The Cranial Nerves (Organization of the Central Nervous System) Part 5

Control of Eye Movements: Role of the Pontine Gaze Center

Whereas CN III, IV, and VI are essential for eye movements, the control of eye movements is under supranuclear control. The precise mechanisms are not totally understood, but several of the key structures have been identified. With respect to the control of horizontal gaze, they include the cerebral cortex, the region adjacent to the abducens nucleus called the pontine gaze center, and the vestibular nuclei.

It is likely that the motor nuclei of CN III, IV, and VI do not receive direct inputs from the cortex. Instead, cortical influences are via indirect pathways. These relationships are depicted in Figure 14-14. Briefly, the major structure for the integration and control of horizontal gaze is the pontine gaze center. It receives inputs from the contralateral cerebral cortex (i.e., frontal eye field). After integrating signals from these regions, the pontine gaze center projects its axons to the nucleus of CN VI on the ipsilateral side and the nucleus of CN III on the con-tralateral side. In this manner, stimulation of the right pontine gaze center by either the ipsilateral vestibular nuclei or contralateral cerebral cortex will result in activation of the ipsilateral CN VI and the contralateral CN III. The effects of stimulation will, thus, cause the right eye to be abducted and the left eye to adduct (i.e., the eyes are directed to the right). Conversely, if there is a lesion of the right pontine gaze center, then the eyes cannot be moved to the right. However, the left pontine gaze center, which remains intact, allows the eyes to be moved to the left. Testing of the horizontal eye movement reflex is done by passively turning the head from side to side, and if the reflex is intact, the eyes will move conjugately in the direction opposite to movement. This is called the doll’s eye (oculocephalic) maneuver. This procedure is applied when a patient is unable to perform voluntary eye movements and serves to determine whether the brain-stem is intact. A lesion affecting the brainstem in the region between the midbrain and pons where vestibular and oculomotor pathways (the MLF) are affected would cause the eyes to move in the same direction as the head. Further discussion of vestibular reflexes is considered in the following sections.

Cortical and Vestibular Control of Extraocular Eye Muscles

Voluntary Control of Eye Movements. As indicated in Figure 14-14, the region of the frontal cortex called the frontal eye fields projects to the contralateral pontine gaze center. Such a connection provides the basis for voluntary control of horizontal eye movements, which can even override certain reflex eye movements associated with inputs to the pontine gaze center from the vestibular nuclei (with the exception of nystagmus). However, if, for example, there is a lesion of the projection from the left cortex to the right pontine gaze center (Fig. 14-16), the ability to gaze to the right will be impaired.

Control of horizontal eye movements serves very important functions. It is used extensively in reading and in looking at stationary and moving objects within our visual field. Horizontal movements can occur quite rapidly, with the duration being less than 50 milliseconds. These are called saccadic movements. If an individual fixates on an object within his or her visual field, the movements change from saccadic to smooth pursuit movements. Such movements most likely involve utilization of primary, secondary, and tertiary regions of the visual cortex, which have connections with the frontal lobe, including the frontal eye fields. Vestibular-Induced Reflexes. Vestibular nuclei receive direct inputs from the semicircular canals of the vestibular apparatus. The vestibular nuclei transmit these inputs to both the pontine gaze center and nuclei of CN VI, IV, and III. The relationship between the vestibular system and the nuclei of the extraocular eye muscles is a very important one. It provides the anatomical basis by which the eyes can continue to fixate upon a given object as the head moves in space. For example, when an individual’s head is rotated to the right, the eyes will turn toward the left. This is because the inertia of the endolymph in the semicircular canals generates a force across the cupula, moving it in the opposite direction to movement (i.e., to the left), which triggers action potentials in the first-order vestibular neurons on the left side that project to the left vestibular nuclei.

The left vestibular nuclei, via the MLF, excite the lateral gaze center and motor nucleus of CN VI on the right side that supply the lateral rectus muscle and excite, through interneurons, motor neurons of CN III on the left side that supply the medial rectus muscle. Other projections will inhibit the lateral gaze center on the left side and its projection targets in left CN VI and right CN III. As the head continues to be rotated, the eyes show a smooth pursuit movement in the opposite direction to continue to fixate upon the object. Continued rotation of the head will eventually bring the object out of the individual’s visual field, and he or she will attempt to fixate on another object. This attempt will result in a rapid (i.e., saccadic) movement of the eyes in the direction in which the head is turning. The entire process results in a number of sequences in which the eyes first display a slow movement in the direction opposite of the movement of the head, which is then followed by a rapid movement in the same direction in which the head is moving. This phenomenon is called the vestibulo-ocular reflex or nystagmus. It is named for the direction of the rapid component of the eye movement (i.e., if the rapid component of the movement is to the right, it is called a right nystagmus).

Nystagmus can be demonstrated experimentally by placing a normal individual in a chair (called a Barony chair) that can be rotated. The individual is then asked to focus on a given object and is spun around rapidly. When the chair stops, the individual displays a period of nystagmus in the direction opposite to that of movement. This is called postrotary nystagmus and is due to the fact that the endolymph continues to move (because of inertia) even after the individual has stopped moving.

Nystagmus can also occur clinically, usually in association with lesions of the MLF at levels rostral to the pontine gaze center. These lesions disrupt the mechanisms that regulate normal conjugate deviation of the eyes, and this disorder is referred to as internuclear ophthalmoplegia. In addition to nystagmus, which is typically present in the abducting eye, there is paralysis of the adducting eye when the individual attempts to look to the opposite side. For example, if a patient who has a lesion of the left MLF attempts to look to the right, his or her left eye cannot be adducted, although his or her right eye can be abducted (Fig. 14-16, lesion #2). Moreover, nystagmus is present in the left (abducting) eye.

Diagram of the anatomical substrates for lateral gaze (left side of figure) and the deficits that occur following lesions at different sites along this pathway (right side of figure). For purposes of illustration, the diagram depicts the mechanisms involved in right conjugate gaze. Voluntary right conjugate gaze is initiated from pathways arising from the left frontal lobe that project to the pontine (lateral) gaze center. Involuntary pathways mediating conjugate gaze are associated with the occipital cortex. Note that the pontine gaze center projects to the ipsilateral abducens (cranial nerve [CN] VI) nucleus and contralateral oculomotor nerve (CN III). The loci of the lesions (1-4) are shown on the left illustration. The corresponding deficits are depicted on the illustration on the right side.

FIGURE 14-16 Diagram of the anatomical substrates for lateral gaze (left side of figure) and the deficits that occur following lesions at different sites along this pathway (right side of figure). For purposes of illustration, the diagram depicts the mechanisms involved in right conjugate gaze. Voluntary right conjugate gaze is initiated from pathways arising from the left frontal lobe that project to the pontine (lateral) gaze center. Involuntary pathways mediating conjugate gaze are associated with the occipital cortex. Note that the pontine gaze center projects to the ipsilateral abducens (cranial nerve [CN] VI) nucleus and contralateral oculomotor nerve (CN III). The loci of the lesions (1-4) are shown on the left illustration. The corresponding deficits are depicted on the illustration on the right side.

Vertical Gaze Center

It is generally an accepted view that a region of the midbrain serves to coordinate the up and down movements of the eyes. This region is called the vertical gaze center. However, much less is known about the mechanisms governing the control of vertical gaze. Experimental studies have suggested that the key region for vertical gaze movements lies in the ventrolateral aspect of the rostral midbrain PAG (the structure is called the rostral interstitial nucleus of the MLF). These cells discharge in response to vertical eye movements and also project their axons to the cell columns of the oculomotor nucleus that supply the extraocular eye muscles. Clinically, disorders involving vertical gaze have been reported and result, in part, from tumor formation in the region of the ventrolateral midbrain PAG and from multiple sclerosis plaques.

Cranial Nerves of the Forebrain

Optic Nerve (Cranial Nerve II)

The optic nerve is a highly specialized sensory cranial nerve that conveys visual signals to the CNS nervous system and is, thus, classified as SSA. It enters the brain at the level of the preoptic region of the diencephalon.

Olfactory Nerve (Cranial Nerve I)

The olfactory nerve is classified as SVA because its receptors are chemoreceptors. The olfactory nerve enters the brain through the cribriform plate of the ethmoid bone and supplies the olfactory bulb.

Clinical Case


Judy is a 29-year-old secretary who has had diabetes since childhood. One morning, she awoke feeling that the left side of her face was drooping and that she was unable to close her left eye.This eye felt dry as well, and noises seemed louder on the left than on the right side. Feeling that it was a transient condition, perhaps resulting from a sleeping position, she went to work anyway, where her supervisor told her that she should go to the emergency room (ER) because it looked as if she was having a stroke.


In the ER, the doctor noted a left-sided facial droop immediately. Because of this, there was some slight slurring of her speech, but there was neither evidence of any problems forming sentences nor problems understanding the content of speech. Her left eye would not close completely and appeared to droop slightly. The corneal reflex was absent on the left side. She was not able to hold air in her cheeks, and only the right side of her mouth was elevated when she was asked to smile. Only the right eyebrow elevated when she was asked to wiggle her eyebrows. She was very sensitive to sounds on her left side, even those that were not especially loud. When sugar water was placed on the left side of her tongue, she was unable to taste it, but was able to taste it when placed on the right side.The doctor drew some blood and gave Judy some medication to take for the condition. He also patched her left eye to prevent it from becoming ulcerated.


Judy has Bell’s palsy, or paralysis of the seventh cranial nerve at or distal to its exit from the facial nerve nucleus in the pons.The motor deficits described on the face are typical of lower motor neuron weakness, in which much of the face is involved. This could not be an upper motor neuron disorder because when there is upper motor neuron weakness,the neurons of the facial nucleus representing the superior third of the face are bilaterally innervated from the cerebral cortex, thus preserving function in this area.This is not preserved in a lower motor neuron lesion.

The loss of taste ipsilateral to a peripheral facial nerve lesion is found when the lesion occurs proximal to the position where the chorda tympani nerve joins the facial nerve.This nerve controls taste function of the anterior two thirds of the tongue.The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, so a facial nerve lesion can also cause weakness of this muscle. Because the function of this muscle is to dampen the motion of the ossicles, which are the small bones within the middle ear modulating quality of sound stimuli, sounds appear louder than they normally would (hyperacusis). The corneal reflex is lost because the facial nerve serves as the efferent arm of the reflex.The result is possible damage to the cornea. Lacrimation, another function governed by the facial nerve, is also diminished and may cause further damage to the cornea.

Often, no definitive cause can be found for most cases of Bell’s palsy. Some causes include diabetes, a blow to the face, and infections and inflammation.


Summary of Cranial Nerves and Their Functions

Cranial Nerve

Nerve Type

Locus of Cell Bodies


Effects of Lesions

Hypoglossal nerve (CN XII)


Dorsomedial medulla (hypoglossal nucleus)

Protrusion of tongue

Deviation of tongue to side of lesion

Spinal accessory nerve (CN XI)


CI-C5 ventral horn cells

Innervation of sternomastoid and trapezius muscles; contralateral turning and lifting of head

Difficulty in moving head to opposite side (sternomastoid muscle) and lowering of shoulder on affected side (trapezius muscle); difficulty in raising head from pillow while lying on back

Vagus nerve (CN X)


Lateral medullary reticular formation (nucleus ambiguus)

Innervates pharynx and soft palate; sounds in speech

Paresis of pharynx (hoarseness, difficulty in swallowing)


Mainly dorsal motor nucleus of vagus nerve (dorsomedial medulla)

Parasympathetic innervations of heart and body viscera; facilitation of peristalsis; slowing of cardiac cycle

Hyperactivity of vagus-stomach ulcers; possible disruption of carotid-sinus reflex (GVE and GVA components); disruption of swallowing, vomiting, and cough reflex (SVE component)


Inferior (nodose) ganglion (aortic arch)

Sensory information from abdominal and thoracic viscera; stretch receptors from aortic arch (baroreceptor inputs, part of baroreceptor reflex)

See comments above for GVE component


Inferior ganglion (aortic body)

Mediates respiratory functions from aortic body; mediates taste from epiglottis and posterior wall of pharynx

Possible loss or some disruption of respiratory functions; possibly some minimal loss of taste functions


Superior ganglion

Somatosensory inputs from skin of back of ear and external auditory canal

Minimal loss of sensation from surface of back of ear

Glossopharyngeal nerve (CN IX)


Lateral medullary reticular formation (nucleus ambiguus)

Innervates stylopharyngeus muscle; elevates upper part of pharynx for speech and swallowing

Weakness of the muscles of the pharynx causing impairment of reflexes (i.e., gag, uvular, and palatal reflexes)


Medullary reticular formation (Inferior salivatory nucleus)

Preganglionic parasympathetic neurons innervating otic ganglion, which, in turn, innervates parotid gland (salivation)

Loss of secretion of parotid gland causing reduction in salivation

Cranial Nerve

Nerve Type

Locus of Cell Bodies


Effects of Lesions


Inferior (petrosal) ganglion in carotid sinus

Responds to changes in blood pressure

Disruption or loss of carotid sinus reflex


Inferior ganglion in carotid body

Mediates changes in blood levels of oxygen and carbon dioxide to reticular formation of medulla essential for normal respiration (afferent limb of reflex contraction of diaphragm); taste inputs from posterior third of tongue to solitary nucleus

Disruption of normal respiratory functions; loss of taste sensation from posterior third of tongue


Superior ganglion

Conveys somatosensory afferents originating from tympanic membrane, skin of external ear, and posterior third of tongue to trigeminal nuclei and then to thalamus and cortex for conscious perception of somatic sensation from these regions

Probable loss of somatosensory sensation from the skin of external ear, tympanic membrane, and posterior third of tongue

Vestibulocochlear nerve (CN VIII)


Vestibular ganglion (for vestibular signals); cochlear ganglion (for auditory signals)

Transmits vestibular and auditory inputs from the inner ear to central neurons mediating these processes

Loss of vestibular inputs can produce ataxia, loss of balance, nystagmus,and related eye movement disturbances; loss of auditory inputs can produce loss of hearing on the side of the affected inner ear

Facial nerve (CN VII)


Facial motor nucleus (in caudal aspect of ventrolateral pontine tegmentum)

Controls muscles of facial expression

Loss of facial expression; hyperacusis on side of lesion


Superior salivatory nucleus in reticular formation of lower pons

Makes synapse with postganglionic parasympathetic ganglia supplying submandibular, sublingual, lacrimal, nasal, and palatine glands

Disturbances in secretion of saliva and reduction or loss of lacrimal secretion


Geniculate ganglion

Conveys taste sensation from anterior two thirds of tongue centrally to solitary nucleus

Loss of taste sensation from the anterior two thirds of tongue


Geniculate ganglion

Cutaneous sensation from back of ear and external auditory meatus; these neurons then synapse with neurons of spinal trigeminal nucleus

Probable loss of some sensation from back of ear and external auditory meatus

Abducens nerve (CN VI)


Abducens nucleus in dorso-medial aspect of posterior pons

Innervate lateral rectus causing eye to be moved laterally

Paralysis of lateral rectus muscle preventing eye from moving laterally, causing medial strabismus (inability of two eyes to focus on same object)

Cranial Nerve

Nerve Type

Locus of Cell Bodies


Effects of Lesions

Trigeminal nerve (CNV)


Motor nucleus of trigeminal nerve in central pons just medial to main sensory trigeminal nucleus

Supplies muscles of mastication to produce biting and chewing

Weakness or paralysis of muscles of mastication; pterygoid muscle damage results in deviation of jaw to affected side


Trigeminal (also called Gasserian or semilunar) ganglion; mesencephalic nucleus located in upper pons

Somatosensory sensation from palate, teeth,gum,face, and cornea; pain and temperature signals to spinal trigeminal nucleus; conscious proprioception, pressure and touch mediated mainly through main sensory trigeminal nucleus; unconscious proprioception (muscle spindles from mandibular branch) to mesencephalic trigeminal nucleus

Loss of pain and temperature on side of face affected by lesion (if lesion is in dorsolateral medulla); general sensory loss if lesion is peripheral or if it affects main sensory trigeminal nucleus;damage to ophthalmic branch can affect corneal reflex; irritation of the trigeminal nerve can produce trigeminal neuralgia; loss of mas-seter reflex

Trochlear nerve (CN IV)


Trochlear nucleus located in caudal aspect of dorsal midbrain just below PAG

Supplies superior oblique muscle, which moves eye downward when in the medial position

Outward rotation of eye; patient has difficulty walking down stairs; head is tilted upon downward gaze

Oculomotor nerve (CN III)


Oculomotor nucleus located in rostral aspect of midbrain just below PAG

Innervates and controls all extraocular eye muscles except superior oblique and lateral rectus muscles plus levator palpebrae superior; moves eyes medially and up and down

Loss of ability to move eye inward or vertically; lateral strabismus of one eye (causing double vision); drooping of eye (ptosis)


Edinger-Westphal nucleus, located adjacent to GSE motor nuclei of CN III

Preganglionic parasympathetic neurons synapse with ciliary ganglion, which then innervates papillary constrictor muscles and ciliary muscles; essential for papillary constriction, near vision, and accommodation reflex

Loss of papillary light reflex and accommodation reflex

Optic nerve (CN II)


Retinal cells

Optic nerve and optic tract mediate visual impulses to central neurons (lateral geniculate nucleus) and then to visual cortex

Blindness, the extent to which is dependent upon where the lesion is located and its size (see Ch. 16 for details)

Olfactory nerve (CN 1)


Olfactory mucosa

Olfactory nerve mediates olfactory sensations to olfactory bulb and through a series of central synapses to prefrontal cortex

Loss or reduction of olfactory sensations (see Ch. 18)

CN = cranial nerve; GSE = general sensory efferent; SVE = special visceral efferent; GVE = general visceral efferent; GVA = general visceral afferent; SVA = special visceral afferent; GSA = general special afferent; SSA = special sensory afferent; PAG = periaqueductal gray matter.

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