|Year : 1985 | Volume
| Issue : 2 | Page : 80-2
Intravenous lignocaine in tinnitus.
SN Merchant, NN Merchant
S N Merchant
|How to cite this article:|
Merchant S N, Merchant N N. Intravenous lignocaine in tinnitus. J Postgrad Med 1985;31:80-2
|How to cite this URL:|
Merchant S N, Merchant N N. Intravenous lignocaine in tinnitus. J Postgrad Med [serial online] 1985 [cited 2022 May 19 ];31:80-2
Available from: https://www.jpgmonline.com/text.asp?1985/31/2/80/5406
Very little treatment is available for tinnitus, a common symptom in E.N.T. practice and whatever is available is unsatisfactory. Goodhill wrote in 1954: "The treatment of tinnitus as a disease is an illogical dream but the management or the patient with tinnitus is an everyday necessity". Encouraged by reports in the literature about the use of intravenous lignocaine in tinnitus, we decided to evaluate its efficacy and safety. This paper describes our preliminary experience.
MATERIAL AND METHODS
A total of 54 patients, 30 men and 24 women, with intractable subjective tinnitus were studied. A detailed history, an E.N.T. and general examination, audiometric evaluation, electrocardiogram and other relevant investigations were perfomed in each patient. The average age of the patients was 52 years (range 19 to 70 years). Tinnitus was present for 2 months to 17 years. It was associated with a sensorineural hearing loss in nearly every case. The causes of hearing loss were presbyacuisis in 15, ototoxicity in 11, noise induced hearing-loss in 8, post-traumatic hearing loss in 3, Meniere's syndrome in 2, idiopathic sensorineural hearing loss in 8, and other causes in 7 cases.
The treatment programme involved an intradermal test dose followed by intravenous injections of lignocaine. A 2% solution of lignocaine hydrochloride without adrenaline or preservative was injected slowly, intravenously in the dose of 3-4 rag/kg body weight, over a period of 5 minutes, under cardioscope monitoring. Upto 200 mg of lignocaine were injected daily for five days. On completion of this course, each patient was asked to evaluate any perceived alteration in tinnitus using a percentage analogue. A control group of 39 patients (mean age: 47 years; range: 16-68 years), also suffering from subjective tinnitus, received an identical treatment regime, under similar conditions, but using intravenous saline as a placebo.
We classified the relief obtained into 5 groups: a 100% relief as total; 76-99% relief as excellent; a 51-75% relief as good; a 26-50% relief as fair; and less than 26% as insignificant. The results obtained in the patient group (lignocaine) and in the control group (saline) are shown In [Table 1]. In one case, the tinnitus which was completely abolished did not return for as long as one year. In the majority, however, the tinnitus returned gradually, over a period of several days to weeks. Even then, it did not reach its pretreatment intensity and remained less disturbing than it was earlier. In a few cases, suppression of tinnitus was only temporary, with the symptoms returning rapidly to their pro-injection level within hours or even minutes.
The beneficial effects of intravenous lignocaine on tinnitus have been reported previously by other investigators.,, The present study confirms the previously reported findings but differs from them in two respects. The present study shows lignocaine to be superior to a placebo in suppressing tinnitus. Further, the dose used was 3-4 mg/kg (maximum-200 mg). This is twice the dose commonly used by other investigators (1-2 mg/kg). It is our clinical observation that low doses of lignocaine (upto 100 mg) frequently lead only to an alteration in the pitch and quality of tinnitus, without diminishing its intensity. Higher doses in the range of 150-200 mg produce the greatest amount of relief, both in terms of magnitude and duration.
Some evidence suggests that tinnitus may arise as a result of central neuronal hyperactivity, perhaps caused by chronic de-afferentiation. Lignocaine is thought to act centrally, probably at the level of the brainstem and reticular formation and suppresses this hyperactivity by virtue of its membrane stabilizing properties. In one of our cases of a proved acoustic neuroma resected surgically with a total section of the eighth nerve, the tinnitus which had persisted in spite of surgery was relieved by lignocaine. In other cases, a caloric test performed during the course of an intravenous lignocaine injection revealed that while the tinnitus disappeared the caloric induced nystagmus remained unchanged. Both these observations suggest that lignocaine acts centrally.
We are grateful to Dr. Mrs. Parshad, Medical Superintendent, Rajawadi Hospital and to the Board of Directors, Dr. Merchants' Hospital for permission to Use the hospital records. We are indebted to Mrs. Sunita Bhavnani for her painstaking secretarial. help. .
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