Middle-ear function with tympanic-membrane perforations. I. Measurements and mechanisms.

Sound transmission through ears with tympanic-membrane (TM) perforations is not well understood. Here, measurements on human-cadaver ears are reported that describe sound transmission through the middle ear with experimentally produced perforations, which range from 0.5 to 5.0 mm in diameter. Three response variables were measured with acoustic stimulation at the TM: stapes velocity, middle-ear cavity sound pressure, and acoustic impedance at the TM. The stapes-velocity measurements show that perforations cause frequency-dependent losses; at low frequencies losses are largest and increase as perforation size increases. Measurements of middle-ear cavity pressure coupled with the stapes-velocity measurements indicate that the dominant mechanism for loss with TM perforations is reduction in pressure difference across the TM; changes in TM-to-ossicular coupling generally contribute less than 5 dB to the loss. Measurements of middle-ear input impedance indicate that for low frequencies, the input impedance with a perforation approximates the impedance of the middle-ear cavity; as the perforation size increases, the similarity to the cavity's impedance extends to higher frequencies. The collection of results suggests that the effects of perforations can be represented by the path for air-volume flow from the ear canal to the middle-ear cavity. The quantitative description of perforation-induced losses may help clinicians determine, in an ear with a perforation, whether poor hearing results only from the perforation or whether other pathology should be expected.

Middle-ear function with tympanic-membrane perforations. II. A simple model.

A quantitative model of the human middle ear with a tympanic-membrane (TM) perforation is developed. The model is constrained by several types of acoustic measurements made on human cadaver ears, which indicate that perforation-induced changes in transmission result primarily from changes in driving pressure across the TM and that perforation-induced change in the structure of the TM and its coupling to the ossicles contributes a substantially smaller component. The model represents the effect of a perforation on the pressure difference across the TM by inclusion of a path for sound coupling through the perforation from the ear canal to the middle-ear cavity. The model implies that hearing loss with perforations depends primarily on three quantities: the perforation diameter, sound frequency, and the volume of air in the middle-ear cavity. For the conditions that produce the largest hearing loss (low frequency and large perforation), the model yields a simple dependence of loss on frequency, perforation diameter, and middle-ear cavity volume. Predictions from this model may be useful to clinicians in determining whether, in particular cases, hearing losses are explainable by the observed perforations or if additional pathology must be involved.

Discrimination reversal conditioning of an eyeblink response is impaired by NMDA receptor blockade.

In the present study we examined the effects of the specific NMDA receptor antagonist CPP on discrimination reversal learning in rabbits. We report two primary findings. First, the institution of NMDA receptor blockade had no effect on a learned discrimination. Second, after stimulus reversal, CPP treatment impaired acquisition of the discrimination reversal. This impairment manifested itself early in training as a retardation in acquisition of a CR to the new CS+ and late in training as an inability to suppress responsiveness to the new CS-. Given the comparability of the present results with previously published results for phenytoin-treated rabbits, we suggest that the effects of phenytoin on learning in this paradigm is at least in part mediated by its effects on NMDA receptors. We further suggest that these findings emphasize the need to better define the role of NMDA receptor activation and hippocampally-mediated circuits in a variety of associative learning paradigms.

How do tympanic-membrane perforations affect human middle-ear sound transmission?

Although tympanic-membrane (TM) perforations are common sequelae of middle-ear disease, the hearing losses they cause have not been accurately determined, largely because additional pathological conditions occur in these ears. Our measurements of acoustic transmission before and after making controlled perforations in cadaver ears show that perforations cause frequency-dependent loss that: (1) is largest at low frequencies; (2) increases as perforation size increases; and (3) does not depend on perforation location. The dominant loss mechanism is the reduction in sound-pressure difference across the TM. Measurements of middle-ear air-space sound pressures show that transmission via direct acoustic stimulation of the oval and round windows is generally negligible. A quantitative model predicts the influence of middle-ear air-space volume on loss; with larger volumes, loss is smaller.

Acoustic responses of the human middle ear.

Measurements on human cadaver ears are reported that describe sound transmission through the middle ear. Four response variables were measured with acoustic stimulation at the tympanic membrane: stapes velocity, middle-ear cavity sound pressure, acoustic impedance at the tympanic membrane and acoustic impedance of the middle-ear cavity. Measurements of stapes velocity at different locations on the stapes suggest that stapes motion is predominantly 'piston-like', for frequencies up to at least 2000 Hz. The measurements are generally consistent with constraints of existing models. The measurements are used (1) to show how the cavity pressure and the impedance at the tympanic membrane are related, (2) to develop a measurement-based middle-ear cavity model, which shows that the middle-ear cavity has only small effects on the motion of the tympanic membrane and stapes in the normal ear, although it may play a more prominent role in pathological ears, and (3) to show that inter-ear variations in the impedance at the tympanic membrane and the stapes velocity are not well correlated.

Middle ear pathology can affect the ear-canal sound pressure generated by audiologic earphones.

OBJECTIVE: To determine how the ear-canal sound pressures generated by earphones differ between normal and pathologic middle ears. DESIGN: Measurements of ear-canal sound pressures generated by the Etymtic Research ER-3A insert earphone in normal ears (N = 12) were compared with the pressures generated in abnormal ears with mastoidectomy bowls (N = 15), tympanostomy tubes (N = 5), and tympanic-membrane perforations (N = 5). Similar measurements were made with the Telephonics TDH-49 supra-aural earphone in normal ears (N = 10) and abnormal ears with mastoidectomy bowls (N = 10), tympanostomy tubes (N = 4), and tympanic-membrane perforations (N = 5). RESULTS: With the insert earphone, the sound pressures generated in the mastoid-bowl ears were all smaller than the pressures generated in normal ears; from 250 to 1000 Hz the difference in pressure level was nearly frequency independent and ranged from -3 to -15 dB; from 1000 to 4000 Hz the reduction in level increased with frequency and ranged from -5 dB to -35 dB. In the ears with tympanostomy tubes and perforations the sound pressures were always smaller than in normal ears at frequencies below 1000 Hz; the largest differences occurred below 500 Hz and ranged from -5 to -25 dB. With the supra-aural earphone, the sound pressures in ears with the three pathologic conditions were more variable than those with the insert earphone. Generally, sound pressures in the ears with mastoid bowls were lower than those in normal ears for frequencies below about 500 Hz; above about 500 Hz the pressures showed sharp minima and maxima that were not seen in the normal ears. The ears with tympanostomy tubes and tympanic-membrane perforations also showed reduced ear-canal pressures at the lower frequencies, but at higher frequencies these ear-canal pressures were generally similar to the pressures measured in the normal ears. CONCLUSIONS: When the middle ear is not normal, ear-canal sound pressures can differ by up to 35 dB from the normal-ear value. Because the pressure level generally is decreased in the pathologic conditions that were studied, the measured hearing loss would exaggerate substantially the actual loss in ear sensitivity. The variations depend on the earphone, the middle ear pathology, and frequency. Uncontrolled variations in ear-canal pressure, whether caused by a poor earphone-to-ear connection or by abnormal middle ear impedance, could be corrected with audiometers that measure sound pressures during hearing tests.

Acoustic mechanisms that determine the ear-canal sound pressures generated by earphones.

In clinical measurements of hearing sensitivity, a given earphone is assumed to produce essentially the same sound-pressure level in all ears. However, recent measurements [Voss et al., Ear and Hearing (in press)] show that with some middle-ear pathologies, ear-canal sound pressures can deviate by as much as 35 dB from the normal-ear value; the deviations depend on the earphone, the middle-ear pathology, and frequency. These pressure variations cause errors in the results of hearing tests. Models developed here identify acoustic mechanisms that cause pressure variations in certain pathological conditions. The models combine measurement-based Thévenin equivalents for insert and supra-aural earphones with lumped-element models for both the normal ear and ears with pathologies that alter the ear's impedance (mastoid bowl, tympanostomy tube, tympanic-membrane perforation, and a "high-impedance" ear). Comparison of the earphones' Thévenin impedances to the ear's input impedance with these middle-ear conditions shows that neither class of earphone acts as an ideal pressure source; with some middle-ear pathologies, the ear's input impedance deviates substantially from normal and thereby causes abnormal ear-canal pressure levels. In general, for the three conditions that make the ear's impedance magnitude lower than normal, the model predicts a reduced ear-canal pressure (as much as 35 dB), with a greater pressure reduction with an insert earphone than with a supra-aural earphone. In contrast, the model predicts that ear-canal pressure levels increase only a few dB when the ear has an increased impedance magnitude; the compliance of the air-space between the tympanic membrane and the earphone determines an upper limit on the effect of the middle-ear's impedance increase. Acoustic leaks at the earphone-to-ear connection can also cause uncontrolled pressure variations during hearing tests. From measurements at the supra-aural earphone-to-ear connection, we conclude that it is unusual for the connection between the earphone cushion and the pinna to seal effectively for frequencies below 250 Hz. The models developed here explain the measured pressure variations with several pathologic ears. Understanding these mechanisms should inform the design of more accurate audiometric systems which might include a microphone that monitors the ear-canal pressure and corrects deviations from normal.

A memory clinic in a department of old-age psychiatry: Its role in clinical and academic research.

Memory clinics are specialist outpatient services offering assessment and evaluation in clinical practice. Memory clinics have been criticized for being preoccupied with research. We analysed the outcomes of 405 referrals to a memory clinic, providing a framework for discussion of the contributions of research to clinical practice. Of the 80% of referrals receiving a formal diagnosis, one-third were recruited on to treatment studies, contributing to clinical research. The remaining two-thirds of patients referred were followed up by specialized care services, and findings from assessment procedures were used to contribute towards academic research. These findings are discussed with reference to the role of research for a memory clinic in clinical practice. The benefits of clinical research are noted, in relation to the percentage of patients involved. The nature of academic research is clarified; it is a dual process, with findings both aiding clinical research and contributing to the body of knowledge about dementia as a possible disease process. It is concluded that memory clinics, as specialized outpatient services, are concerned with research as well as clinical practice, and it is essentially this research which enables clinical practice to develop.

Toynbee Memorial Lecture 1997. Middle ear mechanics in normal, diseased and reconstructed ears.

A review of the structure-function relationships in normal, diseased and reconstructed middle ears is presented. Variables used to describe the system are sound pressure, volume velocity and acoustic impedance. We discuss the following: (1) Sound can be transmitted from the ear canal to the cochlea via two mechanisms: the tympanoossicular system (ossicular coupling) and direct acoustic stimulation of the oval and round windows (acoustic coupling). In the normal ear, middle-ear pressure gain, which is the result of ossicular coupling, is frequency-dependent and smaller than generally believed. Acoustic coupling is negligibly small in normal ears, but can play a significant role in some diseased and reconstructed ears. (2) The severity of conductive hearing loss due to middle-ear disease or after tympanoplasty surgery can be predicted by the degree to which ossicular coupling, acoustic coupling, and stapes-cochlear input impedance are compromised. Such analyses are used to explain the air-bone gaps associated with lesions such as ossicular interruption, ossicular fixation and tympanic membrane perforation. (3) With type IV and V tympanoplasty, hearing is determined solely by acoustic coupling. A quantitative analysis of structure-function relationships can both explain the wide range of observed post-operative hearing results and suggest surgical guidelines in order to optimize the post-operative results. (4) In tympanoplasty types I, II and III, the hearing result depends on the efficacy of the reconstructed tympanic membrane, the efficacy of the reconstructed ossicular chain and adequacy of middle-ear aeration. Currently, our knowledge of the mechanics of these three factors is incomplete. The mechanics of mastoidectomy and stapedectomy are also discussed.

Phenytoin blocks the reversal of a classically conditioned discriminative eyeblink response in rabbits.

PURPOSE: Cognitive deficits associated with chronic treatment with phenytoin (PHT) have been reported. PHT blocks transfer from a signaled appetitive bar press to an active avoidance response in rats. We investigated the effects of PHT and the prodrug fosphenytoin in rabbits required to learn a discrimination and reversal of a classical eyeblink conditioning paradigm. METHODS: Before drug treatment was started, rabbits were trained to produce a discriminated eyeblink response. PHT (n = 7) was administered centrally or the prodrug fosphenytoin (n = 2) was given systemically. Control animals were similarly treated centrally with either saline (n = 3) or no drug treatment (n = 13). Rabbits were then challenged with a stimulus reversal while being maintained on the respective drug. RESULTS: On the first day of reversal training, control animals typically displayed high response rates to both tones, followed by a reduction in responsiveness to the new conditioned stimulus (CS-) in the ensuing days. In contrast, PHT-treated animals failed to suppress responsiveness to the new CS-. CONCLUSIONS: The response patterns observed are similar to those observed in rabbits with hippocampal ablations, leading us to suggest that the adverse effects of phenytoin may be due to actions in the hippocampus.

Analysis of middle ear mechanics and application to diseased and reconstructed ears.

OBJECTIVE: To review current concepts of the mechanical processes of the human middle ear, and to apply them to practical issues in clinical otology and tympanoplasty surgery. BACKGROUND: The wide range of conductive hearing losses associated with middle ear pathology and reconstruction cannot be adequately explained by simple models of middle ear function. METHODS: Variables used to describe the system are sound pressure, volume velocity, and acoustic impedance. The relationship between specific middle ear structures and these variables is described such that inferences can be drawn regarding sound conduction in the normal, diseased, and reconstructed middle ear. RESULTS AND CONCLUSIONS: Sound can be transmitted from the car canal to the cochlea via two mechanisms: the tympano-ossicular system (ossicular coupling) and direct acoustic stimulation of the oval and round windows (acoustic coupling). Acoustic coupling is negligibly small in normal ears, but can play a significant role in some diseased and reconstructed ears. In the normal ear, middle ear pressure gain (which is the result of ossicular coupling) is frequency-dependent and less than generally believed. The severity of conductive hearing loss due to middle-ear disease or after tympanoplasty surgery can be predicted by the degree to which ossicular coupling, acoustic coupling, and stapescochlear input impedance are altered. Hearing after type IV and V tympanoplasty is determined solely by acoustic coupling. The difference in magnitude between the oval- and round-window pressures is more important than the difference in phase in determining cochlear input. In tympanoplasty types I, II, and III, adequate middle-ear and round-window aeration is necessary and the tympanic membrane-ossicular configuration may be less crucial.

Is the pressure difference between the oval and round windows the effective acoustic stimulus for the cochlea?

The assumption that the pressure difference between the cochlear windows is the stimulus that produces cochlear responses is tested experimentally in the ears of anesthetized cats. Cochlear potential is used as a measure of cochlear response. The sound pressures at the oval and round windows are individually controlled with both pressures at the same frequency and amplitude. When the angle difference between the two pressures is varied over one cycle, cochlear-potential magnitude varies by about 40 dB, with a sharp minimum occurring with the angle difference near zero. A linear model of the response to the two input pressures estimates a complex common-mode gain C and a complex difference-mode gain D; magnitude of D is about 35 dB greater than magnitude of C over the frequency range that was tested (75 to 1000 Hz). Thus, except for conditions that make the common-mode input much larger than the difference-mode input, the pressure difference between the oval and round windows is, to a good approximation, the effective acoustic stimulus for the cochlea.

Measurement of acoustic impedance and reflectance in the human ear canal.

The pressure reflectance R (omega) is the transfer function which may be defined for a linear one-port network by the ratio of the reflected complex pressure divided by the incident complex pressure. The reflectance is a function that is closely related to the impedance of the 1-port. The energy reflectance R (omega) is defined as magnitude of [R]2. It represents the ratio of reflected to incident energy. In the human ear canal the energy reflectance is important because it is a measure of the inefficiency of the middle ear and cochlea, and because of the insight provided by its simple frequency domain interpretation. One may characterize the ear canal impedance by use of the pressure reflectance and its magnitude, sidestepping the difficult problems of (a) the unknown canal length from the measurement point to the eardrum, (b) the complicated geometry of the drum, and (c) the cross-sectional area changes in the canal as a function of distance. Reported here are acoustic impedance measurements, looking into the ear canal, measured on ten young adults with normal hearing (ages 18-24). The measurement point in the canal was approximately 0.85 cm from the entrance of the canal. From these measurements, the pressure reflectance in the canal is computed and impedance and reflectance measurements from 0.1 to 15.0 kHz are compared among ears. The average reflectance and the standard deviation of the reflectance for the ten subjects have been determined. The impedance and reflectance of two common ear simulators, the Brüel & Kjaer 4157 and the Industrial Research Products DB-100 (Zwislocki) coupler are also measured and compared to the average human measurements. All measurements are made using controls that assure a uniform accuracy in the acoustic calibration across subjects. This is done by the use of two standard acoustic resistors whose impedances are known. From the experimental results, it is concluded that there is significant subject variability in the magnitude of the reflectance for the ten ear canals. This variability is believed to be due to cochlear and middle ear impedance differences. An attempt was made at modeling the reflectance but, as discussed in the paper, several problems presently stand in the way of these models. Such models would be useful for acoustic virtual-reality systems and for active noise control earphones.