Lidocaine is well known to suppress tinnitus. However, the mechanism underlying tinnitus suppression with lidocaine remains to be established. Recently, the motility of outer hair cells has been considered to be involved in the mechanisms of tinnitus. We have previously investigated that the slow motility of outer hair cells was regulated by the olivocochlear bundle, the efferent nervous system via inositol trisphosphate (InsP3) second messenger system. In the present study, we examined the effects of lidocaine on the InsP3 second messenger system in the cochlear sensory epithelia of the rat. Lidocaine induced the release of inositol phosphates (InsPs) in the dose-dependent manner. This effect of lidocaine was independent of the muscarinic or P2y purinergic receptor-mediated releases of InsPs. Other local anesthetics such as tetracaine, dibucaine and procaine did not markedly induce the release of InsPs, indicating that the mechanism of this effect of lidocaine is not related to its analgesic action. From these results, we hypothesized that lidocaine stimulate the InsP3 second messenger system in the cochlear sensory epithelia, which results in the suppression of tinnitus.
In the present study, the cell proliferation pattern was investigated in the healing process of a perforated tympanic membrane using proliferating cell nuclear antigen (PCNA) as an index. In 40 guinea pigs, a circular perforation with approximately lmm in diameter was made in the posterior superior quadrant of the tympanic membrane in both ears using a high frequency electric knife (Surgitron FFPF, Eliman Co.). The tympanic membrane was then observed periodically, and the histological study was done using HE staining and anti-PCNA antibody. The healing process of the perforated tympanic membrane was divided into 3 stages; epithelial layer stage, middle fibrous layer stage and closed stage. In the epithelial layer stage, increased proliferative activity in the epithelial layer of the perforated edge was observed. The proliferative activity was also reinforced in the periphery of annulus and malleus in a certain distance away from the perforated edge. In this stage, no remarkable change was observed in the middle layer. In the middle layer stage, however, the cell proliferation was markedly increased in the middle layer of the perforated edge. When the perforated hole became progressively smaller, the shift of stage from the epithelial to middle layer was observed. In the closed stage, the proliferative activity was rapidly decreased from the periphery of the middle layer as well as from the closed part of the perforation in the epithelial layer. Since the time and site of onset in which the proliferative activity was differed in the epithelial and middle layer, the mechanisms of closure of the perforation seemed different in each layer.
The effect of basic fibroblast growth factor (b-FGF) on tympanic membrane (TM) perforation was studied in guinea pigs. In 155 guinea pigs, a round perforation of approximately lmm in diameter was made in the posterior superior quadrant of TM of both ears using a high frequency knife (Surgitron FFPF, Ellman Co.). Each guinea pig received 0.2ml of b-FGF solution at different concentrations in the right ear and 0.2ml of placebo in the left ear. Healing was observed under an otomicroscope, and histological examination was performed by HE staining and monoclonal anti-PCNA antibody (DAKO, PC10). The mean duration for closure of perforation was significantly shorter in the ears received 10μg/ml, 100μg/ml b-FGF for three days. With high concentration of b-FGF, severe inflammation was frequently observed. Immunohistochemically, topical application of b-FGF on TM perforation mediated faster healing by inducing rapid proliferation of epithelial layer and middle fibrous layer.
The audiotry brainstem response (ABR) and compound action potential (AP) of the cochlear nerve were measured in guinea pigs using click and 2, 4 and 8kHz tone pip stimuli to investigate age-related alternations in the auditory function. The animals were divided into three groups: group A (3 months of age; 15 animals), B (13 to 14 months of age; 15) and C (23 to 24 months of age; 20). With advancing age, the threshold elevation in both ABR and AP was gradual, and the latencies for wave I, II, III and IV in ABR prolonged among group A, B and C. The difference between group A and other two groups (B and C) were statistically significant. Despite elevation of thresholds, the interpeak latencies (IPL) did not differ one another. Among the frequencies for 2, 4 and 8 kHz, there were not significant differences in each threshold. In the selected animals in group B and C, there were some individual differences in revealing the threshold elevation and prolonged latencies of the ABR and AP among aged animals which was similar to our previous report.
In 32 children with otitis media with effusion (O. M. E), the bacteriological study of the nasopharynx was studied, and the incidence of H. influenzae, S. pneumoniae, S. aureus, and group A steptococcus was about 40%, 20%, 20%, and 10%, respectively. The incidence of these bacteria was higher in the cases with O. M. E. than that in the cases with chronic tonsillitis or control cases. In 28 O. M. E. cases with a-streptococci (87.5%), the incidence of a-streptococci with inhibitory activity against 4 pathogens (H. influenzae, S. pneumoniae, S. aureus, group A streptococcus) was examined. The detection rate of α-streptococcal strains with inhibitory activity against 4 pathogens in the nasopharynx in the cases with O. M. E. was significantly lower than those in the chronic tonsillitis cases and the control cases. Moreover, the detection rate of inhibitory α-streptococci from the nasopharynx was lower than that of the tonsil. These findings suggested that the decrease of inhibitory activity of the bacterial flora against pathogens in the nasopharynx was one of the etiological factors of O. M. E.
The relationship between age and clinical features of acquired cholesteatoma was analyzed in 227 ears. Type of cholesteatoma in every age group was the same, and the development of mastoid pneumatization was inhibited in all age groups. The basic pathogenesis of cholesteatoma appeared to be common in all age groups. Cholesteatoma in pediatric group was aggressive, and high rate of recurrence and residual cholesteatoma was detected. Pathological changes of mucosa were diminished and the recurrence rate was decreased along with aging. Ossicular destruction and bony defect were increased in elderly patients. In pediatric cholesteatoma surgery, staged tympanoplasty using the canal-up technique should be performed to prevent recurrence and residual cholesteatomas. At the second-stage operation in the cases of recurrence, the posterior canal wall was removed in accordance with canal-down technique, and the mastoid cavity was obliterated simultaneously. Because of the low recurrence rate in elderly patients, it was possible to perform the one-stage operation using canal-up technique or canal-down technique with mastoid obliteration.
We have been using a piece of tragal cartilage for reconstructing the ossicular chain in tympanoplasty because of its stability and ease of trimming. Before 1990, the cartilage columella was relatively large and square (4mm×4mm). It was superposed in two or three layers to adapt the height between the head of the stapes and eardrum. Fibrin glue has been used to stabilize a slim cartilage columella (1mm×1mm, length 4 to 6mm) with certainty. From 1990 to 1993 a slim cartilage columella has been used in 56 ears (group I) of tympanoplasty and the postoperative hearing results were compared with that of the 39 ears (group II) with a large columella before 1990. In 41 of 56 ears of the recent series and 25 of 39 ears of the former series, tympanoplasty type III was performed, and the remainder of each series, tympanoplasty type IV was performed. In tympanoplasty type III, the postoperative air-bone gap within 20dB was obtained in 78% and 56% of the cases in group I and group II, respectively. In tympanoplasty type IV, the postoperative air-bone gap within 20dB was obtained in 60% and 36% of the cases in group I and group II, respectively. All subjects were then divided into the following three categories according to the severity of mucosal pathology around stapes: group A: nearly intact mucosa, group B: mucosa with edema, group C: much granulation or adhesion without aeration. In ears in which the slim cartilage columella was used, the postoperative air bone gap within 20dB was achieved in 93%(15/16 ears), 85%(17/20 ears) and 45%(9/20 ears) in group A, B and C, respectively. In contrast, the rate was 50%(5/10 ears), 55%(6/11 ears), and 50%(9/18 ears) in group A, B, C, respectively, when the large columella was used. In group A and B, postoperative hearing of the ears with the slim columella was significantly better than that with the large columella. These results showed that when the aeration around the stapes was present, high success rate in hearing could be obtained by using a slim cartilage columella.
There are two main problems for artificial ossicular chain prosthesis; extrusion and postoperative slippage of prosthesis. We manufacturied a new hydroxylapatite prosthesis “cartilage connecting ossicular chain prosthesis” with a planar-like head portion to contact with a piece of cartilage. As a result, postoperative extrusion rate was 1/41 (2.4%) which seemed lower than the conven tional type, and hearing success rates were 83.8% in modified type III tympanoplasty, 77.8% in modified type IV tympanoplasty. Average improvement on air conduction were 20.0dB in modified type III tympanoplasty, and 24. 5dB in modified type IV tympanoplasty. These good results were explained by that the “cartilage connecting ossicular chain prosthesis” was tightly attached with a reconstructed tympanic membrane and ossicular chain prosthesis might be stable in tympanic cavity.
Three patients presented with chronic otitis media accompanied with extensive bone destruction without evidence of cholesteatoma. Review of literatures suggested that bacterial infection and progressive osteitis were the causes of bony erosion in the first case. Chronic granulation tissue containing cholesterine and an expanding mastoid cyst producing pressure erosion were most likely causative agents of bony destruction observed in case 2 and 3, respectively.
The effect of platelet activating factor (PAF) on mucociliary transport of the eustachian tube was investigated both in vitro and in vivo, in healthy guinea pigs and in healthy chinchillas. Normal ciliated epithelium was carefully obtained from the eustachian tube of guinea pigs and incubated with RPMI 1640 solution in tissue culture. The mucosal specimens were incubated with PAF at concentrations ranging from 10-10M to 10-6M, and ciliary activity was observed under an inverted microscope, recorded on video tapes and photoelectrically quantified on a video monitor. PAF inhibited dosedependently ciliary activity in vitro. For in vivo study, 1 mL each of 10-5M PAF, 10-5M PGE2, 10-5M PAF & PGE2 or the control solution (0.1% methanol/PBS) was directly injected into the tympanic bullae of anesthetized chinchillas with a 27-gauge syringe. The middle ear was examined by otomicroscopy, tympanometry and ABR in relation to time. There was a significant difference in the average peak pressure of tympanograms between PAF-treated and control animals. Furthermore, PGE2 augmented the inhibitory effect of PAF on middle ear clearance although injection of PGE2 showed no significant effects. The threshold average of ABRs in the PAF group was significantly elevated compared with the control, and PGE2 also augmented the effect of PAF. These data suggest that PAF inhibits mucociliary transport of the eustachian tube from the middle ear, and that PGE2 plays an important role in the augmentation of inflammatory disorders.
Case 1 is a 53-year-old man with sudden hearing loss and tinnitus following left perforating ear injury caused by an earpick. An audiogram showed a severe mixed hearing loss in the left ear with no response above 4, 000Hz. Although he did not complain of dizziness just after the accident, he noticed dizziness about 20 days later. This time lag between the accident and onset of dizziness differed significantly from the cases reported previously. He was treated conservatively without improvement in hearing level. Exploratory tympanotomy was performed about 40 days after the accident, and showed the dislocation of the incudostapedial articulation and depression of the stapes into the vestibule. Perilymph was coming out from the oval window. Case 2 is a 66-year-old woman with postero-superior quadrant tympanic membrane perforation with cholesteatoma. When she underwent irrigation of the tympanic cavity through the perforation, she felt severe vertigo and flow of serous fluid from the cavity was noticed. Surgical exploration on the same day demonstrated cholesteatoma matrix around the incudostapedial articulation and a bone defect of the stapes footplate. Perilymph was welling out from the defect of the footplate. Thirty cases with traumatic perilymph fistula secondary to penetrating ear injury were reviewed. There were 15 males and 15 females with the age ranging from 1 year to 63 years. Of the 30 cases, 28 (94%) complained of hearing loss, 25 (83%) vertigo or dizziness and 21 (70%) tinnitus. The pattern of the audiogram showed conductive type in 3 cases, sensorineural type in 3, combined type in 19 and normal or unknown in 5. Out of the 20 cases presented disequilibrium, 13 cases noticed severe vertigo or dizziness such as inability to walk and feeling nauseous on motion. Of the 30 cases, 22 cases demonstrated a perforation of the postero-superior quadrant of the tympanic membrane. Of the 23 cases underwent exploratory tympanotomy, 18 cases demonstrated fistulas in the oval window, 3 in the round window and 2 in the both windows. The dislocation of the incudostapedial articulation was observed in 4 cases, the depression of the stapes into the vestibule in 6, both in 4, normal condition of the articulation and the stapes position in 8 cases which included 3 round window fistula cases. The cases with perilymph fistula in association with traumatic tympanic membrane perforation are rare. However, if a patient would complain of hearing loss, tinnitus and severe vertigo or dizziness just after the ear trauma, we must consider the possibility of the traumatic perilymph fistula secondary to the perforating ear injury.
A 76-year-old female was complaining of vertigo. She noticed ear fullness and tinnitus of the right ear when she swallowed saliva during nasal nebulizer treatment. In the following morning she felt dizzy. Pure tone audiometry revealed marked sensorineural hearing loss in the right ear. Horizontal and rotatory nystagmus to the right was noted. Later, her hearing fluctuated. It was found that she developed perilymph fistula (PLF) during nebulizer treatment. After 2 weeks, vertigo had subsided and audiometry revealed hearing improvement. To explain the mechanism of PLF formation, nasopharyngeal pressure (NP-P) and middle ear pressure (ME-P) were measured. NP-P ranged from 170 to 918 mm H2O with swallowing during nebulizer treatment in 4 healthy people. High NP-P was noted. NP-P and ME-P were simultaneously measured in 2 individuals with traumatic perforation of the eardrum in whom NP-P increased from 150 to 500 mm H2O and ME-P increased from 180-430 mm H2O. High NP-P was transmitted to the middle ear through eustachian tube. High ME-P may predispose to formation of PLF.
Between 1989 and 1994, we successfully treated 4 patients with facial palsy following acute otitis media by mastoidectomy. A child showed typical signs and symptoms of classical mastoiditis secondary to acute otitis media with S. pneumonia. An elderly female with untreated DM demonstrated a classical mastoid infection with S. pyogens. A 50-year-old male with chronic renal failure. showed severe otitis media. In an elderly female patient, the clinical features and course of acute mastoiditis were masked by prior therapy with antibiotics. In all four cases, well developed mastoid cells were observed around the vertical portion of the facial nerve, and these were occupied by edematous granulation.
Labyrinthine lesions of 22 patients (40 ears) with surgically confirmed fenestral otosclerosis were investigated using three CT units with different levels of performance. The patients were classified into three groups as follows: 13 cases (25 ears) of group 1 underwent scanning using the Toshiba TCT60A/60 (the old model); four cases (6 ears) of group 2 were examined by the high resolution mode of the Toshiba TCT -900S; and five cases (9 ears) in group 3 were examined by the super resolution mode of the Toshiba TCT-900S (the newest model). In group 1, six of 25 ears (24.0%) demonstrated an abnormally decreased density zone around the cochlea. The same decreased density zone was found in two of six ears in group 2 (33.3%), and in seven of nine ears in group 3 (77.8%). These were otospongiotic foci basically confined to the labyrinthine capsule, and sensitively detected by the improved CT units. From a detailed comparison of the performance of the CT units, it was speculated that the most important item for detecting the abnormally decreased density zone was spatial resolution controlled by the number of detectors and number of sampling data. The largest number of the patients in group 3, who underwent scanning using the Toshiba TCT-900S (super resolution mode) with high spatial resolution, demonstrated a localized zone of decreased density in the anterior part of the vestibule.
Platinum derivatives such as cisplatin damage cochlea in particular outer hair cells. On the other hand otoacoustic emissions (OAEs) are thought to be the products of outer hair cells movements. So OAE might be affected by platinum derivatives in some way. OAEs of the patients who were treated their malignant neoplasms with platinum derivatives were recorded and their changes were examined. Four of 16 patients showed the suppressive changes of OAEs in various way during their chemotherapy. The first patient showed reduction of the amplitude of evoked otoacoustic emission (EOAE) during treatment without the change of audiogram. And long after the chemotherapy, the ampulitude of OAE recovered to the first level. The second patient showed reduction of the ampulitude of the OAE evoked by 1.5kHz tone burst and simultaneously hearing impairment at high frequency (over 4kHz) was obsered. In the third patient the ampulitude of OAF evoked by 1.5kHz tone burst was reduced and spontaneous otoacoustic emission (SOAE) was disappeared during chemotherapy. In the last patient threshold of OAE evoked by 4kHz tone burst was raised and hearing impairment at high frequency was observed, but OAE evoked by 1.5kHz tone burst was not affected. The results suggested that the early damages of the cochlea by platinum derivatives could be evaluated with OAEs. Particulary in the first and second cases, though the reductive changes were shown in their OAE evoked by 1.5kHz tone burst, no hearing impairment was observed in 1 and 2 kHz. So these results might mean that with OAEs, we could evaluate the early and subtle damages of cochlea by platinum derivatives that did not affect audiogram. In this study only 4 cases showed the changes in OAEs, the other 12 cases showed no change. We evoked OAE by 1.5 or 4kHz tone burst, but the cochlea damages by platinum derivatives are said to occur on higher frequency in the early stage. So to detect the early damages of cochlea, we must use higher frequency stimulation for EOAE. But because of the acoustic specificity of human middle ear it is difficult to record OAE evoked by higher frequency. So to detect the earlier damages of cochlea by platinum derivatives, we should combine the other examinations such as high frequency audiogram or ditortion product OAE (DPOAE) which can be recorded in higher frequency.
Auditory evoked responses (ABRs, MLRs, and SVRs) were recorded in two chronic alcoholics with sudden loss of consciousness. Characteristics of these recordings were as follows. (1) Results of both ears were closely similar in each case. (2) The absolute latencies of wave III and V were exceedingly increased. Thus, the interwave latencies III-V and I-V were increased. (3) No definitive wave was identified in the MLR and SVR tests. It is surmised that the main lesions in both cases were the higher primary auditory tract than the upper brainstem and the non-specific auditory tracts, such as the reticular formation. The auditory evoked response tests are of clinical value in detecting functional abnormalities in chronic alcoholics with an sudden loss of consciousness.