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For over a year, a 47-year-old woman has been having attacks of dizziness and tinnitus. Each episode begins with a feeling of fullness in her left ear, followed within a minute or two by left-sided hearing loss and roaring tinnitus. A few minutes later, vertigo begins, with the environment appearing to spin toward her left. Rapidly increasing in severity, the vertigo is accompanied by nausea and vomiting. During attacks, which last 4 to 5 hours, she is unable to stand and falls toward the left. Her first few attacks were 2 or 3 weeks apart, but they have increased in frequency to one every few days. Head movement does not precipitate them, but it does aggravate the severity of vertigo once present, and during attacks, vertigo is lessened by lying on her side with her left ear uppermost. In recent weeks, she has noticed, while using the telephone, that her hearing is decreased on the left, yet loud noises produce subjective discomfort in that ear.

Examined during an attack, she is agitated, pale, and sweaty, lying on her side, and maintaining as still a posture as possible. There is bilateral conjugate nystagmus on primary gaze, horizontal with a rotatory component, with the fast phase beating toward her left. Following the attack, she feels weak all over but no longer has nystagmus. Hearing is decreased on the left, with bone and air conduction equally affected; the Weber test (a 512-Hz tuning fork placed over her mid-forehead) lateralizes to the right. Audiometric testing reveals hearing loss on the left that is greatest for low-pitched tones. As volume is increased, however, she reports similar subjective loudness in each ear. The left stapedial reflex threshold, determined by impedance measurements, is reduced. Caloric testing, using electronystagmographic recording, reveals a decreased response when warm or cold water is squirted onto the left tympanic membrane. Brain stem auditory evoked response (BAER) testing reveals a delay in the appearance of the first wave on the left.


Ménière disease consists of recurrent attacks of vertigo, hearing loss, and tinnitus. Patients are usually asymptomatic between attacks, but over time, hearing loss becomes cumulatively persistent. Symptoms are the result of increased pressure within the endolymphatic compartment of the inner ear labyrinth, including the cochlea, saccule, utricle, and semicircular canals (see Figure 3–11). Episodic malabsorption of endolymph through the endolymphatic duct and sac causes the endolymphatic compartment to become dilated and ballooned. In some cases, an underlying disease such as trauma or syphilis is identified, but most cases are cryptogenic.

Hearing loss is cochlear in type. As with any sensorineural deafness, bone and air conduction are equally affected, and the Weber test lateralizes sound to the good ear. There is also recruitment, an abnormally increased subjective sense of loudness once threshold is reached. Recruitment is objectively reflected in the abnormal impedance generated ...

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