A woman with a 42-year history of Meniere's syndrome.
The patient had remained symptom-free until 1995, when she developed aural fullness and some intermittent hearing loss in the left ear. The blocked feeling was alleviated by antihistamines.
In March 1997, the woman experienced a severe attack while at work. This time, her symptoms included decreased hearing and aural fullness in the left ear and rotary vertigo with nausea and vomiting. Triamterene hydrochlorothiazide (HCTZ) helped relieve the dizziness, but her symptoms recurred twice in May 1997 and once in June. She tried diazepam, but she experienced yet another recurrence, which was accompanied by left-sided tinnitus. She tried dexamethasone and trimethobenzamide, and that helped to some degree.
One month later, the patient presented to the author for the first time; the visit occurred during one of her symptom-free periods. Other aspects of her medical history included hypercholesterolemia and a hysterectomy 9 years earlier. In addition to triamterene HCTZ, she was taking estrogen and Lipoflavonoid.
Tuning fork testing identified a low-tone hearing loss in the left ear. The patient also had difficulty performing the sharpened tandem Romberg test. Audiology of the left ear detected a mild sensorineural hearing loss (SNHL) at the midtones and a moderate SNHL at 6 and 8 kHz. Her speech reception threshold on the left was 20 dB, and her speech discrimination score was 100% at 60 dB.
Electronystagmography did not reveal any spontaneous or positional nystagmus. The altemate binaural bithermal caloric test elicited a 56% reduced vestibular response (RVR) on the left, and the simultaneous binaural bithermal test yielded a type 2 response and an RVR left. Small-pixel, thin-slice computed tomography of the temporal bones detected evidence of otic capsule otosclerosis without oval window involvement; this finding was more evident in the left ear.
The metabolic evaluation revealed a fasting blood glucose level of 111 mg/dl, which rose as high as 237 mg/dl and did not fall to within the normal range for 4 hours. The patient's total cholesterol level was 316 mg/dl, and her triglyceride level was 204 mg/dl. The triamterene HCTZ and Lipoflavonoid were discontinued because of their effects on blood sugar. She was referred to a nutritionist for counseling and placed on a modified hypoglycemic diet low in fat. She was started on pulsed-dose etidronate (a 2-wk cycle every 6 wk) and daily supplemental therapy with calcium and vitamin D.
The patient returned for follow-up 4 months later in November 1997 and reported no spells of vertigo or hearing symptoms since the previous visit. Her etidronate regimen was continued with 8-week cycles. She returned 7 months later in June 1998 and reported that she had experienced one isolated spell 2 months earlier that had lasted 4 to 5 hours. She had not been fully compliant with her dietary regimen. Her etidronate regimen was extended in 13-week cycles, and fluoride was added.
In September 1998, her left ear became blocked and she noted some fluctuation in her hearing. One month later, she had an episode in which she was unable to focus her eyes while driving; she also experienced imbalance while walking, as well as nausea and vomiting. At this time, she was still not following her diet. A moderate flat heating loss was detected in the left ear.
In January 1999, the patient experienced what has turned out to be her final spell; this episode was of shorter duration and severity. Her hearing in the left ear has continued to fluctuate. In June 2005, she remained free of dizziness. She continues to have difficulty adhering to her diet, and she has also developed non-insulin-dependent diabetes. Her otosclerosis is being treated with risedronate 30 mg twice weekly; this drug is stopped for 2 weeks every 13 weeks and replaced with etidronate at 400 mg/day. She continues taking supplemental calcium, vitamin D, and fluoride daily.
This 42-year history illustrates the effect that the reproductive hormones had in stimulating what eventually became Meniere's syndrome secondary to otosclerosis. Treatment was directed at the otosclerosis and the metabolic abnormalities that were discovered during evaluation. The more severe symptom of dizziness was probably brought under control by the otosclerosis-directed treatment. The heating loss continued to fluctuate, presumably as a result of the effects of the diabetes.
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|Title Annotation:||VESTIBULOLOGY CLINIC|
|Author:||Brookler, Kenneth H.|
|Publication:||Ear, Nose and Throat Journal|
|Date:||Dec 1, 2005|
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