ANATOMY OF VESTIBULAR APPARATUS

ANDPHYSIOLOGY OF EQUILIBRIUM

ByDr. Syed Salman Hussaini

The inner ear has five different organs which are functionally related and establish neural connections in the brain with the oculomotor and postural control systems.

The vestibular system plays a lesser role for the control of posture and balance, but is of great importance clinically due to its common and dramatic involvement during pathological condition affecting the inner ear.

Hearing and vestibular organs contain mechanoreceptors or sensory cells with directionally sensitive ciliary bundles or hairs.

The vestibular organ consists of a delicate system of membranous ducts containing sensory epithelia or mechanoreceptors important for the sense of gravity and balance.

The sensory epithelium is located in the three ampullae of the semicircular canals and in the maculae of the saccule and utricle.

The organ contains endolymph and is surrounded by perilymphatic fluid.

The membranous system, or 'labyrinth' due to its complexity, is connected to the cochlea through the thin reunion duct.

In addition, the various portions of the vestibular organ are interconnected by small canals: the utricular duct and the saccular duct which merge and form the utriculosaccular duct.

This canal runs posteriorly and enters the internal aperture of the bony vestibular aqueduct.

Here, it forms the endolymphatic duct which widens triangularly within the bone of the posterior surface of the petrous bone into the endolymphatic sac.

The endolymphatic sac ends blindly within a dural duplicate in the posterior cranial fossa in close association with the sigmoid sinus and venous drainage of the brain.

The endolymphatic duct and sac, which are closely related to the brain, are thought be involved in the reabsorption of endolymph and regulation of endolymph pressure.

VESTIBULAR SENSORY SYSTEM The vestibular sensory organ is a so-called 'open'

system that rests on a balance of function between the left and right ear.

There is a continuous influx of nerve impulses (over one million per second) from each vestibular nerve to the central nervous system (CNS).

This resting discharge is the source of vestibular tonus.

A viral infection, fracture or a vascular disturbance (enhancement or impairment) in one of the two organs will result in an imbalance between tht sides and give rise to clinical symptoms often perceived as violent by the patient.

Typically is a rotatory type of vertigo.

THE VESTIBULAR NERVE The vestibular nerve contains approximately 18,000

afferent nerve fibres whose size varies between 2 and 15 microns.

The number of ganglion cells has been estimated to be approximately 18,000 in young adults, decreasing to around 12,000 at the age of 80 years.

The vestibular ganglion or Scarpa's ganglion consists of bipolar neurons located in the lateral part the internal auditory canal.

It consists of a superior and an inferior group of cells associated with the superior and inferior vestibular nerve.

The superior branch innervates the cristae of the superior and lateral canals, the macula of the utricle and the anterosuperior part of the the saccule.

The inferior branch supplies the crista of the posterior canal and the main portion of the macula of the saccule.

The nerves contain both large and small nerve fibres;

The larger nerve fibles are predominantly involved in the innervation of type I hair cells located in the central region of the maculae (striola) or the summit of the crista.

The small fibres are more abundant at the slope and the peripheral region of the maculae.

The vestibular ganglion cells are unmyelinated and surrounded by a thin sheath of Schwann cell.

In the internal auditory meatus, the vestibular and cochlear nerves merge.

During their course to the brainstem, the facial nerve becomes located further up the brain.

A small arterial branch from the anterior inferior cerebellar artery (AICA) runs between the VlIth and VIII nerve on the brainstem.

The vestibular nerve contains efferent nerve fibres terminating in both the cochlear and vestibular sensory organs.

Inner ear effererents of central origin arise from the general visceral efferent cell column of the facial nerve and are parts of the nervus intermedius having autonomic functions.

The human vestibular labyrinth is supplied by approximately 200-300 efferent nerve fibres.

There is both an ipsilateral and contralateral origin of vestibular efferents in the brainstem.

There is a bimodal type of innervation where the efferents only make direct contact with the type II cells, while on the type I cells the efferent terminals always contact the afferent nerve fibre or terminal.

Thus a higher or central control of afferent sensory activity could act both at a presynaptic level on the afferent fibres, but also as a direct modulation on the peripheral receptor as can be observed in other sensory systems.

It may allow the primary afferent receptors to both increase and decrease their activity as a response of stimulation.

VESTIBULAR SENSORY CELLS, TYPE I AND TYPE II The sensory epithelia contain two types of sensory cells.

The cells are classified as type I and type II sensory cells.

The type I cells are flask-shaped and surrounded by a nerve chalice formed by the terminal end of the afferent nerve fibre of the vestibular nerve.

Many of the calyces have collateral extensions that end on type II hair cells.

Type II hair cells synapse with these collaterals and also directly with the outer membrane of calyces surrounding type I hair cells.

Efferent nerve endings also terminate on the afferent nerve calyce and on type II hair cells.

Type I cells, correspond to the inner hair cells of the organ of Corti.

Type II cells, resemble outer hair cells of the organ of Corti.

They are cylindrical in shape, but have the same arrangement of stereo- and kinocilia as the type I cells.

The upper surface of the hair cell contains approximately 70 stereocilia and one kinocilium arranged with the longest stereocilia positioned adjacent to the kinocilium.

The stereocilia in the macula are a few microns long, while in the crista they measure up to over 35 microns.

The stereocilia contain actin filaments.

All the cilia within a bundle move together as if joined to one another.

The upper surface of the cell contains a thicker region, called the 'cuticular plate', into which the stereocilia extend their rootlets.

SACCULE AND UTRICLE The utricle is oblong, irregular and slopes anteriorly

upwards.

It lies superior to the saccule .

The macula utriculi, lies in the horizontal plane located in the dilated superior portion of the utricle.

The mean area in adults and children is 4.30 mm2

The macula utriculi contains approximately 33,000 hair cells.

The right and left macula lie in the same plane.

The human saccule lies in a spherical recess in the medial wall vestibule, is hook-shaped and lies in vertical plane.

The mean area in adults is 2.4 mm2.

The saccular macula contains approximately 18,000 hair cells.

Overlying the neuroepithelium is a calcareous material consisting of a multitude of small cylindrical and hexagonally shaped bodies with pointed ends, usually named otoconia.

These otoconia are anchored and partially embedded in a gelatinous substance forming the otoconial membrane.

The hair processes of the sensory cells project into the otoconial membrane and are displaced mechanically by the otoconial mass relative to the sensory epithelium.

Each macula is be divided into two areas by a narrow curved line in its centre termed the 'striola'.

The striola area contains a higher concentration of type I cells.

The sensory cells change orientation along this line so that cells are often 'mirror-shaped' with opposite polarity as to the location of the kinocilium.

In the utricle, the kinocilia face the striola.

In the saccule the kinocilium is polarized away from the striola.

OTOCONIAL LAYER The otoconial membrane consists of a gelatinous layer, a

subgelatinous space and otoconia.

The otoconia measure 3-19 microns in length.

They consist of an organic protein matrix together with inorganic calcium carbonate crystallized in the form of calcite.

Secretion of organic material occurs from the apical cytoplasm of adjacent supporting cells.

The enzyme carbonic anhydrase is located in the epithelium which catalyzes the chemical reaction H

2O +

CO2 ---> H

2C0

3.

The carbonic acid combines with calcium to form crystals of CaC0

3 which is trapped in the matrix leading to the

formation of otoconia.

STRUCTURE AND FUNCTION OF THE AMPULLAAND CUPULA

The three semicircular canals (superior, posterior and lateral) provide a complete coordinate system.

The horizontal canal generally lies in a horizontal plane when the head is oriented in an active position.

The superior opening of the horizontal and superior canal, and the inferior opening of the posterior canal widen into an ampulla which contains the crista ampullaris.

The crest is covered by sensory cells whose kinocilia are directed in the same direction.

In the crista of the lateral semicircular canal, the polarization is towards the utricle, while it is polarized away from the utricle in the superior and posterior canal cristae.

The afferents in the horizontal canal are stimulated when endolymph flows against the utriculus, while the two vertical canals are stimulated when endolymph moves against the ampulla.

The sensory epithelium on the crista is covered by a gelatinous mass called the cupula.

The cupula in the ampulla of the semicircular canal helps in transferring endolymph fluid movement stimuli to the hair cells.

This gives rise to kinetic reflexes.

It contains proteoglycans arranged in a filamentous network.

SUPPORTING AND 'DARK' CELLS

The sensory cells are surrounded by supporting cells whose function is partly secretory in nature.

They provide support and insulation for the sensory cells and also form precursor cells for sensory hair cells.

The membranous labyrinth contains so-called 'dark' cells in all sensory epithelia, except the saccule.

The cells have an irregular surface and resemble the marginal cells of the stria vascularis.

In addition, pigmented cells or melanocytes are often associated with the dark cells, which is similar to the situation in the stria vascularis in the cochlea.

These cells are important for the development and maintenance of the endolymph adjacent to the vestibular mechanoreceptors thereby playing a role for the proper function of the electric activity of the sensory cells and initiating conductive neural responses of afferent nerves.

Degrading otoconia can often be seen on the surface of the dark cells, suggesting that these cells are involved in the degradation and resorption of dislodged otoconia.

VASCULAR SUPPLY OF THE VESTIBULAR ORGAN

The inner ear blood supply derives from the labyrinthine artery, which is a branch of the AICA and vertebrobasilar artery system.

It is an end artery.

The labyrinthine artery divides into the superior vestibular artery, which supplies the vestibular nerve, utricle and parts of the semicircular canals, and the common cochlear artery which divides into the cochlear artery and the vestibulocochlear artery.

This artery divides into vestibular branches at the basal turn of the cochlea and supplies the saccule and the semicircular canals.

The vestibular labyrinth is drained both through a labyrinthine vein running through the meatus and through the vein of the vestibular aqueduct.

PHYSIOLOGY OF EQUILIBRIUM

ROLE OF THE VESTIBULAR SYSTEM: INTRODUCTION

The main function of the mammalian vestibular system is to generate information for the central nervous system with a four-fold purpose:

1. provide general orientation of the body with respect to gravity;

2. enable balanced locomotion and body position;

3. readjust autonomic functions after body reorientation; and

4. ensure gaze stabilization.

Several input systems provide information to the brain, such as the visual, vestibular and proprioceptive systems.

Central processing of all this information in the brain leads to specific outcomes:

• the vestibuloocular reflex (VOR) to ensure gaze stabilization;

• the vestibulospinal reflex (VSR) and the vestibulocollic reflex (VCR) to ensure maintenance of an upright position of the body and trunk and head stabilization in space;

• orientation and navigation and the perception of self-position with respect to the surroundings and gravity, mediated by the vestibular cortex;

• autonomic function adjustments after alterations of body orientation.

Motion decomposition and orientation in the head

Every motion in space can be broken down into three rotational degrees of freedom (yaw, pitch and roll) and three translational degrees of freedom (left-right, up-down, for-aft).

No event in one degree of freedom can be described by the others, hence every movement is uniquely and appropriately described by a combination of all six degrees of freedom.

The anatomical design of the motion sensors in the peripheral vestibular system in the inner ear reflects these six degrees of freedom.

The semicircular canals measure predominantly rotations, whereas the macules of the utricle and saccule detect mainly translations.

The left and right canals are parallel systems, i.e. the left posterior canal is parallel with the right anterior canal which both lie in a plane denoted as the right anterior-left posterior (RALP) plane.

With the right posterior canal, the left anterior constitutes the left anterior-right posterior (LARP) plane.

Both horizontal canals are also parallel with each other in the lateral plane.

The horizontal canal makes an angle of approximately 30° with respect to the horizontal axis of the upright head.

The angles of the vertical canal are approximately 45° with the saggital plane of the head.

Movement detection

Basic laws of physics are responsible for the detection of movement or orientation by the vestibular system.

The first law of Newton states that 'objects in motion will stay in motion until acted upon by a force.

This force can either change the objects direction or speed.

The second law states that a force acting on an object equals mass times acceleration (F = m x a).

The movements are sensed in the vestibular organ by a rigid coupling of sensory epithelium to the bony structure.

Thus, a fluid-filled system is attached to the skull and the inertial forces (upon head acceleration, as well as gravity) drive the fluid.

Motion of the fluid lags behind any motion of the head and this relative displacement is the trigger for movement detection.

To limit the movement of the hair cells triggered by accelerations that drive head movements, the canal system is designed such that the deflection of the hair cells is proportional to the head velocity.

OTOLITH ORGANS The gravitational force acts permanently, hence gravitational

acceleration needs to be detected continuously, and this function is served by the otolith organs, which detect all linear accelerations.

The orientation of the otolith organs, the saccule and utricle, is relatively orthogonal to each other, with the utricle being horizontal and the saccule predominantly vertical.

Consequently, motion in the horizontal plane triggers predominantly the utricle, whereas vertical movements trigger mainly the saccule.

This is enabled by means of an otolithic membrane, i.e. a gelatineous membrane stacked with otoconia (calcium carbonate crystals), which are characterized by a density that is considerably higher than that of the surrounding endolymph.

Hair cells are embedded at the base of the gelatineous membrane, so that any movement of the membrane results in a deflection of the hair cells, which in turn codes for a signal to the brain.

NYSTAGMUS The eye response to a head rotation consists of a

combination of a slow phase or drift until the eye reaches the edge of the outer canthus, and a fast phase to reset the eye in its initial position.

This saw-tooth pattern is called nystagmus.

The direction of the nystagmus is defined by the fast reset phase, since this is the most easy for the clinician to identify.

The slow phase, however, represents the actual vestibular output and is quantified.

An upward excursion, by convention on electronystagmography or video nystagmography, represents eye deviation to the right.

If the slope of the sawtooth is upward to the right, i.e. a positive slope, this corresponds to a slow drift of the eye to the right, followed by a quick leftward reset saccade, as represented by a steep downward trace. This is defined as a left nystagmus.

It is quantified by measurement of the slope of the upward trace, which indicates the speed of the eye movement (degrees/second).

The semicircular canals and the otoliths provide the inputs for the vestibuloocular reflex.

Horizontal VOR compensates for both horizontal rotation and horizontal translation.

The former is due to the canal system where the latter is due to the utricular system.

It is therefore more convenient to use the angular VOR (aVOR) and linear VOR (lVOR).

The semicircular canal system is not designed for sustained rotations, and even rotation at relatively high but constant speeds (> 200 degrees/second) is not sensed by the SCC.

Only the acceleration or deceleration phase is detected.

During constant speed rotations, elastic forces pull the cupula again into its centre position.

However, after sudden cessation of the rotation (e.g. with a deceleration of 400 degrees/second2), the endolymph continues to move within the SCC and a nystagmus in the opposite direction becomes evident for another 20-30 seconds.

The subject has the impression of being spun around in the opposite direction.

VELOCITY STORAGE

The time constant during which the cupula repositions itself is determined as approximately five to seven seconds, which implies that after 12 seconds the cupula is almost entirely restored to its central position.

This gradual decrease in cupular deviation results in a decrease in firing rate of the vestibular neurons to the brain, suggesting erroneously a progressively lower head velocity.

The fact that the nystagmus outlasts this mechanical phenomenon is due to the so-called velocity storage mechanism (VSM), which is a neurophysiological process, taking place mainly in the nucleus prepositus hypoglossus and the adjacent medial vestibular nucleus.

The VSM serves to maintain the VOR at low frequencies (below about 0.02 Hz).

In conditions where visual information of the surrounding rotating world is present during sustained rotations, the optokinetic reflex comes into play and, although slower in response, this takes over the fading performance of the vestibular system.

The transition between both reflexes is facilitated by the VSM.

The VSM not only regulates the dynamics of the VOR, but also accounts for optokinetic (after) nystagmus (OKN), i.e. the reflexive eye movements that are induced by a moving background (e.g. while looking outside the window of a moving train).

The velocity storage mechanism coordinates these two oculomotor responses that are related to self-motion. Whereas the VOR reflects high-frequency behaviour, the OKN reflects low-frequency characteristics.

Matching of their time constants in the brain assures smooth transition from the quick-onset vestibular response into the slow-onset optokinetic response.

Together, the VOR initially, and the OKN subsequently, matched and fine-tuned by the VSM, ensure gaze stabilization.

Semicircular canal stimulation and VOR generation A normal resting discharge rate of approximately 90 spikes

per second is modulated, such that increase of this rate corresponds with an excitation and decrease with Inhibition.

The polarization of the hair cells in the horizontal semicircular canal is such that deflection of the stereocilia in the cupula towards the kinocilium (ampullo or utriculopetal) results in hair cell depolarization and consequently the activity of the primary afferent neurons increases.

Deflection of the stereocilia away from the kinocilium (ampullo or utriculofugal) results in hair cell hyperpolarization and decreased primary afferent neuron activity.

The left and right semicircular canals are oriented in the head such that any movement always induces an antagonistic response in both canals.

In first approximation, this VOR process is a three arc neuron reflex (first order vestibular neurons, second order vestibular neurons and oculomotor plant neurons).

The simplified principle of VOR generation (yaw plane rotation and horizontal SCC) is as follows:

1. During head rest, hair cells in both see have a resting discharge rate of 90 spikes per second.

2. Head rotation is to the right.

3. Endolymph fluid lags behind, i.e. moves relative to the left within each see due to inertia.

4. The cupula bends to the left in each canal.

5. In the (leading) right SCC, the stereocilia bend towards the kinocilium.

6. In the (following) left SCC, the stereocilia bend away from the kinocilium.

7. The discharge rate increases in the leading right ear (e.g. from 90 to 300 spikes per second).

8. The discharge rate decreases in the following left ear (e.g. from 90 to 20 spikes per second).

9. The vestibular nuclei interpret the difference in discharge rates between left and right SCC as movement to the right, and therefore trigger the oculomotor nuclei to drive the eyes to the left to maintain gaze stabilization.

Similar to the horizontal canal, a push-pull principle also governs the vertical canal excitatory and inhibitory functions.

For example, the left anterior canal is excited, while the right posterior canal is inhibited for the same movement.

Also, the vertical canals are direction sensitive, but at this stage ampullopetal movements result in a decreased firing rate.

Thus, the ampullar deflection in the vertical canals, corresponding to excitation, is in the opposite direction to the horizontal sec.

For the horizontal canal, excitation is elicited upon ampullopetal endolymph movement (towards the vestibulum-utricle), whereas for both the vertical posterior and anterior SCC ampullopetal flow is inhibitory.

Every stimulation in whichever direction always evokes the push-pull principle.

When the head is tilted sidewards, a torsional nystagmus is generated, as both posterior and anterior canals are stimulated.

When the head is pitched forward, both left and right anterior canals are stimulated, whereas both posterior canals are inhibited.

This produces an upward eye movement.

The same applies when the head is tilted backwards, but now both posterior canals are stimulated producing a downward compensatory eye movement.

NYSTAGMUS INDUCED BY ACUTE UNILATERAL DEAFFERENTIATION

The push-pull principle is very convenient to explain the origin of the nystagmus observed during acute peripheral lesions.

In the case of an acute unilateral vestibular deafferentiation (u VD) on, for example, the right side, all three right canals and the otoliths cease spontaneous activity (from 90 spikes per second to zero), while the spontaneous activity of the left SCC remains at 90 spikes per second.

Although the head is not moving, the brain perceives an apparent imbalance (R, 0 spikes/second versus L, 90 spikes/second) similar to, for example, when the left system is triggered during head movements towards the left.

This tonic imbalance drives the vestibular and, consequently, the ocular motor nuclei to move the eyes towards the right, as would be appropriate for a head movement towards the healthy side (left).

The brain erroneously interprets the abruptly decreased or absent firing rate of the ipsilateral affected peripheral system as a relative increase of the contralateral system, resulting in a nystagmus that beats away from the acute lesion.

CENTRAL PROJECTIONS OF THE PERIPHERALVESTIBULAR SYSTEM

In the brainstem, four vestibular nuclei (VN) are identified: the superior vestibular nuclei (SVN), lateral vestibular nuclei (LVN), medial vestibular nuclei (MVN) and descending vestibular nuclei (DVN).

From there, several projections are found to the oculomotor nuclei, the lateral and medial vestibulospinal tract, the vestibulocerebellum (floculus, nodulus), the parapontine reticular formation (PPRF), the nucleus prepsositus hypoglossus, nucleus tractus solitarius, and the parietoinsular vestibular cortex (PIVC).

The vestibulocerebellum plays a predominant role in the fine tuning of the vestibular functions.

PROJECTIONS TO THE CENTRAL NUCLEI

Two types of neurons triggered by the lateral SCC input have been traced to the medial vestibular nucleus, namely type 1 and type 2 neurons;

Their resting discharge rates are approximately 80 to 90 spikes/second.

Increased rates, however, can exceed 300 spikes/second.

Some type 1 neurons are excitatory and some are inhibitory.

Primary vestibular afferents synapse with inhibitory, as well as excitatory type 1 neurons.

Upon head rotation to one side, denoted as the ipsilateral side, the ampulla of the ipsilateral horizontal canal is stimulated followed by an immediate increase in firing rate of the neurons, proportional to the velocity of the head turn.

These signals project mainly on to the ipsilateral MVN, but other parts of the vestibular nuclei are also involved.

After passing along the primary afferent, the vestibular signals are relayed into the VN.

From there, axons decussate on to the contralateral abducens nucleus which innervate the lateral rectus of the contralateral eye through the VIth nucleus.

Additionally, the interneurons of the contralateral abducens nucleus project through the longitudinal medial fasciculus to the ipsilateral medial rectus subnucleus in the oculomotor nucleus (III) that activates the medial rectus muscle of the ipsilateral eye.

There is also an accessory pathway that originates from projections of the ipsilateral horizontal canal ampulla on to the ipsilateral magnocellular part of the medial vestibular nucleus.

From there, increased activity is transmitted via the ascending tract of Deiters (ATD) on to the medial rectus subnucleus of the ipsilateral oculomotor nucleus, activating the medial rectus muscle of the ipsilateral eye.

This drives both eyes to rotate towards the side opposite to the direction of the head to stabilize the image on the retina.

In addition to the contraction of the appropriate eye muscles (ipsilaterally the lateral rectus and contralaterally the medial rectus), a relaxation of the antagonist eye muscles has to be initiated in the context of the push-pull principle.

This is generated by inhibitory type 1 neurons in the ipsilateral MVN.

These inhibitory type 1 neurons project on to the ipsilateral abducens neurons and interneurons and, by inhibition, relax the lateral rectus on the ipsilateral eye through the Vlth nerve.

Likewise, the medial rectus of the contralateral eye is relaxed by inhibition of the contralateral oculomotor neurons where the signals come from the ipsilateral superior vestibular neurons and pass through the medial longitudinal fascicle (MLF).

To enhance this mechanism even further, at the same time, the contralateral ampulla is deflected such that the firing rate of the primary afferents is decreased.

This inhibits the contralateral medial vestibular nuclei, resulting in an opposite effect for the antagonist eye muscles, again optimizing gaze stabilization during movement.

To summarize, generation of the VOR is mediated through a combination of signals corning from both labyrinths.

During rotation to the ipsilateral side, the ipsilateral horizontal SCC with ampullopetal endolymph movement will transmit an increased firing rate to the central VN, whereas the contralateral SCC will transmit a decreased firing rate to the contralateral VN due to the ampullopetal endolymph movement.

Commissural pathways In the VN, there are also type 2 secondary vestibular

neurons, which behave exactly in an opposite manner to type 1 neurons.

Activating the inhibitory type 2 neurons silences the neighbouring type 1 neurons.

Whereas type 1 neurons increase their discharge rate upon ipsilateral head acceleration, inhibitory type 2 neurons decrease their firing rate.

For movement towards the contralateral side, ipsilateral type 1 neurons decrease their firing rate and ipsilateral type 2 neurons increase it.

The VOR-generating mechanism is enhanced in a positive feedback loop by commissural pathways where the excited type 1 neurons in the ipsilateral MVN excite the type 2 neurons on the contralateral side that in their turn also silence the contralateral type 1 neurons.

Excitation of the ipsilateral type 1 neurons is increased as the silenced type 1 neurons on the contralateral MVN inhibit the ipsilateral type 2 neurons, so that their inhibitory effect is reduced on the ipsilateral type 1 neurons.

Therefore, type 1 cells receive direct input from the ipsilateral SCC, as well as indirect input from the contralateral SCC.

Principle of the head impulse (thrust) test The head-impulse or head-thrust test, has become

established in clinical examination of the vertiginous patient.

It detects severe unilateral loss of semicircular canal function clinically.

The head-thrust test is positive for the side that causes the refixation saccade upon thrust.

Vestibulospinal reflex This head movement is actually a head nystagmus meant

for gaze stabilization

The extraocular muscles are the effector organs for the VOR, while the extensor muscles of neck, trunk, arms and limbs are those for the vestibulospinal reflex.

Similar to the VOR, the same push-pull mechanisms are used for controlling the balance between extensor and flexor muscles.

Any change in movement, detected by the vestibular organ, is compensated by a series of contractions and relaxations of several muscles.

Since the freedom of motion of the body is much larger than that of the eye, a multitude of muscles are involved in the reaction chain to maintain upright position and stability.

These reflexes are mediated through projections of the vestibular nuclei on to the medial and lateral vestibulospinal tract.

These pathways project to the lower limb and neck muscles to maintain an upright position and balanced locomotion.

The driving input here is mainly gravity detected by the otolith system.

However, proprioceptive and visual information are also necessary to provide the correct body position.