Trace elements have been reported to exist in the active center of the metal-containing enzymes and to play the important roles in the oxidation-reduction reactions in many tissues. Recent works have elucidated that non-protein-bound elements (iron, copper, molybdenum) stimulate the production of superoxides, while protein-bound elements (iron, copper, zinc, selenium, manganese) take part in the elimination of superoxides. It should be noted that iron and copper have influence on both reactions. However, direct measurement of trace elements in the inner ear under the condition of abundant production of free radicals has never been reported. The purpose of the present study is to elucidate the effect of asphyxia on the iron concentration in the cochlear fluids measured by an inductively-coupled plasma atomic emission spectrometer. Samples were collected from young albino guinea pigs before asphyxia, at 3min after the onset of asphyxia, and at 5 and 15min of the reventilation following asphyxia. In the perilymph samples, there was no significant change during asphyxia for 3min. After re-ventilation following asphyxia, however, the non-protein-bound iron concentration significantly increased in the scala tympani perilymph at 5min and decreased rapidly toward the pre-asphyxic level thereafter. In contrast to the rapid decline in the scala tympani perilymph, the elevated level of the non-protein-bound iron concentration was maintained in the scala vestibuli perilymph for further 10min after re-ventilation. In the endolymph, the iron concentration was elevated at the end of asphyxia of 3 minutes' duration and decreased rapidly after re-ventilation. In the serum, there was no significant change at all. It is assumed that the iron increased in the cochlear fluids might be mobilized from the intracellular iron pool under the condition of lower pH or production of free radicals.
The histological changes of the mastoid cavity following simple mastoidectomy was studied using 10 pigs, in which the tympanic bullae has an air cell system resembling the human mastoid air cell system. The right ear was used as the treated group, and the left as the control group. The air cell system of the right ear was drilled open four weeks after birth, and the temporal bone of the animals was subsequently removed one week, two weeks, one month, and two months after the treatment for histological study. One to two weeks after the treatment, the open cavity was filled with granulation tissue, and the interface of the granulation tissue to the middle ear cleft was lined with epithelium. After one month, the epithelium lined the inner surface of the open cavity. The cavity was filled with granulation tissue. After the granulation tissue was absorbed, the epithelium was continuing to grow from the mucosa in the middle ear cleft to the inner surface of the mastoid cavity gradually. The postoperative enlarged tympanic cavity was finally achieved. Repneumatization did not occur after simple mastoidectomy. In the mastoid cavity after mastoidectomy, mucosal lining may be diminished resulting in insufficiency of gas exchange throughout the mastoid mucosa.
Catheterization of the eustachian tube using a metalic catheter is routinely performed and very useful for treatment of ear disaeses. However, this conventional cathetization often lacks reliability, reproducibility and safety owing to invisible method and using a rigid metalic catheter. To improve these disadvantages, we developed a new method using a silicone catheter attached to a flexible fiberscope to visualize the introduction of catheter. Thirty patients with chronic otitis midia were studied with our new catheterization. Our catheterization method obtained better results in reliability and reproducibility compared to the conventional metalic catheterization.
Three cases of lateral healing of the tympanic membrane following canal down tympanoplasty were reported. They received middle ear surgery 20 to 27 years ago two of them underwent canal down tympanoplasty and the rest atticotomy. Following revision surgeries by canaldown technique, the epithelium in the mastoid cavity gradually detached from the bony wall and the tympanic membrane moved laterally. In case 1 and 2, it finally resulted in discontinuity between the tympanic membrane and the ossicular chain. Reoperation succeeded to improve the position of the tympanic membrane and hearing in case 2, but failed in case 1. Reoperation was unnecessary as hearing remained good in case 3.
A 55-year-old female first visited our hospital with complaint of hoarseness and dysphagia. Palsy was found in the soft palate and vocal cord, and facial palsy was subsequently developed. CT scan showed cholesteatoma filled in the attic and mastoid cavity, fistulae in the semicircular canals, and dural exposure. Cholesteatoma was accompanied by severe mastoiditis due to mixed infection of staphylococcus and anaerobic bacteria, and an abscess was also found in the peripheral mastoid cavity. Wide exposure of the facial nerve, fistulae in the lateral and anterior semicircular canals, dural exposure in the middle and posterior cranial fossae, exposure of the sigmoid sinus, and severe inflammation around the sigmoid sinus (sinusphlebitis) were also found. Radical mastoidectomy with facial nerve decompression, and postoperatively palsy of the cranial nerves were inproved.
The retrospective epidemiological study of acute low tone sensorineural hearing loss was conducted. From January 1, 1995 to December 31, 1995, the patients who visited ten medical facilities in Kagoshima Prefecture and were consistent with the criteria such as 1) unknown origin, 2) acute onset, 3) sum of hearing level in three low frequencies (125Hz, 250Hz, and 500Hz) was 100dB or more and that in three high frequencies (2 KHz, 4 KHz, and 8 KHz) was less than 60dB, 4) with no nystagmus and no vertigo, were included in this study. Incidence of this disease was compared among ten medical facilities. Also gender, age, symptoms, prognosis of patients were evaluated, in a total of 89 patients, 21 men and 68 women. In primary medical facilities, more patients were identified than that in secondary facilities. Sum of hearing level in low frequecy at first visit and hearing level of 1 KHz showed no correlations with prognosis of the patients.Any particular combination of treatments showed no improvement in the results. But the patients with earlier consultation showed better prognosis than those with later consultation. Eighteen cases showed relapse.
Idiopathic stenosis of the internal auditory canal is a rare condition characterized by progressive sensorineural hearing loss, tinnitus and vertigo. We present two cases with idiopathic stenosis of the internal auditory canal. A 16-year-old girl complained of progressive hearing loss since she was 13-year-old. The other is a 7-year-old boy who has had hearing disturbance for one year. Common symptoms in these 2 cases were as follows: 1) unilateral mixed hearing loss, 2) they began when these patients were 13-year-old and 6-year-old respectively, 3) lack of vertigo, tinnitus and facial palsy. Characteristic findings on CT imaging were 1) the narrow internal auditory canal for its whole length, 2) septal structure along the midline of internal auditory canal in the latter case 3) no deformity of the bony labyrinth, tympanic cavity and external ear canal.
A 68-year-old man with bullous pemphigoid noticed mucosal ulcers in the oropharynx. In December 1994. He noticed a hearing loss in the left ear in February 1995, following severe recurrent buccal and labial mucosal ulcers. In March, he became dizzy and also noticed a hearing loss in the right ear. Pure tone audiometry on admission revealed a bilateral moderate sensorineural hearing loss (R=57.5dB, L=71.3dB). Short increment sensitivity index (SISI) scores were 100% at 1 kHz in both ears. Gazenystagmus of the horizontal and rotatory type was observed bilaterally. Caloric stimulation (ice water 10ml/10s) demonstrated no response in either ear. He was administered betamethasone and yglobulin for 10 days. However pure tone audiometry showed progressive bilateral profound deafness. Pemphigus vulgaris was diagnosed by biopsy of buccal mucosa. IgG showed a high point in the cerebrospinal fluid (30.8%). The present case developed acute bilateral profound deafness following severe mucosal ulcers. The hearing loss developed in the course of pemphigus vulgaris. It was assumed that autoimmunity was related to development of the hearing loss.
We analyzed statistically the results of audiometrical and vestibular function tests of 75 patients with drug-induced hearing loss and equilibrium disorders who visited our clinic during the past 16 years from 1980 to 1995. 1. Aminoglycoside antibiotics were the etiologic drug in all the cases who developed hearing impairment mainly during 10 years after 1995. In these cases, the hearing impairment was more severe than in those cases from 1980 to 1995. 2. During 1980 to 1995, aminoglycosides were still common among the etiologic drugs, while a new anti-cancer drug, cisplatin, were added to the etiologic drugs. Hearing loss due to cisplatin, although in most cases relatively mild and localized in a high frequency range, tended to increase and came to show a higher incidence than that due to antibiotics in the most recent 10 years. 3. Among the recent cases due to antibiotics, the incidence of associated renal failure was high. As in these cases the degree of the disorders was on average more severe than in other cases, especially strict follow-up observation is necessary when such ototoxic drugs are used.