Dizziness, hyperactive caloric responses, otic capsule demineralization, impaired glucose tolerance, and hyperinsulinemia.

A 51-year-old man reported that 6 months earlier he had experienced a feeling of uneasiness when his eyes were closed while showering. Two months later, on the morning following an airplane flight, he experienced 5 minutes of rotary vertigo upon awakening. Thereafter, he felt perfectly well. However, the same symptoms recurred in a similar fashion on two other occasions. When the most recent dizziness cleared, he began to list to one side for about 2 hours. He began taking meclizine in an attempt to treat these symptoms. Magnetic resonance imaging had been negative, and hearing and balance tests had not provided any insight into the problem.

The patient remained relatively well until about 1 month prior to presentation, when he experienced another episode of rotary vertigo; this time, the vertigo was accompanied by nausea and vomiting. This attack lasted somewhere between 5 and 10 minutes. The next day, he experienced an other bout of rotary vertigo when he turned over in bed.

During that month, the patient experienced two episodes of "spinning in a semicircle" with severe nausea. He was aware of aural fullness in the left ear after these spells, but there was no subjective hearing loss. It was then that he recalled that he had been experiencing weeks-long episodes of aural fullness in the left ear during the first 3 months following the onset of his initial symptoms. He reported no tinnitus.

Findings on physical examination were normal except for a positive sharpened tandem Romberg's test with the left foot forward. Audiometric evaluation revealed normal hearing in both ears to 15 kHz and normal speech test results. Distortion-product otoacoustic emissions were present in both ears, and less robust on the left.

Electronystagmography revealed no spontaneous or positional nystagmus. Hyperactive responses (>25[degrees]/sec) from the left ear were elicited by both warm and cool bithermal stimuli. During the simultaneous binaural bithermal caloric test, a left-beating nystagmus was seen in response to the warm stimulus. This finding is consistent with a hyperactive left ear.

Sinusoidal vertical-axis rotation testing revealed normal gains and phase lags at four frequencies, a finding that is consistent with a peripheral vestibular disorder. A finding of abnormal symmetry toward the left at two frequencies was consistent with an incompletely compensated left peripheral vestibular disorder.

On laboratory evaluation, the complete blood count was normal, as were the lipid panel and thyroid-stimulating hormone level. A 5-hour glucose tolerance test demonstrated impaired glucose tolerance and abnormally elevated insulin levels.

Thin-section axial computed tomography of the temporal bones detected evidence of a demineralized cochlear capsule, such as is seen in patients with inner ear otosclerosis.

The patient was treated with a combination of risedronate 30 mg twice weekly, a calcium supplement with vitamin D, and a calcium supplement with fluoride to address the otic capsular findings. He was placed on a modified hypoglycemic diet to address the blood glucose and insulin findings.

The patient returned after 3 months of treatment. He reported only two spells, which occurred on successive days after he had flown on five airplane flights. Both spells were brief and less severe. Neither the nausea nor the aural fullness on the left returned. Follow-up laboratory data showed a reduction in the serum insulin level, but not to a normal level. Repeat sinusoidal vertical-axis rotation testing elicited evidence of a shift in peripheral vestibular function indicating improvement, although some abnormal symmetry toward the left remained.

When evaluating patients with vestibular symptoms by electronystagmography, the usual expectation is that the source of the vestibular symptoms is hypoactive caloric functioning of the vestibular labyrinth. In the case described herein, the abnormality was reflected as a hyperactive response to the bithermal caloric stimulation in the left ear. The finding that the left ear was the source of the symptoms is consistent with the findings of aural fullness and reduced distortion-product otoacoustic emissions in the left ear.

Demineralization of the bony labyrinthine capsule, as occurs in some forms of otosclerosis, responded to the combination of the bisphosphonate, calcium, vitamin D, and fluoride. The patient's change in diet achieved some success in reversing his hyperinsulinemia. The persistent elevation of the insulin level may explain the brief recurrence of symptoms on the 2 successive days after he had taken five airplane flights.

Kenneth H. Brookler, MD

From Neurotologic Associates, PC, New York City.