The Journal of Laryngology and Otology January 1992, Vol. 106, pp. 44-45
Clinical Records Tinnitus related to eyelid blinking V. RAJAH, M.Med (Otol), F.R.C.S.Ed. (Congella, South Africa)
Abstract Tinnitus due to muscular causes is rare. The commonest pathological muscular cause of tinnitus is palatal myoclonus. A case of bilateral tinnitus, related to eyelid blinking, is presented. This is the first case reported in the literature. Previous reported cases of tinnitus related to eyelid blinking have all been unilateral and associated with recovery from a VII nerve palsy. The treatment of the condition is discussed.
Introduction Tinnitus may be physiological, e.g. circulatory humm, pathophysiological, e.g. temporary noise-induced tinnitus, or pathological. Most patients with pathological tinnitus have associated cochlear pathology and the tonal frequency to which the tinnitus is best matched, tends to be in or close to the frequency zone of the hearing impairment. A small proportion of patients have pathological tinnitus due to other causes, vascular, muscular or respiratory. In this report, a rare case of muscular tinnitus related to eyelid blinking, is presented. The therapeutic problems are discussed.
Initial management consisted of explanation and reassuration, but the tinnitus became louder. A ventilation tube was inserted on the right side, under local anaesthesia. Inexplicably, the tinnitus immediately disappeared on that side. It was planned to insert a ventilation tube on the left side if the relief persisted. The following day, however, the patient sneezed on waking and reported that the tinnitus recurred immediately, and was now associated with right otalgia. The ventilation tube was removed and the patient was then FIFLEX THRESHOLD Y 226Hz ml MANUAL
TEST 1 NON-ACOUSTIC L 20
. 00
Case report A 23-year-old woman presented in July, 1990, complaining of sounds in both ears for the previous three years. The noises were present only when she blinked and occurred with every blink. Blinking only one eye resulted in a sound only in the ipsilateral ear . The sound could not be easily characterized and was neither a click or a buzz, but a combination of both. The tinnitus was apparently of spontaneous onset, but may have been related to an upper respiratory tract infection. There was no hearing loss, otalgia, otorrhoea or vertigo. The patient was on no medication except a low dose oestrogen oral contraceptive pill. There was no history of any systemic illnesses, and the patient had never been hospitalized in the past. General and systemic examination, (including neurological examination) and examination of the nose, postnasal space and larynx wa^ normal. Otoscopy revealed normal tympanic membranes, and s tuning fork tests were normal. Whenever the patient blinked, however, there was a visible medial movement of the tympanic membrane, in the region just posterior to the umbo. There was a simultaneous, upward and backward movement of the uvula. No abnormal sound could be heard on auscultation of the ear and temporal region. Audiology revealed normal hearing thresholds. Tympanometry revealed normal middle ear pressures. The movement of the tympanic membrane related to eye blinking, could be observed with an impedance meter (Fig. 1). The acoustic reflexes were normal. Blood investigations, including a full blood count, urea and eletrolytes, sugar, ESR and WR, were all normal. A CT scan of the brainstem was normal.
• .02
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Y £26Hz
L
. 60
15 sec REFLEX THRESHOLD ml Y 226Hz MANUAL . 00
. 16 ml
I
TEST 2 NON-ACOUSTIC R daP*: 6
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Accepted for publication: 2 September 1991. 44
1
45
CLINICAL RECORDS
prescribed carbamazepine, 100 mg bd orally. After a week, a decrease in the intensity of the tinnitus was noted. The dose was decreased after the second week to 100 mg daily by mouth. Carbamazepine blood levels were estimated weekly, and maintained at between 4-8 mg/ml by this once daily dose. After six weeks, the carbamazepine was tailed off, and after two months was stopped completely. Regular liver function tests, full blood counts, urea and electrolyte estimations were done to asssess possible hepatorenal and haematological toxicity from the drug. After three months, the tinnitus has remained well controlled. Though still present, it is softer, more tolerable and less frequent, occurring approximately once a week. Discussion 'Tinnitus should be considered not only as a symptom of aural disease, but also as a symptom frequently accompanying disorders of other portions of the body.' (Fowler, 1944). It may be, and often is, present in some form in persons who have no apparent aural or other disease (Fowler, 1944). The source of the tinnitus in this patient is probably twofold: (1) from the movement of the soft palate; (2) from the contraction of middle ear muscles. The genesis of the sound from contraction of the soft palate is not clear, but is probably due to either the snapping open of the Eustachian tube (Paparella and Shumrick, 1980) or to the breaking of the surface tension of the mucus at the Eustachian tube opening, (East and Hazell, 1987). The sound is perceived as a click. Tensor tympani contraction is said to produce a clicking sound (Paparella and Shumrick, 1980), whereas stapedius muscle contraction produces a buzzing noise, (Watanabe etal., 1974; Marchiando et al., 1983). The genesis of the tinnitus from stapedial muscle contraction may be from: 1. Propagation of muscle contraction noise 2. Vibration of the tympanic membrane 3. Stimulation of the tympanic plexus 4. Temporary variation of inner ear pressure or cochlear microphonic potential (Watanabe et al., 1974). The action of the stapedius muscle in the middle ear sound conducting system, is more important than that of tensor tympani. Watanabe et al. (1974), described eight cases of tinnitus due to stapedial muscle contraction related to certain facial muscle contraction (either voluntary or involuntary). Unlike the patient discussed in this article, however, all these patients were recovering from facial nerve paralysis, and had unilateral tinnitus. Movement of the tympanic membrane was not visible in relation to the eyelid blinking. All eight patients obtained relief from division of the tendon of the stapedius muscle. Marchiando et al. (1983), reported on two cases of tinnitus produced by stapedius muscle spasm. In both cases, the tinnitus was precipitated by loud noises. Both patients had normal facial nerve function and normal hearing; the tinnitus was relieved by division of the tendon of the stapedius muscle. Shea and Harell (1978) discussed the use of oral carbamazepine in the treatment of tinnitus. In their series of 27 patients, one patient with palatal myoclonus, refractory and to all other Key word: Tinnitus
forms of treatment, had complete relief from a small dose of carbamazepine. This was the basis for the use of carbamazepine in our patient. They used intravenous lignocaine as a test; however, the correlation between the lignocaine test and the response to carbamazepine treatment was not clear. They therefore advised a trial of carbamazepine treatment even if the lignocaine response was minimal. The initial dose used by Shea and Harell (1978), was 100 mg twice daily and blood levels of carbamazepine were measured daily. The dose was increased by 100 mg daily, never exceeding 100 mg four times a day, until a level of 4—8 mg/ml was reached, or until the tinnitus was relieved. Potential complications of bone marrow suppression and abnormal liver and kidney function were monitored by full blood counts, liver function tests, and urea and electrolyte estimations—these were done weekly for eight weeks and then monthly, while the dose of carbamazepine was gradually seduced to nothing. In Shea and Harell's series, the side effects which occurred were temporary, and disappeared when the drug was stopped. East and Hazell, (1987), described the suppression of palatal (or intratympanic) myoclonus by tinnitus-masking devices, using white-noise masking. In their series of twelve cases, three patients became completely symptom-free, four continued to get periods of relief from their clicking sounds with continuous masking and four patients found the distracting effects of white-noise helped them. A white-noise masker was not used in the patient discussed in this article because of reluctance to use an externally visible device. An attempt at masking with a Sony Walkman cassette player was unsuccessful.
References East, C. A., Hazell, J. W. P. (1987) The suppression of palatal myoclonus by tinnitus masking devices. Journal of Laryngology and Otology, 101: 1230-1234. Fowler, E. P. (1944) Head noises in normal and in disordered ears: significance, measurement, differentiation and treatment. Archives of Otolaryngology, 39: 498-503. Marchiando, A., Per-lee, J. H., Jackson, R. T. (1983) Tinnitus due to idiopathic stapedial muscle spasm. Ear, Nose and Throat Journal, 62: 8-13. Paparella, H. M., Shumrick, D. A. (1980) Diseases of the Eustachian tube, Otolaryngology, Vol. II, Chapter 14, W. B. Saunders Co: Philadelphia, p. 1409. Shea, J. J., Harell, M. (1978) Management of tinnitus aurium with lidocaine and carbamazepine. Laryngoscope, 88: 1477-1484. Watanabe, I., Kumagami, H., Tsuda, Y. (1974) Tinnitus due to abnormal contraction of the stapedial muscle. Journal of Otorhinolaryngology, and its Borderlands, 36: 217—226.
Address for correspondence: Dr. V Rajah, Dept. of Otorhinolaryngology, Faculty of Medicine, University of Natal, P. O. Box 17039, Congella, 4013, South Africa.
Clinical Records Tinnitus related to eyelid blinking V. RAJAH, M.Med (Otol), F.R.C.S.Ed. (Congella, South Africa)
Abstract Tinnitus due to muscular causes is rare. The commonest pathological muscular cause of tinnitus is palatal myoclonus. A case of bilateral tinnitus, related to eyelid blinking, is presented. This is the first case reported in the literature. Previous reported cases of tinnitus related to eyelid blinking have all been unilateral and associated with recovery from a VII nerve palsy. The treatment of the condition is discussed.
Introduction Tinnitus may be physiological, e.g. circulatory humm, pathophysiological, e.g. temporary noise-induced tinnitus, or pathological. Most patients with pathological tinnitus have associated cochlear pathology and the tonal frequency to which the tinnitus is best matched, tends to be in or close to the frequency zone of the hearing impairment. A small proportion of patients have pathological tinnitus due to other causes, vascular, muscular or respiratory. In this report, a rare case of muscular tinnitus related to eyelid blinking, is presented. The therapeutic problems are discussed.
Initial management consisted of explanation and reassuration, but the tinnitus became louder. A ventilation tube was inserted on the right side, under local anaesthesia. Inexplicably, the tinnitus immediately disappeared on that side. It was planned to insert a ventilation tube on the left side if the relief persisted. The following day, however, the patient sneezed on waking and reported that the tinnitus recurred immediately, and was now associated with right otalgia. The ventilation tube was removed and the patient was then FIFLEX THRESHOLD Y 226Hz ml MANUAL
TEST 1 NON-ACOUSTIC L 20
. 00
Case report A 23-year-old woman presented in July, 1990, complaining of sounds in both ears for the previous three years. The noises were present only when she blinked and occurred with every blink. Blinking only one eye resulted in a sound only in the ipsilateral ear . The sound could not be easily characterized and was neither a click or a buzz, but a combination of both. The tinnitus was apparently of spontaneous onset, but may have been related to an upper respiratory tract infection. There was no hearing loss, otalgia, otorrhoea or vertigo. The patient was on no medication except a low dose oestrogen oral contraceptive pill. There was no history of any systemic illnesses, and the patient had never been hospitalized in the past. General and systemic examination, (including neurological examination) and examination of the nose, postnasal space and larynx wa^ normal. Otoscopy revealed normal tympanic membranes, and s tuning fork tests were normal. Whenever the patient blinked, however, there was a visible medial movement of the tympanic membrane, in the region just posterior to the umbo. There was a simultaneous, upward and backward movement of the uvula. No abnormal sound could be heard on auscultation of the ear and temporal region. Audiology revealed normal hearing thresholds. Tympanometry revealed normal middle ear pressures. The movement of the tympanic membrane related to eye blinking, could be observed with an impedance meter (Fig. 1). The acoustic reflexes were normal. Blood investigations, including a full blood count, urea and eletrolytes, sugar, ESR and WR, were all normal. A CT scan of the brainstem was normal.
• .02
ml
N0N--ACOUST I C
Y £26Hz
L
. 60
15 sec REFLEX THRESHOLD ml Y 226Hz MANUAL . 00
. 16 ml
I
TEST 2 NON-ACOUSTIC R daP*: 6
- .01 Y 226HZ I NON-ACOUSTIC R MANUAL - / w i M i e*#U«Js\ d 9 P a : 0
. 00
15 sec FIG.
Accepted for publication: 2 September 1991. 44
1
45
CLINICAL RECORDS
prescribed carbamazepine, 100 mg bd orally. After a week, a decrease in the intensity of the tinnitus was noted. The dose was decreased after the second week to 100 mg daily by mouth. Carbamazepine blood levels were estimated weekly, and maintained at between 4-8 mg/ml by this once daily dose. After six weeks, the carbamazepine was tailed off, and after two months was stopped completely. Regular liver function tests, full blood counts, urea and electrolyte estimations were done to asssess possible hepatorenal and haematological toxicity from the drug. After three months, the tinnitus has remained well controlled. Though still present, it is softer, more tolerable and less frequent, occurring approximately once a week. Discussion 'Tinnitus should be considered not only as a symptom of aural disease, but also as a symptom frequently accompanying disorders of other portions of the body.' (Fowler, 1944). It may be, and often is, present in some form in persons who have no apparent aural or other disease (Fowler, 1944). The source of the tinnitus in this patient is probably twofold: (1) from the movement of the soft palate; (2) from the contraction of middle ear muscles. The genesis of the sound from contraction of the soft palate is not clear, but is probably due to either the snapping open of the Eustachian tube (Paparella and Shumrick, 1980) or to the breaking of the surface tension of the mucus at the Eustachian tube opening, (East and Hazell, 1987). The sound is perceived as a click. Tensor tympani contraction is said to produce a clicking sound (Paparella and Shumrick, 1980), whereas stapedius muscle contraction produces a buzzing noise, (Watanabe etal., 1974; Marchiando et al., 1983). The genesis of the tinnitus from stapedial muscle contraction may be from: 1. Propagation of muscle contraction noise 2. Vibration of the tympanic membrane 3. Stimulation of the tympanic plexus 4. Temporary variation of inner ear pressure or cochlear microphonic potential (Watanabe et al., 1974). The action of the stapedius muscle in the middle ear sound conducting system, is more important than that of tensor tympani. Watanabe et al. (1974), described eight cases of tinnitus due to stapedial muscle contraction related to certain facial muscle contraction (either voluntary or involuntary). Unlike the patient discussed in this article, however, all these patients were recovering from facial nerve paralysis, and had unilateral tinnitus. Movement of the tympanic membrane was not visible in relation to the eyelid blinking. All eight patients obtained relief from division of the tendon of the stapedius muscle. Marchiando et al. (1983), reported on two cases of tinnitus produced by stapedius muscle spasm. In both cases, the tinnitus was precipitated by loud noises. Both patients had normal facial nerve function and normal hearing; the tinnitus was relieved by division of the tendon of the stapedius muscle. Shea and Harell (1978) discussed the use of oral carbamazepine in the treatment of tinnitus. In their series of 27 patients, one patient with palatal myoclonus, refractory and to all other Key word: Tinnitus
forms of treatment, had complete relief from a small dose of carbamazepine. This was the basis for the use of carbamazepine in our patient. They used intravenous lignocaine as a test; however, the correlation between the lignocaine test and the response to carbamazepine treatment was not clear. They therefore advised a trial of carbamazepine treatment even if the lignocaine response was minimal. The initial dose used by Shea and Harell (1978), was 100 mg twice daily and blood levels of carbamazepine were measured daily. The dose was increased by 100 mg daily, never exceeding 100 mg four times a day, until a level of 4—8 mg/ml was reached, or until the tinnitus was relieved. Potential complications of bone marrow suppression and abnormal liver and kidney function were monitored by full blood counts, liver function tests, and urea and electrolyte estimations—these were done weekly for eight weeks and then monthly, while the dose of carbamazepine was gradually seduced to nothing. In Shea and Harell's series, the side effects which occurred were temporary, and disappeared when the drug was stopped. East and Hazell, (1987), described the suppression of palatal (or intratympanic) myoclonus by tinnitus-masking devices, using white-noise masking. In their series of twelve cases, three patients became completely symptom-free, four continued to get periods of relief from their clicking sounds with continuous masking and four patients found the distracting effects of white-noise helped them. A white-noise masker was not used in the patient discussed in this article because of reluctance to use an externally visible device. An attempt at masking with a Sony Walkman cassette player was unsuccessful.
References East, C. A., Hazell, J. W. P. (1987) The suppression of palatal myoclonus by tinnitus masking devices. Journal of Laryngology and Otology, 101: 1230-1234. Fowler, E. P. (1944) Head noises in normal and in disordered ears: significance, measurement, differentiation and treatment. Archives of Otolaryngology, 39: 498-503. Marchiando, A., Per-lee, J. H., Jackson, R. T. (1983) Tinnitus due to idiopathic stapedial muscle spasm. Ear, Nose and Throat Journal, 62: 8-13. Paparella, H. M., Shumrick, D. A. (1980) Diseases of the Eustachian tube, Otolaryngology, Vol. II, Chapter 14, W. B. Saunders Co: Philadelphia, p. 1409. Shea, J. J., Harell, M. (1978) Management of tinnitus aurium with lidocaine and carbamazepine. Laryngoscope, 88: 1477-1484. Watanabe, I., Kumagami, H., Tsuda, Y. (1974) Tinnitus due to abnormal contraction of the stapedial muscle. Journal of Otorhinolaryngology, and its Borderlands, 36: 217—226.
Address for correspondence: Dr. V Rajah, Dept. of Otorhinolaryngology, Faculty of Medicine, University of Natal, P. O. Box 17039, Congella, 4013, South Africa.
