Hearing

The principal causes of significant hearing loss among older people are noise exposure, disease, heredity, and senescence. Exposure to industrial noise exceeding 90 dBA for an eight-hour workday over a period of time is known to cause permanent, high-frequency hearing loss. Additionally, a single exposure to very intense sound (exceeding 130 dBA) can also cause a permanent hearing loss that affects either all frequencies or selective, high frequencies. Diseases specific to the ear that affect adults include otosclerosis, Meniere's disease, and labyrinthitis. More than one hundred different abnormal genes causing sensorineural hearing loss have been identified. Although hereditary hearing loss accounts for about 50 percent of congenital childhood deafness, it is also thought to play a role in progressive hearing loss during later adulthood (Fischel-Godshian). At least one report describes a strong family pattern of presbycusis, particularly in women (Gates et al.). Finally, age-related deterioration of structures in the auditory system appears to occur among individuals with no significant history of noise exposure, otologic disease, or familial hearing loss.

The auditory system is housed within the temporal bone of the skull and consists of the outer ear, middle ear, inner ear, nerve of hearing (N. VIII), and central auditory nervous system. Evidence from anatomical studies of temporal bones and physiologic studies of auditory system function in older individuals suggest that age-related changes can occur at each level of the auditory system.

The outer ear consists of the pinna and the ear canal, which collect and amplify acoustic energy as it is transferred toward the tympanic membrane (eardrum). Changes commonly observed in the outer ear of older individuals include an enlargement of the pinnae, an increase in cerumen (earwax) production in the ear canal, and a change in the cartilage support of the ear canals. These factors can affect the sound field-to-eardrum transfer function and thereby alter sound transmission that is received at the tympanic membrane. Excessive cerumen, found in approximately 40 percent of an elderly population, can add a slight-to-mild high frequency conductive overlay to existing hearing thresholds.

The middle ear contains the three tiny bones, or ossicles (malleus, incus, and stapes), that are linked together as the ossicular chain. The principal function of the middle ear is to transmit acoustic energy effectively from the ear canal to the inner ear without an energy loss. The two middle ear muscles, the tensor tympani and stapedius, contract in response to loud sound to protect the inner ear from damage. With aging, the ligaments, muscles, and ossicles comprising the ossicular chain may degenerate, presumably causing a conductive hearing loss. Electrophysiologic measures of middle ear function (tympanometry) further indicate that the middle ear stiffens with age, thereby reducing the transmission of acoustic energy through the middle ear (Wiley et al., 1996).

The inner ear is composed of a fluid-filled bony labyrinth of interconnected structures including the cochlea. The cochlea contains the sensory end organ for hearing (the organ of Corti), which supports the inner and outer hair cells. These microscopic sensory hairs are essential for processing sound. The cochlea analyzes the frequency and intensity of sound, which is transmitted to the nerve of hearing by the inner hair cells. At the same time, the outer hair cells initiate a feedback mechanism resulting in the presence of acoustic energy in the ear canal (otoacoustic emissions). One prominent change in the inner ear with age is a loss of inner and outer hair cells in the basal turn of the cochlea (Schuknecht). Age-related loss of inner hair cells in this region produces a high frequency hearing loss and has been called sensory presbycusis. The loss of outer hair cells is expected to alter the feedback mechanism, possibly causing hearing loss and limited capacity to finely tune the frequency of sound. Electrophysiologic measures of outer hair cell function indicate that thresholds of otoacoustic emissions increase linearly with increasing age, although this age effect is confounded by the presence of hearing loss among older subjects (Stover and Norton). Another prominent change in the inner ear with aging is a decrease in the volume of vascular tissue, the stria vascularis, lining the outer cochlear wall. The stria vascularis maintains the chemical balance of the fluid in the cochlea, which in turn nourishes the hair cells. A loss of the vascular tissue produces a permanent hearing loss affecting most frequencies, called strial presbycusis (Schuknecht, 1993).

Approximately thirty-five thousand neurons comprise the afferent auditory branch of the eighth cranial nerve (N. VIII) in young, healthy adults. The auditory branch of N. VIII recodes the frequency, intensity, and timing information received from the hair cells and transmits it to the nuclei of the central auditory nervous system. With age, there is a loss of auditory neurons that accumulate over the life span. Considerable evidence demonstrates that the neuronal population comprising the auditory nerve is markedly reduced in aged human subjects compared to younger subjects. The effect on hearing, called neural presbycusis, is a mild loss of sensitivity but a considerable deficit in discriminating attributes of sound, including speech.

The nuclei of the central auditory nervous system transmit acoustic signals to higher levels, compare signals arriving at the two ears, recode the frequency of sound, and code other characteristics of the temporal waveform. Final processing of acoustic information is carried out in the primary auditory cortex, located in the superior temporal gyrus. There is a substantial reduction in the number of neurons in each nucleus of the central auditory nervous system with age, with the most prominent decline occurring in the auditory cortex (Willott). These alterations are thought to affect processing of complex acoustic stimuli, including distorted speech signals and sequences of tonal patterns.