Sound Localization. Sound coming from one side of the head will arrive sooner at, and its intensity will be slightly higher in, the ipsilateral ear. Cells in the superior olivary nuclei receive signals from both ears and, therefore, play a major role in the localization of sound. They compare the time of arrival and the intensity and send this information to higher centers for sound localization.
Stapedial Ref ex. Intense sound damages the hair cells in the cochlea and they do not regenerate. The intensity of sound entering the cochlea is decreased by an order of magnitude by the contraction of the stapedius muscle (CN VII) in the stapedial refl ex. Sound from either or both ears projects to both superior olivary nuclei, from which signals are sent to both facial nuclei to drive contraction of the stapedius muscles in both ears. Unfortunately, the onset of muscle contraction does not oc-cur quickly enough to protect the cochlea from the damaging effects of percussive sounds such as hammering or gunshots. Furthermore, the refl ex depends on muscle action and, therefore, will fatigue after prolonged use.
Motor Olivocochlear Pathway. The inhibitory pathway to the outer hair cells, which inhibits electromotility, arises in the superior olivary complex. The role of this pathway is thought to be in sharpening pitch perception.
CASE HISTORY GUIDING QUESTIONS
1. Why did Paul experience “ringing” in his ears before he saw his doctor?
2. What are other causes of hearing loss?
3. In CN VIII lesions, can there be impairment of vestibular function without hearing loss or vice versa?
4. What other CNs can be involved when there is a tumor of CN VIII?
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1. Why did Paul experience “ringing” in his ears before he saw his doctor?
The perception of ringing in the ears in the absence of an external sound source is called “tinnitus” (from the Latin tinnire, to ring). Ten to fi fteen percent of the population experience tinnitus, and for many, it can be bothersome enough that they seek medical help. It is generally accepted that the ringing sensation is due to hyperexcitability in the central hearing pathway, most commonly in the primary auditory cortex and inferior colliculus, in response to sensorineural hearing loss in the cochlea or auditory nerve. In Paul’s case, his auditory nerve damage caused the increased activity in his central auditory pathway. Tinnitus is more common in the elderly, who have presbycusis (hearing loss related to aging). Temporary tinnitus can be caused by high doses of acetyl salicylic acid, which inhibits the cochlear amplifi er.
2. What are other causes of hearing loss?
Hearing loss can occur as a result of a lesion or disease process anywhere along the course of the auditory pathway from the auditory apparatus to the audi-tory cortex. The tympanic membrane, ossicles, and cochlea can be damaged by trauma or infection. Interference with the transmission of sound to the cochlea is defi ned as a conductive hearing loss. The organ of Corti and/or the audi-tory nerve may be damaged by noise exposure, infections, toxic drug exposure, or tumors. The central auditory pathways can be affected by strokes, multiple sclerosis, or tumors. Interference with the transduction mechanism or the trans-mission of impulses to the auditory cortex is defi ned as a sensory hearing loss.
Damage to the transmission mechanism, transduction mechanism, or the audi-tory nerve results in hearing loss only on the affected side. Within the central nervous system, however, hearing signals are carried bilaterally in the lateral lemniscus and represented bilaterally in the auditory cortex. Unilateral lesions in the central nervous system, therefore, do not usually result in hearing loss in the ear on the affected side. In fact, total removal of one cerebral hemisphere of the brain in humans does not result in any major change of auditory sensitivity in either ear.
3. In CN VIII lesions, can there be impairment of vestibular function with-out hearing loss or vice versa?
Although referred to as the “vestibulocochlear nerve,” the nerve is actually two distinct nerves, vestibular and cochlear, that travel together. It is, therefore, pos-sible for only one of the components to be involved in a disease process, but because of the close proximity in their peripheral course through the internal auditory meatus and across the cerebellopontine angle, both are usually involved simultaneously.
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FIGURE VIII–12 An enlarged tumor (schwannoma) in the cerebellopontine angle compromising cranial nerves V, VII, and the vestibular and cochlear divisions of VIII (illustrated in green). This is a sag-ittal section through the jugular foramen.
Once the fibers enter the brain stem and synapse with their nuclei, the axons take different courses and are less likely to be affected simultaneously.
4. What other CNs can be involved when there is a tumor of CN VIII?
Tumors such as schwannomas and meningiomas typically compress CN VIII at the cerebellopontine angle. Other CN involvement is a refl ection of the close proximity of these nerves to CN VIII. CN VII is most often affected because it traverses the internal auditory meatus and the cerebellopontine angle beside CN VIII (see Fig.
VIII–12). Facial nerve damage results in ipsilateral facial paralysis. CN V can also be involved resulting in facial numbness, tingling, and sometimes facial pain. As the tumor enlarges, it can also compress CNs IX and X.
In addition to the peripheral CNs, an expanding cerebellopontine angle tu-mor may compress the brain stem and interfere with transmission of sensory and motor signals between the cerebrum and the spinal cord. The magnetic resonance imaging (MRI) scan (Fig. VIII–13) shows significant compression of his brain stem and cerebellum.
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