Functional Neuroanatomy of CN III, IV, and VI Flashcards
This slide lists only some of the disease entities that may alter eye movements and pupillary function
This slide demonstrates the location of the four lower motor neuron nuclei involved in eye movement and pupil control. This is a dorsal view of the brainstem with the cerebral hemispheres and cerebellum removed.
Note that all four nuclei lie near the midline and are located dorsally (that is closer to the 4th ventricle) in the brainstem.
Note that CNs III and IV lie in the midbrain just ventral to what structures?
the superior and inferior colliculi respectively. Note that CN VI lies in the caudal half of the pons. I have added the Edinger Westphal nuclei (shown in red) to the drawing.
This slide presents a left lateral view of the brain stem shown on the right side of the slide with the relevant nuclei shown in color. The nuclei are enlarged to demonstrate the complex multinuclear structure of CN III. This multinuclear structure relates to the fact that CN III controls five separate eye muscles and accordingly has five separate nuclei.
The Edinger-Westphal nucleus is closely associated with CN III but is considered a separate nucleus.
What does the Edinger-Westphal nucleus do?
It is a parasympathetic pathway supplying the constrictor muscles of the iris.
The dorsal nuclei of CN III serve what muscle?
the inferior rectus muscle
The intermediate nucleus of CN III serves what muscle?
the inferior oblique muscle
The medial nucleus of CN III serves what muscle?
the superior rectus
The ventral nucleus of CN III serves what muscle?
the medial rectus.
The central caudal nucleus of CN IIII serves what?
the levator palpebrae superioris muscle.
This slide presents a dorsal view of the brainstem and nuclei that control eye movement and pupil constriction.
Note once again the midbrain location of CNs III and IV just ventral to what structure?
the quadrigeminal plate, i.e. the superior and inferior colliculi.
. Note the location of the abducens nucleus (CN VI) in the caudal half of the pons.
Recall that CN VII sends its axons over the top of CN VI creating what?
the facial colliculus. The facial colliculus is seen in the floor of the 4th ventricle as a raised bump and CN VI lies immediately below this bump.
CN III central nuclei, i.e. the Edinger-Westphal nucleus and the caudal nucleus provide bilateral input to their respective muscles. The remaining left and right paired CN III nuclei serve their respective ipsilateral muscles except for the medial nucleus that serves the contralateral superior rectus muscle.
However, the clinical significance of this ipsilateral, contralateral, and bilateral output of one or another of the CN III subnuclei is inconsequential since the CN III complex is small and near the midline and only in the rarest of conditions does it suffer a lesion localized to only the left or right half of the complex. Nevertheless, the fascicles, i.e. the axons from the subnuclei, join together and quickly lateralize. Thus lateralized lesions of the midbrain can produce unilateral eye movement and pupillary abnormalities as do lesions of CN III after it leaves the brainstem.
A ventral view of the brain stem showing the exit of CN III where?
at the junction of the midbrain and pons
CN IV exiting dorsally
Where does CN VI exit the midbrain?
at the pontomedullary junction.
Note that CN III exits ventrally at the level of the midbrain. CN __ is the only CN that exits the brainstem dorsally.
IV. Note it exits just caudal to the inferior colliculus.
How does CN IV act?
The trochlear nerve crosses over from its dorsal exit from the brainstem caudal to the inferior colliculus to innervate the contralateral super or oblique muscle; accordingly the left trochlear nucleus controls the right superior oblique and vis versa (see also Slide 14).
Which two cranial nerve nuclei controlling eye movement serve contralateral eye muscles?
the trochlear nucleus and the medial nucleus of CN III.
This slide presents a frontal view of the eyes and several brain stem sections depicting the location of CNs III, IV, and VI nuclei and their respective nerves.
Note the ipsilateral innervation of the lateral rectus muscle by the CN VI,
the ipsilateral innervation of the superior rectus, medial rectus, inferior rectus, and inferior oblique muscles by CN III,
and the contralateral innervation of the superior oblique by CN IV.
I36 takes you to C4
Note the error in this figure; the figure mistakenly shows the left CN III nuclei sending efferents fibers to the left superior rectus muscle when in fact the right medial nucleus of CN III is the source of this muscles innervation.
Be aware that the axons from the medial nucleus immediately cross over and join the contralateral fascicle such that there is no error in the figure regarding CN III fascicle within the brainstem.
T or F. A lesion of the oculomotor nucleus on one side would disrupt upgaze in both eyes.
T.
Loss of the CN III nucleus would remove what?
the source of fibers supplying the superior rectus on the opposite side. The lesion would also destroy the crossed fibers from the opposite intact oculomotor nucleus affecting the ipsilateral superior rectus. Neither superior rectus muscle would receive nerve impulses to contract the muscles. This is a primary characteristic of a dorsal midbrain stroke.
This slide presents a cross section through the midbrain. Note the locations of CNs III, IV, and VI and their proximity to the cerebral blood vessels.
Of particular importance is the route of CN III as it passes between what arteries?
the superior cerebellar artery and the posterior cerebral artery and then alongside the posterior communicating artery and underneath the internal carotid artery. The juxtaposition of CN III with these intracranial arteries subjects it to compression and injury from vascular outpouchings called aneurysms that not uncommonly develop in arterial branch points at the base of the brain.
To help you navigate future MTI and CT images, note the apparent Mickey Mouse face created by structures comprising the midbrain in the left figure. This region of the brain stem is seen on CT and MRI scans of the brain as shown on the right.
Familiarity with Mickey’s face allows for the approximation of these structures on brain scans. Mickey’s ears are created by the cerebral peduncles and the substantia nigra, his eyes by the red nuclei, his nose by the periaqueductal gray and cerebral aqueduct of Sylvius, and his chin by the superior colliculi.
This slide presents a coronal section through the cavernous sinus at the level of the pituitary gland. Recall that the cavernous sinus is a maze of venous sinusoids located lateral to what structures?
the pituitary gland and sphenoid sinus. The cavernous sinus drains blood from the eyes and cortical veins to empty eventually into the jugular vein.
What CNs pass through the cavernous sinus?
Note that CNs III, IV, VI (red boxes) and the V1, V2 (green boxes) divisions of the trigeminal nerve travel within the sinus.
Note also that the internal carotid artery travels within the sinus and begins a hairpin turn within the sinus, called the carotid siphon, before entering the subarachnoid space.
What else travels through the cavernous sinus?
Sympathetic fibers traveling with the internal carotid artery on their way to dilator muscles of the pupil also travel through the cavernous sinus.
It is important to recognize that hemorrhage from a ruptured internal carotid artery aneurysm, tumors, infections, and inflammatory diseases such as Tolosa-Hunt syndrome may affect the cavernous sinus to produce a syndrome called the cavernous sinus syndrome. Lesions of the cavernous sinus may produce symptoms and signs affecting all or just some of the structures passing through the sinus.
This slide presents a lateral view of the orbit, its contents, and the innervation of the eye muscles and eye lid. Its purpose is to allow you to trace the pathways from the Edinger-Westphal nucleus, CN III and the sympathetic fibers traveling initially with the internal carotid artery as they innervate their target organs.
Note the parasympathetic innervation of the pupillary constrictors and ciliary muscles.
The sympathetic innervation of the Tarsal muscle provides autonomic elevation of the eye lid that is not subject to voluntary control.
Note the sympathetic innervation of the pupil dilator muscles as well
What innervates of the levator palpebra superioris, which allows for voluntary elevation of the upper eye lid
CN III.
What does the ciliary muscle do?
produces changes in lens shape as the eyes converge on a target moving toward the eyes. The resulting pupillary constriction produces the accommodation reflex.
This slide presents the four recti muscles with their CN innervation and the primary direction that they move the eye. Note that the medial and lateral recti move the eye globe towards the nose (adduction) or away from the nose (abduction) respectively. Note that while the slide depicts pure vertical movement for the superior and inferior recti, in fact these muscle will produce a degree of torsional movement because of the manner in which they are anatomically connected to the eye.
For the purposes of this course and for the ease of clinical examination when you become practicing physicians (unless you specialize in ophthalmology) we will disregard all torsional movements for the superior and inferior recti muscles.
This slide presents the two oblique muscles with their CN innervation and the primary direction that they move the eye.
How do the superior obliques move the eye? Inferior obliques?
They cause intorsion of the eye and the inferior oblique causes extorsion.
To understand how you can disregard the torsional eye movements when examining patients, you need to comprehend the material in the next two slides.
First, notice the axis of the eye shown as a line drawn through the center of the lens back to the fovea of the retina. In fact this axis is the most direct path of light traveling through the lens to reach the fovea, the area of the retina with the most acute vision.
Now, contraction of the lateral or medial rectus muscles moves the eye globe in such a way that the axis of the eye does not rotate about itself, that is there is no intorsion or extorsion.
In contrast, the other four eye muscles connect to the globe in such a manner that when they contract the eye globe does rotate about its axis, that is the eye intorts or extorts. Importantly, it is possible to eliminate most of this rotational movement of the eye globe if the eyes are examined in specific positions. I will explain this on the next slide and then present the steps to examine eye movement
This slide attempts to explain the physics that permits examination of the eyes without dealing with the torsional movements. It presents a dorsal view of the eyes and extraocular muscles.
Note that when the eyes look to the right the superior rectus of the right eye becomes almost parallel with the axis of the right eye. Thus when the right superior rectus contracts, it will not cause the right eye to rotate around its (the right eye) axis, that is there will be no intorsion or extorsion.
Accordingly, with the eye in an abducted position, that is looking laterally, the superior rectus can be simply tested by asking the patient to look upward.
Similarly, when the left eye looks to the right, that is, it is placed in the adducted position, the superior oblique muscle becomes almost parallel with the axis of the left eye. When the left superior oblique contracts it cause the left eye to look downwards without accompanying intorsion or extorsion. The superior oblique causes the eye to look downward because it loops around the trochlear before inserting on the posterior portion of the eye. If these physical relationships are unclear, then simply review and remember the next two slides to be able to examine patients without remembering the torsional functions of the extraocular muscles.
This slide presents the primary fields of gaze for testing the patient’s right eye without having to consider torsional movements.
The slide is oriented with you as the examiner looking directly at the face and eyes of your patient. By focusing on the right eye and asking the patient to look to his right (abducted) or left (adducted) and then asking him to look up and then down you are able to isolate the movements of all six extraocular muscles of the right eye without having to consider torsional movements.
When either eye is in the abducted position, that is looking laterally, elevation of the eye is controlled primarily by the superior rectus muscle. Accordingly, weakness of elevation of an abducted eye means that the superior rectus is weak or the nerve innervating it is injured.
To fully abduct either eye the lateral rectus muscle on that side must function normally; if the eye does not fully abduct, then the lateral rectus is weak or CN VI is not functioning normally.
In the abducted position, depression of the eye is controlled primarily by the inferior rectus muscle and its CN. In the adducted eye, the inferior oblique is responsible for elevation, the superior oblique is responsible for depression, and the medial rectus for adducting the eye. Weakness in any one of these directions of the adducted eye translates into weakness of the responsible muscle or its CN.
This slide simply presents the primary gaze field for testing eye movement in your patients. When you face your patient and ask them to look to their right, up, and then down you are testing in order the lateral rectus, superior rectus, and inferior rectus of their right eye and simultaneously testing the medial rectus, inferior oblique, and superior oblique muscles of their left eye.
Clinical Note: The 3rd cranial nerve may be completely damaged or partially damaged. A lesion causing the former causes complete paralysis of all 3rd nerve muscles including the levator palpebrae superioris with resultant eye closure. Incomplete lesions produce paresis (weakened or incomplete movement) of 3rd nerve muscles and the eye lid will be only partially closed.
What does the levator palpebrae do?
raise the eyelid (voluntary control of eyelid elevations)
What innervates the levator palpebrae?
CN III
What does the superior tarsal muscle (Muller’s) do?
raise the eyelid (involuntary elevation of the eyelid)- innervated by the sympathetic nerve
The next series of slides reviews the parasympathetic innervation of the pupillary constrictors and the ciliary muscle, as well as the sympathetic innervation of the dilator muscle.
Describe the pathway and its primary neurons of the sympathetic pathway to the dilator muscle.
1) The pathway originates in the hypothalamus, and then
2) travels through the lateral brainstem and eventually synapses with secondary neurons located in the intermediolateral gray area of the spinal cord at the C8 - T2 level.
What are the next steps of the sympathetic pathway to the dilator muscle?
3) The secondary neurons sends their axons out the ventral roots into the paravertebral sympathetic ganglia chain and travel up to synapse in the superior cervical ganglion.
4) The tertiary neurons in the superior cervical ganglion send their fibers along with the internal carotid artery within the carotid sheath and enter the calvarium with the internal carotid artery.
5) Intracranially, the sympathetic fibers join the _____ nerve to innervate the superior tarsal muscle and the _______ nn. to innervate the dilator muscle of the pupil.
nasociliary
long and short ciliary nerves
This slide demonstrates the pupillary light reflex. This is a dorsal view of a silhouetted brain, brain stem, and eyes. Describe the initial parts of this pathway.
1) A bright light flashed in front of the left eye sends afferent signals via the optic nerve through the optic chiasm and optic tract to synapse in the left and right pretectal nuclei. The latter are located in the midbrain just under the superior colliculi.
What is the next step in pupillary reflex?
2) Secondary neurons in the pretectal nuclei send bilateral axons to the Edinger-Westphal or EW nuclei, shown here as two separate nuclei, but recall the EW nucleus is a single midline nucleus that projects bilaterally to both pupils. Thus light coming from either eye will stimulate the EW nucleus neurons to send signals to both the left and right pupillary constrictor muscles.
When examining the integrity of the pathway for the pupillary light reflex, light shown in one eye, for example the right, will produce constriction of the right pupil and this is designated the ‘direct’ light reflex response. However, due to the bilateral EW connections, the left pupil will also constrict and this is designated the ‘indirect’ or ‘consensual’ light reflex response.
To summarize, shining a light in one eye causes a direct light reflex (that is pupillary constriction) in that eye and a consensual pupillary constriction in the contralateral eye. By shining the light in one eye you are testing the integrity of the afferent pathway, that is fibers from the retina and optic nerve traveling to the EW nucleus. You are also testing the efferent pathways, that is the EW projections to both eyes via the ciliary ganglia to produce pupillary constriction.
Note the Edinger-Westphal nucleus is outlined as a single midline structure just above the nose of the upside down Mickey Mouse. The nose is the cerebral aqueduct as you may recall from slide #10.
The pathway of the parasympathetic fibers from the EW nucleus to the pupil constrictors is via ____
CN III
This slide presents some of the clinically relevant nuances of the Edinger-Westphal parasympathetic path to the pupil constrictor muscles. Note this is a frontal view of the eyes and brain stem with the optic nerves (in yellow), brain stem (in tan), and an enlarged section of CN III (in orange).
Note once again that the figure presents two separate Edinger-Westphal nuclei rather than correctly presenting a single midline nucleus.
Focus your attention to the enlarged section of CN III. Note the location of the blood vessels serving the periphery of the nerve and also separate blood vessels serving the center of the nerve.
Note also the darker band lying along the dorsal medial surface of the nerve. This band represents the parasympathetic fibers from the Edinger-Westphal nucleus. Their position along the dorsal medial surface of CN III figures into the clinical presentation of two neurological syndromes that have markedly different causes and prognosis.
Where do the parasympathetic fibers from the Edinger-Westphal nucleus lie on CN III?
the dorsal medial surface
Recall that CN III passes between what arteries?
the posterior cerebral artery and the superior cerebellar artery and then adjacent to the posterior communicating artery and internal carotid artery.
Aneurysms (balloon like enlargements) occur at arterial branch points and in this scenario, Posterior Communicating Artery Aneurysms or PCOM aneurysms are the most common to compress CN III. When they compress CN III, the peripherally located parasympathetic pupillary constrictors are compromised first and hence, a unilateral pupillary dilatation may be the first clue of an enlarging aneurysm. As the aneurysm enlarges further, the entire third nerve may be injured producing unilateral paresis of all the extraocular muscles innervated by this nerve. Thus the acute onset of a unilateral enlarged pupil and paresis of CN III muscles is a neurologic emergency since rupture of a cerebral aneurysm carries a 30 to 40% incidence of death or permanent disability.
What is compressed first on CN III due to a Posterior Communicating Artery Aneurysms or PCOM aneurysm?
When they compress CN III, the peripherally located parasympathetic pupillary constrictors are compromised first and hence, a unilateral pupillary dilatation may be the first clue of an enlarging aneurysm.
As the aneurysm enlarges further, the entire third nerve may be injured producing unilateral paresis of all the extraocular muscles innervated by this nerve. Thus the acute onset of a unilateral enlarged pupil and paresis of CN III muscles is a neurologic emergency since rupture of a cerebral aneurysm carries a 30 to 40% incidence of death or permanent disability.
The second, more common and less dangerous development of oculomotor paresis occurs without enlargement of the pupil. How?
This presentation is typically caused by occlusion of the small arteries suppling the center of CN III. This small vessel disease occurs as a result of diabetes mellitus and sometimes other vasculopathies.
Note that the superficial placement of the parasympathetic fibers along with the superficial blood vessels that are less prone to diabetic involvement and occlusion. This protects the parasympathetic fibers from central ischemia of CN III. Since about one in twenty cases of pupil-sparing oculomotor paresis is still caused by aneurysm, these patients need to have urgent vascular imaging with CT angiography or MRA (MRI angiography) to exclude the possibility of aneurysm.
What is the accommodation reflex?
The accommodation reflex consists of convergence of the eyes along with parasympathetic mediated constriction of the pupil and thickening of the lens to allow for near vision.
What mediates the accommodation reflex?
1) Contraction of the ciliary muscle causes the suspensory ligaments attached to the lens to relax and thus the lens increases its diameter.
What are the first two steps of the accomodation reflex?
1) The accommodation reflex is initiated by a combination of cortical areas including the prefrontal eye fields and the occipital-parietal fields.
2) These cortical areas cause pretectal activation that triggers parasympathetic output through Edinger-Westphal nucleus to produce pupil constriction and lens thickening in conjunctions with activation of CN III bilaterally to produce eye convergence.
T or F. The accommodation reflex activation of CN III nuclei is independent of the medial longitudinal fasciculus (MLF) pathway connecting the contralateral abducens nucleus to CN III nuclei.
T. Thus, the eyes can still converge, that is bilateral activation of CN III nuclei permits accommodation in the face of a lesion of the MLF.
To this point we have discussed cranial nerve nuclei, their nerves, and target muscles that control eye movements and the shape of the pupil and lens. These functions represent the output of the lower motor neurons.
Upper motor neuron regulation of these lower motor neurons is equally complex
Supranuclear or upper motor neuron control of eye movements follows the same general organizational pattern that we discussed for voluntary control of the body musculature. Thus, cortical areas activate pattern generators located in the brainstem, and this process is modified by the basal ganglia and the cerebellum.
Horizontal movement of the eyes requires a coordinated contraction of one lateral rectus with the contralateral medial rectus. Since these two muscles are controlled by separate nuclei, their actions must be linked and regulated simultaneously. How is this achieved?
To achieve this, neurons located in the abducens nucleus activate the contralateral ventral nucleus of CN III nuclei.
This connection between CN VI and III nuclei is achieved via what?
the medial longitudinal fasciculus or MLF.
How does the internuclear pathway work?
The fibers from the abducens nucleus immediately cross the midline and travel rostrally via the MLF to synapse on the ventral nucleus of CN III. Thus activation of CN VI to initiate abduction of the ipsilateral eye simultaneously activates the contralateral ventral nucleus of CN III to cause adduction of the contralateral eye.
This results in conjugate lateral eye movement.
Any failure of thw conjugate movement of the MLF will cause what?
dysconjugate gaze, misalignment of the eyes and diplopia (double vision) since the two eyes will present the visual cortex with slightly or markedly displaced images.
The phasic firing of this conjugate link between the abducens nucleus and the contralateral ventral nucleus of CN III is regulated by what?
the paramedian pontine reticular formation or PPRF, also known as the horizontal gaze center and the parabducens nucleus. Thus, activation of the left PPRF triggers the left abducens nucleus to simultaneously activate contraction of the left lateral rectus muscle and the right oculomotor nucleus to activate the right medial rectus muscle.
The vestibular system is also an additional important regulator of extraocular movement. Head movement strongly influences eye movement, and this is mediated via the semicircular canals, the vestibular nerve, and vestibular nuclei. Note that this diagram is a significant over-simplification of the vestibular regulation of eye movement.
Describe the vestibulo-ocular reflex (VOR)
Rotation of the head to the right in the horizontal plane stimulates the right horizontal semicircular canal. This prompts the vestibular apparatus to signal the right medial vestibular nucleus via the right vestibular nerve.
How does the right vestibular nucleus react?
It, in turn, activates the contralateral PPRF, that activates the left abducens nucleus and the right ventral nucleus of CN III to contract the eye muscles to move the eyes to the left.
The consequence of turning the head suddenly to the right is a compensatory reflex movement of the eyes to the left so that a person can maintain visual fixation on an object of interest. This is called the vestibulo-ocular reflex or VOR.
We exploit the VOR reflex during our examination of patients under several conditions.
For example, in comatose patients we use this reflex to test the structural integrity of the midbrain to the pons. If integrity is preserved, the eyes will move conjugately in the opposite direction of rotation when the head is quickly turned to the right or left. This is called the oculocephalic maneuver or the Doll’s eyes maneuver. Absence of eye movement indicates the nuclei and tracts mediating the VOR are not functioning either due to a severe metabolic derangement or due to a structural lesion such as infarction or hemorrhage.
Three cortical centers that are important in eye movements, namely:
the visual cortex,
the frontal eye fields, and
the parietal-occipito-temporal (POT) area
The visual cortex functions in concert with both the frontal eye field and the POT area.
Eye movements are characterized by two general types:
fast conjugate movements called saccades and slow conjugate movements called pursuit movements.
NOTE: There is a third type of slow conjugate movement that we have already described, that is the vestibulo-ocular reflex movements.
Saccadic eye movement, shown in the left figure, is under the control of what?
the frontal eye fields and is either voluntarily triggered or reflexive. For example, if you hold your head still and look with only your eyes from one corner of the room to the other, you are voluntarily activating your saccadic system.
If a bug crawling on the wall in your peripheral vision causes you to automatically look at it, you have experienced a reflexive saccade involving so-called ______ ______.
collicular vision
How does the saccadic pathway from one frontal eye field travel?
It travels with the ipsilateral corticobulbar fibers through the internal capsule to the ipsilateral superior colliculus and on to the CONTRALATERAL PPRF.
Thus the right frontal eye field activates the left PPRF which in turn activates the left abducens nucleus and right ventral nucleus of CN III causing the eyes to conjugately look to the left.
Since the right hemisphere controls the left arm/hand, if you are catching a ball with your left hand you naturally want you head and eyes turned to the left to guide your hand to the ball. Thus the right frontal eye field generates saccades to the left and the left frontal eye field produces saccades to the right.
Slow pursuit eye movements are under the control of the POT area and in contrast to the frontal eye field, the POT area directs eye movement in the ipsilateral direction.
The pathway from the POT area to brain stem control centers is more complex than that involved in saccadic control. For the purposes of this course, simply recall that the _________ and _________ participate in this control mechanism.
contralateral cerebellum and vestibular nuclei
You can demonstrate smooth pursuit in yourself by holding your index finger up in front of you, fix your eyes on it and slowly move your hand from right to left keeping you eyes fixed on your finger. As your eyes track your finger to the left, recognize that your left POT area is controlling this movement.
How do neurologists test the integrity of the saccadic and smooth pursuit eye movements?
with the use of an opticokinetic (OKN) strip.
How does an OKN strip work?
an OKN strip of cloth has alternating vertical stripes or bars of red and white. It is held in front of a patient’s eyes and moved from right to left and then left to right. The patient is asked to fix on the stripes. As the strip moves, the eyes will transiently pursue one stripe and quickly snap back to the midline to pick up the next stripe.
The initial slow pursuit movement is controlled by the ipsilateral POT area and the quick snap back (saccade) is controlled by the contralateral frontal eye field. Lesions in either of these areas will impair one or the other component of the OKN test. Thus, as the striped bars are moving in your visual field from right to left, the right POT tracks with slow pursuit and the left frontal eye field causes the eyes to saccade back toward the right for the next stripe. The OKN nystagmus shows the fast component (saccadic) beating to the right.
This slide presents an artists drawing of two men, one (A) with a lesion of the left frontal cortex causing right hemiparesis and eyes looking away from the paretic side and
a second man (B) with a lesion of the left brain stem at the pontine level causing the same right hemiparesis as A but now with eyes looking toward the paretic side.
Note that the diagram on the left of the frontal eye field pathway to the PPRF shows only the right PPRF and the lesion B corresponds to injury to the left PPRF.
What does Lesion of left frontal lobe produce?
Eyes Away From Paresis (Frontal Corex Lesion)
produces a right hemiparesis and loss of input to the right PPRF allowing the combination of the right frontal eye field and the left PPRF to drive the eyes towards the left, i.e. away from the paresis.
What does a left pontine lesion produce?
Lesion of the left pons (B) produces a right hemiparesis and loss of function of the left PPRF allowing the right PPRF to drive the eyes towardsthe right, i.e. towards the paresis.
