Damage to the cochlea, especially to the hair cells of the organ of Corti, produces sensorineural hearing loss by several means. Prolonged exposure to loud occupational or recreational noises can lead to hair cell damage, including mechanical disruption of the stereocilia. Such damage is localized in the outer hair cells along the basilar membrane at a position related to the pitch of the sound that produced it. Antibiotics such as streptomycin and certain diuretics can cause rapid and irreversible damage to hair cells similar to that caused by noise, but it occurs over a broad range of frequencies. Diseases such as meningitis, especially in children, can also lead to sensorineural hearing loss.
In carefully selected patients, the use of a cochlear implant can restore some function to the profoundly deaf. The device consists of an external microphone, amplifier, and speech processor coupled by a plug-and-socket connection, magnetic induction, or a radio frequency link to a receiver implanted under the skin over the mastoid bone. Stimulating wires then lead to the cochlea. A single extra-cochlear electrode, applied to the round window, can restore perception of some environmental sounds and aid in lip-reading, but it will not restore pitch or speech discrimination. A multielectrode intracochlear implant (with up to 22 active elements spaced along it) can be inserted into the basal turn of the scala tympani. The linear spatial arrangement of the electrodes takes advantage of the tonotopic organization of the cochlea, and some pitch (frequency) discrimination is possible. The external processor separates the speech signal into several frequency bands that contain the most critical speech information, and the multielectrode assembly presents the separated signals to the appropriate locations along the cochlea. In some devices the signals are presented in rapid sequence, rather than simultaneously, to minimize interference between adjacent areas.
When implanted successfully, such a device can restore much of the ability to understand speech. Considerable training of the patient and fine-tuning of the speech processor are necessary. The degree of restoration of function ranges from recognition of critical environmental sounds to the ability to converse over a telephone. Cochlear implants are most successful in adults who became deaf after having learned to speak and hear naturally. Success in children depends critically on their age and linguistic ability; currently, implants are being used in children as young as age 2.
Infrequent problems with infection, device failure, and natural growth of the auditory structures may limit the usefulness of cochlear implants for some patients. In certain cases, psychological and social considerations may discourage the advisability of using of auditory prosthetic devices in general. From a technical standpoint, however, continual refinements in the design of implantable devices and the processing circuitry are extending the range of subjects who may benefit from cochlear implants. Research directed at external stimulation of higher auditory structures may eventually lead to even more effective treatments for profound hearing loss.
vertical (superior) canal and the posterior vertical canal, which are perpendicular to each other. The planes of the anterior vertical canals are each at approximately 45° to the midsagittal section of the head (and at 90° to each other). Thus, the anterior canal on one side lies in a plane parallel
The vestibular apparatus in the bony labyrinth of the inner ear. The semicircular canals sense rotary acceleration and motion, while the utricle and saccule sense linear acceleration and static position.
with the posterior canal on the other side, and the two function as a pair. The horizontal canals also lie in a common plane.
Near its junction with the utricle, each canal has a swollen portion called the ampulla. Each ampulla contains a crista ampullaris, the sensory structure for that semicircular canal; it is composed of hair cells and supporting cells encapsulated by a cupula, a gelatinous mass (Fig. 4.24). The cupula extends to the top of the ampulla and is moved back and forth by movements of the endolymph in the canal. This movement is sensed by displacement of the stereocilia of the hair cells. These cells are much like those of the organ of Corti, except that at the "tall" end of the stereocilia array there is one larger cilium, the kinocilium. All the hair cells have the same orientation. When the stereocilia are bent toward the kinocilium, the frequency of action potentials in the afferent neurons leaving the ampulla increases; bending in the other direction decreases the action potential frequency.
The role of the semicircular canals in sensing rotary acceleration is shown on the left side of Figure 4.25. The mechanisms linking stereocilia deflection to receptor potentials and action potential generation are quite similar to those in the auditory hair cells. Because of the inertia of the endolymph in the canals, when the position of the head is changed, fluid currents in the canals cause the deflection of
The sensory structure of the semicircular canals. A, The crista ampularis contains the hair (receptor) cells, and the whole structure is deflected by motion of the endolymph. B, An individual hair cell.
the cupula and the hair cells are stimulated. The fluid currents are roughly proportional to the rate of change of velocity (i.e., to the rotary acceleration), and they result in a proportional increase or decrease (depending on the direction of head rotation) in action potential frequency. As a result of the bilateral symmetry in the vestibular system, canals with opposite pairing produce opposite neural effects. The vestibular division of cranial nerve VIII passes the impulses first to the vestibular ganglion, where the cell bodies of the primary sensory neurons lie. The information is then passed to the vestibular nuclei of the brainstem and from there to various locations involved in sensing, correcting, and compensating for changes in the motions of the body.
The remaining vestibular organs, the saccule and the utricle, are also part of the membranous labyrinth. They communicate with the semicircular canals, the cochlear duct, and the endolymphatic duct. The sensory structures in these organs, called maculae, also employ hair cells, similar to those of the ampullar cristae (Fig. 4.26). The macular hair cells are covered with the otolithic membrane, a gelatinous substance in which are embedded numerous small crystals of calcium carbonate called otoliths (otoconia). Because the otoliths are heavier than the endolymph, tilting of the head results in gravitational movement of the otolithic membrane and a corresponding change in sensory neuron action potential frequency. As in the ampulla, the action potential frequency increases or decreases depending on the direction of displacement. The maculae are adapted to provide a steady signal in response to displacement, in addition, they are located away from the semicircular canals and are not subject to motion-induced currents in the endolymph. This allows them to monitor the position of the head with respect to a steady gravitational field. The maculae also respond proportionally to linear acceleration.
The vestibular apparatus is an important component in several reflexes that serve to orient the body in space and maintain that orientation. Integrated responses to
Head rotation Semicircular canal Utricle
Slow eye movements
The role of the semicircular canals in sensing rotary acceleration. This sensation is linked to compensatory eye movements by the vestibuloocular reflex. Only the horizontal canals are considered here. This pair of canals is shown as if one were looking down through the top of a head looking toward the top of the page. Within the ampulla of each canal is the cupula, an extension of the crista ampullaris, the structure that senses motion in the endolymph fluid in the canal. Below each canal is the action potential train recorded from the vestibular nerve. A, The head is still, and equal nerve activity is seen on both sides. There are no associated eye movements (right column). B, The head has begun to rotate to the left. The inertia of the endolymph causes it to lag behind the movement, producing a fluid current that stimulates the cupulae (arrows show the direction of the relative movements). Because the two canals are mirror images, the neural effects are opposite on each side (the cupulae are bent in relatively opposite directions). The reflex action causes the eyes to move slowly to the right, opposite to the direction of rotation (right column), they then snap back and begin the slow movement again as rotation continues. The fast movement is called rotatory nystagmus. C, As rotation continues, the endolymph "catches up" with the canal because of fluid friction and viscosity, and there is no relative movement to deflect the cupulae. Equal neural output comes from both sides, and the eye movements cease. D, When the rotation stops, the inertia of the endolymph causes a current in the same direction as the preceding rotation, and the cupulae are again deflected, this time in a manner opposite to that shown in part B. The slow eye movements now occur in the same direction as the former rotation.
The relation of the otoliths to the sensory cells in the macula of the utricle and sac-cule. The gravity-driven movement of the otoliths stimulates the hair cells.
vestibular sensory input include balancing and steadying movements controlled by skeletal muscles, along with specific reflexes that automatically compensate for bodily motions. One such mechanism is the vestibuloocular reflex. If the body begins to rotate and, thereby, stimulate the horizontal semicircular canals, the eyes will move slowly in a direction opposite to that of the rotation and then suddenly snap back the other way (see Fig. 4.25, right). This movement pattern, called rotatory nystagmus, aids in visual fixation and orientation and takes place even with the eyes closed. It functions to keep the eyes fixed on a stationary point (real or imaginary) as the head rotates. By convention, the direction of the rapid eye movement is used to label the direction of the nystagmus, and this movement is in the same direction as the rotation. As rotation continues, the relative motion of the endolymph in the semicircular canals ceases, and the nystagmus disappears. When rotation stops, the inertia of the endolymph causes it to continue in motion and again the cupulae are displaced, this time from the opposite direction. The slow eye movements are now in the same direction as the prior rotation,- the postrotatory nystagmus (fast phase) that develops is in a direction opposite to the previous rotation. As long as the endolymph continues its relative movement, the nystagmus (and the sensation of rotary motion) persists. Irrigation of the ear with water above or below body temperature causes convection currents in the endolymph. The resulting unilateral caloric stimulation of the semicircular canal produces symptoms of vertigo, nystagmus, and nausea. Disturbances of the labyrinthine function produce the symptoms of vertigo, a disorder that can significantly affect daily activities (see Clinical Focus Box 4.2).
Related mechanisms involving the otolithic organs produce automatic compensations (via the postural and ex-traocular musculature) when the otolithic organs are stimulated by transient or maintained changes in the position of the head. If the otolithic organs are stimulated rhythmically, as by the motion of a ship or automobile, the distressing symptoms of motion sickness (vertigo, nausea, sweating, etc.) may appear. Over time, these symptoms lessen and disappear.
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