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Table 3–1. Functional Classes of Human Eye Movements
Class of Eye Movement Main Function
Movements holding images
steady on the retina
Visual fixation Holds the image of a stationary object on the
fovea when the head is still
Vestibular Holds images steady on the retina during brief
head rotations or translations
Optokinetic Holds images steady on the retina during
sustained head rotation
Movements directing the
fovea to an object of interest
Saccades Bring images of objects of interest rapidly onto
the fovea
Nystagmus quick phases Reset the eyes during prolonged rotation and
direct gaze toward the oncoming visual scene
Smooth pursuit Holds the image of a small moving target
on the fovea; aids optokinetic responses to
stabilize gaze during sustained head rotation
Vergence Moves both eyes in opposite directions so that
images of a single object are simultaneously
placed on the fovea of each eye
(2) microsaccades (average 0.1 degrees, 120 Hz); and
(3) microdrift (<0.3 deg/ sec). The role of these movements in visual fixation is unclear, though they may be
important for preventing peripheral vision fade of stable objects due to habituation of a persistent stimulus.
Vestibular
The vestibulo-ocular reflex holds images of the seen
world steady on the retina by producing compensatory
eye movements during brief head rotations or translations. These phylogenetically old reflexes are generated
with a much shorter latency than visually mediated eye
movements and are critical for maintaining stable vision
during natural activities such as walking and running.
Optokinetic
Optokinetic eye movements are those generated by
movement of a large visual scene and serve to hold
images of the world steady on the retina during sustained head rotation. They supplement the vestibularinduced eye movements that begin to decline during
prolonged rotation. Optokinetic eye movements consist of a slow phase in the direction of visual scene
motion and a nystagmus quick phase to reset the eye
in the opposite direction.
Saccades
Saccades are rapid, brief, conjugate eye movements
that shift the line of sight to bring target images onto
the fovea. They may be volitional (elective and purposeful), reflexive (generated to novel stimuli occurring unexpectedly in the environment), predictive (in
anticipation of or in search of the appearance of a target
at a particular location), memory guided (to the location of a previous target), command (generated on cue),
or spontaneous (seemingly random in the absence of
any specific task). Saccades are critical for exploring a
visual scene and reading, among other things.
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Nystagmus Quick Phases
The quick phases of nystagmus generated during
vestibular and optokinetic stimulation are a form of
saccades. The evolutionary forerunner of volitional
saccades, they serve to reset the eyes during prolonged
rotation and direct gaze toward the oncoming visual
scene.
Smooth Pursuit
Smooth pursuit allows the image of a small, slowly
moving target to be held on the fovea while the head
is still. Smooth pursuit is primarily voluntary, driven
by retinal slip from visual motion and modulated by
attention and motivation. The pursuit system is also
required to track an object on a complex moving background and to suppress reflexive vestibular and optokinetic responses during combined head and eye tracking.
Vergence
As opposed to versional eye movements, which conjugately move both eyes in the same direction by the
same amount, vergence eye movements move the eyes
in opposite directions (convergence or divergence) so
that images of a single object are placed or held simultaneously on the fovea of each eye. Vergence is provoked
by either the retinal blur (loss of image sharpness) or
retinal disparity (image separation when images fall
on noncorresponding areas of each retina) that occurs
with changes of target image distance during binocular
fixation, such as when shifting gaze from a distant to a
very near object.
THE FINAL COMMON PATHWAY
FOR
EYE MOVEMENTS
Orbital Muscle Gross Anatomy
The extraocular muscles reside within the bony confines of the cone-shaped orbit. At the orbital apex, the
four rectus muscles and superior oblique originate
from the dense fibrous annulus of Zinn through which
the optic nerve passes. The four rectus muscles course
anteriorly through orbital fat and terminate as tendinous tissue on the sclera. The superior oblique passes
through a ring of connective tissue called the trochlea
at the upper nasal portion of the orbital frontal bone
to terminate on the lateral posterior portion of the
sclera. The inferior oblique originates in the inferior
nasal orbital wall, laterally crosses the orbital floor,
and inserts on the lateral posterior globe. The globe is
suspended and supported in the orbit by a fibrous sac
of fascia called Tenon’s capsule.
Extraocular Muscle Actions
and
Innervation
Six extraocular muscles control the movements of
each eye: medial rectus, lateral rectus, superior rectus,
inferior rectus, superior oblique, and inferior oblique
(Figure 3–1). The medial rectus, superior rectus, inferior rectus, and inferior oblique are innervated by the
oculomotor nerve (cranial nerve III). The lateral rectus
is innervated by the abducens nerve (cranial nerve VI).
The superior oblique is innervated by the trochlear
nerve (cranial nerve IV).
Coordinated extraocular muscle action facilitates
movement of the eyes in three directional planes (horizontal, vertical, and torsional) about three axes (craniocaudal, interaural, and naso-occipital). Nomenclature
for these directions is described in Table 3–2. The
actions of each muscle are dependent on the muscle’s
origin and terminal insertion, the center of rotation of
the eye, and the optical axis of the eye. Growing evidence also suggests that fibromuscular pulleys just
behind the rectus muscles’ insertion sites contribute to
extraocular muscle kinematic properties (Demer, 2006).
The muscles of each eye work in agonist/antagonist
pairs. In order to facilitate rotation of the eye, increased
innervation to the agonist results in an equal amount of
decreased innervation to the antagonist (Sherrington’s
law of reciprocal innervation). Muscle actions may
vary depending on the position of the globe in the
orbit. Each extraocular muscle has a primary action,
and all but the medial and lateral recti also have secondary and tertiary actions. Horizontal eye movements
are controlled by the antagonistic medial rectus and lateral rectus muscles. The primary and only action of the
medial rectus is adduction, and the primary and only
action of the lateral rectus is abduction. Vertical and
torsional eye movements are controlled by two antagonist pairs: the superior and inferior recti and the superior and inferior oblique muscles. The contribution of
a given muscle to vertical eye movement depends on
the horizontal position of the eye. When the eye is in
an abducted position, the superior and inferior rectus muscles are the principal elevator and depressor
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figure 3–1. Orbital anatomy. A. The relative position of the five muscles
just behind the left eyeball.
lateral rectus;
plane of this section is shown in (C). B.
and lateral rectus (shown in the shaded area), which are responsible
for horizontal eye movements. Only a small segment of the superior
rectus is shown in order to show the optic nerve beneath it. C.
superior and inferior obliques have a similar axis of rotation but opposite pulling direction. D. Axis of rotation of the superior rectus (shaded
region) and the inferior rectus located directly beneath it.
and inferior recti mainly move the eye vertically. From Handbook of
Balance Function Testing, Jacobson et al., 1997.
MR, medial rectus; IR, inferior rectus; ON, optic nerve. The
SR, superior rectus; SO, superior oblique; LR,
muscles, respectively. When the eye is in an adducted
position, inferior oblique action causes elevation, and
superior oblique action causes depression. The superior oblique and superior rectus muscles are intorters of
the eye, and the inferior oblique and inferior rectus are
extorters. The primary, secondary, and tertiary actions
of each muscle are shown in Table 3–3.
In addition to each eye’s antagonistic pairs with
opposite directions of action, the extraocular muscles
exist as “yoked” pairs between eyes to generate con-
Top view with the medial rectus
The
The superior
jugate eye movements. The three yoked pairs include
(1) the medial rectus in one eye and the lateral rectus
in the other eye, (2) the superior rectus in one eye and
the inferior oblique in the other eye, and (3) the inferior
rectus in one eye and the superior oblique in the other
eye. “Yoked” muscle pairs receive equal and simultaneous innervation generated from premotor control
systems, stimulating the cranial nerve nuclei to elicit
the conjugate eye movement (Hering’s law of equal
innervation).
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table 3–2. Nomenclature for Eye Movement Direction
Eye Movement Type Directional Definition
Duction:
movements of each eye
Version:
movements, rotating both
eyes in the same direction
by the same amount
Monocular
Conjugate eye
Abduction: horizontal movement about the craniocaudal axis
away from the median plane
Adduction:
toward the median plane
Elevation:
Depression:
Intorsion:
pole of the eye rotates toward the median plane
Extorsion:
pole of the eye rotates away from the median plane
Dextroversion:
craniocaudal axis
Levoversion:
craniocaudal axis
Elevation:
Depression: both eyes rotating downward about the interaural
axis
Dextrocycloversion:
occipital axis so that the top pole of the eyes rotate toward the
subject’s right
Levocycloversion: both eyes rotating about the naso-occipital
axis so that the top pole of the eyes rotate toward the subject’s
left
horizontal movement about the craniocaudal axis
upward rotation about the interaural axis
downward rotation about the interaural axis
rotation about the naso-occipital axis so that the top
rotation about the naso-occipital axis so that the top
both eyes rotating to the right about the
both eyes rotating to the left about the
both eyes rotating upward about the interaural axis
both eyes rotating about the naso-
Vergence:
movements, rotating the two
eyes in opposite directions
Disjunctive eye
table 3–3. Extraocular Muscle Actions with the Eye in Central Position
Muscle Primary Action Secondary Action Tertiary Action
Medial rectus Adduction
Lateral rectus Abduction
Superior rectus Elevation Intorsion Adduction
Inferior rectus Depression Extorsion Adduction
Superior oblique Intorsion Depression Abduction
Inferior oblique Extorsion Elevation Abduction
Convergence: both eyes rotating horizontally about the
craniocaudal axis toward the median plane
Divergence:
craniocaudal axis away from the median plane
Incyclovergence:
axis so that the top pole of both eyes rotates toward the median
plane
Excyclovergence: both eyes rotating about the naso-occipital
axis so that the top pole of both eyes rotates toward the median
plane
both eyes rotating horizontally about the
both eyes rotating about the naso-occipital
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Ocular Motor Nuclei and Nerves
Abducens Nerve (Cranial Nerve VI)
Paired abducens nuclei are located in the dorsomedial
pons at the floor of the fourth ventricle, in close proximity to the fascicle of the facial nerve (Figure 3–2). Each
nucleus contains abducens motor neurons that form
the abducens nerve and interneurons that decussate
at the level of the nucleus and ascend in the contralateral medial longitudinal fasciculus (MLF) to the oculo-
motor medial rectus subnucleus to facilitate conjugate
horizontal gaze in the direction ipsilateral to the abducens nucleus of origin. The abducens fascicles arise
from the ventral surface of the nucleus, traverse the
brainstem, emerge from the ventral pontomedullary
sulcus, and travel as the abducens nerve in the subarachnoid space where it ascends along the clivus. It
pierces the dura, travels through the cavernous sinus
lateral to the internal carotid artery, and enters the
superior orbital fissure to innervate the ipsilateral lateral rectus muscle.
Figure 3–2. Brainstem structures involved in eye movements. A parasagittal section
of the monkey brainstem shows the location of key structures responsible for saccadic eye movements. Excitatory burst neurons (EB
the paramedian pontine reticular formation (PPRF). Inhibitory burst neurons (IBN) for
horizontal saccades lie in the medullary reticular formation (MedRF). EBN for vertical
and torsional saccades lie in the rostral interstitial nucleus of the medial longitudinal
fasciculus (riMLF). Some vertical IBN may reside in or close to the interstitial nucleus
of Cajal (INC). EBN and IBN project to ocular motor neurons lying in the abducens
nucleus (VI), trochlear nucleus (IV), and oculomotor nucleus (III). Omnipause neurons (OPN, indicated by an asterisk) lie in the nucleus raphe interpositus in the midline of the pons between the rootlets of the abducens nerve (C
the activity of EBN and IBN. The mesencephalic reticular formation (MRF) may help
keep the OPN inhibited until a saccade is complete and the eye is on target. CG:
central gray; MB: mammillary body; CN III: rootlets of the oculomotor nerve; CN IV:
trochlear nerve; CN VII: genu of facial nerve; ND: nucleus of Darkschewitsch; NRTP:
nucleus reticularis tegmenti pontis; NPH: nucleus prepositus hypoglossi: PC: posterior
commissure; TR: tractus retroflexus. Reproduced from Ramat et al. (2007) with permission from Dr. Jean Büttner-Ennever and Oxford University Press.
N) for horizontal saccades lie in
N VI) and influence
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a superior rectus subnucleus that innervates the contra-
Clinical Correlation:
Abducens Nucleus and Nerve Palsies
A lesion of the peripheral abducens nerve or its
fascicles within the lower pons will both produce
an isolated ipsilateral lateral rectus muscle weakness. The two may often be distinguished by the
presence of additional central neurological signs in
a pontine lesion, such as contralateral arm and leg
weakness from involvement of the corticospinal
tract. In either case, the lateral rectus is weak for all
classes of eye movements (saccades, pursuit, vestibular), and thus ipsilateral eye movements will
be slow, of limited range, or absent. However, if
the abducens nucleus is intact, abducens interneurons innervating the contralateral medial rectus
subnucleus of CN III will still produce adduction
upon attempted lateral gaze. If, on the other hand,
the lesion affects the abducens nucleus (including
the abducens motor neurons and interneurons),
the result is a complete ipsilesional horizontal
gaze paralysis of all eye movement classes, often
producing a contralateral gaze deviation. In this
case, the eyes cannot be brought past the midline
even by the vestibulo-ocular reflex (VOR).
lateral superior rectus muscle; and an Edinger–Westphal nucleus supplying preganglionic parasympathetic
output to the iris sphincter and ciliary muscles. A single
midline caudal central subnucleus provides innervation to both levator palpebrae superioris muscles.
Clinical Correlation:
Internuclear Ophthalmoplegia
Unilateral inactivation of the MLF results in ipsilaterally slowed or absent adduction with abducting nystagmus in the contralateral eye during
attempted contralateral gaze (internuclear ophthalmoplegia [INO]), in combination with a skew
deviation with ipsilateral hypertropia. Bilateral
MLF inactivation results in bilateral impairment
of adduction with bilateral dissociated abducting nystagmus (bilateral INO), impaired vertical
smooth pursuit, and reduced vertical VOR gain.
Clinical Correlation:
One-and-a-Half Syndrome
Trochlear Nerve (Cranial Nerve IV)
Paired trochlear nuclei lie very close to the dorsomedial
surface of the midbrain just below the inferior colliculus. The fascicles emerge from the nuclei and briefly
course dorsally before exiting the dorsal midbrain. The
trochlear nerves are the only cranial nerves to emerge
from the dorsal brainstem surface. After emerging, the
nerves decussate within the anterior medullary velum
and wrap around the surface of the midbrain to travel
ventrally within the subarachnoid space toward the
cavernous sinus. In the cavernous sinus, the trochlear
nerve is located in the lateral dural wall, inferior to the
oculomotor nerve. From the cavernous sinus, the nerve
passes into the superior orbital fissure and ultimately
innervates the superior oblique muscle contralateral to
the nucleus of origin.
Oculomotor Nerve (Cranial Nerve III)
Paired oculomotor nuclei are located in the dorsal midbrain ventral to the periaqueductal gray matter at the
level of the superior colliculus. Each nuclear complex
includes individual subnuclei innervating the ipsilateral inferior rectus, medial rectus, and inferior oblique;
Occasionally a lesion affects the abducens
nucleus on one side and the ipsilateral MLF containing interneurons from the contralateral abducens nucleus that have already crossed and are
destined for the ipsilateral oculomotor nucleus.
The result is a complete conjugate horizontal gaze
paralysis toward the side of the lesion as described
earlier, plus an INO for gaze in the opposite direction. Thus, the patient loses all conjugate gaze
ipsilesionally (the “one”) and can only abduct
the contralateral eye with attempted contralateral
gaze (the “half”).
Third-nerve fascicles originate from the ventral
surface of each nucleus and traverse the midbrain,
passing through the red nucleus and in close proximity to the cerebral peduncles before emerging as ventral
rootlets in the interpeduncular fossa. The rootlets converge into a third-nerve trunk that continues ventrally
through the subarachnoid space toward the cavernous
sinus, passing between the superior cerebellar artery
and the posterior cerebral artery. In the cavernous
sinus, the third nerve is located in the dural sinus wall,
just lateral to the pituitary gland. From the cavernous
sinus, the third nerve enters the superior orbital fissure.
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Just prior to entry, the nerve anatomically divides into
superior and inferior divisions. The superior division
innervates the superior rectus and the levator palpebrae superioris, and the inferior division innervates
the inferior and medial recti, the inferior oblique, and
the iris sphincter and ciliary muscles. Prior to innervating the ciliary and sphincter muscles, parasympathetic third-nerve fibers synapse in the ciliary ganglion
within the orbit.
Internuclear Connections
The MLF is a paramedian pathway that lies in the dorsal brainstem and carries ocular motor and vestibular
signals between the medulla and midbrain. As noted
above, the MLF carries signals from the abducens
nucleus to the contralateral medial rectus portion of
the oculomotor nucleus. These signals allow conjugate
horizontal eye movements with synchronous contraction of the ipsilateral lateral rectus and contralateral
medial rectus muscles (Figure 3–3). The MLF also carries signals for vertical gaze from the vestibular nuclei
in the medulla to the midbrain vertical gaze control
centers important for vertical smooth pursuit and vestibular eye movements.
CENTRAL VESTIBULAR
STRUCTURES AND PATHWAYS
The basic three-neuron arc of the VOR consists of the
vestibular ganglion and nerve, vestibular nuclei, and
ocular motor nuclei (Figure 3–4). The VOR serves to
maintain stable gaze direction by compensating for
head movement. The drive for the VOR is vestibular rather than visual and thus can operate at a much
shorter latency than could occur if visual information
had to reach the visual cortex and then be relayed to
the brainstem. However, the cerebellum has important
connections that fine-tune the VOR to changing visual
requirements.
from the otolith organs, affecting the linear (translational) VOR, vertical ocular alignment, and vestibulospinal reflexes.
Cerebellum
The cerebellum receives input from the vestibular nuclei
as well as directly from vestibular nerve afferents that
bypass the vestibular nuclei. These inputs travel in the
juxtarestiform body of the inferior cerebellar peduncle
to the ipsilateral vestibulocerebellum (flocculonodular
lobe, consisting of the flocculus, paraflocculus, nodulus, and ventral uvula). Additionally, the cerebellum
receives visual and ocular motor signals from regions
such as the pontine nuclei, nucleus reticularis tegmenti
pontis, paramedian tract, and inferior olivary nuclei.
Thus, although not part of the three-neuron arc of
the VOR, the cerebellum is critical for adapting the
gain (ratio of eye movement to head movement) and
direction of the VOR to new visual requirements, as
occurs in disease states like unilateral vestibular loss or
even when changing spectacle prescriptions (Versino,
Hurko, & Zee, 1996; Walker & Zee, 1999).
Central Organization of the
Vestibulo-
The function of the VOR is to generate compensatory
conjugate eye movements in the opposite direction
of brief head movement and thereby maintain stable
gaze and clear vision. The VOR can be subdivided
into canal-ocular reflexes, with input from the semicircular canals driving the angular VOR (aVOR), and
otolith-ocular reflexes driving the translational VOR
(tVOR). An additional otolith-mediated VOR, ocular
counterrolling, occurs in response to change in the
static orientation of the head with respect to gravity in
the roll (frontal) plane; a small change in the static torsion (counterrolling) of the eyes occurs in the opposite
direction with sustained head tilt.
Canal-Ocular Reflexes
Ocular Reflex
Vestibular Nuclei
Four nuclei form the vestibular nuclear complex on
each side in the dorsal medulla: The rostral portions
(medial and superior vestibular nuclei) predominantly
receive input from the semicircular canals (SCCs), with
their central projections most important for generating the rotational (angular) VOR. The caudal portions
(lateral and inferior nuclei) mainly receive projections
Stimulation or inhibition of a single SCC leads to slowphase eye movements that rotate the eye in a plane
parallel to the canal. Thus, the affected canal can be
inferred from the pattern of nystagmus, such as the
mixed vertical-torsional nystagmus of benign paroxysmal positional vertigo occurring from inappropriate
stimulation of the posterior SCC. Central mechanisms
are used to suppress the effect of persistent vestibular imbalance and thereby compensate for vestibular
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figure 3–3. Anatomic scheme for the synthesis of signals for horizontal eye movements. The abducens nucleus
(CN VI) contains abducens motor neurons that innervate the ipsilateral lateral rectus muscle (LR) and abducens internuclear neurons that send an ascending projection up the contralateral medial longitudinal fasciculus
(MLF) to reach the medial rectus (MR) motor neurons in the contralateral oculomotor nucleus (CN III). From the
horizontal semicircular canal, primary vestibular nerve afferents project mainly to the medial vestibular nucleus
(MVN), where they synapse and then send an excitatory connection to the contralateral abducens nucleus and
an inhibitory projection to the ipsilateral abducens nucleus. Saccadic inputs reach the abducens nucleus from
the ipsilateral excitatory burst neurons (EBN) and contralateral inhibitory burst neurons (IBN). The neural integrator
within the nucleus prepositus hypoglossi (NPH) and adjacent MVN send eye position information to the abducens
nucleus. The medial rectus motor neurons in CN III also receive commands for vergence eye movements. Putative
neurotransmitters for each pathway are shown: Ach: acetylcholine; asp: aspartate; glu: glutamate; gly: glycine.
The anatomic sections on the right correspond to the level of the arrow heads on the schematic on the left. Abd.
nucl.: abducens nucleus; CN VI: abducens nerve; CN VII: facial nerve; CTT: central tegmental tract; ICP: inferior cerebellar peduncle; IVN: inferior vestibular nucleus; Inf. olivary nucl.: inferior olivary nucleus; MRF: medullary reticular
formation; SVN: superior vestibular nucleus. Reproduced from Leigh and Zee (2006) with permission from Oxford
University Press.
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figure 3–4. Excitatory projections from individual semicircular canals on the right side
to the extraocular muscles.
lateral rectus;
LC: lateral canal; MLF: medial longitudinal fasciculus; ATD: ascending tract of Deiters; BC:
brachium conjunctivum;
medial);
from Fife (2010) with permission from Elsevier.
SR: superior rectus; MR: medial rectus; AC: anterior canal; PC: posterior canal;
III: oculomotor nucleus; IV: trochlear nucleus; VI: abducens nucleus. Reproduced
SO: superior oblique; IO: inferior oblique; IR: inferior rectus; LR:
VN: vestibular nuclei (S = superior; I = inferior; L = lateral; M =
lesions. The brisk nystagmus seen in acute peripheral
vestibular lesions will gradually decrease in intensity
as the central vestibular system compensates for the
imbalance. In addition, visual fixation may significantly suppress the spontaneous nystagmus of an acute
vestibular lesion, necessitating the use of examination
techniques that eliminate fixation.
To generate the aVOR, the vestibular nuclei send
excitatory and inhibitory signals to specific ocular
motor nuclei in order to activate yoked pairs of extraocular muscles (and inhibit their antagonists) (Fife,
2010). This reflex leads to activation of specific muscles
that move the eyes in the same plane but in the opposite direction as the semicircular canal being stimulated, regardless of the initial position of the eye in the
orbit. The horizontal aVOR is the simplest and most
commonly tested. Activation of the lateral semicircular canal by ipsilateral head rotation leads to vestibular
nerve excitation synapsing on the vestibular nuclei.
From there, second-order excitatory projections course
rostromedially and then cross the midline to synapse
on the contralateral abducens nucleus. As with generation of other conjugate eye movements, abducens
motor neurons and interneurons are activated within
the abducens nucleus, leading to activation of the lateral rectus (contralateral to the vestibular stimulus) and
via the MLF to the oculomotor nucleus, activation of
the opposite medial rectus (ipsilateral to the vestibular
stimulus). Some neurons also connect directly from the
vestibular nuclei to the ipsilateral medial rectus subnucleus in the ascending tract of Deiters, but its functional
significance is uncertain. For each extraocular muscle
activated, its antagonist must be inhibited to permit
rotation of the eye in the orbit. Thus, for each excitatory pathway, the vestibular nuclei send inhibitory
projections to antagonist muscles (for the horizontal
aVOR this is the ipsilateral lateral rectus and contralateral medial rectus). In addition, during head rotation, the semicircular canal being inhibited (such as the
right horizontal canal during leftward head rotation)
reduces its tonic firing rate, thereby facilitating relaxation of the antagonist muscles. The eye movements
elicited by vestibular stimulation constitute the vestibular slow phase eye movements. However, sustained
vestibular stimulation in an awake person leads to nystagmus quick phases opposite the slow phase direction
(toward the side of vestibular stimulation). The nystagmus direction is named based on quick phase direction.
The vertical semicircular canal projections are
more complicated but follow the same principles. Each
anterior (superior) SCC sits in the same plane as the
contralateral posterior SCC. Thus, in natural states of
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movement, one canal is activated while its contralateral functional pair is inhibited. The anterior SCC is
oriented along the same axis of rotation as that produced by activation of the ipsilateral vertical recti and
contralateral obliques. Stimulation of the anterior canal
leads to excitation of the ipsilateral superior rectus and
contralateral inferior oblique via brainstem connections between the vestibular nuclei and the two oculomotor subnuclei. Activation of the posterior canal
produces excitation of the contralateral inferior rectus
and ipsilateral superior oblique. Thus, with the eyes in
the straight ahead position, stimulation of an individual vertical SCC will produce a combination of vertical
and torsional eye movement based on the actions of
the muscles activated. For example, excitation of the
right posterior SCC produces vestibular slow phases
that are downward and with torsion where the top
poles of the eyes roll toward the subject’s left (extorsion of the left eye and intorsion of the right eye), with
nystagmus quick phases that are upward and with
oppositely directed torsion. Because of the fact that the
trochlear nucleus and superior rectus subnucleus of
CN III innervate contralateral muscles, vertical excitatory projections from the vestibular nuclei to ocular
motor nuclei cross the midline, but vertical inhibitory
connections do not.
During dynamic head roll in the frontal plane (tilting the head alternately to the right and left shoulder),
the dynamic torsional VOR generates compensatory
slow-phase torsional eye movements in the opposite
direction predominantly by the vertical semicircular
canals. Rolling to the right stimulates the right anterior
and posterior canals while inhibiting the left anterior
and posterior canals. Provided that brainstem saccade networks are intact, torsional nystagmus quick
phases occur opposite the slow phases. The gain of the
dynamic torsional VOR is between 0.4 and 0.7, lower
than that of the horizontal or vertical VOR.
Otolith-Ocular Reflexes
The otolith-ocular reflexes refer to compensatory eye
movements evoked by stimulation of the utricle or saccule. The two types include (1) the translational VOR
(tVOR) in response to linear head acceleration, and
(2) ocular counterrolling (or static torsional VOR) in
response to static head tilt in the roll plane.
The central otolith projections for the tVOR are less
studied than for the aVOR but must take into account target distance and eccentricity. It appears that the horizontal tVOR may arise from stimulation of the lateral portion
of the utricle during ipsilateral linear head translation,
with polysynaptic connections to the lateral vestibular
nuclei then projecting (possibly via the cerebellum) con-
tralaterally to the abducens nucleus and driving oppositely directed conjugate slow phase eye movements.
Projections from the medial portion of the utricle
may be more important for signaling head tilt and
generating compensatory counterrolling using vertical torsional eye muscles. The medial portion of
the utricle would be excited by sustained ipsilateral
head tilt, synapsing on the lateral vestibular nucleus,
with connections via the MLF to the midbrain ocular
motor nuclei, producing counterrolling of the eyes in
the opposite direction via excitation of the ipsilateral
superior oblique and superior rectus and contralateral
inferior oblique and inferior rectus.
The brain is evidently able to use contextual cues
to resolve the ambiguity of whether the head is being
linearly translated or tilted relative to gravity despite
the fact that the shear forces on the utricular macula
would be the same for each. This may be based upon
the frequency of linear acceleration input, with lowfrequency input interpreted as tilt and high-frequency
Clinical Correlation: Ocular Tilt Reaction
A lesion anywhere along the otolith ocular pathway between the utricle and vertical/torsional
ocular motor nuclei in the midbrain (including
in the MLF) can lead to the ocular tilt reaction
(OTR) (Brodsky, Donahue, Vaphiades, & Brandt,
2006). For example, a lesion of the left utricle or
its peripheral or central connections disrupts the
normally symmetric utricular input and leads to a
shift in the patient’s internal estimate of true vertical (gravity) in the roll plane to the left. Thus, the
brain erroneously registers that the head is tilted
to the right with respect to gravity. This results
in an OTR to the left with the pathologic triad of
head tilt to the left to realign the head’s verti-
(1)
cal axis with the perceived but incorrect vertical
gravitational axis, (2) torsional ocular counterrolling of the top pole of the eyes to the left to
realign the eyes’ vertical meridian with the perceived but incorrect vertical gravitational axis,
and (3) skew deviation (the left eye depresses and
right eye elevates) to realign the eyes’ horizontal
meridian with the perceived but incorrect internal estimate of the earth-horizontal (Figure 3–5).
Because central utricular pathways cross at the
pontomedullary junction to enter the MLF, a
lesion of the utricular nerve or medulla will cause
an ipsilesional OTR, while a lesion in the pons or
midbrain after the projections have crossed will
cause a contralesional OTR.
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