VESTIBULAR SYSTEM

The vestibulocochlear nerve (VIII) has the dual function of serving both the sense of hearing (via cochlear fibers) and proprioception (via vestibular fibers).

THE VESTIBULAR APPARATUS

A cavernous network called the bony labyrinth exists within the temporal bone on either side of the head. Within this bony labyrinth is a membranous labyrinth of roughly the same shape filled with endolymph, the same fluid present in the cochlear duct of the inner ear (Fig-1). The endolymph in both the vestibular and cochlear systems is continuous, and is formed in the endolymphatic sac, which makes contact with the fluid of the temporal dura. The space between the membranous and bony labyrinths is filled with perilymph. The membranous labyrinth is composed of three semicircular canals. Each canal is twice connected to the utriculus, a large endolymph-containing sac. The endolymph of each canal is continuous with that in the utriculus at one end, and separated from it at the other end by a flexible mechanosensitive barrier called the crista ampullaris. The crista is located in the enlarged end of each canal known as the ampulla. The anterior and posterior canals are essentially vertical when a person holds his head erect and they are at right angles to each other. The lateral canal is almost horizontal (actually elevated 23° anteriorly) and forms a plane at right angles to the other two. This geometric arrangement provides the vestibular system with the capability of detecting movements of the head in all directions. The utriculus is continuous with a second endolymphatic enlargement, the sacculus. A mechanosensitive structure, the macula acustica, is located in the wall of the utriculus with a second macula located in the saccular wall. The three cristae and two maculae are the actual proprioceptive units in each vestibular apparatus. The cristae and maculae are in neural contact with the central nervous system through SSA VIII nerve fibers. Mechanosensitive hair cells in the cristae and maculae form two-element receptors with these fibers.

Fig-1

Figure-2 illustrates the distribution of the vestibular nerve fibers to the membranous labyrinth. Notice that one branch of the nerve is distributed to each ampulla, where it distributes to the crista ampullaris hair cells. Separate branches of the nerve are also distributed to the maculae of the utriculus and sacculus, where they form two-element receptors with the macular hair cells. The Crista Ampullaris The crista ampullaris is a mechanosensitive flexible barrier to the flow of endolymph between one end of the semicircular canal and the utriculus (Fig-3). A number of sensitive hair cells are interposed with supporting cells at the base of the crista within the ampulla. The hair cell hairs project into a gelatinous mass, the cupola, which projects upward to form a flexible barrier across the space of the ampulla. The cupola behaves like an elastic diaphragm rather than like a swinging door. Angular movements of the head cause the endolymph to push against the cupola so that it bows in one direction or the other. Deflection toward the utriculus is utriculopetal deflection, while deflection away from the utriculus is utriculofugal deflection. Deflecting the cupola bends the hairs, excites the hair cells, and produces impulses in the SSA VIII nerve fibers. In this way the CNS is informed of movements of the head.
	Fig-2	Fig-3

There are two types of hair cells in the vestibular apparatus. Type I hair cells are somewhat spherical in shape with 60 to 70 small hairs (stereocilia) emerging from the cuticle (Fig-4). A particularly long hair process, the kinocilium, stands at one end of the stereocilia. Type II hair cells are more cylindrical in shape but their stereocilia and kinocilia are identical with type I cells. SSA VIII nerve fibers are in close contact with both types of cells, although they form more extensive processes around the base of type I cells. In addition to the SSA fibers, there is evidence that small-diameter efferent fibers of unknown origin also innervate the hair cells. They form direct synaptic contacts with the type II cells but appear instead to terminate on SSA fibers of the type I cells. The origin and function of these efferent fibers is unknown. It seems likely that they may in some way influence the excitability of the hair cells and their potential for producing impulses in the SSA VIII nerve fibers. Hair Cell Stimulation and Cochlear Nerve Discharge The stereocilia and kinocilium of each hair cell project up into the gelatinous cupola. Consequently, whenever the cupola is displaced, either toward the utriculus or away from it, the hairs are also deflected. Deflection of the hairs toward the kinocilium produces a change in the hair cell sufficient to increase the firing rate in the SSA VIII nerve fibers. Conversely, deflection away from the kinocilium decreases the firing rate (Fig-5).
	Fig-4	Fig-5

The hair cells in a given crista ampullaris are all orientated in the same direction so that deflection of the cupola either bends all the hairs toward the kinocilia or away from it. Thus deflection of the cupola either increases or decreases the firing rate of the SSA VIII nerve fibers.

In the lateral canals, the kinocilia all face the utriculus. In the vertical canals they all face away from the utriculus, toward the canal. Thus, utriculopetal deflection in the lateral canals produces an increase in the firing rate, while utriculofugal deflection produces a decrease. However, just the opposite is true concerning the vertical canals. Here the hair cell kinocilia are oriented in the opposite direction so that utriculopetal deflection causes a decrease while utriculofugal deflection produces an increase in the firing rate.

Coplanar Canals are Functional Units The anterior canal on one side of the head and the posterior canal on the opposite side are in the same plane. Thus the two canals are a functional unit since any head movement which causes utriculofugal deflection in the anterior canal on one side will be matched by utriculopetal deflection in the posterior canal on the opposite side (Fig-6). A similar relationship exists with the two lateral canals and they also form a functional unit (Fig-7).

Fig-6	Fig-7

Hair cells stimulate SSA VIII nerve fibers via chemical synapses. Because a fairly steady resting discharge of 40 to 60 impulses per second can be recorded in the nerve fibers, it is assumed that a small amount of transmitter chemical (possibly a catecholamine) is constantly being released. It has been proposed that displacement of the hairs toward the kinocilium increases the firing rate by increasing the rate or amount of transmitter released by the hair cell. Likewise, displacement of the hairs in the opposite direction decreases the firing rate by lowering the rate or amount of release.

In contrast to the stereocilia, which are embedded in the cuticle, the base of the kinocilium is in direct contact with the hair cell cytoplasm. The kinocilium plunging inward (with the aid of the stereocilia leaning against it) may depolarize the hair cell membrane and establish a receptor potential, which in turn causes transmitter release. Alternatively, deflection of the stereocilia away from the kinocilium pulls the kinocilium outward, hyperpolarizing the membrane and decreasing transmitter release.

The cristae are particularly sensitive to changes in angular acceleration and deceleration of the head. The greatest change in firing rate along nerve fibers from the cristae occur at the beginning and end of angular movements of the head. As Fig-7 shows, the inertia of the endolymph when the head first starts rotating to the left produces utriculopetal deflection in the left canal and utriculofugal deflection in the right canal. Thus we see a large initial change in firing rate from each canal at the beginning of the movement. However, if the rotation of the head to the left continues, we see no further change in firing rates until the rotation begins to slow down (decelerate). At this point. the inertia of the endolymph causes the cupola to deflect in the opposite direction, once again causing a change in the firing rate. This time, however, there is a decrease in the left canal and an increase in the right canal. Thus one can see that the canal system is particularly adept at signaling changes in acceleration and deceleration of the head's angular movements. Further, because the canals are arranged in three planes, angular movements in all directions are easily detected by the canal system. No doubt angular movements which are not exactly parallel with a single coplanar canal system are detected by the brain through some "weighted" input from two or more coplanar functional units.

The Macula Acustica The macula acustica is a mechanosensitive structure in the utriculus and sacculus. It is similar to the crista in that the base of the structure is composed of type I and type II hair cells (Fig-8). Likewise, the base of the hair cells forms contacts with SSA VIII nerve fibers. Maculae are also called otolith receptors because the hair processes project into a low-lying gelatinous structure which is impregnated with dense calcareous formations called otoliths or otoconia. The otolith receptors respond to static gravitational pull and are therefore well equipped to signal the position of the head in space at any given time. A basal discharge rate of the SSA VIII fibers from the utriculus is observed when the head is in the normal erect position. This rate increases to a maximum when the head is moved to a position 90° from normal (i.e., 90° forward, backward, or to either side). In addition to their gravitational or static response, utricular otolith receptors also respond to linear acceleration and deceleration of the head, thus exhibiting a dynamic response characteristic as well. Saccular otolith receptors respond only to the static position of the head in space and demonstrate no appreciable dynamic response.

Fig-8

VESTIBULAR SYSTEM INTERACTIONS

Vestibular Control of Eye Movements An interesting cooperative relationship exists between the vestibular system and the extraocular muscles of the eye. Those eye movements caused by vestibular stimulation are generally compensatory in nature, attempting to keep to the visual axis relatively fixed when the head is moved in space. This aids both vision and the maintenance of posture. As an example, a cooperative relationship exists between the lateral canals on both sides of the head that is designed to keep the eyes directed toward a reference point in the visual field as the head is moved in a lateral plane (Fig-9). Unless consciously overridden, the eyes move slowly to the left as the head is turned slowly to the right, main­taining a constant reference point in the visual field. These reflex conjugate eye movements are produced by changes in activity of the extraocular eye muscles in response to vestibular activity. A close exam­ination of Fig-9 shows that when the head is turned to the right, the endolymph in the right lateral canal deflects the cupola toward the utriculus (utriculopetal), while the endolymph of the left lateral canal deflects its cupola away from the utriculus (utriculofugal). Now if we remember that utriculopetal deflection in the lateral canals increases the firing rate while utriculofugal deflection decreases it, an examination of the neural circuitry in Fig-9 explains the slow shift of the eyes to the left. The lateral rectus muscle of the left eye and medial rectus of the right eye both contract, while their antago­nists relax, pulling the eyes slowly to the left. A similar cooperative relationship exists between the anterior canal on one side and the posterior canal on the other. The anterior canals are able to produce stimulation of the ipsilateral su­perior rectus muscle and the contralateral inferior oblique. The posterior canals produce stimulation of the ipsilateral superior oblique and the contralateral inferior rectus muscle. In this way the eyes can maintain their reference point when the head is moved through any plane. The Vestibulospinal System While the vestibular system responds primarily to movements of the head, it is able to produce far-reaching postural changes throughout the body. The vestibular system can regulate alpha and gamma motor neuron activity in the spi­nal cord through the lateral and medial vestibulospinal tracts (Fig-7). The vestibulospinal tracts originate in the vestibular nuclei of the brainstem. Those fibers which originate in the lateral vestibular (Deiter's) nucleus descend ipsilaterally in the anterior funiculus and form the lateral vestibulospinal tract. The fibers of this tract terminate in laminae VII, VIII, and IX at all levels of the cord. Arising from the medial vestibular nucleus are the fibers of the medial vestibulospinal tract. While there is a small crossed component, most of its fibers descend ipsilaterally only as far as the midthoracic level, where they too synapse in laminae VII, VIII, and IX. The vestibulospinal tracts facilitate extensor and inhibit flexor alpha and gamma motor neurons. Input to the vestibular nuclei via fibers of cranial nerve VIII from the vestibular apparatus presupposes an antigravity or postural role for the vestibulospinal tracts. Activity in these tracts is also influenced by input to the vestibular nuclei from the cerebellum, and through it, the peripheral proprioceptors of muscles, tendons, and joints.

Fig-9

The Vestibular System and the Cerebellum

Because of the role the vestibular system plays in the maintenance of posture and muscle control, it is not surprising to find that the system has a close rela­tionship with the cerebellum. Both first- and second-order vestibulocerebellar fibers end as mossy fibers on the granular cells of the cerebellar cortex of the flocculonodular lobe. In addition, the fastigial and dentate cerebellar nuclei also receive vestibular input. Presumably the cerebellar cortex integrates the vestibular input with other proprioceptive input from all parts of the body. The cerebellum is then in a position to exert influence on the postural musculature via output to the vestibular, reticular, and red nuclei. Vestibulospinal, reticulospinal, and rubrospinal fibers influence muscle activity at the spinal cord level, while cerebellar output through the thalamus to the cerebral cortex modifies motor activity at the cortical source.

Vestibulocortical Projections

In order to be consciously aware of position and movements of the head in space, it is necessary that vestibular information reach the cerebral cortex. The kinesthetic sense (conscious awareness of body position and movement) requires cortical input from peripheral proprioceptors as well as from the vestibular system. The cortical area which receives this information is located in the postcentral gyrus near the somatosensory projection of the mouth. Vestibulocortical projections appear to be primarily contralateral with intermediate synapses in the ipsilateral vestibular nuclei and the contralateral thalamus.

Vestibular System and Autonomic Effects

The effects of vestibular activity on autonomic function are well known and are grouped under the heading "motion sickness." They include effects on the vasomotor system (typically a vasodepressor action with a blood pressure drop), an increase in the rate and depth of respiration, decreased salivation, increased sweating, pupillary dilation, and disturbances of the gastrointestinal tract. Most of these effects are mediated through the sympathetic nervous system.

Tests for the Integrity of the Semicircular Canals

Certain bodily responses to vestibular stimulation are reflexly predictable, such as conjugate movements of the eyes and other postural adjustments of the body. The integrity of the various canals can be tested by their capacity to produce the expected responses. The rotation (swivel chair) test and the caloric test are both designed to do this.

The rotation test allows maximum stimulation of the horizontal and vertical canals. Maximum deflection of the cupola of a particular canal occurs when the movement of the head is in the same plane as the canal which contains that cupola. This is accomplished in the swivel chair by placing the head in various positions and then rotating the chair. Recall that maximum deflection in a canal on one side of the head is accompanied by maximum deflection in its functional counterpart on the opposite side.

Predictable responses observed with rotation tests are nystagmus, vertigo, and past pointing. Nystagmus refers to rapid to-and-fro movements of the eyes. As previously noted, the eyes slowly shift to the left as the head is turned slowly to the right. Of course there is a limit to how far left the eyes can shift if the head continues turning to the right. When they have pulled as far left as possible, they suddenly "snap" back to the right and "fix" on a new reference point in the visual field. This alternating slow phase to the left followed by a fast phase to the right continues as the head keeps rotating to the right unless consciously overridden. While nystagmus technically refers to the eye shifts in both directions, neuroscientists typically refer to nystagmus as the direction of the fast phase. For example, nystagmus is to the right in the case just described.

Because cupola deflection directly controls eye movements, and because this deflection is in one direction during the acceleration phase of the angular rotation and in the opposite direction during the deceleration phase, it follows that nystagmus is in one direction during rotation (perrotation) and in the opposite direction after rotation (postrotation). Perrotational nystagmus is in the same direction as the rotation. However, if the rotating chair is suddenly stopped, the canals cease to rotate but the inertia of the endolymph is not so easily overcome. Consequently the cupolae are deflected in the opposite direction for a brief period of time, producing a postrotational nystagmus in the direction opposite the rotation.

Vertigo and past pointing are also predictably observed following rotation in a normal individual. Vertigo is the sensation of a movement when no such movement exists. This is caused by the fact that once the actual turning stops, the inertia of the endolymph remains for a while, deflecting the cupolae and sending signals to the brain that turning is still occurring. Normally the vertigo (false sense of movement) is in the same direction as the postrotational nystagmus. The body will ordinarily attempt to reflexly make postural adjustments for the vertigo just as it would for a real movement. Thus, predictable leaning of the whole body (a reflex attempt to correct for the false movement) is typically observed following a period of rotation. Specifically, the body leans in the direction opposite the postrotational nystagmus, An extended arm also points in the direction opposite the post rotational nystagmus. This is past pointing,

The rotation test has the disadvantage of not allowing the canals on each side of the head to be tested separately. However, caloric tests, which involve the introduction of hot or cold solutions into the auditory canal, allow the clinician to test each side of the head separately. A hot water solution introduced into the auditory canal causes the endolymph to expand, deflecting the cupola in a predictable direction. This is later followed by the use of a cold water solution which cools the endolymph, producing deflection in the opposite direction. Like the rotation test, predictable changes in nystagmus, vertigo, and past pointing can be observed.