Disorders of the brainstem or cerebellum that may also cause vertigo include tissue ischemia secondary to atherosclerosis, tumors, or conditions such as psychiatric disorders, migraine headaches, or multiple sclerosis. However, in these cases, additional neurologic signs and symptoms are typically present. Drugs may also cause vertigo (alcohol, anticonvulsants, sedatives). Management of vertigo is usually aimed at the cause if known. Medications such as antihistamines and anticholinergics can be helpful.1

Sometimes no symptoms are present and the foreign body is discovered on routine examination. If the foreign body is an insect, beating of its wings and movement may cause distress. When symptomatic, however, foreign bodies can cause pain or drainage of pus from the ear. The external ear canal is very sensitive to touch and bleeds easily, which increases the risk for subepithelial hematomas from minor trauma. Therefore, removal of solid foreign bodies carries a risk of additional trauma to the ear canal, as well as tympanic membrane rupture, if the individual is not completely cooperative or removal is difficult. Light anesthesia may be necessary. Firm materials may be removed from the canal with loop or hook instruments, taking care not to push the object further into the canal. Irrigation should not be performed on organic foreign bodies (beans, peas) because water may cause them to swell. Living insects may be immobilized with lidocaine before removal.3 Excess cerumen may be removed with gentle irrigation.

Otosclerosis is a progressive conductive, sensorineural, or mixed hearing impairment caused most often by stapedial fixation. Resorption of bone is followed by the formation of new spongelike bony lesions usually occurring on and around the ossicles of the middle ear. Lesions involving the footplate of the stapes cause decreased transmission of sound waves to the oval window. However, when otosclerotic lesions impinge on the cochlea, permanent sensorineural hearing loss can occur. The basic initiating factors are unknown, but up to 50% of individuals with clinical otosclerosis have a history of the disease in the family.6 Several types of inheritance patterns have been suggested. The disease is most common in Caucasian middle-aged women. Pregnancy may accelerate the otosclerotic process.⁶ Viral infections and autoimmune processes are also thought to be possible causes. The age of onset is variable due to the insidious progression of the disorder, but the most common ages are between 15 and 45. There may be periods of symptom worsening, followed by times of little apparent change.

The diagnosis of otosclerosis is made through careful history taking and radiologic studies, along with audiometric studies. Generally, hearing loss begins in one ear, but 80% to 90% of affected individuals will develop bilateral impairment.6 Although hearing loss may be severe, speech discrimination is preserved except in the instance of cochlear involvement. The individual may report being able to hear better in a noisy environment than in a quiet one. Tinnitus is often present. Hearing tests reveal a conductive loss of varying severity.

Management of otosclerosis at this point is generally surgical, in an effort to prevent the conductive hearing loss. The limitation on treatment options for otosclerosis is related largely to the lack of exact knowledge regarding the cause and pathogenesis of the disease. The universally accepted operation for otosclerosis is stapedectomy, or removal of the focus of the disease by removing the stapes and inserting a prosthesis. In the case of otosclerosis involving the cochlea, treatment with oral sodium fluoride and bisphosphonates is associated with some decrease in development of the sensorineural hearing loss.⁷ Amplification with hearing aids is another approach.

Acquired sensorineural hearing loss caused by chronic, repeated exposure to loud sounds is common in the U.S. population. Four million people work each day in an environment with damaging levels of noise, and in 2008 approximately 2 million employees were exposed to workplace noise levels that put them at risk for hearing loss.9 Noise-induced hearing loss can be associated with the use of firearms, personal stereo systems, and power tools and with occupations such as firefighting, construction, agriculture, mining, manufacturing, transportation, and the military.

The loudness of sound/noise is measured in the logarithmic units of decibels (dB). A normal whisper is measured at approximately 30 dB, a conversation at 3 feet at 50 to 60 dB. In contrast, ambulance sirens have been measured at 120 dB, lawnmowers and motorcycles at 90 dB.¹⁰ Sounds exceeding 85 dB are considered potentially injurious, and chronic noise exposure is the most damaging. If exposure is severe enough, most structures of the inner ear can be damaged, including the organ of Corti. Sensory hair cells and supporting cells are lost because of overexposure. Noise-induced hearing loss typically is bilateral and affects higher (speech) frequencies first.³

Noise exposure has two phases: the first is a temporary threshold shift. When the ear is exposed to a loud sound, it will show a loss of sensitivity (a rise in the threshold for sound). If the hearing returns to normal after the sound has been removed, the shift was temporary and no permanent damage has occurred. If hearing does not return to normal, damage has occurred and the hearing impairment is permanent. Such a permanent threshold shift is the second phase of the damage. The ears of some individuals are more easily affected by noise, and considerable damage may occur before individuals are aware of the hearing loss.

Sensorineural hearing impairment can also occur with head trauma and subsequent damage to the structures of the inner ear. If blood is coming from the ear or the temporal bone is fractured, damage should be suspected. As a rule, hearing loss from trauma or head injury is permanent if the cochlea is damaged. A rare condition of sudden sensorineural hearing loss usually occurs in adults with middle ear problems. A viral or ischemic pathology is postulated. Prompt evaluation and treatment are necessary for these individuals. The prognosis is mixed but hearing may be recovered with intratympanic infusion of steroids.3

Four categories of presbycusis have been theorized: (1) sensory, characterized by atrophy and degeneration of the sensory and supporting cells; (2) neural, typified by loss of neurons in the cochlea and central nervous system; (3) metabolic, characterized by atrophy of the wall of the cochlea affecting central auditory processing; and (4) mechanical, in which the middle ear undergoes changes in properties with a resulting conductive hearing loss.3,8,11,12 Some of these age-related changes are shown in the Geriatric Considerations: Changes in Hearing box. An endless list of genetic, environmental, and disease states can also cause hearing loss in an older adult, many of which may occur concurrently. Thus uncertainty remains regarding the exact cause of presbycusis.

Assessment of an individual with suspected presbycusis should begin with exclusion of all other causes of hearing impairment. Diseases such as diabetes, stroke, and heart disease may produce effects similar to those seen with hearing loss and must be ruled out. The diagnosis is made by obtaining a thorough history and performing audiometric studies. Individuals with presbycusis respond well to hearing aids that amplify sound. Many simple lifestyle adjustments that will be mentioned at the end of this section can dramatically improve the quality of life for an individual experiencing presbycusis. It is important in these patients to avoid excessive noise exposure and ototoxic drugs, which may cause further deterioration of hearing loss.8

Etiology and pathogenesis

Meniere disease is an excessive accumulation of endolymph in the membranous labyrinth. The volume of endolymph increases with distention of the scala media until the

GERIATRIC CONSIDERATIONS

Changes in Hearing

Presbycusis, or age-related hearing problems, occurs after age 50 and is thought to be caused by structural changes in the organs of hearing. Ankylosis of the ossicles can lead to a functional decrease in transmission of sound to the inner ear.

In the inner ear or cochlea, degeneration of hair cells, changes in the basilar membrane, or atrophic changes can lead to decreased hearing of higher tones. With these changes is also noted a decline in pitch discrimination. As hearing is progressively lost, even lower pitch tones will be more difficult to hear.

membrane ruptures. Consequently, the neural end organs of the cochlea degenerate. Many conditions including allergies, viral and bacterial infections (such as syphilis), head trauma, metabolic derangements, and chronic stress have been suggested as causative agents, but the precise cause cannot be established in most cases.3,13 Men and women are equally affected by this disorder, and the onset of symptoms is typically in the fourth decade of life.¹³

Clinical manifestations of Meniere disease include tinnitus, fluctuating sensorineural hearing loss, vertigo, and sensations of ear fullness. In the early stages, hearing loss fluctuates, with return to normal after the rupture heals. Remissions and exacerbations are typical. The hearing loss is usually in the low tones. As the disease progresses, hearing loss becomes permanent. Symptoms initially usually are unilateral; the mean time for the manifestation of bilateral symptoms is approximately 7 years.13

Episodes of vertigo may be immediately preceded by the sensation of pressure in the ear, increased hearing loss, increased tinnitus, or an alteration in the quality of these symptoms. The onset of vertigo is usually sudden, reaches maximal intensity within a few minutes, usually lasts for an hour or more, and either subsides completely or continues as a sensation of unsteadiness for several hours or days. The tinnitus is typically a low buzzing or blowing sound and is frequently louder before the attack of vertigo. The attacks are not precipitated by positional changes and may be several weeks or months apart. In the initial stages of the disease they may be years apart. If not treated, the episodes may become more frequent and severe. Nystagmus, which occurs only during acute attacks, may be directed to the side opposite the involved ear.

Physical examination, including neurologic and otolaryngologic examination, is generally normal in those with Meniere disease. Radiologic studies are often used to rule out other causes of the symptoms of Meniere disease such as acoustic neuroma. Electrophysiologic studies, such as auditory brainstem response testing and electrocochleography, and audiometric tests as well as glycerol dehydration testing can lead to a diagnosis of Meniere disease.13 Caloric testing (irrigating the ears with warm and cool water) commonly reveals loss or impairment of thermally induced nystagmus on the involved side.¹³

Treatment for Meniere disease consists of providing symptomatic relief during acute episodes with antiemetics and anticholinergics such as meclizine. Between acute attacks, eating a low-sodium diet and using diuretics may help reduce the volume of endolymph. Cessation of smoking, management of stress, and elimination of caffeine from the diet are also suggested.

Several surgical interventions are used to manage Meniere disease. Shunts can be placed to drain excess endolymph, and ablation of portions of the eighth cranial nerve and destruction of the labyrinth are options. In refractory cases, patients may undergo intratympanic corticosteroid or gentamycin injections. These interventions have different indications, risks, and benefits associated with them. Almost all patients who choose surgical intervention have failed to respond to medical treatment.³