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Not all hearing loss in the elderly is presbycusis. Ototoxic drugs such as aminoglycoside antibiotics, loop diuretics, and antineoplastic agents (especially cisplatin) may contribute to hearing loss in the elderly. Patients especially at high risk for injury to the auditory system from ototoxic drugs include those with a preexisting hearing loss, those undergoing simultaneous treatment with multiple ototoxic drugs, and those with renal insufficiency. The risk of ototoxic injury can be significantly reduced by monitoring ototoxic exposure with serial audiometry. Of course, serum peak-and-trough levels should be measured to establish the lowest possible dose compatible with therapeutic efficacy. Substitution with nontoxic therapy, whenever feasible, is paramount for prevention.
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Sudden Sensory Hearing Loss
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Sudden loss of hearing in one ear is a relatively common occurrence in the elderly. Most cases are the result of thrombotic or embolic obstruction of the internal auditory artery. Although complete losses seldom recover, most partial losses experience some degree of spontaneous improvement within a few weeks to months. Empirical therapy with oral prednisone appears to be of some benefit. Although most sudden losses are idiopathic and presumably vascular, other etiologies, such as acute endolymphatic hydrops, perilymphatic fistula, tertiary syphilis, brainstem ischemia or infarction, demyelinating disease, and vestibular schwannoma, should be considered.
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Asymmetric Hearing Loss
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Most hearing losses in the elderly are bilateral and symmetric. Unilateral or asymmetric sensorineural hearing loss is atypical and demands further investigation to exclude disease of the central auditory system, such as vestibular schwannoma. The most common symptoms of vestibular schwannoma are sensorineural hearing loss, tinnitus, and dysequilibrium.
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The initial screening test for the evaluation of asymmetric hearing loss is the auditory brainstem response (ABR), which records the changes in the electroencephalogram evoked by sound stimulation. Five waves may be observed in the first 10 ms, corresponding to the activation of the eighth cranial nerve (Wave I), the cochlear nucleus (Wave II), the superior olive (Wave III), the lateral lemniscus (Wave IV), and the inferior colliculus (Wave V). Absent ABR response or interaural latency differences in Wave V >0.3 ms are suggestive of retrocochlear pathology and warrant further radiological evaluation. Gadolinium-DTPA-enhanced MRI scanning is the gold standard for evaluating diseases involving the cerebellopontine angle and the internal auditory canal. MRI scanning may also detect brainstem pathology, such as multiple sclerosis or infarction, which can mimic the clinical presentation of vestibular schwannoma.
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Other Types of Hearing Losses
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Less common causes of sensorineural hearing loss in the aged are numerous and include metabolic derangements (eg, diabetes, hypothyroidism, hyperlipidemia, and renal failure); infections (eg, measles, mumps, and syphilis); autoimmune disorders (eg, polyarteritis and lupus erythematosus); physical factors (eg, radiation therapy); and hereditary syndromes (eg, Usher syndrome). The identification of metabolic, infectious, or autoimmune sensory hearing loss is especially important because these hearing losses are occasionally reversible with medical therapy.
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Vertebrobasilar Insufficiency
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In the elderly, vertebrobasilar insufficiency is an important cause of vertigo and dysequilibrium. It usually results from arteriosclerosis with insufficient collateral circulation, but may also be due to compression of vertebral arteries by cervical spondylosis, postural hypotension, or the subclavian steal syndrome. The full-blown clinical presentation of vertebrobasilar ischemia includes vertigo with head motion (especially looking up), dysarthria, numbness of the face, hemiparesis, headache, and diplopia. Less frequently, visual disturbances occur including oscillopsia, field defects, transient blindness, cerebellar ataxia, and dysphagia; drop attacks may also occur, reflecting ischemia of the brainstem and cerebellum. Vertigo or dysequilibrium may occur without other neurological signs or symptoms. A definitive diagnosis may be established by four-vessel cerebral angiography, but is seldom indicated. Presently, there is no effective medical or surgical treatment for vertebrobasilar insufficiency, although rehabilitative measures may be beneficial.
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A plethora of systemic disorders may affect equilibrium and balance in the elderly, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, neurological disorders, visual impairment, metabolic disease, and musculoskeletal problems. Therapeutic drugs are frequently responsible for dysequilibrium and postural instability, especially the antihypertensive, antidepressant, and sedative-hypnotic classes.
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Peripheral Vestibular Disorders
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A host of peripheral vestibular disorders may cause vertigo, including benign paroxysmal positional vertigo (BPPV) or cupulolithiasis, labyrinthitis, vestibular neuronitis, Meniere syndrome, labyrinthine concussion due to trauma, superior canal dehiscence, and perilymph fistulas, among others. In younger patients, BPPV is usually secondary to trauma, whereas in the elderly it is usually a result of degenerative processes. Patients complain of intermittent, irregular episodes of vertigo precipitated by rapid head motion. Vestibular suppressant medications are of limited usefulness except during periods of exacerbation. The severity of symptoms may diminish with repetition because of habituation. Patients usually respond to vestibular exercises, and spontaneous resolution occurs within 1 year in most cases.
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Meniere syndrome is characterized by episodic severe vertigo, fluctuating sensorineural hearing loss, tinnitus, and ear “fullness.” Pathologically, there is distention of the endolymphatic system throughout the inner ear, presumably due to dysfunction of the endolymphatic sac. The clinical course is highly variable, with clusters of severe episodes interspersed with periods of remission of variable duration. Management may include a sodium-restricted diet, diuretics, vasodilators, vestibular suppressants, and, occasionally, surgery to decompress the endolymphatic system.
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Probably a viral infection of the inner ear, acute labyrinthitis, causes both severe vertigo and hearing loss. Typically, it runs its course over a period of 1–2 weeks, although residual hearing loss and the periodic recurrence of vertigo are common sequelae. Vestibular neuronitis also presents with vertigo similar to labyrinthitis, but is unaccompanied by auditory symptoms.