The Cranial Nerves (Organization of the Central Nervous System) Part 4

Cranial Nerves of the Pons and Midbrain Associated With the Control of Eye Movements

Abducens Nerve (Cranial Nerve VI)

Components: GSE. The abducens nerve is a pure motor nerve whose principal function is to move the eye laterally (i.e., abduct the eye). The cell bodies of origin of the abducens nerve lie in the abducens nucleus in the dorsomedial aspect of the posterior pons. The axons pass ventrally and exit the brain in a medial position at the pons-medulla border. The abducens nerve courses ventrally into the cavernous sinus and exits the skull through the superior orbital fissure, as do CN IV and III. Peripherally, the fibers innervate the lateral rectus muscle on the ipsilateral side (Fig. 14-10). Stimulation of the abducens nerve results in a contraction of the lateral rectus muscle and causes the eye to be moved laterally.

Clinical Disorders. A peripheral or central lesion involving the abducens nucleus produces paralysis of the lateral rec-tus muscle. This results in medial strabismus, which is the inability for both eyes to be focused on the same object. This is due to the fact that the affected eye cannot abduct and that the affected eye will tend to lay medially when looking forward. The resulting effect is double vision. To eliminate the double vision, the patient moves his or her head so that the affected eye is facing the object directly, while the unaffected eye then compensates for a change in position of the object in the visual field. The function of this nerve is tested by asking the patient to focus on an object that is placed in the lateral aspect of his or her visual field without moving his or her head. Because the affected eye cannot move beyond the midline of the visual field as a result of the unopposed action of the medial rec-tus muscle, the patient (with the normal eye closed) will be unable to identify the object located in the lateral aspect of his or her visual field, and the disorder is thus easily identified.


Trochlear Nerve (Cranial Nerve IV)

Components: GSE. The trochlear nerve is unique in that it is the only nerve that exits the brain dorsally and is also crossed. The cell bodies lie in a medial position just below the midbrain periaqueductal gray (PAG) at the level of the inferior colliculus in proximity to the medial longitudinal fasciculus ([MLF] Fig. 14-11). The fibers pass dorsally and caudally, cross over to the contralateral side, and emerge from the brain just behind the inferior colliculus. The fibers continue anteriorly and enter the cavernous sinus. These fibers enter the orbit through the superior orbital fissure and supply the superior oblique muscle. The primary action of this muscle is to move the eye downward when it is located in a medial position. Clinical Disorders. When there is a paralysis of the trochlear nerve, there is an outward rotation of the eye due to the unopposed action of the inferior oblique muscle. Therefore, when these patients attempt to look downward and inward, such as when walking down a staircase, they experience double vision and will tend to fall down. Patients will frequently compensate for this double vision by tilting their heads. Tilting of the head upon downward gaze thus provides a clue of the presence of a trochlear lesion. Clinically, one could test for fourth nerve lesions by asking patients to follow an object as it is moved downward within their medial fields of vision without moving their heads. Again, failure to do so would indicate the likelihood of a fourth nerve lesion.

Origin and distribution of cranial nerves (CN) VI, IV, and III, which innervate extraocular eye muscles. The focus of the upper part of this figure includes the abducens nerve (CN VI) and the general somatic efferent component of the oculomotor nerve (CN III), which are essential for horizontal gaze. The lower part of this figure depicts the muscles of the eye and their relationship with CN III, IV, and VI.

FIGURE 14-10 Origin and distribution of cranial nerves (CN) VI, IV, and III, which innervate extraocular eye muscles. The focus of the upper part of this figure includes the abducens nerve (CN VI) and the general somatic efferent component of the oculomotor nerve (CN III), which are essential for horizontal gaze. The lower part of this figure depicts the muscles of the eye and their relationship with CN III, IV, and VI.

Origin and distribution of the trochlear nerve (cranial nerve IV) to the superior oblique muscle. As indicated in the cross section of the brainstem, note that this nerve exits the brain from the dorsal aspect, and it is the only nerve that is crossed. Arrow indicates direction of movement of the bulb downward and inward.

FIGURE 14-11 Origin and distribution of the trochlear nerve (cranial nerve IV) to the superior oblique muscle. As indicated in the cross section of the brainstem, note that this nerve exits the brain from the dorsal aspect, and it is the only nerve that is crossed. Arrow indicates direction of movement of the bulb downward and inward.

Diagram illustrating the direction of actions of the extraocular muscles of the eye (indicated by arrows). The lateral rectus muscle is innervated by the abducens nerve, the superior oblique muscle is innervated by the trochlear nerve, and the remaining muscles are innervated by the oculomotor nerve.

FIGURE 14-12 Diagram illustrating the direction of actions of the extraocular muscles of the eye (indicated by arrows). The lateral rectus muscle is innervated by the abducens nerve, the superior oblique muscle is innervated by the trochlear nerve, and the remaining muscles are innervated by the oculomotor nerve.

Oculomotor Nerve (Cranial Nerve III)

Components: GSE, GVE. The oculomotor nerve controls both skeletal and smooth muscles (via a postganglionic neuron). The GSE component of the third nerve provides innervation to all of the extraocular eye muscles (skeletal muscle) except for the lateral rectus and superior oblique muscles (Fig. 14-12). The GVE component provides pre-ganglionic parasympathetic innervation to the pupillary constrictor and ciliary muscles (smooth muscle) through connections with postganglionic parasympathetic neurons in the ciliary ganglion.

GSE: Origin, Distribution, and Function. The oculomotor nucleus is located in a medial position just below the floor of the midbrain periaqueductal gray at the level of the superior colliculus (see Fig. 12-6). The nucleus actually consists of a group of subnuclei, each of which gives rise to axons that innervate skeletal muscle or the ciliary ganglion. The nerve fibers pass ventrally in the medial aspect of the mid-brain, exit the brain medial to the cerebral peduncle, pass through the interpeduncular fossa, enter the cavernous sinus, and then enter the orbit through the superior orbital fissure. The GSE component of the oculomotor nerve supplies the superior, medial, and inferior rectus muscles as well as the inferior oblique and levator palpebrae superior muscles. The action of the medial rectus muscle is to move the eye medially; the superior and inferior rectus muscles move the eye up and down, respectively; the inferior oblique muscle elevates the eye when it is in the medial position; and the levator palpebrae superior muscle elevates the upper eyelid.

GVE Component. As described earlier, the cells that give rise to the GVE component of the oculomotor nerve, called the Edinger-Westphal nucleus, are located close to the GSE component and are situated around the midline (Figs. 14-13 and 14-14). Fibers from the Edinger-Westphal nucleus, which constitute preganglionic parasympathetic neurons, project to the ciliary ganglion. Postganglionic parasympathetic fibers from the ciliary ganglion then innervate the pupillary constrictor muscles and the ciliary muscles. Note that the pupillary dilator muscles of the eye receive their innervation from postganglionic sympathetic fibers that arise from the superior cervical (sympathetic) ganglion.

Origin and distribution of the oculomotor nerve (cranial nerve [CN] III). The anatomical organization of the general somatic efferent (GSE) cell columns of the oculomotor nerve (CN III) complex, whose axons innervate all of the extraocular eye muscles except the lateral rectus and superior oblique muscles, is shown; the Edinger-Westphal nucleus, whose axons (general visceral efferent) serve as preganglionic parasympathetic neurons, innervate the ciliary ganglia. The postganglionic parasympathetic neurons from the ciliary ganglia (not shown in figure) innervate the constrictor muscles of the pupil and the ciliary muscle.

FIGURE 14-13 Origin and distribution of the oculomotor nerve (cranial nerve [CN] III). The anatomical organization of the general somatic efferent (GSE) cell columns of the oculomotor nerve (CN III) complex, whose axons innervate all of the extraocular eye muscles except the lateral rectus and superior oblique muscles, is shown; the Edinger-Westphal nucleus, whose axons (general visceral efferent) serve as preganglionic parasympathetic neurons, innervate the ciliary ganglia. The postganglionic parasympathetic neurons from the ciliary ganglia (not shown in figure) innervate the constrictor muscles of the pupil and the ciliary muscle.

Contraction of the pupillary constrictor muscles results in a constriction of the size of the pupil. Likewise, constriction of the ciliary muscles causes a release of tension from the suspensory ligament of the lens, thus causing it to bulge (i.e., increase its curvature). Accordingly, the GVE component of the oculomotor nerve is capable of regulating both the size of the pupil (i.e., the amount of light that enters the eye) and the shape of the lens.

Diagram illustrating the anatomical substrates underlying conscious and unconscious regulation of conjugate gaze and the vestibular-ocular reflex. (A) Several of the key relationships revealing the connections between the cerebral cortex and the pontine gaze center as well as the linkage between cranial nerves (CN) VI and III are shown. Concerning conscious regulation of conjugate gaze, this process originates from the frontal lobe, where axons project to the contralateral horizontal gaze center (1). In this manner, activation of the left frontal eye field will result in movement of the eyes to the right because of excitation of the right abducens and left oculomotor nucleus. Involuntary regulation of conjugate gaze begins in part in the occipital cortex and projects bilaterally to CN III (2). The pontine gaze center projects ipsilaterally to CN VI and contralat-erally to CN III (3). The connections of CN III (4) to the medial rectus muscle and CN VI to the lateral rectus muscle (5) are also indicated.

FIGURE 14-14 Diagram illustrating the anatomical substrates underlying conscious and unconscious regulation of conjugate gaze and the vestibular-ocular reflex. (A) Several of the key relationships revealing the connections between the cerebral cortex and the pontine gaze center as well as the linkage between cranial nerves (CN) VI and III are shown. Concerning conscious regulation of conjugate gaze, this process originates from the frontal lobe, where axons project to the contralateral horizontal gaze center (1). In this manner, activation of the left frontal eye field will result in movement of the eyes to the right because of excitation of the right abducens and left oculomotor nucleus. Involuntary regulation of conjugate gaze begins in part in the occipital cortex and projects bilaterally to CN III (2). The pontine gaze center projects ipsilaterally to CN VI and contralat-erally to CN III (3). The connections of CN III (4) to the medial rectus muscle and CN VI to the lateral rectus muscle (5) are also indicated.

(B) This diagram illustrates other important relationships essential for conjugate gaze and the regulation of the vestibular-ocular reflex. An essential element in this relationship includes vestibular inputs to vestibular nuclei (6). Vestibular nuclei project to the ipsilateral cranial nerve (CN) VI, which is inhibitory, and to the contralateral CN VI, which is excitatory (3). Projections from CN VI to the contralateral CN III are also excitatory (7). The medial longitudinal fasciculus contains fibers passing from vestibular nuclei and the pontine gaze center to CN VI and III as well as fibers passing from CN VI to the contralateral CN III. To illustrate how these relationships function, assume that the head is rotated to the left. The net result is that the eyes are rotated to the right. In order for this to be achieved, there must be contraction of the right lateral rectus and left medial rectus muscles. Activation of these muscles is induced by initial activation of vestibular nerve fibers originating from the left horizontal semicircular canal, which project to vestibular nuclei. Projections from left vestibular nuclei to the right abducens nucleus are excitatory, causing contraction of the lateral rectus muscle of the right eye. Because the projection from the right abducens nucleus to the left oculomotor nucleus is also excitatory, activation of the right abducens nucleus results in excitation of the left medial rectus muscle. Because the projection from the left vestibular nucleus to the ipsilateral (left) abducens nucleus is inhibitory, the left lateral rectus muscle will have a greater tendency not to contract; likewise, the excitatory projection from the left abducens nucleus to the right oculomotor nucleus would not be activated because of the inhibitory input from the vestibular nuclei; therefore, reducing the likelihood of excitation of the right medial rectus muscle.

FIGURE 14-14 (B) This diagram illustrates other important relationships essential for conjugate gaze and the regulation of the vestibular-ocular reflex. An essential element in this relationship includes vestibular inputs to vestibular nuclei (6). Vestibular nuclei project to the ipsilateral cranial nerve (CN) VI, which is inhibitory, and to the contralateral CN VI, which is excitatory (3). Projections from CN VI to the contralateral CN III are also excitatory (7). The medial longitudinal fasciculus contains fibers passing from vestibular nuclei and the pontine gaze center to CN VI and III as well as fibers passing from CN VI to the contralateral CN III. To illustrate how these relationships function, assume that the head is rotated to the left. The net result is that the eyes are rotated to the right. In order for this to be achieved, there must be contraction of the right lateral rectus and left medial rectus muscles. Activation of these muscles is induced by initial activation of vestibular nerve fibers originating from the left horizontal semicircular canal, which project to vestibular nuclei. Projections from left vestibular nuclei to the right abducens nucleus are excitatory, causing contraction of the lateral rectus muscle of the right eye. Because the projection from the right abducens nucleus to the left oculomotor nucleus is also excitatory, activation of the right abducens nucleus results in excitation of the left medial rectus muscle. Because the projection from the left vestibular nucleus to the ipsilateral (left) abducens nucleus is inhibitory, the left lateral rectus muscle will have a greater tendency not to contract; likewise, the excitatory projection from the left abducens nucleus to the right oculomotor nucleus would not be activated because of the inhibitory input from the vestibular nuclei; therefore, reducing the likelihood of excitation of the right medial rectus muscle.

In this reflex, light shown into one eye results in a constriction of the pupil in both eyes. Constriction of the pupil in the same eye that received the light is called the direct light reflex, and the constriction in the other eye is called the consensual light reflex. The pathway for this reflex involves afferent signals passing in the optic nerve and optic tract whose fibers terminate, in part, in the pretectal region. Fibers from the pretectal region innervate the oculomotor nucleus bilaterally (Fig. 14-15A). When the oculomotor nucleus on each side is stimulated, impulses are transmitted along the preganglionic neurons to the pupillary constrictor muscles on each side via postganglionic neurons in the ciliary ganglion.

The pathways mediating (A) the pupillary light and (B) accommodation reflexes.

FIGURE 14-15 The pathways mediating (A) the pupillary light and (B) accommodation reflexes.

A second reflex is called the accommodation reflex (Fig. 14-15B). This reflex occurs when an individual attempts to focus on a near object after looking at more distant objects. The responses that occur include:

(1) pupillary constriction; (2) medial convergence of the eyes by the simultaneous actions of medial recti muscles; and (3) focusing of the eyes on the near object, which requires contraction of the ciliary muscles, causing the suspensory ligament to relax and the lens to bulge. This reflex occurs by the activation of the following pathways: (1) descending cortical fibers from the occipital cortex to the oculomotor complex via a synapse in the pretectal region;

(2) activation of both somatic motor fibers that cause the medial rectus muscle on each side to contract; and

(3) activation of the visceral motor neurons that stimulate the ciliary ganglion, resulting in both pupillary constriction and a bulging of the lens, which allows the light rays to properly focus on the near object.

Clinical Disorders. Lesions involving the third nerve can affect both GSE and GVE components. Concerning the GSE component, lesions will produce lower motor neuron paralysis of the extraocular eye muscles supplied by this nerve. The most common forms of deficits include: (1) the inability to move the eye inward or vertically (because of the loss of all of the recti muscles, except the lateral rectus muscle, as well as the loss of the inferior oblique muscle); (2) lateral strabismus, in which the eye on one side is now not coordinated with the opposite eye whose extraocular eye muscles are intact, causing diplopia (double vision); and (3) drooping of the eyelid (called ptosis), which results from damage to the nerves innervating the levator palpe-brae superior muscle.

Lesions of the GVE components will produce the following autonomic effects: (1) loss of the pupillary light reflex; and (2) accommodation, which includes the convergence reactions. It is also possible that, as a result of a lesion, the pupil will remain small, but pupillary constriction will be brisk during accommodation. This disorder results from syphilis and is referred to as the Argyll Robertson pupil, but the locus of the lesion for this disorder remains unknown.

If lesions involving the third nerve are located within the CNS rather than peripherally, it is likely that a constellation of deficits will be present. The most typical case involves a lesion located near the ventromedial aspect of the midbrain. Such a lesion i nvariably affects both fibers of the third nerve and corticospinal fibers contained within the crus cerebri because of the proximity of one fiber system to the other.In such a condition, the patient displays both third nerve paralysis as well as upper motor neuron paralysis of the contralateral limbs. This is referred to as Weber’s syndrome or superior alternating hemiplegia.

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