Clinical Neuroanatomy, 27 ed.

CHAPTER 17. The Vestibular System

The vestibular system participates in the maintenance of stance and body posture; coordination of body, head, and eye movements; and visual fixation. It includes the peripheral vestibular receptors, vestibular component of the VIII nerves, and the vestibular nuclei and their central projections.


The membranous labyrinth, filled with endolymph and surrounded by perilymph, lies in the bony labyrinthine space within the temporal bone of the skull base (Fig 17–1). Two special sensory systems receive their input from structures in the membranous labyrinth: the auditory system, from the cochlea (see Chapter 16), and the vestibular system, from the remainder of the labyrinth.


FIGURE 17–1 The human ear (compare with Fig 16–1).

The static labyrinth gives information regarding the position of the head in space; it includes the specialized sensory areas located within the saccule and the utricle (see Fig 17–1). Within the utricle and saccule, otoliths (small calcium carbonate crystals, also termed otoconia) are located adjacent to hair cells clustered in macular regions. The otoliths displace the hair cell processes and excite the utricle and saccule in response to horizontal and vertical acceleration.

The kinetic labyrinth consists of the three semicircular canals. Each canal ends in an enlarged ampulla, which contains hair cells, within a receptor area called the crista ampullaris. A gelatinous partition (cupula) covers each ampulla and is displaced by rotation of the head, displacing hair cells so that they generate impulses. The three semicircular canals are oriented at 90° to each other, providing a mechanism that is sensitive to rotation along any axis.


The peripheral branches of the bipolar cells in the vestibular ganglion course from the specialized receptors (hair cells) in the ampullae and from the maculae of the utricle and the saccule. The central branches run within the vestibular component of cranial nerve VIII to enter the brain stem and end in the vestibular nuclei (Figs 17–1 and 17–2; see also Chapter 7).


FIGURE 17–2 Principal vestibular pathways superimposed on a dorsal view of the brain stem. Cerebellum and cerebral cortex removed. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

Some vestibular connections go from the superior and lateral vestibular nuclei to the cerebellum, where they end in the cerebellar cortex within the flocculonodular component (see Chapter 7). Others course from the lateral vestibular nuclei into the ipsilateral spinal cord via the lateral vestibulospinal tracts, from the superior and medial vestibular nuclei to nuclei of the eye muscles, and to the motor nuclei of the upper spinal nerves via the medial longitudinal fasciculi (MLF) of the same and opposite sides (Fig 17–2). The medial vestibulospinal tract (the descending portion of the MLF) connects to the anterior horn of the cervical and upper thoracic cord; this tract is involved in the labyrinthine righting reflexes that adjust the position of the head in response to signals of vestibular origin. Some vestibular nuclei send fibers to the reticular formation. Some ascending fibers from the vestibular nuclei travel by way of the thalamus (ventral posterior nucleus) to the parietal cortex (area 40).


As previously noted, the vestibular nerve conducts two types of information to the brain stem: the position of the head in space and the angular rotation of the head. Static information about the position of the head is signaled when pressure of the otoliths on the sensitive areas in the utricle and saccule is transduced to impulses in the inferior division of the vestibular nerve (Figs 17–1 and 17–3). Dynamic information about rotation of the head is produced by the three semicircular canals (superior, posterior, and lateral) (Fig 17–4). Within each ampulla, a flexible crista changes its shape and direction according to the movement of the endolymph within the canal, so that any rotation of the head can affect the crista and its afferent nerve fibers (Fig 17–5). Acting together, the semicircular canals send impulses along the superior division of the vestibular nerve to the central vestibular pathways.


FIGURE 17–3 Macular structure. (Reproduced, with permission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 11th ed. McGraw-Hill, 2005.)


FIGURE 17–4 Diagram of a crista in an opened ampulla.


FIGURE 17–5 Schematic illustration of the effects of head movements (top) and the subsequent cessation of movement (bottom) on the crista and the direction of endolymph flow.

The vestibular apparatus thus provides information that contributes to the maintenance of equilibrium. Together with information from the visual and proprioceptive systems, it provides a complex position sense in the brain stem and cerebellum.

When the head moves, a compensatory adjustment of gaze, the vestibulo-ocular reflex, is required to keep the eyes fixed on one object. Clockwise rotation of the eyes is triggered by counterclockwise rotation of the head so as to maintain fixation of the eyes on a target in the external world. The pathways for the reflex are via the medial longitudinal fasciculus and involve the vestibular system and the motor nuclei for eye movement within the brainstem (see Fig 8–7).


Nystagmus is an involuntary back-and-forth, up-and-down, or rotating movement of the eyeballs, with a slow pull and a rapid return jerk. (The name comes from the rapid jerking component, which is a compensatory adjustment to the slow reflex movement.) Nystagmus can be induced in normal individuals; if it occurs spontaneously, it is a sign of a lesion. The lesions that cause nystagmus affect the complex neural mechanism that tends to keep the eyes constant in relation to their environment and is thus concerned with equilibrium.

Physiologic nystagmus can be elicited by turning the eyes far to one side or by stimulating one of the semicircular canals (usually the lateral) with cool (30 °C) or warm (40 °C) water injected into one external ear canal (Fig 17–6). Cool water producesnystagmus toward the opposite side; warm water produces nystagmus to the same side. (A mnemonic for this is COWS: cool, opposite, warm, same.) Peripheral vestibular nystagmus results from stimulation of the peripheral vestibular apparatus and is usually accompanied by vertigo. Fast spinning of the body, sometimes seen on the playground, is an example: If children are suddenly stopped, their eyes show nystagmus for a few seconds. Professional skaters and dancers learn not to be bothered by nystagmus and vertigo. Central nervous system nystagmus is seldom associated with vertigo; it occurs with lesions in the region of the fourth ventricle. Optokinetic (railroad or freeway) nystagmus occurs when there is continuous movement of the visual field past the eyes, as when traveling by train. Nystagmus may occur during treatment with certain drugs. For example, nystagmus is often seen in patients treated with the anticonvulsant phenytoin. Streptomycin and other drugs may even cause degeneration of the vestibular organ and nuclei.


FIGURE 17–6 Example of caloric test with normal results. Stimulation of left ear for 40 s with cool (30 °C) water produces nystagmus lasting 110 seconds.

Vertigo, an illusory feeling of spinning, falling, or giddiness with disorientation in space that usually results in a disturbance of equilibrium, can be a sign of labyrinthine disease originating in the middle or internal ear. Adjustment to peripheral vestibular damage is rapid (within a few days). Even though a labyrinth is not intact or functioning, balance is still remarkably good when vision is present: Visual information can even compensate for the loss of both labyrinths. Vertigo can also result from tumors or other lesions of the vestibular system (eg, Meniere’s disease, or paroxysmal labyrinthine vertigo) or from reflex phenomena (eg, seasickness).

Vestibular ataxia, with clumsy, uncoordinated movements, may result from the same lesions that produce vertigo. Nystagmus is often present. Vestibular ataxia must be distinguished from other types: cerebellar ataxia (see Chapters 7 and 13) and sensory ataxia (caused by lesions in the proprioceptive pathways; see Chapter 5).

Interruption of the pathway between the nuclei of nerves VIII, VI, and III (the medial longitudinal fasciculus, pathway of the vestibulo-ocular reflex) may occur. This results in internuclear ophthalmoplegia, an inability to adduct the eye ipsilateral to the lesion (Fig 17–7).


FIGURE 17–7 Internuclear ophthalmoplegia interrupting the medial longitudinal fasciculus on the left (a left internuclear ophthalmoplegia). Eye movement command from the lateral gaze center in the paramedian pontine reticular formation on the right cannot reach the left oculomotor nucleus (see Fig 8–7). As a result, the left eye cannot voluntarily turn beyond the midline to the right. (Reproduced, with permission, from Aminoff ML, Greenberg DA, Simon RP: Clinical Neurology, 6th ed. McGraw-Hill, 2005.)


A 38-year-old male clerk saw his doctor because of sudden episodes of nausea and dizziness. These attacks had started 3 weeks earlier and seemed to be getting worse. The abnormal episodes at first lasted only a few minutes, during which “the room seemed to spin.” Lately, they had been lasting for many hours. A severe attack caused the patient to vomit and to hear abnormal sounds (ringing, buzzing, paper-rolling sounds) in the left ear. He thought that he was becoming deaf on that side.

The neurologic examination was within normal limits except for a slight sensorineural hearing loss in the left ear. Computed tomography examination of the head was unremarkable.

What is the probable diagnosis?

Cases are further discussed in Chapter 25.


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