Post-lesional plasticity following unilateral labyrinthectomy is considered as an excellent model of plasticityof the adult central nervous system. Indeed, the static and dynamic postural and oculomotor syndromesobserved at the acute stage largely disappear over time in all species of vertebrates that have been studied.First, we have briefly summarized the studies of our group, which have used electrophysiological and moleculartechniques together with morphological methods to investigate the neuronal basis of vestibular compensation.Second, the main characteristics of the compensation process in vestibular patients were summarized.An attempt was made to link the findings of various clinical studies on that topicwith the results of previousinvestigations in animal models. Such a comparison may open new directions for clinical research on vestibulartests and vestibular syndromes and could suggest new pathways of investigation for vestibular rehabilitation.

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My method of surgery for cholesteatoma has changed overtime and can be split into four terms inchronological order. Tympanoplasty was performed in all cases, but in each term the method and approachchanged as follows.
The first: 1955-1964 Canal wall down tympanoplasty
The second: 1965-1874 Canal wall up tympanoplasty
The third: 1975-1989 Canal wall down tympanoplasty with mastoid obliteration
The fourth: 1990-2002 Canal wall down tympanoplasty with mastoid obliteration and without atticobliteration
The reasons for these changes in surgical method and approach were influenced by the incidence of complicationssuch as mastoid cavity problems in the first term and recurrent cholesteatoma in the second term.In the change from the third term to the fourth term obliteration technique was no longer performed in theattic region to obtain a better surgical result. Then, a stable postoperative course is observed.

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We have devised new operative procedures for cholesteatoma, which involve a minimal risk of postoperativerecurrence even as the posterior wall of the external ear canal is preserved. Any one of the three proceduresmay be selected depending on the characteristics of the cholesteatoma, which can be classified into thefollowing three types:
(A) Cases in which the cholesteatoma is confined to the attic, and the ossicular chain is preserved;
(B) Cases in which the cholesteatoma has extended to the mastoid antrum, but the ossicular chain is stillpreserved;
(C) Cases in which the ossicles are destroyed.
For type (A), transcanal atticotomy is performed. For type (B), transcanal atticotomy combined withcortical mastoidectomy is performed. In both of these types in which mucosa of the middle ear is intact andthe attic is well aerated, only reconstruction of the lateral wall of the attic using fascia and a cartilage plate isrequired.
For type (C), a combination of transcanal atticotomy and cortical mastoidectomy is first performed. Inthis type of cholesteatoma, the mucosa is diseased and recurrent cholesteatoma is likely to develop. For thisreason, the space between the attic and the mastoid antrum needs to be closed by a bone pate and cartilageplate. In addition, of course, reconstruction of the sound transmission system is also necessary.

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the treatment of cholesteatoma employing intact canal wall tympanoplasty, staging the operation isrequired to re-establish aeration of the tympanic cavity and to eradicate possible causes of recurrence, cholesteatoma residue, and retraction pocket. The planned staged tympanoplasty with preventive measuresfor recurrence has evolved. The first stage operation is carried out to remove cholesteatoma, to controlinflammation, and to reestablish well aerated middle ear. Posterior tympanotomy with removal of the incusand head of the malleus allows wide view enough to remove the cholesteatoma under an operation microscope.For safe and total removal oto-endoscopy is of great help. The new methods of silastic sheeting and amastoid cortex plasty are described. Scutum defect must be repaired using bone pate. The second stageoperation is performed between 9 and 12 months after the first stage operation. At the second-stage operation, one of the following three types of operations was performed according to the finding of the middle ear: type S-I ; ossiculoplasty and mastoid cortex plasty, type S-II; ossiculoplasty, scutum plasty and mastoid cortexplasty and type S-III; ossiculoplasty, scutum plasty, and mastoid obliteration. The type S-I operation isindicated for an ear with a perfectly aerated middle ear lined with normal mucosa and without a defectivetympanic scute. The type S-II operation is indicated for an ear with a defective tympanic scute, but a partiallyaerated middle ear. The type S-III operation is indicated for an ear with a poorly aerated middle ear cavityand a defective tympanic scute. The surgical concept, indication, and technique are briefly describedtogether with the long-term results.

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Sensorineural hearing loss and vertigo are known to be a significant sequelae of otitis media. However, the pathophysiology of such a hearing loss and vertigo in otitis media still remains unknown. The presentstudy revealed that the development of inner ear disorders is closely related to the formation of free-radicals.Endotoxin can penetrate the inner ear via multiple routes such as, via round window, via blood vessel or lymphatics, and/or interscala exchange, resulting in a disturbance of not only in the cochlea but also of vestibularend organs. Radical scavengers and steroid may be useful for the treatment of inner ear disorders. Clinically, it might be important to detect earlier signs of inner ear disorders and to start treatment as early as possible.

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Influence of otitis media upon the cochlear function was examined clinically on patients with severaltypes of otitis media, and the following findings were obtained.
1. In otitis media with effusion, abnormality in the bone conduction probably due to middle ear negativepressure and/or fluid retention was observed at least in 30% of children, but actual sensorineural hearingloss was revealed as rare as approximately 3%. Cases whose mean bone conduction threshold was worsethan 20 dB even after myringotomy and removal of effusion were revealed high-risk cases in terms of permanentsensorineural hearing loss.
2. In chronic non-cholesteatomatous otitis, sensorineural hearing loss tended to progress more than that byaging particularly in aged population.
3. Sensorineural hearing loss was found to progress with the length of disease course also in primary cholesterolgranuloma of the middle ear, and its treatment including steroid (P.O.) and tympanostomy tubeinsertion was found to be effective particularly in young patients. It seems, therefore, desirable to treatthis disease as early as possible.
4. Worsening of the bone conduction hearing often observed in acute otitis media or mastoiditis cannot necessarilybe considered as the cochlear sensorineural damage, because it is often reversible and alsobecause loss of vestibular function is not often observed. We tried to test our hypothesis that this boneconduction worsening may be caused by mechanical impairment of sound conduction through the temporalbone due to fluid retained in the mastoid and middle ear using a dry human temporal bone, but failedto demonstrate it.

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Neurosensory hearing loss has been reported as one of the major complications of acute and chronic otitismedia. However, the effect on the vestibular function is not well known. In this report, we have reviewedthe vestibular function of 3964 patients with acute and chronic otitis media (excluding cholesteatoma) whovisited Aichi Medical University Hospital between 1998 and 2003.
1) Vestibular complication due to acute otitis media.
Vertigo occurred in approximately one percent (1%) of the acute otitis media patients. Nystagmus oftendisappeared within a week. Treatment options included antibiotic medications, ATP agents, and myringoto-my and/or tube ventilation.
2) Vestibular complication due to chronic otitis media.Vertigo occurred in approximately five percent (5%) of the chronic otitis media patients. Fifty percent (50%) of the patients showed various patterns of nystagmus.Although it is not well documented, BPPV canalso be caused by chronic otitis media.
3) Vestibular complication due to eosinophilic otitis media.Hearing loss can occur in the early stages of eosinophilic otitis media.Whereas, vertigo seldom occurs inthe early stages of acute and chronic otitis media.Vestibular damage became more frequent when the averagehearing level exceeded 60dB.
Conclusions: We have reviewed the vestibular function of the patients with acute and chronic otitismedia (including eosinophilic otitis media). Findings revealed vestibular damage may be recognized as havinga more mild effect on the vestibular function than on cochlear damage, but this requires more follow-up.Caloric testing mainly stimulates the horizontal semicircular canal, and it only imparts a -0.01Hz low frequencystimulation. Further analysis is needed to clarify the findings of vestibular damage in patients with acuteand chronic otitis media.

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The widespread use of antimicrobial agents has made intracranial otogenic complications increasing infrequent, but they still occur even following non-cholesteatomatous ears, such as adhesive otitis media, chronicsuppurative otitis media and acute otitis media. The classic clinical pictures are often modified by previousantibiotic treatment making diagnosis and management difficult. We present three such cases of otogeniccomplications, i.e. brain abscess, petrous apicitis and lateral sinus thrombosis, which were diagnosed definitivelywith a combination of computed tomography and magnetic resonance imaging. The general treatment ofintracranial complications is also outlined.

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In order to establish experimental autoimmune labyrinthitis model, the present study investigated todefine organ specificity of inner ear antibodies in the mouse model which were induced by repeated immunizationwith bovine crude inner ear antigens (blEAgs). Serum from model mouse reacted with severalblEAgs which were 220, 160, 70-60, 46, 42, 33, 30, 26, 22kDa. However, this serum also reacted with severalantigens of the other mouse kidney, liver, lung and brain. IgG deposition was seen at many sites of all theseorgans, but was unable to distinguish specific reaction from non specific reaction, since the control mice withBSA immunization showed the same deposition of IgG in the inner ear as the model mice. These resultsdemonstrated that crude IEAgs contained specific as well as non-specific inner ear antigens, indicating thenecessity to establish inner ear specific autoimmune labyrinthitis model by inner ear specific antigens.

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Although otogenic intracranial complications are considered relatively rare, it is still a potentially lifethreateningdisease. We report our experiences on 7 patients with otogenic intracranial complications, whowere treated at the University of Tsukuba Hospital from 1988 to 2003. The patients were successfully treatedwith intravenous antibiotics and oto-and/or neuro-surgical interventions. It is important to reduce mortalityfrom otogenic intracranial complications by precise diagnosis and treatment in the early stages of the disease.

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We report six ears in which stapedectomy or stapedotomy was perfomed for tympanosclerotic stapes fixation.Hearing gain of more than 15 dB was archived in 4 ears (66.7%) more than one year after the surgery.Sensorineural hearing loss greater than 15 dB at 4 and 8 kHz occurred in one ear, but the averagepostoperative bone conduction level at 0.5, 1 and 2 kHz was unchanged in all of 6 ears. This report demonstratesthat stapedectomy or stapedotomy is safe and efficient for tympanosclerotic stapes fixation.

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During the past nine years, seventeen ears of traumatic perforation of the tympanic membrane havebeen operated on at our department. In 17 ears, 13 ears had a large perforation classified as grade i and IV.The average period from the injury to the operation in 17 ears was 5.9 months. Type-I tympanoplasty wasperformed in 15 ears and myringoplasty was performed in 2 ears. In 15 ears with type-I tympanoplasty, only one ear failed to close the perforation, on the other hand, all 2 ears with myringoplasty obtained the closureof the perforations. Success of hearing recovery was observed in 16 ears except for the ear failed in closureof the perforation ear. Early and aggressive treatment is desirable for the cases with a large perforation.

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A 73-year-old man presented with a complaint of recurrent deep neck abscess in spite of repeateddrainage at a local hospital. He had suffered from stenosis of the left external auditory canal due to injurywhile Judo training. CT scan showed a diffuse cloudiness of the mastoid cavity with bony destruction and anabscess formed behind the left sternocleidomastoid muscle. Radical mastoidectomy and drainage of the neckabscess were performed under general anesthesia. The mastoid cavity was filled with pus and cholesteatomadebris. Concomitant diabetes mellitus seemed to have facilitated exacerbation of infection inside of the earcanal stenosis. Postoperative course was uneventful.

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Herein we report a 3-year-old boy brought to the Department of Otolaryngology-Head and Neck Surgery, Saga Medical School because of tugging of the left ear in July 2000. He had never been treated for otitismedia. A small white sphenical mass was seen at the left tympanic membrane. The mass was extirpatedunder surgical microscopy, and the mucosal layer was preserved. The patient was diagnosed withcholesteatoma. Congenital cholesteatoma of the tympanic membrane is relatively rare, and congenitalcholesteatoma of the tympanic membrane without otitis media is extremely rare. The aetiopathogenesis ofthis lesion is still unclear. An embryologic origin was suspected because there was no previous history ofinflammatory process of the external or middle ear. We propose that the cholesteatoma within the tympanimembrane would be added in the originating site classification of the congenital cholesteatoma.

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