The trochlear nerve enters the wall of the cavernous sinus and lies between the oculomotor nerve and the ophthalmic division of the trigeminal nerve (see Figure­ 12-6).5,16 While in the sinus, the trochlear nerve sends sensory fibers (likely proprioceptive) to the ophthalmic nerve. It enters the orbit through the superior orbital fissure above the common tendinous ring, outside the muscle cone (see Figure 12-11). The trochlear nerve runs with the frontal nerve to the medial side of the orbit above the levator and superior rectus muscles and enters the upper surface of the superior oblique muscle.10

ABDUCENS NERVE: CRANIAL

NERVE VI

The abducens nerve innervates the lateral rectus muscle.

Abducens Nucleus

The abducens nucleus is located near the inferior dorsal midline of the pons beside the floor of the fourth ventricle (see Figure 12-8). The fibers from the nucleus pass through the pons and lie adjacent to the corticospinal tract for part of their path32; they exit in the groove between the pons and the medulla oblongata. The abducens nucleus also contains internuclear neurons that communicate with the nucleus for the contralateral medial rectus muscle in the oculomotor complex via the medial longitudinal fasciculus.36 This is the pathway for conjugate horizontal eye movements. This pathway receives information from higher CNS centers, including the paramedial pontine reticular formation, the cerebellum, and the vestibular nucleus. Thus coordinated movement of the ipsilateral lateral rectus muscle and the contralateral medial rectus muscle results in conjugate horizontal eye movement.36

Abducens Nerve Pathway

In its long, tortuous, intracranial course, the abducens nerve runs along the occipital bone at the base of the skull and up along the posterior slope of the petrous portion of the temporal bone, makes a sharp bend over the petrous ridge (see Figure 12-10), and enters the cavernous sinus.5,13,37 Within the sinus it lies near the lateral wall of the internal carotid artery6,38 (see Figure 12-6). Small sympathetic branches leave the internal carotid plexus and travel with the abducens nerve. The abducens carries these autonomic fibers and sensory fibers, which are possibly proprioceptive, to the ophthalmic division of the trigeminal nerve.38 The abducens nerve enters the orbit through the superior orbital

fissure within the common tendinous ring and innervates the lateral rectus muscle on the medial surface (see Figure­ 12-11).

SUPERIOR ORBITAL FISSURE

The trochlear, frontal, and lacrimal nerves as well as the superior ophthalmic vein are located in the superior orbital fissure above the muscle cone. The superior and inferior divisions of the oculomotor nerve, the abducens nerve, and the nasociliary nerve are located within the superior orbital fissure and the common tendinous ring. The inferior ophthalmic vein lies below the fissure and the tendinous ring (see Figure 8-15).

CONTROL OF EYE MOVEMENTS

Communication among areas of the CNS is necessary to produce controlled and coordinated eye movements. The corticonuclear tract contains fibers that travel from the cerebral hemispheres to the nuclei of CNs III, IV, and VI; the tectobulbar tract connects the superior colliculus to the CN III, IV, and VI nuclei. The medial longitudinal fasciculus extends from the midbrain into the spinal cord and connects the vestibular nucleus, the oculomotor nucleus, the abducens nucleus, and the trochlear nucleus, providing a connection between eye movement control and the vestibular apparatus (see Figure 12-8).

FACIAL NERVE: CRANIAL NERVE VII

The facial nerve has two roots: the large motor root innervates the facial muscles, and the smaller root contains sensory and parasympathetic fibers. The sensory fibers carry taste sensations from the tongue. The parasympathetic nerves supply secretomotor fibers to various glands of the face; those supplying the lacrimal gland are discussed in Chapter 14.

Facial Nucleus

The motor nucleus of the facial nerve is located in the reticular formation of the pons. The upper segment of the nucleus supplies the frontalis, procerus, corrugator superciliaris, and orbicularis muscles, and the lower segment supplies the remaining facial muscles.39,40

Facial Nerve Pathway

The fibers leave the facial nucleus, arch around the abducens nucleus, and emerge as the facial nerve from the brain stem at the lower border of the pons. The facial nerve enters the internal acoustic foramen in the petrous portion of the temporal bone and runs through a canal in the bone. While in the temporal bone, parasympathetic

Pons

Facial nucleus

Internal acoustic foramen

Stylomastoid foramen

Facial

nerve

FIGURE 12-12

Facial nerve pathway. Motor pathway of facial nerve to facial muscles of orbit.

Temporal nerve

Zygomatic nerve

fibers en route to the lacrimal gland are given off as the greater petrosal nerve.39,40 The motor fibers of the facial nerve emerge through the stylomastoid foramen, pass below the external auditory canal, travel over the mandibular ramus, and divide into several branches (Figure 12-12). The upper two — the temporal and zygomatic branches — supply the frontalis, procerus, corrugator, and orbicularis muscles.

The following Clinical Comments discuss damage to the cranial nerves, specifically the oculomotor, trochlear, and abducens nerves, caused by involvement of adjacent cranial and orbital structures and the resulting clinical presentation.

Clinical Comment: Cranial Nerve

Damage

Injury to sensory cranial nerve fibers results in anesthesia,

a loss of sensation in the innervated area. Injury to a cranial motor nerve causes either a partial loss (paresis) or a total loss (paralysis) of muscle function. Paresis or paralysis of an extraocular muscle can result in diplopia if the involvement is acquired; in congenital involvement, diplopia usually is

not a complaint because the brain has learned to disregard the double image, resulting in suppression.

Nerve fibers can be ischemic, damaged by a compromised blood supply caused by vascular diseases (e.g., hypertension, atherosclerosis, diabetes mellitus) or by space-occupying lesions (e.g., aneurysms, hemorrhages, tumors) that exert pressure on the nerve fibers. The location of the involvement will influence the presenting signs and symptoms.

In some studies of isolated extraocular muscle nerve paralysis, the sixth cranial nerve is reported to be affected most often, and the fourth cranial nerve affected least often.41-43 The tortuosity and length of the abducens nerve make it susceptible to compression and stretching injuries and may explain why it is damaged so frequently.16

A number of clinical signs and symptoms accompany damage to the motor nerves that innervate the extraocular­ muscles­ . Muscle paresis or paralysis will be evident in testing­ ocular motility (as described in Chapter 10). In acquired

extraocular muscle impairment, a patient often attempts to minimize diplopia by carrying the head in a compensatory position. If a horizontal deviation is present, the head will be turned to the right or left. With a vertical deviation, the head is raised or lowered, and if a torsional deviation occurs the head is tilted toward the shoulder usually away from the involved side.35 With right superior oblique involvement the head may be turned to the left, positioned down, and tilted toward the left shoulder44,45 (Figure 12-13).

FIGURE 12-13

Patient tilts head toward the left shoulder and turns head to the left and down, resulting from right superior oblique ­dysfunction. (From Eskridge JB: Evaluation and diagnosis of incomitant ocular deviations, J Am Optom Assoc 60[5]:378, 1989.)

Clinical Comment: Oculomotor

Damage

MIDBRAIN INVOLVEMENT 

A lesion in the midbrain can affect the entire oculomotor nucleus or selectively affect only some subnuclei; however, such selective damage is unusual.28 If the lesion affects the entire oculomotor nucleus, the muscles involved are the ipsilateral medial rectus, inferior rectus, and inferior

oblique, contralateral superior rectus, and both levators. The ipsilateral superior rectus might be involved as well because the decussating fibers pass through the contralateral superior rectus nucleus.28,32 Dilation of the pupil may also be present. The trochlear nucleus is near the oculomotor nucleus, and if it too is involved, the contralateral superior oblique muscle will be affected. The clinical presentation would show the ipsilateral eye positioned out in primary position and only able to move in as far as the midline. The contralateral eye would be unable to elevate in abduction and unable to depress in adduction.

INTRACRANIAL INVOLVEMENT

The oculomotor nerve lies near several blood vessels in its intracranial path and frequently is affected by an aneurysm of the posterior communicating artery.46An aneurysm of the superior cerebellar artery or the posterior cerebral artery could also impinge on the nerve, damaging fibers.

Once the oculomotor nerve exits the midbrain, all its fibers supply the ipsilateral eye, and the dysfunction is unilateral. Damage to the nerve results in ptosis because of levator muscle paralysis; in primary position, the eye is positioned out because of the unopposed action of the superior oblique and lateral rectus muscles (Figure 12-14, A and B). (Because the superior oblique muscle is unaffected, the eye also should be positioned down, but clinically this is not always evident.47) The eye cannot adduct (Figure 12-14, D) and,

in the abducted position, cannot move up or down (Figure 12-14, E and F).2 If injury involves the cerebral peduncles, a contralateral hemiparesis will be present.48 In paralysis of the iris sphincter and ciliary muscle, the pupil will be dilated, and accommodation will not occur.

Incomplete lesions of the oculomotor nerve are possible. In external ophthalmoplegia, the extraocular muscles are paralyzed and the intrinsic muscles (those to the iris sphincter and the ciliary muscle) are spared; in internal ophthalmoplegia the internal muscles are paralyzed and the extraocular muscles are spared. As the oculomotor nerve exits the midbrain, the parasympathetic fibers

are superficial, and as the nerve nears the orbit, the parasympathetic fibers move into the center of the nerve and therefore are better protected in compressive lesions. The parasympathetic fibers are often spared in ischemic lesions, accounting for normal pupillary responses usually seen with diabetic ophthalmoplegia.28,49-51 Third nerve palsies that include a dilated pupil are highly suspicious of a compressive lesion.

CAVERNOUS SINUS INVOLVEMENT

The lateral wall of the cavernous sinus contains the ­oculomotor nerve as well as the trochlear, ophthalmic, and maxillary nerves. A lesion that affects all these nerves would leave only the lateral rectus muscle still functioning. The eye would be positioned out in primary gaze and could move only from the lateral position to the midline. Anesthesia of the facial areas served by the ophthalmic and maxillary nerves would be present in addition to the impaired ocular motility.

ORBITAL INVOLVEMENT

Both divisions of the oculomotor nerve are located within the muscle cone, together with the abducens and nasociliary nerves. A retrobulbar tumor or inflammation

involving these nerves would leave only the superior oblique muscle functional. In primary position, the eye would be positioned downward and outward slightly and would

be fairly immobile. Corneal sensitivity could be decreased because of nasociliary nerve involvement.

ABERRANT REGENERATION OF THE OCULOMOTOR NERVE

After injury, the brain may attempt to repair a nerve, and some attempts may be misdirected, eliciting an unusual clinical presentation. Lid elevation might occur with downward gaze or adduction.32 Some cases even can involve pupil responses; fibers going to the inferior oblique may sprout branches that also innervate the sphincter, causing pupillary constriction on elevation. Fibers innervating the medial rectus may send sprouts that innervate the sphincter, causing miosis with adduction or convergence.

Clinical Comment: Trochlear

Damage

When the superior oblique muscle is affected by trochlear nerve damage, the eye is elevated in primary gaze and is unable to move down in the adducted position. The head may be tilted toward the opposite shoulder to compensate for the unopposed extortion of the inferior oblique muscle5

(see Figure 12-13). Under the age of 10 years, palsies involving the trochlear nerve are usually congenital, and between 21 and 40 years of age the usual cause is trauma; otherwise the palsy may be idiopathic.52-54

MIDBRAIN INVOLVEMENT

Damage to the trochlear nucleus will affect the ­contralateral superior oblique muscle. Because of the ­proximity of the oculomotor nucleus, a lesion could affect both cranial nerve nuclei, resulting in the clinical ­presentation just discussed.

INTRACRANIAL INVOLVEMENT

For the most part, the trochlear nerve follows the same path as the oculomotor nerve and is susceptible to the same ­injuries. Damage to the trochlear nerve affects the ­ipsilateral superior oblique muscle, causing the eye to be elevated in primary gaze and unable to move down in the adducted position (Figure 12-15).

CAVERNOUS SINUS INVOLVEMENT

A lesion in the lateral wall of the cavernous sinus could affect the trochlear nerve. It could also affect the

­oculomotor, ophthalmic, and maxillary nerves, causing the ­previously described clinical presentation.

ORBITAL INVOLVEMENT

The trochlear nerve lies above the muscle cone near the frontal nerve, and injury affecting both nerves could impair the superior oblique muscle, limiting depression in the adducted position. Decreased sensitivity of the areas of the skin and scalp innervated by the branches of the frontal nerve might be observed.

FIGURE 12-15

Fourth nerve palsy OS, limitation in downgaze when adducted. (From Kanski JJ: Clinical ophthalmology: a systematic approach, ed 5, Oxford, UK, 2003, Butterworth-Heinemann.)

Clinical Comment: Abducens

Damage

Damage to the abducens nerve results in paralysis of the lateral rectus muscle; because of the unopposed action by the medial rectus muscle, a convergent strabismus is

evident.55 The eye will be unable to abduct (Figure 12-16). The patient might try to compensate for the diplopia by turning the face toward the paralyzed side.5