The postoperative results after tympanoplasty have recently improved remarkably, however, cases without expected results after the operation also still remain. The purposes of this panel discussion were to analize the causes of unsuccess and to consider these counterplans and the indication for re-operation. The six cases presented here were as follows: 1) frequent perforations after myringoplasty, 2) lateralization of the ear drum or stenosis of the external meatus after tympanoplasty, 3) development of cholesteatoma after tympanoplasty, 4) frequent dislocation of the reconstructed ossicular chain, 5) fixation of the ossicular chain after tympanoplasty, and 6) inadequate indication for tympanoplasty.
From the view point of education for young surgeons, the technical procedures for prevention of complications during the surgery were also discussed.

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Due to recent advances in treatments for chronic otitis media, the results of tympanoplasty have markedly improved. However, not all cases achieve a well inflammation-free middle ear cleft and satisfactory hearing results after surgery. There are several reasons for these unsuccessful cases. In particular, unexpected trauma during the operation is the most severe problem. Sensorineural hearing loss, vertigo and tinnitus are typical inner ear symptom caused by reckless procedures near the otic capsule. High speed drilling of the temporal bone should not be performed close to the ossicles or the otic capsule, and should never touch these regions directly. Sufficient water irrigation should be applied along with drilling to avoid increased temperature in the otic capsule. Complete understanding of the temporal bone's anatomy and safe and skillful techniques are importamt way to avoid these accidents.

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The sequential changes of cochlear compound action potentials (CAPs) following transient cochlear ischemia was studied in the gerbil to reveal if transient ischemia causes delayed neuronal death of the organ of Corti. For chronic reading of the CAPs, a platinum wire electrode was inserted into the facial canal through the stylomastoid foramen. Cochlear ischemia was created by occluding the bilateral vertebral arteries for 5 minutes, as the posterior cerebral communicating arteries are lucking and the labyrinthine arteries are supplied only by the vertebral arteries in the gerbil. Occlusion of the vertebral arteries caused remarkable increase in the CAP threshold, which subsequently recovered after recirculation. Hearing impairment recovered completely during the 1st and 3rd day of ischemia in all animals (n=6). However, the threshold increased again after the 5th day. The increase was more than 10dB at the 10th day in 3 of 6 (50%) animals.

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The findings in the temporal bone of a 62-year-old male patient who died of generalized metastasis of malignant melanoma are reported. Autopsy revealed multiple metastatic foci in the brain and cranial pia mater. Histopathological examination of the temporal bone revealed invasion of bilateral internal auditory canals by malignant melanoma cells. The mode of invasion of the temporal bone by the malignant melanoma cell appear to reflect diffuse leptomeningeal carcinomatosis. None of the clinical manifestations, such as hearing loss, tinnitus, vertigo, or facial paralysis, were noted in this patient, because of no degeneration of the nervous tissue in the auditory canal.

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There are some cases of acute otitis media (AOM) in children which have repetitive courses and finally develop intractable chronic otitis media with effusion (COME). In these cases, infection could be one of the major background factors. What kinds of infectious lesions in the tympanic cavity, mastoid and Eustachian tube will lead these sequelae? Microscopic findings of the tympanic membrane and the findings at paracenthesis procedure were evaluated with the findings of CT scan.
There were two groups of AOM that showed bulging of the tympanic membrane.
The one was without infectious lesions and the other was with infectious lesions of the mastoid air cells found on CT scan. The former showed a mixture of air and fluid in the tympanic cavity only and were treated by administration of antibiotics. The latter showed partial absorption of effusion in the mastoid and as a result developed retraction of the tympanic membrane with residual effusion in the tympanic cavity.
Even in the aerated mastoid after resolution of the initial COME, if there was repeating infections, severe inflammation developed in the total mastoid, and the case resulted in intractable COME.
I concluded that mastoid lesions influenced tubal function and were important to determine the prognosis of AOM in children.

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A 24-year-old woman was complaining of hearing loss in the right ear since 1996. Microscopic examination of the right ear revealed attic retraction and a white lesion behind the posterosuperior quadrant of the tympanic membrane. High-resolution CT demonstrated softtissue density masses in the mastoid antrum, attic and mesotympanum. Audiograms showed a conductive hearing loss of average 52.5dB in the right ear. She had no past history of otitis media and myringotomy.
On the first surgery, 4 solitary open-type cholesteatomas were found in the mastoid antrum, the aditus ad antrum, around the tensor tympani tendon and adjacent to the posterosuperior part of the tympanic annulus. None of cholesteatomas had contact with the tympanic membrane. Ossicular abnormalities, defect of the incus and fixation of the stapes were noted independent of cholesteatomas.From the above findings, diagnosis of multiple congenital cholesteatomas associated with ossicular abnormalities was made. Eight months later, the removal of residual cholesteatomas and mastoid obliteration were performed on a secondlook operation.

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Petrous bone cholesteatoma extending beyond the labyrinth involves the petrous pyramid and internal auditory canal. The treatment of the petrous bone cholesteatoma is difficult because of the hearing preservation and its anatomical characteristics. In this paper, we described the clinical findings of two cases treated in our hospital in order to elucidate the surgical strategies for treatment of petrous bone cholesteatoma.
Case 1 was a 66-year-old male with 6 years' history of dizziness. An attic type cholesteatoma was observed in his right middle ear. CT examination revealed that the cholesteatoma extended from the antrum inferiorly, the superior semicircular canal to the upper part of the internal auditory canal. The cholesteatoma was removed completely by translabyrinthine approach with supuralabyrynthine route.
After cholesteatoma matrix was removed from the canal foramen, liquorrhea was observed. His left hearing level was decreased more than 30 dB postoperatively.
Case 2 was a 55-year-old male with 7 years' history of left facial paralysis and left deafness. For the last two years his gait has become ataxic. His left eardrum was adhered completely to the promontory. All middle ear ossicles were sclerotic.
CT and MRI revealed that there was a massive destructive petrous bone cholesteatoma. The lesion was removed by the tranmastoid-translabyrinthine approach. In deeper part of the sino-dural angle, the middle fossa dura was locally so atrophic that the arachnoid membrane was exposed. The cavity was obliterated with the temporal muscle.
In general, lateral skull base approach to the petrous apex can be classified into two procedures, passing through the otic capsule and conserving the otic capsule.
Approach through the otic capsule are including the translabyrynthine and the transcochlear approach. On the other hand, approaches conserving the otic capsule (extra labyrinthine) which are consisted of the middle fossa approach passing above the otic capsule and the retrosigmoid-retrolabyrinthine approach passing behind it are most popular. Decision making of surgical strategy depends on not only the localization and the extension of cholesteatoma, but the remaining function of labyrinth. It can also be necessary that postoperative follow-up study with CT and MRI should be regularly performed in addition to the surgery.

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Thirty nine ears of recurrent cholesteatoma after closed tympnoplasty were reviewed. The mean period between the previous operation and the reoperation was 5.3 years with a range from 2 to 20 years. The mean age at the reoperation was 41.9 years old with a range from 8 to 68 years old. The opposite ear was normal in twenty five ears (64.1%), cholesteatoma in 10 ears (25.6%), otitis media with effusion in 2 ears (5.1%), adhesive otitis media in one ear (2.6%) and chronic suppurative otitis media in one ear (2.6%). In the reoperation, closed tympanoplasty was performed in 13 ears (33.3%), open tympanoplasty in 18 ears (46.2%), total mastoid obliteration in 4 ears (10.3%) and partial mastoid obliteration in 4 ears (10.3%). No cases showed common findings of recurrent cholesteatoma in the previous operation. Recurrent cholesteatoma ocurred again in 2 ears (15.4%) and a deep retraction pocket in 2 ears (15.4%) of 13 ears operated on with closed tympanoplasty in the reoperation. Recurrent cholesteatoma should be operated with open tympanoplasty or mastoid obliteration technique because of the high risk of recurrent cholesteatoma after closed tympanoplasty. Cholesteatoma in the only hearing ear, bilateral ears, aged patients or with medical complications should be operated on with open tympanoplasty in the first operation. To evaluate operative results of closed tympanoplasty needs at least 6 years, because the mean periods between the previous operation and the reoperation was 5.3 years.

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There are two possible causes for Cholesteatoma in the external ear canal: Keratosis obturance (KO) and External auditory canal cholesteatoma (EACC). KO is caused by the pressure on embolus, and mainly a transformation of bone at the time of its remodeling. The posterior wall is sustained for long period of time, thus cholesteatoma takes a long time to get into the mastoid. The anterior wall also shows an intense transformation resulting in so-called ballooning. In EACC, inflamation of bone produces destruction, and cholesteatoma goes into mastoid within a short period of time. Therefore, the anterior and inferior walles shows minimal transformation.
Since both EACC and KO develop into a tumor like lesion with essentially the same nature, we call these advanced cases “external auditory canal cholesteatoma”. As for their early stages in the external ear canal, “epidermal keratosis” and “localized cholesteatoma” seem to be clinically appropriate.

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DFN3, an X-linked non-syndromic mixed deafness, is associated with mutations of BRAIN-4 (POU3F4) which encodes a POU transcription factor. The clinical hallmarks of DFN3 are a conductive hearing loss with perilymphatic gusher during surgery and progressive sensorineural deafness. We generated a mouse model of DFN3 by a targeting disruption of Brain-4 (Brn-4) and elucidated the pathology of deafness and the underlying mechanisms.
The hearing of mutant mice was assessed by auditory brainstem response (ABR) as compared with that of wild-type control mice. Wild-type mice (12W) exhibited normal ABR waveforms and thresholds (23±3dB SPL, n=9). Mice homozygous for Brn-4 deletion (12W) showed a significant elevation of ABR thresholds (90±5dB SPL, n=8). The middle ear including the ossicular chains of homozygous mutant mice appeared grossly normal, indicating that the deafness of Brn-4 deficient mice is unlikely to be conductive in origin. To further elucidate the site responsible for the deafness, the endocochlearpotential (EP) was measured through the cochlear lateral wall. The wild-type mice showed 101±9mV of the EP (n=9). On the other hand, the EP averaged 45±7mV (n=7) in homozygous mutant mice.
Electron microscopy revealed that suprastrial fibroblasts in mutant mice were lacking in irregular processes or plasma membrane outfoldings. The volume of the cytoplasm and the number of mitochondria were also decreased. Fibroblasts filling the area between the stria vascularis and bony otic capsule were devoid of processes of the cell or mitochondria. Extracellular fibrous strands were sparse in mutant mice as compared with those in wild mice. On the other hand, the organ of Corti, the spiral ganglion cells, and the stria vascularis are grossly normal appearance. Brn-4 message was intensively observed in the spiral ligament and suprastrial cells as well as the cochlear capsule using non-isotopic in situ hybridization.
These findings suggest that Brn-4 plays a critical role in the development of fibroblasts along the cochlear duct, contributing to the generation of the EP and the responsible site for DFN3.

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