A. The otolith organs (Utricle and Saccule) detect tilting of the head and linear acceleration.
The otolith organs include two endolymph-filled chambers within the labyrinth, the utricle and the saccule (
- Hair cells are located in a sensory epithelium called the macula.
- The tips of hair cell stereocilia project into a gelatinous cap, which is covered in small calcium carbonate crystals called otoliths.
- Movement of the head displaces otoliths and bends the stereocilia, resulting in development of a receptor potential in the same way as that described for auditory hair cells.
- The otolith organs transduce two types of information, the static angle (tilting) of the head and the presence of linear acceleration.
- Tilting of the head changes the angle between the otolith organs and the direction of the force of gravity. Different degrees of tension are placed on hair cell stereocilia, depending on their orientation. All possible angles are represented because the macula of each utricle is oriented horizontally and the macula of each saccule is oriented vertically.
- Linear acceleration (e.g., starting and stopping when riding in a vehicle) also displaces the otoliths and excites hair cells in the maculae. (Note: When traveling at a constant velocity, there is no acceleration, resulting in the sensation of being perfectly still.)
B. Three semicircular ducts (anterior, posterior, lateral) detect angular acceleration produced by rotation of the head.
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 vestibular ganglion is located in the internal auditory canal which is a bony canal within the petrous part of the temporal bone of the skull.
More specifically, it sits in the fundus (the lateral end) of the internal auditory canal, near where the canal divides into its superior and inferior branches. It contains the bipolar cell bodies of the vestibular nerve (the vestibular division of cranial nerve VIII — the vestibulocochlear nerve).
These neurons carry sensory information about balance and head position from the vestibular apparatus of the inner ear (the utricle, saccule, and three semicircular canals) to the brainstem.
The central branches run within the vestibular component of cranial nerve VIII to enter the brain stem and end in the vestibular nuclei
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).
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.
Macular structure. (Reproduced, with permission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 11th ed. McGraw-Hill, 2005.)
Diagram of a crista in an opened ampulla.
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.
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, 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).
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.