The vestibular end organs communicate via the vestibular branch of the eighth cranial nerve with targets in the brainstem and the cerebellum that perform much of the processing necessary to compute head position and motion. As with the cochlear nerve, the vestibular nerves arise from a population of bipolar neurons, the cell bodies of which in this instance reside in the vestibular nerve ganglion (also called Scarpa's ganglion; see Figure 14.1). The distal processes of these cells innervate the semicircular canals and the otolith organs, while the central processes project via the vestibular portion of cranial nerve VIII to the vestibular nuclei (and also directly to the cerebellum) (Figure 14.10). Because vestibular and auditory fibers run together in the eighth nerve, damage to this structure often results in both auditory and vestibular disturbances. The vestibular nuclei are important centers of integration, receiving input from the vestibular nuclei of the opposite side, as well as from the cerebellum and the visual and somatic sensory systems.

Figure 14.10

Connections underlying the vestibulo-ocular reflex. Projections of the vestibular nucleus to the nuclei of cranial nerves III (oculomotor) and VI (abducens). The connections to the oculomotor nucleus and to the contralateral abducens nucleus are excitatory (more...)

One of the main functions of the vestibular system is to coordinate head and eye movements (other functions include protective or escape reactions; see Box D). The vestibulo-ocular reflex (VOR) in particular is a mechanism for producing eye movements that counter head movements, thus permitting the gaze to remain fixed on a particular point (Box C; see also Chapter 20). For example, activity in the left horizontal canal induced by leftward rotation of the head excites neurons in the left vestibular nucleus and results in reflexive eye movements to the right. This effect is due to excitatory projections from the vestibular nucleus to the contralateral nucleus abducens that, along with the oculomotor nucleus, help execute conjugate eye movements. For instance, horizontal movement of the two eyes toward the right requires contraction of the left medial and right lateral rectus muscles. Vestibular nerve fibers originating in the left horizontal semicircular canal project to the medial and lateral vestibular nuclei (see Figure 14.10). Excitatory fibers from the medial vestibular nucleus cross to the contralateral abducens nucleus, which has two outputs. One of these is a motor pathway that causes the lateral rectus of the right eye to contract; the other is an excitatory projection that crosses the midline and ascends via the medial longitudinal fasciculus to the left oculomotor nucleus, where it activates neurons that cause the medial rectus of the left eye to contract. Finally, inhibitory neurons project from the medial vestibular nucleus to the left abducens nucleus, directly causing the motor drive on the lateral rectus of the left eye to decrease and also indirectly causing the right medial rectus to relax. The consequence of these several connections is that excitatory input from the horizontal canal on one side produces eye movements toward the opposite side. Therefore, turning the head to the left causes eye movements to the right. In a similar fashion, head turns in other planes activate other semicircular canals, causing other appropriate compensatory eye movements. The rostro-caudal set of cranial nerve nuclei involved in the VOR (i.e., the vestibular, abducens and oculomotor nuclei), as well as the VOR's persistence in the unconscious state, make this reflex especially useful for detecting brainstem damage in the comatose patient (see Box C).

Box D

Mauthner Cells in Fish.

Loss of the VOR can have severe consequences. A patient with vestibular damage finds it difficult or impossible to fixate on visual targets while the head is moving, a condition called oscillopsia. If the damage is unilateral, the patient usually recovers the ability to fixate objects during head movements. However, a patient with bilateral loss of vestibular function has the persistent and disturbing sense that the world is moving when the head moves. The underlying problem in such cases is that information about head and body movements normally generated by the vestibular organs is not available to the oculomotor centers, so that corrective eye movements cannot be made.

Descending projections from the vestibular nuclei are essential for postural adjustments of the head and body. As with the VOR, these postural reflexes are extremely fast, in part due to the small number of synapses interposed between the vestibular organ and the relevant motor neurons (Box D). Axons from the medial vestibular nucleus descend in the medial longitudinal fasciculus to reach the upper cervical levels of the spinal cord (Figure 14.11). This pathway regulates head position by reflex activity of neck muscles in response to stimulation of the semicircular canals from rotational accelerations of the head. For example, during a downward pitch of the body (e.g., tripping), the superior canals are activated and the head muscles reflexively pull the head up. The dorsal flexion of the head initiates other reflexes, such as forelimb extension and hindlimb flexion, to stabilize the body and protect against a fall (see Chapter 17).

Figure 14.11

Descending projections from the medial and lateral vestibular nuclei to the spinal cord. The medial vestibular nuclei project bilaterally in the medial longitudinal fasciculus to reach the medial part of the ventral horns and mediate head reflexes in (more...)

The inputs from the otolith organs project mainly to the lateral vestibular nucleus, which in turn sends axons in the lateral vestibulospinal tract to the spinal cord (see Figure 14.11). The input from this tract exerts a powerful excitatory influence on the extensor (antigravity) muscles. When hair cells in the otolith organs are activated, signals reach the medial part of the ventral horn. By activating the ipsilateral pool of motor neurons innervating extensor muscles in the trunk and limbs, this pathway mediates balance and the maintenance of upright posture. Decerebrate rigidity, which is characterized by rigid extension of the limbs, arises when the brainstem is transected above the level of the vestibular nucleus. The tonic activation of extensor muscles in this instance suggests that the vestibulospinal pathway is normally strongly suppressed by descending projections from higher levels of the brain, especially the cerebral cortex (see also Chapter 17).