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CHAPTER 41 OTOLOGIC DISORDERS

CHAPTER 41 OTOLOGIC DISORDERS
Practice of Geriatrics
CHAPTER 41 OTOLOGIC DISORDERS
Bradford S. Patt, M.D., F.A.C.S.
External Auditory Canal
Middle Ear
Inner Ear
Vertigo
Auditory Dysfunction
Otologic disorders can affect the aged in many ways, causing problems that involve the external auditory canal, the middle ear, and the inner ear. Sensorineural hearing loss and aural rehabilitation are two other areas that have significant ramifications in the aged.
EXTERNAL AUDITORY CANAL
Anatomy
Changes in the auditory canal associated with aging are better understood in the light of knowledge of the normal anatomy of the ear. The external canal extends from the opening of the ear laterally to the tympanic membrane medially (Fig. 41-1). The skin of the outer or lateral portion of the canal is thick and contains numerous hair follicles and sebaceous and cerumen glands. It also includes well-developed dermal and subcutaneous layers. The skin of the medial portion, in contrast, overlies the periosteum and is thin; it is firmly attached to the underlying bone and has few hair follicles and glands.1

Figure 41-1 Types of hearing loss. This cross section demonstrates the external, middle, and inner regions of the ear. The type of hearing loss is also classified according to the region of the ear involved. M = malleus; I = incus; S = stapes.

Age-Related Changes
Two kinds of hair grow within the external auditory canal. Minute vellus hairs cover almost all of the ear canal, while larger tragi hairs are laterally situated in the external canal. The tragi hairs are a secondary sex characteristic and become coarser, larger, and more noticeable in the third or fourth decades of life. The tragi are also found on the auricle but only in males.1
Cerumen glands are actually modified apocrine sweat glands. In the ear canal they are responsible for the distinctive odor of cerumen. Cerumen glands open onto the skin or into hair follicles just external to the opening of sebaceous gland ducts. In the hair follicle, sebum, apocrine secretions, and desquamated epithelial cells combine to form wet or dry cerumen depending on a person’s phenotype. Cerumen glands atrophy in the ear canals of the elderly, leading to an increased impaction of wax in the older male population.
Impactions
Cerumen impactions occur more often in elderly men because of the large tragi in the external ear canal that trap the drier wax secondary to atrophy of the cerumen glands. Impactions can be remedied in several ways. If the wax is soft, gentle irrigation of the canal with warm water may be attempted. Dry, firm wax may be softened with ceruminolytic agents (e.g., Debrox or Ceruminex) and then irrigated. Wax that remains after irrigation should be carefully extracted using a curette and an otoscope or microscope. It is important to avoid trauma to the skin of the canal because it can lead to bleeding, hematoma, or infection.2
Dermatitis
Itching in the external auditory canal is also due to atrophy of the glands in the canal. Dermatitis presents as a constant itching in the canal, and a cycle of itch-scratch-itch ensues, leading to desquamation of the canal.3 Occasionally a normal appearing canal can itch, but normally the lack of cerumen in the canal is a good clue to the onset of dermatitis.
Treatment is aimed at adding moisture to the external ear using lubricating agents such as glycerin or mineral oil. Overuse of alcohol-based mixtures should be avoided because these tend to dry the ear further. Instillation of steroid-based creams in the external canal with a syringe may be effective in more resistant cases. Always be aware that itching can be a sign of early infection, and a complete examination of the canal is warranted before initiating any treatment.
Infections
Aging is associated with an increased incidence of fungal infections in the external canal due to the aforementioned age-related changes in the canal. Fungal otitis is caused by increased moisture in the external canal resulting from hearing aid use or trapped moisture due to cerumen impaction. Unlike bacterial infection, fungal otitis presents as persistent itching without acute pain, although some tenderness may be present. There is usually some discharge or odor from the external canal. Treatment consists of debridement of the discharge within the ear, culture of the discharge, and use of antifungal medication. Because the most common organisms involved are Candida and Aspergillus species, clotrimazole (Lotrimin) drops, usually mixed with a steroid-type liquid, are used to resolve the infection.3 Other drops used include those based on acetic acid or boric acid (e.g., Otic Domeboro or Vo-Sol Otic ear drops); antifungal creams may also be used. Fungal infections can be recalcitrant to any treatment, and frequent debridement of the canal may be the only way to resolve the problem. Systemic treatment is not warranted in most cases of fungal otitis.
Bacterial otitis externa presents as acute pain of the ear canal associated with tragal tenderness, canal erythema and edema, and foul discharge.2,3 Treatment includes thorough cleansing of the canal and the instillation of antibiotic and steroid-based drops (e.g., Cortisporin Otic). Severe swelling of the canal may require intubation of the canal with a cotton or Merocel wick to allow medication to enter the canal. Persistent symptoms may require systemic antibiotics and culture of the canal. Antibiotics used should cover gram-negative organisms, especially Pseudomonas aeruginosa. If pain continues despite these measures, or if the patient is diabetic or otherwise immunocompromised, malignant otitis externa should be suspected.
Tumors
Tumors involving the external canal usually involve the auricle and include actinic keratosis, basal cell carcinoma, and squamous cell carcinoma. These lesions present most commonly in patients 50 to 60 years old. Any nonhealing lesion in the elderly should undergo biopsy. Treatment in the early stages involves excision with adequate margins and immediate reconstruction. In patients with larger lesions excision with delayed reconstruction or radiation therapy may be required.
MIDDLE EAR
Anatomy
The middle ear includes the tympanic membrane, the tympanic cavity, two muscles (the tensor tympani and the stapedius), and three bony ossicles (malleus, incus, and stapes).
Age-Related Changes
The middle ear undergoes senile changes that affect the ossicles and their respective articulations. Erosive changes within the joint capsule may range from mild to severe and can occasionally lead to narrowing of the joint space between the ossicles. Severe changes may lead to calcification of the joint capsule, diffuse calcification of the articular cartilages and disk, and obliteration of portions or all of the joint space. All individuals over 70 years of age show moderate to severe degeneration of the middle ear. Fortunately, even complete obliteration of the joint space within the ossicles causes no identifiable loss of sound transmission through the middle ear. Aging does not directly affect the conductive hearing mechanism.
INNER EAR
Anatomy
The inner ear is encased in a dense capsule, which includes the vestibule, three semicircular canals (balance organs), the cochlea (hearing organ), and the cochlea and vestibular aqueduct.4 The common denominator of function of the vestibule and cochlea is the hair cell. Degeneration of the hair cells in the vestibular and cochlear systems causes loss of function in these areas, leading to vertigo and hearing loss, respectively.
VERTIGO
Dizziness, disequilibrium, and vertigo are common complaints of the elderly. By age 65, 90% of adults have listed imbalance as the primary reason for visiting the doctor.5 An estimated 13 million persons over age 65 in the United States are significantly affected by vertigo or some type of balance disturbance. To understand the management of vertiginous patients, it is important to understand the general principles of balance control. Loss of balance is a common denominator in many elderly patients’ complaints of dizziness.
Balance is maintained by the accurate and rapid integration of three primary sensory inputs—visual, vestibular, and somatosensory—within the brain, leading to the delivery of appropriate task-specific motor signals to the eye, trunk, and limb musculature. A sense of imbalance, therefore, can come from (1) an absence of two or more sensory inputs, (2) an orientationally incorrect sensory input, (3) poor central nervous system integration of sensory information, or (4) faulty motor signal or motor response.6,7 In patients with dizziness resulting from altered sensory information, imbalance does not occur until either the sensory input from vision and proprioception is reduced and vestibular cues are faulty, or the conflict between different sensory cues cannot be resolved quickly enough to produce the correct motor response. In contrast, central causes of dizziness imply an improper integration of normal yet conflicting sensory information and the production of appropriate muscle action. The treatment of balance disorders must not be limited solely to the role of the inner ear taken in isolation but should also focus on the interaction with sensory inputs from the central nervous system and proprioception.7,8
Another issue is the symptoms created by acute inner ear dysfunction versus those generated by either abnormal visual and somatosensory cues or problems with the resolution of sensory conflicts. Acute unilateral dysfunction presents as true vertigo (a false sense of motion). Defective sensory selection or conflict resolution between the senses leads to persistent feelings of disequilibrium rather than episodic illusions of motion. Vertigo, therefore, is the most distinct sensation and is most likely created by paroxysmal changes in eighth cranial nerve function. The problem with evaluating a patient with vertigo is the nervous system’s remarkable ability to compensate for peripheral (eighth cranial nerve) vestibular disease. In many instances, vertigo experienced by the patient produces a paucity of physical findings on examination. In many cases, longitudinal follow-up and repeated examinations are necessary to document changes in vestibular function.8
Evaluation of the Dizzy Patient
HISTORY
Seventy-five percent of dizzy patients can be diagnosed on the basis of a complete history using a live interview and a written questionnaire. The questionnaire should include six major categories: (1) A description of the dizzy sensation without using the word dizzy. In most cases of vertigo, the patient has no trouble in describing the illusion of motion. In all other forms of dizziness or disequilibrium, the patient usually struggles to describe what he or she experiences. (2) Direct questions about the history of vertigo. Questions may include those about the sensations the patient experiences during the dizzy spells or what initiates the attacks of vertigo. (3) Typical accompanying symptoms of peripheral vestibular disease. The presence of distinct attacks, nausea, worsening of symptoms with movement, and a duration of vertigo from seconds to hours are all clues that support a diagnosis of a peripheral etiology of vertigo. (4) Typical accompanying symptoms of central vestibular disease. Associated neurologic deficits, syncope, and altered mentation all indicate the presence of posterior fossa–cerebellar disease. (5) Typical hearing complaints. Unilateral tinnitus, fullness, or hearing loss are important lateralizing symptoms. (6) General history, including the use of habit medications. Sedative medications, caffeine, tobacco, alcohol, and stress all play a potential role in the dizzy patient.5,6
Based on the history alone, patients with distinct attacks of vertigo and episodic unilateral auditory complaints are likely to have a disorder of the eighth cranial nerve. Patients with vertigo with auditory symptoms may still have neuronitis or benign paroxysmal vertigo (BPV) or a variety of extralabyrinthine problems. Patients with unilateral auditory complaints without vertigo may have either a nonvestibular disease or a slowly compensating unilateral disease (e.g., acoustic neuroma). Finally, patients without vertigo or unilateral auditory complaints belong to a large group of patients with either partially compensated vestibular disease, diffuse central, metabolic, or vascular disorders, or psychogenic disorders.6
PHYSICAL EXAMINATION
Every dizzy patient requires a full medical evaluation, including blood pressure and cardiac and pulmonary examinations as well as neurologic and neuro-otologic examinations. General medical causes of vertigo, including hypertension, hypotension, and cardiac arrhythmias, must be excluded. Furthermore, vision checks are important to rule out simple problems with acuity.
The otologic examination focuses on tympanic membrane and middle ear abnormalities and on the presence of vertigo or nystagmus with pneumatic otoscopy. In the neuro-otologic examination one looks for cranial nerve deficits as well as the presence of nystagmus. Nystagmus may be spontaneous, positional, or gaze-related or may be present on headshake. Cerebellar tests of the upper and lower extremities are performed to detect dysmetria. Finally, the Romberg test and gait testing are used to evaluate the patient’s static and dynamic postural control.
LABORATORY TESTS
Vestibular function tests are performed to quantify the degree to which a person is affected by vertigo and may identify the source of the problem. Unfortunately, these tests can show great variability in results, especially in the elderly population. Vestibular testing is used to determine the primary source of the disorder, whether peripheral or central, and whether the disorder is unilateral or bilateral. Quantitative testing includes electronystagmography (ENG) with caloric stimulation, rotary chair testing, and computerized posturography. Magnetic resonance imaging (MRI) with gadolinium is an important test that is used to rule out vascular loops, tumors, or other central nervous system problems (e.g., multiple sclerosis, infarcts).9
DIFFERENTIAL DIAGNOSIS
Vertigo can be related to acute unilateral peripheral dysfunction, acute central dysfunction, or secondary peripheral involvement with a systemic process.
Acute Unilateral Dysfunction
Acute unilateral dysfunction generates vertigo by sending asymmetrical labyrinthine signals to the vestibular nuclei; this asymmetry is misinterpreted as motion, which the patient senses. In such cases, the duration of the spell gives a clue to the cause. Vertigo lasting seconds frequently implies the presence of benign paroxysmal positional vertigo (BPPV). Vertigo lasting minutes to hours may accompany a hydrops attack or mild neuronitis. Spells lasting up to 24 hours with constant vertigo frequently imply neuronitis. Rarely does acute labyrinthine dysfunction cause constant vertigo lasting for days. Other, less common causes are a perilymph fistula (which causes Valsalva-related vertigo and fluctuating hearing loss), labyrinthitis (which causes hearing loss and vertigo), and acoustic neuroma (which rarely presents with vertigo).6,7
Acute Central Dysfunction
Acute central dysfunction generates vertigo by interrupting vestibular-related brain stem or cerebellar connections at the pontomedullary junction. Most commonly, ischemia resulting from significant small vessel disease or even a full-blown transient ischemic attack (TIA) causes vertigo that lasts for seconds to minutes and is frequently produced or exacerbated by antigravity movements. Demyelination plaques may also affect the brain stem pathways, causing vertigo as well as other symptoms of multiple sclerosis. Tumors of the cerebellopontine angle rarely cause acute attacks of vertigo because of their slow growth and gradual compensation of the brain stem. Infarcts of the brain stem or cerebellum generate severe vertigo and gait ataxia, which can be confused with the vertigo of peripheral origin. Finally, migraine-induced vertigo may take a variable course and can mimic peripheral vertigo.5
Secondary Labyrinthine Involvement
Labyrinthine dysfunction may occur with systemic diseases that impair either the circulation or metabolism or that directly attack the membranous labyrinth. Hypertension, hypercholesterolemia, diabetes mellitus, and advanced atherosclerosis all affect oxygen delivery to the labyrinth and can sometimes produce vertigo. In some patients with systemic connective tissue disease, autoimmune-mediated hearing loss and vertigo may occur.6
Generally speaking, symmetrical bilateral labyrinthine dysfunction (ototoxicity, presbycusis [age-related hearing loss]), slowly progressive unilateral dysfunction (acoustic neuroma), and diffuse CNS disease produce disequilibrium rather than vertigo. Disorders of sensory conflict resolution belong in this category also, as described earlier.
THERAPY
Acute Vertigo
The CNS compensates rapidly for an isolated episode of acute vertigo or peripheral vertigo within days to weeks after the spell, given adequate visual and proprioceptive activity. Thus, the elderly may have a more prolonged recovery with an attack of acute vertigo. In such instances, treatment consists of vestibular suppressants and antiemetics for the acute episode only, along with encouragement for activity and reassurance. As an initial regimen, prochlorperazine (Compazine) suppositories, 25 mg per rectum every 6 hours, and meclizine (Antivert), 25 mg by mouth three times a day for 48 to 72 hours, are often sufficient to control vomiting and vertigo. In recalcitrant cases, diazepam (Valium), 2 to 10 mg by mouth every 6 hours, may help but carries a significant risk of sedation and addition. In certain patients dehydration occurs, and the patient requires intravenous resuscitation along with diazepam, 5 to 10 mg intramuscularly, droperidol, 2.5 mg intramuscularly, or ondansetron (Zofran), 4 mg intravenously, to successfully control emesis. In patients in whom neuronitis is suspected, tapering doses of oral or intravenous steroids appear to shorten the attack and lessen its severity. Early ambulation and regular exercise tend to hasten full recovery. Minor episodes of dizziness may occur months after an initial episode, but routine use of vestibular suppressants is not warranted and may in fact delay recovery.
Recurrent Vertigo
Treatment of recurrent vertigo depends on the cause of the attack. For instance, BPV is treated effectively with repeated head-positioning exercises with no need for prolonged medication use.8 Endolymphatic hydrops attacks, however, require adequate sedation and antiemetics during the severe episodes but no suppressants between attacks. As in isolated cases of acute vertigo, the use of steroids during hydrops attacks has been successful. Recalcitrant cases of vertigo secondary to hydrops may require surgical intervention.
Central Vertigo
Vertigo of central origin can be difficult to manage depending on the location and extent of the injury in relation to the central balance center. For patients with diffuse small vessel cerebrovascular disease, cessation of smoking, increased exercise, control of blood pressure and cholesterol, and antiplatelet aspirin therapy have proved useful. In patients with demyelination, high-dose steroid therapy seems to lessen the severity of the symptoms. Of course, tumors of the CNS require surgical removal. Postoperatively, the patient’s balance may in fact become worse and may require extensive formal balance retraining and medication.
Vestibular Rehabilitation
Patients with nonfluctuating, poorly compensated, unilateral peripheral disease, bilateral vestibular disease, limited central disease, head trauma, and disorders of sensory conflict resolution are excellent candidates for formal vestibular rehabilitation therapy. Using this approach, a specially trained physical therapist designs an exercise program consisting of progressively more challenging oculomotor and postural tasks that are learned by the patient and incorporated into daily life. Patients learn to augment existing vestibular cues, substitute vision and proprioception for lost vestibular input, resolve sensory conflict among visual, vestibular, and proprioceptive input, and avoid tasks that are deemed beyond their balance capability.8 It is important to note that there is no place for rehabilitation training in patients with acute peripheral vertigo because the brain cannot adjust to changing peripheral input by repetition and habituation.
AUDITORY DYSFUNCTION
Types of Hearing Loss
Hearing impairment is classified as conductive, sensorineural, or mixed. Conductive hearing loss may be caused by anything that precludes the normal transmission of sound energy through the external auditory canal, tympanic membrane, or middle ear. Various conditions that frequently result in conductive hearing loss include impacted cerumen, tympanic membrane perforation, otitis media, and discontinuity or fixation of the ossicles (e.g., otosclerosis). Sensorineural hearing loss results when the inner ear, auditory nerve (eighth cranial nerve), brain stem, or cortical auditory pathways do not function properly. A mixed hearing loss is a conductive hearing loss superimposed on a sensorineural hearing loss.
Presbycusis
Presbycusis, a sensorineural form of hearing loss, is the most common form of hearing loss in the elderly. Studies have indicated that approximately 25% of people between 65 and 74 years of age and 50% of people 75 years of age or older experience hearing difficulties.10 The cause of hearing loss due to presbycusis remains unclear. Studies have attempted to link the effects of diet, metabolism, arteriosclerosis, noise, stress, and heredity on hearing, but no clear correlation has emerged. Presbycusis remains a diagnosis of exclusion, and other causes of bilateral progressive sensorineural hearing loss must be ruled out before the diagnosis is made. Some research has correlated long exposure to environmental noise with presbycusis, but it would be overly simplistic to assume that noise is the only etiologic factor. Research has yet to elucidate the exact cause of presbycusis, but it probably has many sources, including degeneration of the cochlea and disorders in central auditory processing that occur with increasing age.10
Presbycusis is not a simple entity but a complex disorder involving a wide range of problems varying from loss of speech processing to decreased word intelligibility. The elderly require careful explanations of their problem to help prevent the isolation and frustration that may result from progressive hearing loss. Auditory rehabilitation plays an important role in keeping the older person with a hearing deficit from withdrawing from society.
To develop an optimum rehabilitation plan it is necessary to look beyond the standard audiogram. Multiple factors, acoustic and nonacoustic, influence a person’s success in the rehabilitation process. Intervention decisions should be based on a careful study of the elderly patient’s auditory and nonauditory performance. The need for patient counseling is an important element of the rehabilitation process.
Audiologic Evaluation
The audiologic evaluation involves obtaining an objective picture of a patient’s hearing deficit. It helps to identify the possible cause of a person’s hearing loss. Initial evaluation begins with a complete head and neck examination. An adequate history is taken to further elucidate the source of the hearing loss. An audiogram is performed to identify the nature and degree of hearing impairment. An audiogram, however, does not provide information about the effect of the hearing loss on the patient’s ability to function. Because each person responds to a loss of hearing in a different manner, assumptions should not be made about a patient’s hearing handicap based solely on interpretation of the audiogram. A self-assessment hearing handicap scale can be used to fully evaluate the actual hearing handicap an elderly patient is experiencing.10 A number of self-assessment scales are available for clinical use. These scales can provide information about the difficulties experienced by hearing-impaired people in a variety of listening conditions, the impact of hearing loss on psychosocial function, and the self-perception of the hearing-impaired person.11,12
Amplification Selection
A number of amplification options are available to the elderly person who is hearing impaired. Levitt in 198713 suggested that we refer to this group of devices as rehabilitation technology for the hearing impaired. He divided the technology into four categories: (1) sound enhancement technology, (2) television enhancement technology, (3) telecommunication technology, and (4) signal-alerting technology.13,14
Sound enhancement technology refers to amplification systems that are used to assist in the reception of sound. Included in this group are traditional and programmable hearing aids, assistive listening devices such as hardware, infrared, and frequency modulation (FM) systems, and cochlear implants.
Television enhancement technology refers to equipment used to improve the auditory perception of television. Included in this group may be sound enhancement technology such as infrared or FM systems and closed caption decoding devices.
Telecommunication technology refers to systems that improve the ability to communicate over the telephone. Included in this group are specific devices such as amplified telephone handsets, portable strap-on telephone amplifiers, and the telephone device for the deaf (TDD).
Signal-alerting technology refers to equipment used to alert a hearing-impaired person to the presence of sound by using either a visual or tactile signal. Included in this group are lights that flash in the presence of sound, vibrating alarm systems, and hearing ear dogs.
A complete assessment of a hearing-impaired person’s needs must be done to determine the appropriate choice for amplification. All areas of communication should be considered when making this decision.
Hearing aids (Fig. 41-2) are the sound enhancement device most commonly recommended for hearing-impaired patients. In addition to the degree and configuration of the hearing loss, many nonacoustic factors, such as motivation, financial ability, manual dexterity, cognitive ability, and cosmetic concerns, may influence the patient’s choice of a hearing aid. A number of choices are available; however, it must be stressed that no hearing aid can improve communication ability if the hearing-impaired patient is unable to use it.

Figure 41-2 Types of hearing aids. A, Bone-conduction aid. B, Behind the ear (BTE). C, In the ear (ITE). D, In the canal (ITC). E, Completely in canal (CIC).

The growing complexity of hearing aid devices increases the need for hearing aid orientation. The type of hearing aid prescribed depends on the needs and capabilities of the patient and the exact nature and configuration of the hearing loss.15,16 In general, binaural aids are more useful than single aids in the bilaterally hearing-impaired person. Contralateral routing of signal (CROS) aids can be used for people who perceive a need for bilateral input when only a unilateral loss exists. Smaller in-the-ear or in-the-canal aids may be cosmetically appealing, but they provide only limited amplification and require considerable dexterity on the part of the patient to use. Eyeglass hearing aids are limited by the ability of the dealer to adjust the aid without causing the patient to lose the use of the glasses temporarily.
A hearing aid alone may not offer sufficient help to enable a hearing-impaired person to hear in the presence of background noise, in a highly reverberating environment, or over the telephone. Many assistive listening devices are effective in such adverse conditions. Success with these devices is due to the increased signal-to-noise ratio, which helps to reduce the perception of background noise.
The clinician should possess an understanding of an elderly person’s communication needs and should determine the most effective plan to meet those needs.15,16,17 and 18 This plan may include a prescription for either short- or long-term counseling. Cooperation among hearing-impaired patients, their families, the clinician, and the audiologist allows optimum auditory rehabilitation.
CHAPTER REFERENCES

1.
Perry ET: The Human Ear Canal. Springfield, IL, Charles C Thomas, 1957, pp. 57–70.

2.
Glasscock ME III, Shambaugh GE Jr: Surgery of the Ear, 4th ed. Philadelphia, WB Saunders, 1990.

3.
Senturia BH, Marcus MD. Lucente FE: Diseases of the External Ear: An Otologic-Dermatologic Manual. New York, Grune & Stratton, 1980.

4.
Maceri DR: Sensorineural hearing loss: Sudden, fluctuating, and gradual. In Meyerhoff WL, Rice DH (eds): Otolaryngology: Head and Neck Surgery. Philadelphia, WB Saunders, 1992.

5.
Sloane P, Baloh RW: Persistent dizziness in geriatric patients. J Am Geriatr Soc 1989;37:1031–1038.

6.
Gacek RR, Ham R: A clinical approach to the management of geriatric disequilibrium. Ear Nose Throat J 1989;68:958–960.

7.
Baloh RW, Honrubia V: Clinical Neurophysiology of the Vestibular System. Philadelphia, FA Davis, 1990.

8.
Barber HO, Sharpe JA: Vestibular Disorders. Chicago, Mosby-Yearbook, 1988.

9.
Baloh RW, Sakala SM, Yee RD, et al: Quantitative vestibular testing. Arch Otolaryngol Head Neck Surg 1985;92:145–156.

10.
Meyerhoff WL: Diagnosis and Management of Hearing Loss. Philadelphia, WB Saunders, 1984.

11.
American Speech-Language and Hearing Association: Definition of and competencies for aural rehabilitation. ASHA 1984;26:37–41.

12.
High W, Fairbanks C, Glorig A: Scale of self-assessment of hearing handicap. JSHD 1964;29:215–230.

13.
Malinoff R, Weinstein B: Measurement of hearing aid benefit in the elderly. Ear Hear 1989;10:354–356.

14.
Schow R, Nerbonne M: Communication screening profile: Use with elderly clients. Ear Hear 1980;3:135–148.

15.
Ventry I, Weinstein B: The hearing handicap inventory for the elderly: A new tool. Ear Hear 1982;3:128–134.

16.
Traynor R: Hearing aid counseling and orientation. In Hull R (ed): Rehabilitative Audiology. New York, Grune & Stratton, 1982.

17.
Shumway-Cook A, Horak FB: Rehabilitation strategies for patients with vestibular deficits. Neurol Clin 1990;8:441–457.

18.
American Academy of Otolaryngology and American Council of Otology: Guidelines for evaluation of hearing handicap. JAMA 1979;241:2055–2059.

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