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.
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. Nystagmus can be induced in normal individuals; if it occurs spontaneously. It can be a sign of a lesion. 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 produces nystagmus 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 with the anticonvulsant phenytoin. Streptomycin and other drugs may even cause degeneration of the vestibular organ and nuclei.
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, Ménière'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).
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 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.
Neurologic examination was within normal limits except for a slight sensorineural hearing loss in the left ear. Computed tomography was unremarkable.
What is the probable diagnosis?
Cases are further discussed in Chapter 25.
BOX 17–1 Essentials for the Clinical Neuroanatomist After reading and digesting this chapter, you should know and understand:
Labyrinth and peripheral vestibular receptors
Vestibular pathways: vestibular nuclei
Clinical correlations: nystagmus and vertigo
Internuclear opththalmoplegia (Figs 8–6 and 17–7)