esotropia, Möbius syndrome, Duane syndrome).

Pathophysiology

Only the ipsilateral lateral rectus that is solely innervated by the involved peripheral sixth cranial nerve is affected; therefore, only deviations in the horizontal plane are produced. In isolated cases of peripheral nerve lesions, no vertical or torsional deviations are present. Central nervous system lesions of the abducens nerve tract are localized easily secondary to the typical findings associated with each kind of lesion. Damage to the sixth nerve nucleus results in an ipsilateral gaze palsy. The lack of a contralateral adduction defect makes it easy to differentiate a nuclear lesion from a fascicular or nonnuclear lesion.2

Abducens nerve palsy is frequently seen as a postviral syndrome in younger patients and as an ischemic mononeuropathy in the adult population.

Frequency

United States

Sixth nerve palsies fall into the following categories: 8-30% idiopathic, 10-30% miscellaneous, 3-30% trauma, 0-6% aneurysm, and 0-36% ischemic.

The sixth cranial nerve is the most commonly affected of the ocular motor nerves. In children, it is the second most common after the fourth nerve, with an incidence of 2.5 cases per 100,000 in the population.

Mortality/Morbidity

A young patient should have an aggressive workup because of the greater likelihood of a neoplasm causing the palsy. Patients older than 40 years require a less aggressive workup because of the greater likelihood of the etiology being more benign in nature (eg, ischemic mononeuropathy, vasculopathy).

Age

Cranial nerve VI palsy can occur in all age groups; however, the etiology varies depending on the age group.

Clinical

History

Clinical history includes the following:

  • Esotropia
  • Head-turn
  • Binocular diplopia (worse at distance)
  • Vision loss
  • Pain
  • Hearing loss
  • Symptoms of vasculitis, particularly giant cell arteritis
  • Trauma

Physical

Physical findings include the following:

  • An esodeviation that increases on ipsilateral gaze and is often greater at a distance
  • An isolated abduction deficit
  • Slowed ipsilateral saccades
  • Papilledema (if increased intracranial pressure)
  • Nystagmus (usually in children, ie, secondary to pontine glioma)
  • Otitis media
  • Orbital wall fracture
  • Tender, enlarged, nonpulsatile temporal arteries in giant cell arteritis

Causes

Not all abduction deficits are cranial nerve VI palsies. Mimickers are orbital lesions, medial wall fractures, Duane syndrome, thyroid disease, and myasthenia gravis.4

  • Elevated intracranial pressure can result in downward displacement of the brainstem, causing stretching of the sixth nerve secondary to its anatomic location within the Dorello canal. This is believed to be the reason that about 30% of patients with pseudotumor cerebri have an isolated abducens nerve palsy.
  • Subarachnoid space lesions can be causes of abducens nerve palsy (eg, hemorrhage, infection, inflammation, space-occupying tumor, cavernous sinus mass). Inflammatory (eg, postviral, demyelinating, sarcoid, giant cell arteritis)
  • Vascular
  • Metabolic (eg, vitamin B, Wernicke-Korsakoff syndrome)
  • Neoplasm (children) - Pontine glioma
  • Infectious (eg, Lyme disease, syphilis)
  • Congenital absence of the sixth nerve (eg, Duane syndrome)5
  • Trauma, particularly if it results in a torsional head motion6,7,8,9
  • Post–lumbar tap10

More on Abducens Nerve Palsy

Overview: Abducens Nerve Palsy
Differential Diagnoses & Workup: Abducens Nerve Palsy
Treatment & Medication: Abducens Nerve Palsy
Follow-up: Abducens Nerve Palsy
References

References

  1. Evans NM. Ophthalmology. 2nd ed. Oxford University Press Inc; 1995.

  2. Kline LB, Bajandas FJ. Neuro-ophthalmology Review Manual. 3rd ed. University of Alabama, Birmingham; 1988.

  3. Yanoff M, Duker JS. Ophthalmology. Mosby International Ltd; 1999.

  4. Ayberk G, Ozveren MF, Yildirim T, et al. Review of a series with abducens nerve palsy. Turk Neurosurg. Oct 2008;18(4):366-73. [Medline].

  5. Denis D, Dauletbekov D, Girard N. Duane retraction syndrome: Type II with severe abducens nerve hypoplasia on magnetic resonance imaging. J AAPOS. Feb 2008;12(1):91-3. [Medline].

  6. Calisaneller T, Ozdemir O, Altinors N. Posttraumatic acute bilateral abducens nerve palsy in a child. Childs Nerv Syst. Jul 2006;22(7):726-8. [Medline].

  7. Dwarakanath S, Gopal S, Venkataramana NK. Post-traumatic bilateral abducens nerve palsy. Neurol India. Jun 2006;54(2):221-2. [Medline].

  8. Kurbanyan K, Lessell S. Intracranial hypotension and abducens palsy following upper spinal manipulation. Br J Ophthalmol. Jan 2008;92(1):153-5. [Medline].

  9. Hanu-Cernat LM, Hall T. Late onset of abducens palsy after Le Fort I maxillary osteotomy. Br J Oral Maxillofac Surg. Dec 16 2008;[Medline].

  10. Anwar S, Nalla S, Fernando DJ. Abducens nerve palsy as a complication of lumbar puncture. Eur J Intern Med. Dec 2008;19(8):636-7. [Medline].

  11. Rhee DJ, Pyfer MF. The Wills Eye Manual: Office and Emergency Room diagnosis and treatment of eye disease. Lippincott Williams & Wilkins; 1999.

Further Reading

Keywords

abducens nerve palsy, sixth nerve palsy, VI nerve palsy, 6th nerve palsy, cranial nerve VI palsy

Contributor Information and Disclosures

Author

Michael P Ehrenhaus, MD, Director, Department of Cornea, External Disease & Refractive Surgery, Assistant Professor, Department of Ophthalmology, State University of New York Downstate Medical Center
Michael P Ehrenhaus, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and Contact Lens Association of Ophthalmologists
Disclosure: Nothing to disclose.

Coauthor(s)

Mohammedyusuf E Hajee, MD, Clinical Instructor, Staff Physician, Department of Ophthalmology, Director, Blood Flow Laboratory, State University of New York-Downstate Medical Center
Mohammedyusuf E Hajee, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, and National Medical Association
Disclosure: Nothing to disclose.

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Brian R Younge, MD, Professor of Ophthalmology, Mayo Clinic School of Medicine
Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

James P Gills, MD, Founder, St Luke's Cataract and Laser Institute; Professor, Department of Ophthalmology, University of South Florida College of Medicine
James P Gills, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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