Volume 69 March 1976
Section of Otology President Alan G Gibb FRCS
Meeting 7 November 1975
President's Address Tympanosclerosis
occasion on which this English term was used
by Alan G Gibb FRCS (Department of Otolaryngology, University ofDundee, Ninewells Hospital, Dundee, DD2 1 UD)
This renaissance was intimately related to the introduction of the operating microscope, which not only permitted a much closer study of the condition but also opened the way to its microsurgical treatment. A detailed description by House & Sheehy (1960) and a comprehensive thesis by Harris (1961) signalled the growing interest in the condition; despite this, our present understanding and knowledge of this strange healing process remains very limited. From a personal point of view I appear to have recognized intra-tympanic tympanosclerosis for the first time in 1961, when I made the following operation record of the middle ear findings on a case listed for stapedectomy:
Tympanosclerosis must surely be regarded as the Cinderella of middle ear diseases. First recognized centuries ago it remained in almost total obscurity until the last twenty years. Since then it has gradually emerged as onc of the most fascinating conditions affecting the middle ear. The revival of interest corresponded with the introduction of the modern operating microscope, opening as it did new vistas for the ,otologist, who was at last able to view in detail the beautiful and remarkable structure of this unusual condition. Tympanosclerosis of the tympanic membrane the familiar chalk patch or calcareous deposit was recognized by Cassebohm (1734) in his anatomical studies of the ear, but the first reference to tympanosclerosis affecting the middle ear cavity is attributed to Von Troltsch of Wurzburg just over a century ago. In 1869 he described the occurrence of thickening of the tympanic mucosa with solidification and decrease in its elasticity to which he gave the name 'sclerosis'. Shortly after this a full description was given by Politzer (1883). Before the turn of the century further descriptions followed (Habermann 1892, Walb 1893), but either because of lack of effective treatment or, as Harris (1961) suggests, because of 'astonishing amnesia' on the part of the otologist, tympanosclerosis remained in obscurity for more than half a -
century. Interest was rekindled by Zbllner & Beck (1955). In the same year Zollner read a paper entitled 'Tympanosclerosis' at the Institute of Laryngology and Otology in London the first -
'The initial appearance was striking. Everything was enclosed in a very white coating of mucous membrane. This was thick, and not resilient; even the stapedius tendon was coated. The crura of the stapes looked extremely thick and fixation was complete. Mucous membrane was stripped in layers, a tremendous amount being removed from the region of the footplate which was eventually uncovered and found to be blue and thin. Diagnosis - tympanosclerosis with or without otosclerosis.'
This case in particular clarified my concept of tympanosclerosis and stimulated a lasting interest in the condition. The present paper is based on a review of 138 operations in the course of which tympanosclerosis was encountered: it should be appreciated that numerous additional cases seen in clinic during the same period, but for various reasons not operated on, have also influenced my ideas on the condition.
Definition and Classification Tympanosclerosis is not a disease per se, but appears to represent an unusual healing response
Proc. roy. Soc. Med. Volume 69 March 1976
to a past episode or episodes of otitis media. There is frequently blear-cut evidence of the preceding infection, most commonly in the form of scarring or perforation of the tympanic membrane. On this basis, I have already suggested classification into closed and open tympanosclerosis, depending on the integrity or otherwise of the drumhead (Gibb 1971, 1973).
Clinical Features The condition is easily recognized by the presence of white plaques in the tympanic membrane or in the middle ear. These plaques are of mesodermal origin and lie in the submucosa - in the stratum fibrosum of the tympanic membrane or between mucosa and periosteum within the middle ear. They are normally covered with an intact mucosa. Plaques occurring in the tympanic membrane are frequently known as 'chalk patches'. These invariably occur in the pars tensa and vary from small, clinically insignificant, deposits to very large plaques occupying the entire drum surface. Plaques within the tympanic cavity and mastoid may occur with or without associated deposits in the drumhead (Table 1) and in both open and closed forms of tympanosclerosis. At times the deposits are enormous and may virtually obliterate the tympanic air space. The distribution of plaques throughout the tympanum follows a characteristic pattern (Table 2). The most common sites of election comprise the stapes-oval window region, the incudostapedial joint, the adjacent fallopian canal and promontory and the 'sub-fallopian
Table 1 Distribution of tympanosclerosis (138 cases) Percentage of cases
Tympanic membrane Middle ear and mastoid Combination of both
24 32 44
Table 2 Intratympanic tympanosclerosis distribution of plaques (138 cases)
Promontory Oval window, stapes, incudostapedial joint Fallopian canal Attic Stapedius tendon Subfallopian groove Tensor tympani Round window niche Eustachian tube area Mastoid Hypotympanum Diffuse massive plaques
Percentage incidence 29 27 16 16 15 14 6 4 2 2 I 9
groove'. The epitympanum is involved in a considerable proportion of cases - possibly higher than is evident in the present series, since the epitympanum was explored only if attic tympanosclerosis or attic cholesteatoma was suspected. Tympanosclerosis of the mastoid was relatively uncommon but did occur. There was a relative absence of localized tympanosclerotic deposits in the round window niche, around the mouth of the eustachian tube and especially in the hypotympanum. Occasionally, massive plaques of tympanosclerosis were seen extending downwards into these regions but they appeared for the most part to arise elsewhere; small discrete deposits limited to the areas indicated have in my experience been noticeably uncommon.
Pathology Soft tissue changes: The otologist is able, with the assistance of the operating microscope, to distinguish two distinct types of tympanosclerotic tissue: (l) A softer form, creamy in colour, with a rubbery or cartilaginous texture which peels off in onion layers. (2) An extremely dense, hard, white form often firmly adherent to the surrounding bone which may fracture when the plaque is removed. Histological examination shows that the plaques are covered with a rather flattened epithelium and are composed of birefringent collagenous masses almost totally devoid of cells. The collagen is generally arranged in bundles, many of which show an irregular fibrillar structure, but in other areas the collagen assumes an amorphous hyaline appearance. Deposition of calcium is common and areas of bone may be encountered. Generally the latter has a fibrous woven architecture unlike the normal bone of this area. The formation of new bone in tympanosclerotic plaques is not unexpected provided mesenchymal cells are present, since it has long been recognized that ectopic bone may form without the help of 'professional osteoblasts' (Keith 1927): any primitive uncommitted mesenchymal cell can deviate from its intended progression to a fibroblast by altering course to become an osteoblast with formation of ectopic bone. Changes in surrounding bone: Ossicles which have been buried in tympanosclerotic tissue frequently appear porous, moth-eaten and brittle when viewed with the operating microscope: extra care is necessary during manipulations because of the risk of fracture. More extensive bone erosion may result in ossicular discontinuity. Microscopic sections of the affected bone show the eroded areas filled with typical tympanosclerotic tissue.
Section of Otology
Electronmicroscopy in our hands has been helpful in confirming the presence of collagen fibres with their periodicity around 64 nm. We are indebted to Bonnaud (1971), Won Chang (1969) and others for comprehensive descriptions of the electronmicroscopic findings. The chemical structure of the tympanosclerotic deposits has been examined in a number of cases by infrared spectroscopy. This is an extremely delicate method of analysis which depends on vibrational changes of the microparticles on exposure to infrared irradiation. The resulting absorption spectrum provides qualitative and quantitative information about the molecular structure, functional groups and character of chemical bonding of the parent compound. This form of analysis is particularly sensitive for detecting phosphate and oxalate compounds - more so than the X-ray diffraction technique used by Won Chang (1969). Absorption analysis of tympanosclerotic material showed the presence of a calcium compound exhibiting all the characteristics of carbonate apatite.
sclerosis can be recognized - an initial stage of active collagenesis and a later inactive phase featured by the presence of masses of mature collagen. In the earliest stages of collagenesis the clinical features of tympanosclerosis are absent and one sees only masses of tough semi-organized fibrous tissue in the middle ear at the sites oe election of tympanosclerosis. The histological appeafancesare those of maturing fibrous tissue with variable amounts of collagen - presumably this is a precursor stage of tympanosclerosis. However, in a small proportion of cases with clinically recognizable tympanosclerosis definite activity can be detected histologically, especially in young patients with a relatively recent history of otitis media. This active phase provides an interesting insight into the probable mode of plaque formation. Typically one sees a submucosal cellular inflammatory reaction merging on its deeper aspect with a zone of fibroblastic activity beneath which successive layers of collagen deposition, hyalinization, calcification and bone formation can be recognized: such a picture indicates the essential stages in the process of collagen maturation resulting from one or more inflammatory episodes in the middle ear. Bone destruction may occur in this active phase of tympanosclerosis but like House & Sheehy I believe that bone destruction takes place primarily during the course of the preceding otitis media. Even in this so-called 'active' phase, tympanosclerosis is only very slowly progressive and it seems likely that clinical tympanosclerosis normally takes many years to develop: certainly in most cases there is a lapse of 10-30 years between the onset of the original infection and the time the clinician sees the full-blown picture of tympanoscierosis: on the other hand tympanosclerosis may at times develop much more rapidly and I have observed tympanosclerosis in a mastoid cavity where none existed 20 months previously. In the passive phase of tympanosclerosis characterized by the presence of mature collagen, I consider that any invasive tendencies which may have been present previously no longer exist: it seems possible nevertheless that lowgrade bone necrosis may take place as a result of slow strangulation of the ossicles by the surrounding sheath of avascular hyaline tissue. Surjan & Juhasz (1971) offer support to this argument by suggesting: 'It is not impossible that the pressure and the ischemia caused by the sclerotic masses have a role in the destruction of the bone and of the ossicles, in particular of the stapes and of the long process of incus.' With the foregoing conception in mind I consider that tympanosclerosis initially shows a low grade of activity and slight invasive tendencies
Discussion ofthe Pathological Picture At this point it may be appropriate to consider the foregoing findings in relation to the clinical behaviour of tympanosclerosis, keeping in mind three questions: (1) Is tympanosclerosis progressive? (2) Does it invade surrounding structures ? (3) Is it likely to recur after removal ? A survey of the literature highlights the widely divergent views expressed in answer to these questions. House & Sheehy (1960) regarded tympanosclerosis as inactive and non-invasive and stated that 'plaques can be safely removed without fear of recurrence inasmuch as hyaline degeneration is a final process and does not tend to recur or increase in size'. They considered that ossicular erosion resulted from a previous episode of otitis media and preceded the tympanosclerotic process. Harris & Weiss (1962), on the other hand, separated tympanosclerosis into two distinct types: (1) A non-invasive superficial form, 'sclerosing mucositis', in which the adjacent mucosa and periosteum remained intact and there was little tendency to recurrence after removal. (2) 'Osteoclastic mucoperiostitis', which they regarded as invasive to surrounding structures and showing a tendency to destroy bone. Doubtless the truth lies somewhere between these differing interpretations of the tympanosclerotic process, and my own experience supports this view. While I am not convinced of the existence of frankly invasive tympanosclerosis and believe that Harris & Weiss were in many instances describing concomitant keratoma (cholesteatoma) as part of the tympanosclerotic process, I believe that two stages of tympano-
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but later in its mature state, when it is most commonly encountered by the otologist, the condition is inactive, non-invasive and nonrecurrent. A single instance of recurrence after removal was encountered in this series of cases doubtless an isolated incident resulting from a chance combination of circumstances similar to those responsible for the initial fibrogenesis rather than to a true recurrent tendency on the part of the tympanosclerosis. I believe that surgery should be planned on the premise that tympanosclerosis will not recur after removal and consider that radical surgical excisions are unnecessary for its elimination.
narrow or cul-de-sac areas where inflammatory exudates tend to get trapped during the course of an acute infection: the reduction of air space combined with limited gland secretion and absence of ciliary function compromise their elimination so that organization and possible conversion to tympanosclerotic plaques may occur. This theory presupposes mucosal destruction during the preceding acute necrotizing infection with subsequent mucosal regeneration in order to account for the eventual submucosal site of the organized deposit. The observations of Tos & Bak-Pedersen (1974) concerning the gland population in the tympanic mucosa may also be relevant to plaque distribution. In comparing tympanosclerosis with chronic secretory otitis, adhesive otitis and granulating otitis, they found that the middle ear mucosa exhibits 'considerably less secretory activity in tympanosclerosis than in the other named diseases': not only was the mean gland density low but practically all the existing glands were devoid of secretory activity. Thus tympanosclerosis may tend to favour sites where glandular activity is virtually absent - hence its affinity for those parts of the middle ear where the gland population is lowest and hence possibly its tendency to occur in the wake of an inflammatory process sufficiently acute to destroy or severely damage glandular function. This theory would also explain why. tympanosclerosis and secretory otitis media co-exist only occasionally (2% in this series). In summary, the clinical evidence points to tympanosclerosis arising from one or more episodes of severe acute otitis media with gland destruction and mucosal damage. While a severe middle ear infection may act as a trigger to the development of tympanosclerosis it would be naive to regard it as the cause of this complex problem. Clearly not all severe acute infections cause excessive collagen formation and one must therefore probe deeper for the cause of this abnormal collagenesis. For this reason it may be appropriate to consider the possible causes of excessive collagenesis (or fibrogenesis) as a lead to future research. In theory this condition may result from excessive production of collagen with a normal turnover or normal production with a diminished turnover. In the former group, a fibrogenesis-stimulating factor may be released by macrophages activated in a variety of ways. (1) By organization of thrombus or fibrin due either to an antibodymediated immunological reaction, e.g. farmer's lung, or to tissue trauma, e.g. infarction. (2) By chemical irritation as in silicosis. A mechanism analogous to that caused by chemical irritation may be initiated by certain systemic drugs, e.g.
Etiology The exact etiology of tympanosclerosis is unknown but before speculating on possible causes I shall consider the clinical evidence which emerges from this study and discuss its significance. The following features were observed in most patients in this survey: (1) There was a history of previous otitis media. (2) The ears were almost invariably dry (83 Y.). (3) The perforations were large in a high percentage of cases (84%). (4) All the perforations were confined to the pars tensa. The foregoing features are atypical of the average clinical picture encountered in chronic otitis media; on the contrary they suggest a previous episode or episodes of acute otitis media of the necrotizing type which was frequently encountered in the past in association with the acute infectious fevers. One must therefore consider the possibility of a severe acute otitis media of viral or bacterial origin rather than a chronic middle ear infection as the precursor of tympanosclerosis. Support for this concept is forthcoming if one accepts, as I do, that the coexistence of tympanosclerosis and cholesteatoma is uncommon: although opinions differ on this point my own view coincides with that of Plester (1972), who regards the association of these conditions as no more than accidental. A further clinical feature of special interest, and perhaps significance, was the rather unusual distribution of plaques throughout the middle ear. As has already been mentioned plaques were commonest around the ossicles and on the adjacent part of the promontory. They were infrequent in the hypotympanum, sinus tympani and eustachian area which have certain features in common: (1) They represent the widest parts of the tympanic cavity. (2) The gland population of the mucosa is heaviest in these areas (Sade 1966). (3) The mucosa is ciliated in these areas
(Sade 1966). When one considers the above facts it is apparent that tympanosclerosis occurs mainly in
practolol, and it is theoretically possible that locally applied drugs could do the same. (3) By cell mediated immunity. A good example of this mechanism is found in chronic fibrocaseous tuberculosis. The above immunological responses are frequently interrelated and may be activated simultaneously in a complex fashion. Excessive fibrogenesis may possibly also result from an idiosyncratic increase in fibroblast activity, as for example in keloid. The mechanism of druginduced fibrogenesis and that occurring in keloid is purely speculative: it is possible that in these instances the excessive collagenesis may be due to diminished collagen turnover with normal production. One must finally ask the question, where does tympanosclerosis fit into the above pattern ? Clinical evidence has shown that there is no known link with other connective tissue diseases nor is there any connexion with keloid. The question of a drug-induced mechanism, e.g. drugs applied locally in the treatment of otitis media, is as yet unresolved: difficulties in reaching a solution arise from the time-lag between the onset of tympanosclerosis and the end stage with which the otologist is familiar. It seems probable that the excessive collagenesis in tympanosclerosis is initiated by a severe infection which triggers off several of the mechanisms already referred to and leads to the release of a fibrogenesis-stimulating factor which results in the typical clinical picture seen by the otologist.
with a surgical problem far more complicated than he anticipated and with a much poorer prognosis than he may have indicated to the
Diagniosis Tympanosclerosis affecting the tympanic membrane as chalk patches seldom presents difficulties. The diagnosis of intratympanic tympanosclerosis is less easy except in the 'open' type where plaques may be visible through the perforation, usually in the oval window area or on the promontory. In 'closed' tympanosclerosis the diagnosis may be difficult since confusion with otosclerosis or other forms of ossicular stiffness may arise. Tympanosclerosis should be suspected in the following circumstances: (I) If 'chalk patches' are visible in either tympanic membrane. (2) If the tympanic membrane shows evidence of scarring. (3) If there is no family history of otosclerosis. (4) If there is a history of past otitis media followed by nonprogressive conductive deafness. (5) If the mastoid is radiologically acellular. Accurate diagnosis is extremely important since the surgical treatment of tympanosclerosis is in many instances much more complicated than that of any other type of conductive deafness. Thus tympanosclerosis, unsuspected preoperatively and manifesting itself for the first time at tympanotomy, confronts the otologist
patient. Tympanosclerosis may also be confused with cholesteatoma: careful examination under the operating microscope will generally help to distinguish the conditions. In other cases the two conditions may co-exist: this happens less often than one might expect especially in open tympanosclerosis where the presence of a perforation lays the middle ear open to infection and epithelial invasion. In this survey cholesteatoma was encountered in 19 cases (14%): however, in 3 of these the condition may well have been iatrogenic foljowing previous grafting procedures.
Distuirbance of Fiunctioni The effect of tympanosclerosis on middle ear function depends on its severity. In -mild cases there is no noticeable or measurable alteration. More severe involvement results in hearing impairment due to interference with the soundconducting apparatus in one or more of the following ways: (I) Reduced mobility. (2) Loss of continuity. (3) Reduction of tympanic air space. Tympaniic Membrante The mobility of the tympanic membrane may be impaired by massive plaque formation covering a large area of drum surface; by adherence of a large plaque to the annulus tympanicus, to the handle of the malleus or to both; or by a massive deposit lying against the promontory. The most typical situation encountered in practice is a huge plaque involving the whole anterior portion of the drum and fixed to the annulus in front and to the handle of the malleus behind: such a plaque not only affects the mobility of the drum but immobilizes the malleus at the same time. In tympanosclerotic ears perforations of the tympanic membrane are present in about twothirds of the cases: as already stated the perforations are generally large (84%) and as such constitute an important cause of hearing impairment especially in those cases with no associated ossicular disturbance. Ossicitlar Chain Stiffness of the ossicular chain results from the splinting effect of the tympanoscierotic envelope which can be likened to a layer of creamy cement poured over the ossicular chain or, in more severe cases, to a mass of thick cement within which the ossicles are embedded. Tympanosclerosis most frequently involves the oval window niche causing reduced mobility of the
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stapes (30% of all cases): upper ossicular fixation is also common (22 %), partly due to the narrowness of the air space between the ossicles and attic walls: the liability to epitympanic fixation is increased if the deposits become calcified or ossified. Erosion of the ossicular chain affects mainly the long process of incus leading in many cases to discontinuity of the incudostapedial joint: the latter was present in 45 % of cases in this series. Erosion of the stapedial arch (5%) and malleus handle (3 %) were encountered less commonly. Reduction of tympanic air space is caused by massive deposits of tympanosclerosis: these at times almost entirely obliterate the cavity and reduce its efficiency as a resonating chamber.
majority of cases; the results have been consistently good and it is now my standard procedure in all myringoplasty operations: grafts are placed deep to the handle of the malleus and are normally supported in position with Sterispon: drying and crushing are avoided. The middle ear is irrigated routinely with an antibiotic solution prior to graft insertion. Myringoplasty (only) was carried out in 58 cases with a 96.5% take rate: 7 ears were wet or unstable at the time of operation: of the 2 failures, cholesteatoma was removed from one at the time of grafting.
Treatment In general treatment is directed towards the relief of deafness and plaques not interfering with sound conduction are as a rule left alone. The three basic principles of treatment are as follows: (1) Restoration of mobility to stiffened or fixed structures. (2) Repair of defects in the soundtransmitting structures. (3) Circumvention of severely affected areas by creation of a by-pass.
Tympanosclerosis of the Tympanic Membrane Plaque removal: Plaques are excised if they interfere with sound transmission. Preservation of the overlying epithelium is frequently possible if the following technique is employed. The plaque is pushed inwards by applying firm pressure to its outer surface via the drum: this manceuvre mobilizes the plaque if it is fixed and initiates separation at the edges. An elevator is then inserted between the plaque and the outer layer of the drum, via an existing perforation or by way of a stapes approach if the drum is intact. As the plaque is freed it is pushed inwards until all its attachments to the drum are separated: the plaque is then removed leaving the epithelial layer of the drum intact. Myringoplasty: In suitable cases of open tympanosclerosis grafting of the perforation is undertaken together with plaque removal, where appropriate. It is not always necessary or advisable to remove plaques adjacent to a perforation as the latter almost inevitably becomes enlarged due to epithelial retraction or occasionally to tearing. Furthermore, grafts 'take, surprisingly well when placed on these avascular areas: Z6llner's (1963) early anxieties regarding late graft necrosis would appear to be without foundation. Removal of plaques by the technique already described automatically denudes the inner surface of the drum of its mucosal layer thus creating an ideal bed for an underlay graft. The underlay technique using temporal fascia was employed in the
Tympanosclerosis of the Ossicular Chain In mild cases of tympanosclerosis removal of plaques with restoration of ossicular mobility has proved a justifiable and often rewarding operation: preservation of an intact ossicular chain is normally possible and good hearing is often well maintained over a considerable period. In more severe cases, plaque removal is usually combined with some tympanoplastic procedure depending on the area involved. Stapes fixation: While stapes mobility may sometimes be restored by plaque removal, e.g. a plaque fixing the stapedius tendon, severe localized involvement of the stapes is generally best treated by stapedectomy. This operation may, however, be complicated by certain factors peculiar to tympanosclerosis: (I) Footplate fixation is generally caused by a surface layer of collagen, although annular ligament invasion, first reported by Habermann (1892), may occur from time to time. Removal of the collagenous layer normally frees the fixed stapes and a floating footplate may occur unless special care is exercised to prevent this. (2) The long process of the incus is frequently demineralized or eroded and in general is poorly endowed for the attachment of a prosthesis. (3) It is believed by many otologists that tympanosclerosis is associated with increased cochlear fragility leading to a marked increase in the incidence of sensorineural deafness following stapedectomy. Modifications of the standard technique may be necessary to combat these problems. At present, the stapedectomy technique which I favour involves the creation of a small circular window in the footplate into which a piston of appropriate diameter is inserted so as to produce a snug fit, yet permit free movement. I believe that this method causes less cochlear disturbance than most other techniques. In this series 17 stapedectomy operations were performed: of these 14 were standard operations and 3 were malleus-oval window procedures. The overall results from both procedures showed a 65% closure rate of the air-bone gap to 1OdB.
Section of Otology
These figures were disappointing and fell far short of the standard one would expect in otoscierosis. Careful analysis, however, revealed certain factors of significance:
to the formation of fibrous, or bony adhesions following surgery. Care must always be taken to exclude tympanosclerosis in the attic prior to undertaking stapedectomy with prosthetic replacement. Upper ossicular fixation missed at operation or developing at a later date may prove a serious problem since the stapedectomy must be 'undone' prior to further surgery in the attic to protect the cochlea from transmitted vibrations.
(1) The failures occurred mainly in cases of widespread tympanosclerosis affecting all the middle ear structures or in cases with concomitant otosclerosis. (2) Several of the operations were carried out in the early years of stapedectomy employing methods which are now outdated and technical skills which have improved considerably. (3) Although there was a 35% 'failure' rate, all but one case showed some postoperative hearing gain: in several cases there was significant audiometric and social improvement yet these are classified as failures merely because they did not meet the 10 dB criterion of air-bone closure: included in this group is one case with an I dB and another with a 12 dB air-bone gap closure. It is my impression that while in otosclerosis a 10 dB closure level is a reasonable measure of success or failure the application of the same criterion to a condition not necessarily confined to the stapes area is unduly harsh. (4) One 'dead' ear occurred in this small series; in this particular case it is not possible to incriminate the operation with any degree of certainty; the hearing loss was a slowly progressive one starting prior to the operation and becoming total four years later: it seems probable that the operation merely accelerated a progressive cochlear degeneration. I have found no convincing evidence of increased cochlear fragility in tympanosclerosis: at the same time I am aware that stapedectomy tends to be carried out as a secondary procedure much more frequently in tympanoscierosis than in otosclerosis and it is possible that in these circumstances the cochlea may be rendered more sensitive by the preceding ear surgery. (5) The results of the present investigation suggest that a much greater hazard after stapedectomy is a late conductive regression which occurred in varying degree in 6 of the cases. I have not as yet had the opportunity to re-open any of the affected ears, and I can only speculate on possible factors peculiar to tympanosclerosis which may be responsible for this occurrence: (a) Recurrence of tympanosclerosis with refixation of stapes. This is unlikely as recurrences are very rare: only one case in this series showed any such tendency. (b) Diminution of blood supply to the long process of incus. Attachment of a prosthesis to a poorly nourished incus may accelerate its erosion and absorption. (c) Recurrence of ossicular stiffness elsewhere in the chain, due either to progression of the tympanosclerosis or
Attic fixation: Inspection of the attic is essential in selected cases to exclude tympanosclerosis in that area. Exposure may be carried out by permeatal atticotomy, by an inspection window or via the mastoid. It might be argued that thorough inspection of the attic and middle ear by posterior tympanotomy should be carried out routinely in all cases of tympanosclerosis: personally, I believe this to be unnecessary and undesirable. Such a procedure, however, has one significant advantage, namely, to overcome the hazard of undiscovered cholesteatoma. As a rule, attic tympanosclerosis results in reduced mobility or total fixation of the malleus and incus. The stapes even on careful inspection may also appear fixed although in actual fact it is mobile: its mobility can be readily established by disarticulating the incudostapedial joint: this procedure in my opinion is justified in all cases of doubt. Mobilization of the ossicular chain by removal of plaques from the attic is seldom successful and should only be considered in very mild forms of tympanosclerosis - even so, there is a considerable risk of ossicular refixation especially if the plaques are calcified or ossified, The methods I employ in dealing with attic tympanosclerosis vary according to the state of the stapes:
(1) Stapes intact and mobile: If the stape is intact and mobile I prefer to by-pass the fixed structures in the attic as this eliminates the risk of epitympanic refixation - an ever-present danger with the ossicles preserved intact. The incus and head of malleus are removed and an ossiculoplasty is then performed by reinserting either the incus or head of malleus, suitably modified or modelled if necessary, between the handle of malleus and head of stapes. This technique is also employed in cases of ossicular discontinuity provided the stapes is normal. Nineteen cases were treated in this manner using the incus in 10 and the malleus in 9: while I personally prefer utilizing the head of malleus, the results obtained by both methods were roughly comparable in this series. A Type III tympanoplasty is favoured by some surgeons as an alternative method, but the overall results of this procedure in my hands
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are poor and I have employed this technique only once in the present series. (2) Stapes superstructure missing, footplate mobile: In cases where the stapes superstructure has been eroded, the remains of the incus or, failing this, a homograft malleus is placed between the handle of malleus and the mobile stapes footplate. Five cases were treated in this fashion (incus 4, homograft malleus 1). (3) Stapes fixed: If the stapes is fixed special problems arise. In mild cases, if the superstructure is intact, it may be possible to restore mobility by removal of plaques and then proceed as in the case of an intact mobile stapes. In more severe cases, I favour removal of the incus and head of malleus and the creation of a malleusoval window by-pass: a Sheehy wire or a Teflon piston may be utilized depending on the anatomical relationships of the particular case or on the surgeon's individual preference. I have found the results of this procedure somewhat unpredictable but, if successful, the hearing improvement is generally a lasting one. Of the 3 cases operated on in this series there was complete air-bone gap closure in one; a second obtained a useful hearing improvement but without air-bone gap closure; and the third case is too recent to assess. An alternative procedure is fenestration of the horizontal semicircular canal: while this method has no chance of closing the air-bone gap and has the disadvantage of creating an open mastoid cavity it does provide a single-stage procedure for a difficult problem. This operation should probably be reserved for cases of widespread ossicular involvement together with gross plaque formation or scarring in an intact membrane. In these circumstances tympanoplastic repair would almost certainly involve multiple operations with no certainty of a successful outcome: fenestration on the other hand offers a one-stage procedure with a reasonable chance of a good hearing gain: restoration of mobility to the tympanic membrane so vital in tympanoplasty can be ignored in a fenestration procedure so long as a phase difference is created between the oval and round windows. When one considers the moderate success rate of stapedectomy in widespread tympanosclerosis, a postoperative air-conduction level of 20-30 dB, such as may be anticipated after fenestration, must be considered highly acceptable, especially if achieved by a single-stage procedure. Fenestration was carried out only once in this series, but the result fully justified the return to this now little used technique.
methods in the course of time will doubtless be replaced with more effective techniques, possibly in the nature of block transplants. For h'e present, the condition of tympanosclerosis continues to present one of the major challenges to the otologist and to those in other disciplines who assist him in his efforts to solve the mystery of this strange healing process.
The methods of treatment which I have described are those which I have employed pergonally in the series of cases analysed. These
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Meeting S December 1975
The subject was Middle Ear Homografts and the following papers were read: Ten Years of Experience in Tympanoplasty by Using Homologous Implants Professor J Marquet
(University of Antwerp, Belgium) The Preserved Tympano-ossicular Homograft Dr P van den Broek and Dr W Kuypers
(St Radboud Hospital, Nijmegen, Holland) Early Impressions of the Tympanic Membrane and Ossicular Chain Homograft in Reconstructive Surgery of the Middle Ear Mr W M S Ironside (Royal Inifirmary, Huddersfield, HD3 3EA)
This meeting may be published in the Journal ofLaryngology and Otology