Abducens Nerve Palsy

Abducens Nerve Palsy

Clinical Anatomy

The abducens nucleus lies just lateral to the midline of the pons at its junction with the medulla. The genu of the facial nerve passes close to its dorsal and lateral surface. The medial longitudinal fasciculus is just medial to the nucleus. There are two cell populations in the abducens nucleus: Motor neurons of the abducens nerve and interneurons of the contralateral medial longitudinal fasciculus that pass to the medial rectus subnucleus of the contralateral third nerve nucleus. The fascicular portion of the abducens nerve courses ventrally through the pons. Structures near the fascicle include the motor nucleus and fascicle of the facial nerve, the motor nucleus of the trigeminal nerve, the spinal tract and nucleus of the trigeminal nerve, the superior olivary nucleus, the central tegmental tract, and the corticospinal tract.

The extra-axial portion of the sixth nerve turns rostral along the base of the pons lateral to the basilar artery. The nerve ascends through the subarachnoid space along the clivus and penetrates the dura about 1 cm below the crest of the petrous bone. It then passes under the petroclinoid ligament to enter the cavernous sinus. Within the cavernous sinus, the abducens nerve is not situated within the lateral wall, as are the oculomotor and trochlear nerves, but it lies in the body of the sinus close to the carotid artery. The sixth nerve enters the orbit through the superior orbital fissure within the annulus of Zinn, adjacent to the lateral rectus muscle. The nerve ramifies in the posterior orbit, and its branches enter the lateral rectus muscle diffusely. The classic notion is that the vulnerability of the abducens nerve is attributable to its long intracranial course.215

Because the abducens nerve is about one third the length of the trochlear nerve, however, its vulnerability probably results from other structural and vascular relationships.215 A sixth nerve nuclear lesion paralyze ipsilateral horizontal gaze, because cell bodies of lateral rectus motoneurons and medial longitudinal fasciculus (MLF) interneurons are juxtaposed in the nucleus.373 Because these lesions usually have some spillover to involve the adjacent abducens nerve, these patients often have concurrent esotropia. Brainstem lesions involving the sixth nerve frequently damage nearby structures, and some localizing syndromes have been named. A large dorsal pontine lesion can produce a horizontal gaze palsy with a variable combination of other signs, including ipsilateral facial palsy, analgesia of the face, peripheral deafness, and loss of taste from the anterior two thirds of the tongue (Foville syndrome). A ventral pontine lesion involving the pyramidal bundles and tegmentum can produce lateral rectus weakness with or without ipsilateral facial paralysis, and contralateral hemiplegia (Millard–Gubler syndrome).369

The sixth nerve is particularly vulnerable to traumatic, inflammatory, or compressive injury as it leaves the pons and passes vertically through the subarachnoid space to enter the dura overlying the clivus. Blunt trauma may injure the sixth nerve at this point, as may a clivus chordoma or petrous ridge tumor.127,227,466,494,536,560,613 Basilar meningitis preferentially affects the subarachnoid portion of the abducens nerve. After entering the cavernous sinus, the abducens nerve is especially prone to damage from intracavernous lesions because of its location in the body of the sinus next to the carotid artery, although intracavernous tumors and aneurysms are more rare in children than in adults.281,404 Abducens palsies from cavernous sinus lesions may not be distinguishable from those caused by superior orbital fissure lesions, as associated cranial neuropathies are similar in both cases. Sympathetic fibers have been demonstrated to leave the carotid plexus and join the abducens nerve in the posterior cavernous sinus.425 The coexistence of a sixth nerve palsy and an ipsilateral Horner syndrome localizes a lesion to the cavernous sinus.202

Clinical Features

Because the sixth nerve innervates only the lateral rectus muscle, the sole action of which is to abduct the eye, the clinical features of a sixth nerve palsy are more straightforward than those of oculomotor or trochlear nerve palsies. Children with an acute sixth nerve palsy present either with a head turn toward the side of the lesion or with a horizontally noncomitant esotropia that increases in gaze toward the affected eye and decreases or disappears in gaze away from the affected eye. The esodeviation is usually greater at distance than at near fixation. It is also greater when the child fixates with the paretic eye. Infants and children with sixth nerve palsy who avoid looking into their diplopic field of gaze may appear to have a gaze palsy.28 Examining versions with the child’s head in its neutral position or spinning an infant to stimulate the vestibulo-ocular reflex should reveal the noncomitancy of the deviation.

A child with an acute complete sixth nerve palsy has about 35 prism diopters of esotropia when fixating with the nonparetic eye at near. In the recovery phase, a significant esotropia may persist despite almost full recovery of abduction. This could result from a residual imbalance in the ratio of phasic to tonic lateral rectus innervation from secondary medial rectus contracture, or from decompensation of a preexisting esophoria. Small sixth nerve palsies can unleash small physiologic hyperphorias, which persist with head tilt to either side in patients with peripheral lesions, and switch sides with head tilt to either side in central lesions.604