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Cranial Nerve VI Palsies

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Title: Cranial Nerve VI Palsies

Author (s): Dan Jones, MSIV University of Utah

Photographer: Drawings done by David Morton, Ph.D.

Date: 10/15/20

Keywords/Main Subjects: Cranial Nerve Palsies, diplopia

The sixth cranial nerve, also known as the abducens nerve, innervates only one structure: the lateral rectus muscle of the eye. The function of this muscle is to abduct the eye, or in other words, move it laterally. It also coordinates with the medial rectus muscle, which moves the eye medially, to center the eye horizontally in the primary position (looking straight ahead) (Figure 1).

Figure 1. Extraocular muscle anatomy. The sixth cranial nerve innervates the lateral rectus muscle, which facilitates eye abduction.

Therefore, individuals with sixth nerve palsy are unable to properly abduct or center their affected eye(s), resulting in esotropia (and consequently, diplopia) that varies with gaze (Figure 2). While gazing towards the affected side, the affected eye is impaired to varying degrees depending on the severity of the palsy/paresis. In the primary position, the affected eye is often directed medially (esotropic) due to the unopposed tone of the medial rectus pulling the eye inward.

The primary presenting symptom of sixth nerve palsy is horizontal binocular diplopia—meaning double vision (diplopia), with the displaced images appearing side-by-side (horizontal), and only when both eyes are open (binocular). Furthermore, the image displacement is usually worse at a distance. Patients often compensate for sixth nerve palsies by turning their head towards the affected side, which minimizes utilization of the lateral rectus muscle, thereby alleviating their diplopia.  However, this compensatory head position doesn’t apply to patients with bilateral 6^th nerve palsies. These patients instead present with both eyes directed medially at rest, and worsening esotropia when gazing in either direction.

The most common etiologies of sixth nerve palsies are traumatic, congenital, neoplastic, and increased intracranial pressure (e.g. meningitis, idiopathic intracranial hypertension, intracranial tumors). The etiology may also be postviral in the pediatric patient, or ischemic in patients with diabetes and/or multiple vascular risk factors. The sixth nerve is especially vulnerable to increased intracranial pressure (ICP) due to its positioning between the brainstem and clivus in the subarachnoid space (Figure 3).

Figure 3. Course of the sixth cranial nerve. CN VI originates in the pons, courses up and over the clivus, over the cavernous sinus, and then enters the orbit via the superior orbital fissure. Sixth nerve palsies may be caused by a lesion or impingement anywhere along this path.

A careful history is essential in all cases of 6th nerve palsies.  New cases where there is not a clear traumatic, ischemic or post-viral etiology warrant neuro-imaging, the urgency of which should parallel the timing of onset. The treatment will depend on the underlying cause. Potential avenues include alternate patching, prism therapy, and strabismus surgery; however, spontaneous recovery is possible, even in traumatic etiologies, so watchful waiting is often a first step.

References:

1. Bienfang DC. (2017) Overview of diplopia. Wilterdink JL, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com (Accessed on June 20, 2018).
2. Brazis PW, Lee AG. (1999) Acquired binocular horizontal diplopia. Mayo Clin Proc. 74(9):907-16.
3. Lee AG, Brazis PW. (2017) Sixth cranial nerve (abducens nerve) palsy in children. Wilterdink JL, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com (Accessed on June 20, 2018).
4. Patel SV, Holmes JM, Hodge DO, Burke JP. (2005) Diabetes and hypertension in isolated sixth nerve palsy: a population-based study. Ophthalmology. 112(5):760-3.

Faculty Approval: Griffin Jardine, MD