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Clinical Correlation: Smooth Pursuit Abnormalities
Pathways serving smooth pursuit are widespread
throughout the cerebral hemispheres, brainstem,
and cerebellum, so pursuit abnormalities commonly
accompany lesions throughout the central nervous
system. Reduced pursuit gain (the ratio of eye velocity to target velocity) manifests as “choppy” or “saccadic” pursuit, as small saccades are made to catch
up with the moving target as the eyes fall behind.
One must recognize that pursuit gain declines normally with advancing age, especially at high velocities, but also becomes impaired in Parkinson disease,
progressive supranuclear palsy, cerebellar disorders,
and large cerebral lesions. While diffuse disorders
cause omnidirectional pursuit abnormalities, large
unilateral cerebral lesions (especially of the parietooccipital cortex and underlying white matter but
also of the MST visual cortex and the FEF) cause
pursuit tracking deficits predominantly to the side
of the lesion, independent of homonymous hemianopia or visual neglect. This asymmetric pursuit
can be demonstrated with an “optokinetic” tape or
drum. Directional pursuit abnormalities may also be
encountered with unilateral lesions of the descending pursuit pathways, including the midbrain tegmentum, DLPN, and cerebellum. Because of the
double decussation of the pursuit pathway, lesions
of the pontocerebellar projections and vestibular
nuclei may impair either ipsilateral or contralateral
smooth pursuit. Unless the VOR is also impaired by
a disease process, smooth pursuit deficits are generally accompanied by impairment of VOR suppression during combined eye–head tracking.
Isolated defects of vertical pursuit are less common. Bilateral INO from MLF lesions impair vertical
pursuit (and the vertical VOR), as the MLF transmits pursuit and vestibular signals from the vestibular nuclei to CN III and IV serving vertical eye
movements. An unusual disturbance can occur with
cavernous angiomas of the middle cerebellar peduncle, where vertical pursuit is accompanied by torsional nystagmus, suggesting that pursuit signals
processed through the cerebellum may be encoded
in the same reference planes as the semicircular
canals.
for calibrating the VOR, while the vermis and fastigial nucleus are critical for pursuit initiation (Krauzlis,
2004; Thier & Ilg, 2005).
Cerebellar influenCes on gaZe
The cerebellum optimizes or refines eye movements
so that they are calibrated to improve accuracy and
ensure clearest vision. In order to perform this role, the
cerebellum receives both sensory and motor information regarding the eye movement and must compare
the predicted eye movement based on the command
with the desired eye movement and generate a signal
to decrease the error between predicted and desired to
get the eyes accurately on target. Three primary regions
of the cerebellum are involved with ocular motility:
the flocculus and paraflocculus; (2) the dorsal ver-
(1)
mis (oculomotor vermis) and caudal fastigial nucleus;
and (3) the nodulus and ventral uvula.
As part of the vestibulocerebellum, the paired
flocculi lie adjacent to the paraflocculi, ventral to the
inferior cerebellar peduncle and next to the vestibulocochlear nerve (CN VIII) (Figure 3–11). The flocculi
and paraflocculi receive mossy fiber input from the
vestibular nuclei, NPH, NRTP, DLPN, and paramedian tract cell group and climbing fiber input from
the contralateral inferior olivary nucleus. The main
output from the floccular and parafloccular Purkinje
cells is to the ipsilateral superior and medial vestibular
nuclei. The flocculus appears more important for
calibrating the VOR, while the paraflocculus mainly
contributes to smooth pursuit. The flocculus and
paraflocculus also contribute inhibitory influence to
counteract the inherent tonic upward VOR bias otherwise favoring the anterior over posterior SCC pathways, as lesions of these cerebellar structures often
lead to upward slow phases and downbeat nystagmus, as would be seen with unopposed anterior canal
activation.
Lobules VI and VII of the dorsal vermis (Figure 3–12) receive mossy fiber inputs from the PPRF,
NRTP, DLPN, NPH, and vestibular nuclei as well as
climbing fiber input from the contralateral inferior olivary nucleus. Projections coming from the NRTP relay
information necessary for planning saccades, whereas
those from the DLPN are more important for smooth
pursuit. Dorsal vermis Purkinje cells discharge prior to
contralateral saccades as well as encode target veloc-
3. PRACTICAL ANATOMY AND PHYSIOLOGY OF THE OCULAR MOTOR SYSTEM 65
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Area MST
Dorsolateral
pontine nuclei
Flocculonodular
lobe and paraflocculus
Ocular motor
nuclei
Medial and
superior
vestibular
nuclei
figure 3–11. Role of the vestibulocerebellum (flocculonodular lobe
and paraflocculus) in the control of eye movements.
of the flocculonodular lobe, adjacent uvula and ventral paraflocculus (vestibulocerebellum) is the control of certain eye movements.
The nodulus and uvula receive vestibular inputs both directly from
the labyrinth and via the vestibular nuclei; inputs from the frontal eye
fields and the middle superior temporal (MST) area via the dorsolateral pontine nuclei; and inputs from the ocular motor control network
via the nucleus prepositus hypoglossi and the nuclei of the paramedian tracts (not shown).
medial and superior vestibular nuclei predominantly for control of the
horizontal and vertical vestibulo-ocular reflexes and smooth pursuit.
Reprinted with permission from Dr. Eduardo Benarroch (Benarroch,
2006) and Mayo Foundation for Medical Education and Research.
The flocculus and paraflocculus project to the
Uvula
Paraflocculus
FlocculusNodulus
The main role
ity during pursuit and combined eye–head tracking.
Dorsal vermis Purkinje cells project to the caudal part
of the deep cerebellar fastigial nucleus, coined the fas-
tigial oculomotor region, which also receives collaterals
from the same climbing and mossy fiber inputs destined for the dorsal vermis. The main projection from
the fastigial nucleus crosses through the other fastigial
nucleus and enters the uncinate fasciculus in the border
of the superior cerebellar peduncle to reach the premotor burst neurons and OPN in the brainstem. Fastigial
neurons discharge prior to and during contralateral
saccades (facilitating them) and discharge late for ipsilateral saccades (perhaps serving as a stop signal to end
a saccade on target).
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Frontal ey
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e field
Fastigial oculomotor region
Superior
colliculus
Saccadic
burst
generator
Dorsal vermis
Nucleus reticularis
tegmenti pontis
figure 3–12. Role of the dorsal vermis and fastigial oculomotor region
for control of saccades.
oculomotor region, controls the amplitude and direction of saccadic
eye movements. These structures receive inputs from the paramedian
pontine reticular formation, which contains the excitatory burst neurons for horizontal saccades, and from the nucleus reticularis tegmenti
pontis, which relays saccadic signals from the frontal eye fields and
superior colliculus. The fastigial nucleus projects to the saccadic burst
generator of the brainstem via the uncinate fasciculus to control the
amplitude of ipsilateral and contralateral saccades. Reprinted with
permission from
Foundation for Medical Education and Research.
Dr. Eduardo Benarroch (Benarroch, 2006) and Mayo
The posterior or dorsal vermis, via the fastigial
The nodulus, which is the midline portion of the
flocculonodular lobe, and the adjacent ventral uvula
control the velocity-storage mechanism of the VOR.
This central vestibular mechanism functions to enhance
the responsiveness of the VOR to low-frequency stimuli
such as sustained rotation. Without a velocity-storage
mechanism, the discharge from vestibular nuclei driving
the VOR would quickly decay during sustained rotation,
based on the mechanical properties of cupular deflection
in the semicircular canals. Velocity storage prolongs the
raw vestibular signal so that the angular VOR can better transduce the low-frequency components of head
rotation. The neural substrate for velocity storage may
be the medial vestibular nuclei and their interconnections, since sectioning the vestibular commissure abolishes velocity storage. Purkinje cells of the nodulus send
GABAergic projections to the vestibular nuclei to control
the velocity-storage mechanism of the VOR.
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Clinical Correlation: Cerebellar Syndromes
Three principal ocular motor syndromes may occur
in the setting of cerebellar disease depending on the
location of dysfunction, with overlap being common due to more widespread cerebellar dysfunction
(Versino et al., 1996).
Lesions of the Flocculus and Paraflocculus
Focal dysfunction of the flocculi and paraflocculi,
such as may be seen in Chiari malformation, produces several abnormalities. Gaze-evoked nystagmus results from loss of the cerebellar contribution
to the fidelity of the brainstem neural integrator.
Downbeat nystagmus and rebound nystagmus are
other common sequelae. Smooth pursuit is impaired
(choppy or saccadic), as is the ability to suppress the
VOR during combined eye –head tracking or during
caloric irrigation by fixating on a stationary target.
Finally, patients cannot adapt the VOR to changing
visual needs, such as new spectacle correction.
Lesions of the Dorsal Vermis and Fastigial Nucleus
Dorsal vermis and fastigial nucleus lesions cause
saccadic dysmetria (inaccurate saccades), typically
hypometria if the vermis alone is involved and
hypermetria if the fastigial nuclei are involved.
Unilateral lesions of the dorsal vermis would cause
ipsilateral hypometria and mild contralateral hypermetria of saccades. A unilateral lesion of the fastigial nucleus would cause ipsilateral hypermetria
and contralateral hypometria of saccades as well
as cause the eyes to tonically deviate ipsilaterally
(ipsipulsion). While such asymmetric dysfunction is
rarely seen clinically, since the fastigial projections
cross within the opposite nucleus, the same functional effect occurs in Wallenberg syndrome (below).
Because those crossed projections ascend in the contralateral uncinate fasciculus of the superior cerebellar peduncle, a lesion in the uncinate fasciculus can
cause contrapulsion of saccades. Finally, dorsal vermis and fastigial lesions can impair smooth pursuit
initiation.
Lesions of the Nodulus and Ventral Uvula
Nodulus and ventral uvula lesions lead to loss of the
GABAergic inhibition of the velocity-storage mechanism, thus maximizing the velocity-storage effect
in circumstances that would usually reduce it, such
as pitching the head forward during post-rotatory
nystagmus. The most clinically important result
of a nodulus lesion is periodic alternating nystagmus (PAN), where the velocity-storage mechanism
becomes unstable, and short-term vestibular adaptation leads to sustained horizontal nystagmus that
reverses directions every two minutes. Although
in pure form, PAN is only present in darkness, it
may be present during attempted visual fixation
if the adjacent flocculus and paraflocculus are also
involved (because of their role in VOR suppression).
Infarction of the dorsolateral medulla (generally
from occlusion of the ipsilateral vertebral or posterior inferior cerebellar arteries or vertebral dissection) causes Wallenberg syndrome, consisting of
ipsilateral impairment of facial pain and temperature sensation, Horner’s syndrome, limb ataxia, and
bulbar disturbances leading to dysarthria and dysphagia. Contralaterally, pain and temperature sensation are impaired in the trunk and limbs. Patients
commonly report vertigo and a variety of unusual
sensations of body and environmental tilt, including the room being tilted on its side or upside down.
Lateropulsion, a compelling sensation of being
pulled to one side (in this case toward the side of
the lesion), is a common complaint.
Clinical Correlation: Wallenberg Syndrome
Several ocular motor abnormalities are characteristic of Wallenberg syndrome and may be the
main or sole manifestation (Baloh, Yee, & Honrubia,
1981; Brazis, 1992). Lateropulsion of saccades develops because the lesion affects the inferior cerebellar
peduncle carrying climbing fibers from the inferior
olivary nucleus to the dorsal cerebellar vermis, leading to the functional equivalent of a fastigial nucleus
lesion. Lateropulsion of the eyes is easy to detect at
the bedside. If the patient is asked to fixate straight
ahead and gently close the eyes, the eyes will conjugately deviate toward the side of the lesion, requiring a refixation saccade back to the straight-ahead
position after opening the eyes again. Horizontal
saccades are hypermetric toward the side of the
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lesion (ipsipulsion) and hypometric contralateral to
the lesion. Vertical saccades take an oblique trajectory, with an inappropriate horizontal component
toward the side of the lesion (requiring a horizontal corrective saccade once the vertical saccade is
complete).
The lesion’s involvement of the vestibular
nuclei can produce spontaneous nystagmus (often
mixed horizontal-torsional), with slow phases usu-
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4
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Practical Anatomy and Physiology
of the Vestibular System
Jamie M. Bogle and Robert F. Burkard
introduCtion
The vestibular system is responsible for detecting head
motion and translating this information into postural
control and gaze stability. The vestibular system detects
head motion (both angular and linear accelerations) and
transmits this information into the central vestibular
system. The subsequent reflex pathways lead to vestibular-mediated reflexes involved in maintaining appropriate body posture and gait, as well as in the ability to
keep clear vision when in motion (gaze stabilization).
This chapter provides a brief overview of the
anatomy and physiology of the vestibular system.
Additionally, this chapter describes several vestibular
reflexes that help achieve postural and gaze stability.
Note that this system is quite complex and not fully
understood. Readers are encouraged to follow up with
the referenced material for detailed information on the
various aspects covered in this chapter.
PeriPheral Vestibular system anatomy
The inner ear is located within the otic capsule in the
petrous portion of the temporal bone. The bony structure, or labyrinth, houses the membranous labyrinth
comprising the tubes and sacs of the vestibular system.
The membranous labyrinth is cushioned from the bony
labyrinth by perilymph, an extracellular fluid high in
sodium (Na+) composition and found throughout the
inner ear. The vestibular membranous labyrinth is
filled with endolymph, a fluid with high concentration
of potassium (K+) (Smith, Lowry, & Wu, 1965). The
vestibular membranous labyrinth contains five structures: three semicircular canals and two otolith organs
(Figure 4–1). These five sensory structures are responsible for transmitting information about motion through
the vestibulocochlear nerve (cranial nerve VIII) and
into the central nervous system. This system is highly
complex, and research continues to better understand
its function as well as how vestibular information integrates with other sensory systems.
There are two types of vestibular sensory end
organs. The three semicircular canals (SCCs) sense
angular accelerations such as rotational head turns.
Based on their orientation in space, they are labeled as
the horizontal, superior, and posterior SCCs. They are
also known as the lateral, anterior, and inferior SCCs
(Lysakowski, McCrea, & Tomlinson, 1998). The remaining two vestibular end organs are the utricle and saccule, collectively called the otolith organs. These organs
are responsible for sensing linear acceleration, including gravity (Goldberg et al., 2012; Leigh & Zee, 2006).
Within each of these end organs are sensory structures
containing hair cells. Once stimulated, the hair cells
transmit bioelectric information through CN VIII to the
subsequent vestibular reflex pathways.
69
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Figure 4–1. Anatomy of the peripheral vestibular labyrinth. The sensory structures include the three
semicircular canals (horizontal canal, superior canal, posterior canal) and two otolith organs (utricle,
saccule). Each end organ contains its own sensory epithelium, the crista ampullaris for the semicircular canals and the maculae for the otolith organs.
mechanical energy into neural impulses encoding acceleration information.
vestibular nerve branch innervates the horizontal and superior semicircular canals and utricle, while
the inferior vestibular nerve branch innervates the posterior canal and saccule. Used with permission
of
Mayo Foundation for Medical Education and Research, all rights reserved.
Semicircular Canals
The hair cells within the sensory epithelium transmit
Note that the superior
plane that connects the bony portion of the external
auditory canal to the floor of the bony rim of the orbit
The SCCs are responsible for encoding angular acceleration. These structures are curved tubes with connections to the utricle at each end. The canals create an
arch of approximately 240°. The membranous tubes of
the SCCs are quite small, with diameters of approximately 0.4 mm and lengths of approximately 6.5 mm
(Ramprashad, Landolt, Money, & Laufer, 1984). The
horizontal SCC is responsible for sensing angular acceleration in the yaw (or horizontal) plane. This SCC is
oriented approximately 30° from the horizontal plane
or approximately 20° upward from Reid’s baseline, a
(Della Santina, Potyagaylo, Migliaccio, Minor, & Carey,
2005). The superior and posterior SCCs are oriented
orthogonally — or approximately at 90° angles — from
the horizontal SCC (Della Santina et al., 2005). The
relative angles of the canals vary across individu-
als (Bradshaw et al., 2010). This orientation of SCCs
is important as it allows each canal to sense angular
acceleration within a specific plane. The SCCs create a
three-dimensional model of the angular accelerations
of the head. Because the inner ear is interconnected via
fluid channels, and due to the less than perfect orthog-
4. PrACtiCAl AnAtomy And PHysiology oF tHE vEstiBulAr systEm 71
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onal relationship of the SCCs, it is likely that at least
two SCC sensory organs are stimulated with each head
movement (Barin & Durrant, 2000).
Each SCC has two ends, one that houses the sensory epithelium, and one that is open to the common
vestibule (utricular space) and allows for endolymph
to flow unrestricted into the SCCs (see Figure 4–1).
The horizontal SCC directly connects to the vestibule,
while the superior and posterior SCCs merge to form
the common crus prior to connecting to the vestibule.
The opposite end of this opening is the ampulla, an
enlargement in the SCC which houses the sensory epithelium. These areas contain the sensory hair cells and
nerve fibers for each vestibular end organ. The ampulla
is located at the anterior portion of the horizontal and
superior SCCs, and at the inferior portion of the posterior SCC. Within the ampulla is the sensory epithelium
called the crista ampullaris. Sitting atop the crista ampullaris is the cupula, a gelatinous structure that extends
completely across the SCC duct (Hillman & McLaren,
1979; Scherer, 2001). The cupula maintains a fluid-tight
seal across the SCC but does not actually attach to the
canal (Lysakowski et al., 1998). The cupula has the same
specific gravity as the surrounding endolymph, and
thus it does not respond to linear translations.
Otolith Organs
The two remaining vestibular end organs are the otolith organs, the utricle and saccule, which are housed
within the vestibule of the bony labyrinth (see Figure 4–1). These sac-like structures are responsible for
detecting linear accelerations such as gravity, head tilt,
and centripetal forces (Leigh & Zee, 2006). The utricle
is located directly behind the eyes, and is oriented in
a similar plane as the horizontal SCC. The utricle is
responsible for transmitting information about horizontal linear translations. Remember that the SCCs
also connect into the utricular space, allowing for the
free flow of endolymph throughout the vestibule. The
endolymphatic duct also connects to this space. It is
thought that this structure produces and absorbs endolymph, thus controlling endolymph volume and pressure from the membranous labyrinth (Gulya, 1997).
The saccule lies within the vertical plane at an approximate right angle to the utricle. The saccule is near the
cochlea, and the ductus reuniens links the endolymphatic fluid channel of the saccule and the cochlea.
The sensory epithelia of the otolith organs are flattened structures called the maculae. These structures
are quite small, measuring less than 1 mm in diame-
ter. The utricular macula is a kidney-shaped structure
located on the anterior wall. The saccular macula is
more gently curved and is located on the ventrolateral wall (see Figure 4–1). This orientation allows for
accurate transduction of both horizontal (utricle) and
vertical (saccule) linear translations. As previously
described for the cupula in the SCCs, the gelatinous
macula of the otolith organs, or otolithic membrane,
has the same specific gravity as the surrounding endolymph. However, the maculae are embedded with calcium carbonate crystals (otoconia) (Lundberg, Zhao,
& Yamoah, 2006). There are thousands of otoconia
embedded into each otolith macula (Lindeman, 1973).
While small (approximately 10 µm) (Walther et al.,
2014), the otoconia increase the specific density of the
macula, providing inertial mass and allowing the sensory hair cells to be stimulated by linear acceleration.
Vestibular Nerve
The vestibular branch of CN VIII innervates the vestibular end organs and then travels through the internal
auditory canal (or meatus) and cerebellar pontine angle
to the brainstem. The cell bodies of the vestibular nerve
are located within Scarpa’s ganglion (Brodal, 1981).
There are two branches of the vestibular nerve to each
labyrinth. The superior branch of the vestibular nerve
innervates the horizontal and superior SCCs as well as
the utricle. The inferior branch of the vestibular nerve
innervates the posterior SCC and the saccule (Naito,
Newman, Lee, Beykirch, & Honrubia, 1995). Interestingly, a small portion of the saccule is also innervated
by the superior branch of the vestibular nerve (Lindeman, 1969).
The vestibular nerve contains between 15,000 and
25,000 fibers in humans. While there is wide variability in the number of afferent fibers across individuals,
increasing age is also associated with declining afferent fibers (López, Honrubia, & Baloh, 1997; Park, Tang,
López, & Ishiyama, 2001; Richter, 1980). The superior
and inferior branches travel together to the pontomedullary junction, where they enter the vestibular nucleus
(VN). The VN has four divisions: the superior (SVN),
inferior (IVN), lateral (LVN), and medial (MVN). The
afferent fibers from the superior branch of the vestibular nerve synapse in the SVN, MVN, and LVN, with
some nerve fibers projecting directly to the cerebellum
(Brodal & Brodal, 1985; Furuya, Kawano, & Shimazu,
1975; Goldberg, 2000; Korte & Mugniani, 1979). Fibers
from the inferior vestibular nerve synapse in the MVN,
LVN, and IVN (Naito et al., 1995).
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Blood Supply
Blood supply to the vestibular end organs is through
the labyrinthine artery. The labyrinthine artery typically arises from the anterior inferior cerebellar artery,
but may also arise from the superior cerebellar artery or
basilar artery (Baloh & Honrubia, 2001). This supply
follows a similar path as the afferent nerve innervation and contains two branches. One branch, called the
superior vestibular artery, supplies the horizontal and
superior SCCs as well as the utricle. The second branch,
called the common cochlear artery, flows into the posterior SCC and saccule, as well as the cochlea. Venous
drainage follows a similar path to remove blood from
the inner ear.
VESTIBULAR AFFERENT PHYSIOLOGY
Within the inner ear, the hair cell is the mechanism for
transmitting mechanical forces into neural potentials.
The vestibular end organs are mechanoreceptors. Each
sensory epithelium contains hair cells that transduce
mechanical energy into neural responses. These hair
cells are arranged in bundles of 20 to 100 stereocilia and
1 kinocilium. The stereocilia are arranged in a stairstep
fashion so that the tallest stereocilia are adjacent to the
kinocilium. Each stereocilia is connected to its neighbor by small filaments called tip-links (Jeffries, Pickles,
Osborne, Rhys-Evans, & Comis, 1986; Pickles, Comis,
& Osborne, 1984), which allows for the whole hair cell
bundle to deflect together (Figure 4–2). The orientation
of hair cell bundles is important, as deflections toward
and away from the kinocilium produce an increase
or decrease of the vestibular afferent discharge rate,
respectively (Lowenstein & Wersäll, 1954).
Semicircular Canals
The saddle-shaped crista ampullaris contains the hair
cells and supporting cells for each SCC. The hair cell
bundles emerge from the cuticular plate at the top
of the hair cells and are embedded into the cupula.
The orientation of the kinocilium within the crista
ampullaris varies across canals and thus influences
the excitation or inhibition of the hair cells and eighth
nerve fibers (see Figure 4–1). The kinocilia of the horizontal SCC are oriented toward the vestibule. Remember that the membranous labyrinth is filled with
endolymph. As the head turns, the endolymph (which
has mass) lags behind, moving opposite to the head
movement and pushing on the cupula. When endolymph flows toward the ampulla, the stereocilia move
toward the kinocilium and depolarizes (excites) the
hair cell; the flow is described as ampullopetal. Conversely, when endolymph flows away from the
ampulla, the stereocilia move away from the kinocilium and hyperpolarizes (inhibits) the hair cell; the flow
is described as ampullofugal. The anterior and posterior SCCs are oriented differently, with kinocilia oriented away from the vestibule. Therefore, endolymph
flow toward the ampulla (ampullopetal) in the vertical canals inhibits, while flow away from the ampulla
(ampullofugal) excites the sensory epithelium (Lysakowski et al., 1998).
The SCCs between the ears work in a push-pull
mechanism to encode angular acceleration. This is
described as “coplanar function.” As such, the horizontal SCCs work as an agonist pair, as a head turn leading
to excitation (ampullopetal flow) of one horizontal SCC
will also inhibit (ampullofugal flow) the opposite side.
The vertical canals are oriented differently, as the superior SCC and the contralateral posterior SCC are paired.
Excitation (ampullofugal flow) of the superior SCC will
lead to inhibition (ampullopetal flow) of the contralateral posterior SCC and vice versa. The right superior
SCC and left posterior SCC are paired and describe the
right anterior (superior)/left posterior (RALP) plane.
Conversely, the left superior SCC and right posterior
SCC describe the left anterior (superior)/right posterior (LARP) plane. This coplanar relationship is quite
important in transmitting adequate vestibular excitation and inhibition information by enhancing the differences in neural firing between the pairs. The cupula
is an important component to the functionality of the
vestibular system. Displacement of this structure is
responsible for deflection of the underlying stereocilia,
leading to neural stimulation. The physiology of this
structure has been mathematically modeled in order to
predict the frequency and acceleration response characteristics of this system. For further reading on the pendular model of cupular physiology, see Leigh and Zee
(2006) and Goldberg et al. (2012).
Otolith Organs
The hair cell bundles are oriented differently within the
otolith organs than in the SCCs. Each organ contains
an invisible “reversal line” where the orientation of
the hair cell bundles changes direction. This reversal
figure 4–2. Endolymph flow in the semicircular canals. The membranous labyrinth of the vestibular system contains
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endolymph which flows opposite to head movement. Note in this figure that head rotation leads to an opposite
flow of endolymph that pushes on the cupula, deflecting it and leading to changes in hair cell polarity. Remember
that in the vertical canals, the kinocilia is oriented away from the vestibule. Endolymphatic flow from the vestibule
pushes on the cupula, deflecting and depolarizing the hair cells. Used with permission of Mayo Foundation for
Medical Education and Research, all rights reserved.
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