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An approach to tinnitus management.

A 46-year-old man presented with a 4-month history of tinnitus. Six months earlier, he had experienced a dental infection. Two months later, he noticed the tinnitus one day upon awakening. He also noticed bi-frontal pressure in his head that extended across the temporal area and a feeling of dizziness with associated nausea. He remained in bed for the rest of that day, and when he awoke the next morning, his symptoms were completely gone.

A day or two later, the patient experienced a recurrence of all symptoms except dizziness. He also noticed some aural fullness and hypersensitivity to sound. He was treated with a variety of agents, including selenium, magnesium, ginkgo biloba, and flavonoids. These agents seemed to provide some degree of improvement, but it was not sustained. He was next placed on a diuretic and later switched to a corticosteroid and then to alprazolam, but these drugs provided only temporary relief.

Eventually, the patient was referred to the author. He reported that at times his symptoms would completely disappear. His hyperacusis seemed to have diminished during the month prior to presentation. He had no subjective hearing loss. When present, the degree of aural fullness and tinnitus was about equal on both sides. His current medications included alprazolam, eszopiclone, and hydrochlorothiazide. His family history was positive for hearing loss. He was a nonsmoker, had stopped drinking alcohol upon the onset of symptoms, and had been on a low-salt diet for 3 months.

The neurotologic examination revealed an anxious and hyperactive patient who had minimal to mild difficulty performing the sharpened tandem Romberg test. Physical examination revealed occipital muscle tenderness and spasm on the left.

Audiology demonstrated normal hearing in both ears to 2 kHz and a moderate dropoff beginning at 3 kHz and continuing through to 8 kHz; the decrease was slightly greater in the right ear.

[FIGURE 1 OMITTED]

Speech reception was normal in quiet, but there was a significant drop in discrimination in the right ear during simulated background noise (figure 1). Tympanometry was normal in both ears. Acoustic stapedial reflexes were absent with contralateral stimulation in the left ear at 0.5 and 4 kHz, and they elicited a response indicating a chochlear site in the right ear at 4 kHz. There was no stapedial reflex decay. Otoacoustic emissions--both transient-evoked and distortion-product--were present in both ears, less so in the right (figure 2).

Electronystagmography was negative for spontaneous, positional, neck torsion, and vertical nystagmus. Caloric stimulation with the closed-loop caloric irrigator was administered with the alternate binaural bithermal (ABB) and the simultaneous binaural bithermal (SBB) tests. The ABB test showed a 31% reduced vestibular response right and a 69% directional preponderance to the right. The SBB test elicited a type 3 response with a right-beating nystagmus produced with either of the bithermal stimuli; the latter is compatible with the directional preponderance to the right on the ABB test.

[FIGURE 2 OMITTED]

The sinusoidal vertical-axis rotation test revealed normal gains and a lag or borderline lag at three frequencies--findings that are consistent with a peripheral vestibular disorder. Symmetry was normal and consistent with the patient's lack of vestibular symptoms. Fixation suppression was present throughout caloric and rotatory testing.

The salient laboratory findings were abnormalities on the glucose tolerance test and a deficiency of vitamin D. The serum glucose levels fluctuated normally for the first 2 hours, but then they fell from 119 mg/dl at the second hour to 49 mg/dl at the third hour. Simultaneous insulin levels were elevated according to the criteria established by Kraft. (1) The 25-hydroxy vitamin D level on liquid chromatography was 20.8 ng/ml (normal: 32 to 100).

Overlapping thin-section (0.6 mm) axial and coronal computed tomography (CT) of the temporal bones was obtained. The basal turn of the cochlea contained a mixed sclerotic and spongiotic plaque in the right ear from the base at the footplate to the apex and a sclerotic plaque in the left ear from the base at the posterior internal auditory canal to the apex. These findings were consistent with inner ear otosclerosis. The patient was placed on a diet to address his serum glucose and insulin findings. To address the otosclerosis, he was placed on risedronate 30 mg twice weekly plus daily supplementation with calcium/vitamin D, vitamin [D.sub.3], and fluoride.

At follow-up 3 months later, the patient said his tinnitus had become less intense and remained intermittent. When present, it lasted 2 or 3 days. The hyperacusis, headaches, and neck pain were present only when the tinnitus was. He had experienced no dizziness but did feel a wave of weakness and heaviness in his head for 24 hours when he would try to focus his eyes. The aural fullness had disappeared after the first week of treatment.

Repeat audiometry revealed similar pure tones and speech findings, and an improvement in noise in the right ear only to 80%. Otoacoustic emissions testing revealed similar transient-evoked findings and an increase in the range of the distortion-product findings in the right ear. The 25-hydroxy vitamin D level was now normal. Etidronate 400 mg daily for 2 of every 6 weeks was added to the patient's continued medical regimen; risedronate was discontinued during the 2-week periods on etidronate.

At another follow-up visit 3 months later, the patient said he had initially experienced no change in the severity, number, or duration of his tinnitus episodes, and the hyperacusis was not as bad as it had been. He continued to have some difficulty hearing in background noise. The aural fullness had not returned, but beginning with the second cycle of etidronate, the tinnitus intensified for 11 of the next 30 days; this was accompanied by an off-balance feeling. Again, the headaches and neck pain paralleled the tinnitus.

[FIGURE 3 OMITTED]

Audiometry revealed an improvement in the pure tones in both ears at the higher frequencies. Speech testing was similar in quiet with a reduction in discrimination in noise to 68% in both ears. His tinnitus was matched in both ears at 3.6 to 3.7 kHz in both ears at the limit of the electrical audiometer and could not be suppressed with continued electrical stimulation. Transient-evoked otoacoustic emissions were less than they had been at the previous visit. The distortion-product emissions were present in both ears--more so on the left--and they were improved over the previous test only on the left.

The treatment regimen was changed so that etidronate was taken for 2 of every 8 weeks. Because the tinnitus increased with etidronate use, the patient insisted on another contrast-enhanced MRI despite counseling against it; the MRI was negative. Follow-up laboratory testing identified a marked increase in his serum glucose and insulin levels. On further questioning, the patient admitted that he had enlarged the portions of the nutritionally acceptable foods he ate because he had been losing weight on his diet. He was encouraged to return to the original diet.

Four months later, the patient volunteered that for 7 days in a row, his tinnitus had stopped by 9 a.m., but 2 1/2 weeks before this visit, the tinnitus had returned and had persisted until the day before. It was worse than it had been during his follow-up visits, but not as bad as it had been at the onset of his original symptoms approximately 10 months earlier. The hyperacusis and headaches continued to parallel the tinnitus, but the neck stiffness had abated somewhat. He still had not experienced any recurrence of his aural fullness or dizziness.

Follow-up blood testing demonstrated a continuing elevation in the patient's serum insulin level. Pure-tone audiometry and speech in quiet remained the same as before, and speech discrimination in noise improved to 92% in the right ear and 84% in the left ear. Otoacoustic emissions testing revealed improvement in both transient-evoked and distortion-product findings in both ears (figure 3). Treatment was continued with the etidronate for 2 of every 13 weeks.

This case brings up several discussion points. Based on a minimal history of vestibular symptoms, the findings of a peripheral vestibular disorder on electronystagmography and no abnormal symmetry on sinusoidal vertical-axis rotation testing indicate a longstanding inner ear disorder. With a pre-existing inner ear disorder, a dental infection 2 months before the onset of symptoms (significant enough for the patient to include in his history) could have acted as an inflammatory stimulus for the subsequent findings. The fact that his symptoms abated spontaneously and briefly suggests an element of reversibility. The presence of head pressure with tinnitus and hyperacusis is consistent with the activation of the vestibilucollic reflex that produced the occipital muscle spasm.

While the tinnitus did not localize to one ear or one side of the head, three findings point to a predominantly right-sided lesion: speech discrimination in noise, the results of ABB electronystagmography, and the distortion-product otoacoustic emissions.

Thin-slice CT of the temporal bones revealed cochlear capsule lesions consistent with those seen in otosclerosis. The laboratory evaluation showed a vitamin D deficiency that readily responded to supplemental vitamin [D.sub.3]. The patient's serum glucose level fluctuated significantly and his insulin level was also sufficiently elevated to adversely affect inner ear function.

Treatment directed at the otosclerosis and diet directed at the metabolic factors initially resulted in periods when the absence of symptoms was more common than their presence and when the overall intensity of the tinnitus was less. But then the addition of a nonamine bisphosphonate (etidronate) to an aminecontaining bisphosphonate (risedronate) initially intensified the symptoms. This effect, which has been reported by others as an indicator of the drug's effect on the inner ear, paradoxically resulted in subsequent improvement. After 7 months on the bisphosphonate combination, the patient was already experiencing longer symptom-free periods. Follow-up glucose tolerance testing after he had begun to eat more revealed serum glucose levels consistent with a diagnosis of diabetes and an elevation in serum insulin to levels much higher than they had been at the outset. These findings suggest that his metabolic condition was evolving into the insulin resistance syndrome and ultimately to type 2 diabetes.

The use of otoacoustic emissions testing in the diagnosis and monitoring of the response to treatment is helpful in the management of the tinnitus patient. It is widely held that dyssynchrony in the output of the auditory periphery is a basis for the symptoms of tinnitus. In this case, the dyssynchrony was demonstrated with distortion products before treatment. While these distortion product results 10 months into treatment indicated no overwhelming improvement, they did indicate at least some improvement, especially in the previously more abnormal right ear.

External sound devices have enjoyed some popularity and success in the treatment of tinnitus. But they address tinnitus only by possibly reorganizing the dyssynchrony; they do not address the underlying etiology. The symptom of tinnitus could herald a progressive hearing loss or a severe vestibular disorder that might be avoided if the underlying etiology could be found and treated. Such a development might also result in a permanent cure of tinnitus.

Reference

(1.) Kraft JR. Hyperinsulinemia: A merging history with idiopathic tinnitus, vertigo, and hearing loss. Int Tinnitus J 1998;4(2):127-30.

Kenneth H. Brookler, MD, MS, FRCSC; Mohamed A. Hamid, MD, PhD From Neurotologic Associates, PC, New York City (Dr. Brookler), and the Cleveland Hearing and Balance Center, Beachwood, Ohio (Dr. Hamid).
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Title Annotation:AUDITORY AND VESTIBULAR MEDICINE CLINIC
Author:Brookler, Kenneth H.; Hamid, Mohamed A.
Publication:Ear, Nose and Throat Journal
Article Type:Clinical report
Geographic Code:1USA
Date:Nov 1, 2008
Words:1891
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