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IV. FUNCTIONS AND PATHPHYSIOLOGY OF THE MIDDLE EAR

The middle ear is a crucial component in the transmission of sound from the external world to the inner ear. Disorders of the middle ear are common in the clinic. Understanding the way in which the middle ear functions is crucial to understanding the hearing loss that results when it malfunctions.Moreover, middle ear disease may herald more serious medical problems, and an understanding of middle ear function is necessary to understand to onset and progress of these disease states. We first take up the normal function of the middle ear in some detail, and then go on to describe the hearing loss that results from a wide variety of conditions.

Objectives: At the end of this section you should be able to:

1. Describe the properties of the middle ear which facilitate transfer of sound energy from air to fluid of the inner ear, including impedance matching.

2. State the function of the round window.

3. Describe the effect upon sound conduction of static pressure difference in the middle ear cavity and the consequent importance of normal Eustachian tube function.

4. Describe the basic attributes of a vibrating mechanical system, including mass, stiffness, friction, resonance, frequency response, and how they are associated with middle ear function.

5. State was is meant by a conductive hearing loss, how this can be differs from a sensorineural hearing loss and how it is measured.

6. Describe common middle ear disorders and how they interfere with hearing.

THE MIDDLE EAR

Objective 1: The middle ear functions to transmit sound efficiently from air to fluid

Although we have seen that the acoustic properties of the outer ear and external canal substantially increase sound pressure at the eardrum above that in a free sound field for the middle frequency range, the middle ear constitutes another important mechanism to increase auditory sensitivity. Recall that the auditory receptors of the inner ear operate in a fluid environment, and that the inner ear is really an "underwater" sound receiver. When sound in air strikes a fluid boundary (a boundary between media with different acoustic impendances) there is a theoretical loss of 99.9% of the energy in a sound wave in air (due to reflection). This 99.9% loss is equivalent to 30 dB; a reduction in stimulus intensity of this amount is quite noticeable to a listener. In order to overcome this mismatch in the impedance of air and fluid, the middle ear is interposed between the tympanic membrane and the oval window. The process is referred to as impedance matching. Impairment in the transmission of sound through the middle ear creates a conductive hearing loss.

Impedance matching

The middle ear acts as a kind of hydraulic press in which the effective area of the eardrum is about 21 times that of the stapes footplate. Thus, the force caused by a given sound pressure in the air acting on the area of the eardrum is concentrated through the ossicles onto the small area of the footplate, resulting in a pressure increase proportional to the ratio of the areas of the two structures which, in humans, is about 21:1. It also happens that the lever arm formed by the malleus in rotating about its pivot is somewhat longer than that of the incus, giving another factor of about 1.3 in pressure increase. FigureIV-1 shows these relationships.

The 21x of the drum/footplate area ratio, multiplied by the 1.3x lever arm factor, yields about a 27.3x increase in pressure, which is 29 dB, thus just about overcoming the theoretical 30 dB loss due to the air/liquid interface. We say that the middle ear matches the acoustic impedance between the air and the fluid, thus maximizing the flow of energy from the air to the fluid of the inner ear.

Objective 2: The round window allows for fluid displacement in the cochlea

The tympanic membrane moves in and out under the influence of the alternating sound pressure. Motion of the eardrum causes the malleus and incus to rotate as a unit about a pivot point; rotation of the long process of the incus about this pivot causes the stapes to rock back and forth in the oval window, setting up a wave of sound pressure in the fluid of the inner ear. Because fluid of the inner ear in noncompressible, inward movement of the stapes footplate is allowed because of the yielding of the thin membrane which covers the round window. This is essential to the transmission process, since it provides elastic relief for the fluid of the inner ear, thus permitting movement of the stapes and the structures of the inner ear.

Objective 3: The Eustachian tube functions to equalize pressure

The middle ear operates normally when it is filled with air at atmospheric pressure. The Eustachian tube, which connects the middle ear cavity to the nasopharynx, normally opens and closes periodically thereby insuring that the static pressure in the middle ear will remain the same as atmospheric pressure. When the Eustachian tube fails to open, a negative pressure immediately begins to build in the middle ear cavity due to absorption of the trapped air by the middle ear mucosa. There is an increased stiffness in the middle ear mechanical transmission system. The transmission loss is greater for low frequencies and has been observed to be of the order of 20 dB for frequencies below 1000 Hz. A pressure difference may also be experienced when the Eustachian tube fails to open during ascent or descent in an airplane.

Reflex contractions of the middle ear muscles.

The tensor tympani and stapedius tensor muscles in the middle ear contract reflexly in response to loud sounds. Both muscles increase the stiffness of the ossicular chain when they contract and thus reduce sound transmission by up to 15 dB, depending on frequency. In humans the stapedius tensor is much more effective than the tensor tympani. The reflexes are generally thought to be primarily a protective mechanism to shield the inner ear from damage due to intense sound but, because the latency of contraction is at least 10 milliseconds, they cannot protect against impulsive sounds such as a pistol shot. Since the reflexes primarily reduce the transmission of low frequencies, they also act to improve the discrimination of speech sounds in the presence of loud, low frequency background noise.

Objective 4: Attributes of a vibrating system - mechanical resonace in the middle ear

In order to understand the physiological implications of several kinds of pathological change which can occur in sound conduction in the middle ear it is helpful to consider some of the basic properties of a vibrating mechanical system, which the middle ear ossicles are one example. In general, a vibrating system includes three elements: mass, stiffness and friction. The corresponding three types of forces which act on the system are: 1) an inertia force given by the product of the mass and its acceleration; 2) a stiffness force proportional to the deflection of the spring from its resting position; 3) a frictional or damping force which dissipates energy in the form of heat when movement occurs. When such a system is subjected to a sinusoidal driving force of constant magnitude, but which varies in frequency, the resulting amplitude of vibration is maximum at a frequency known as the resonant frequency.

A plot of vibration amplitude vs. driving frequency, referred to as a resonance curve, gives the frequency response of the system as shown in Figure IV-2A. At resonance the inertia and stiffness forces are equal in magnitude but out of phase in time and thus cancel, leaving only the frictional force to limit the amplitude of vibration.

If the stiffness of the system is increased with the mass and friction remaining unchanged, the resulting amplitude is reduced for frequencies below the resonant frequency and the resonant frequency is increased (Figure IV-2B). Conversely, if the stiffness of the original system is not changed but the mass is increased, the response amplitude is little changed for frequencies below the resonant frequency but is reduced for frequencies above resonance and the resonant frequency is lowered (Figure IV-2C).

Objective 5: Conductive hearing loss

We have seen how the normal outer and middle ears participate in sound conduction. When one or more parts of these systems do not function properly a conductive hearing loss results. A conductive hearing loss is the result of a physical blockade of sound transmission to the inner ear. Conductive hearing loss is a problem in the outer ear, the middle ear, or both. A sensorineural hearing loss occurs when there is damage to the cochlear receptor organ, to the fibers of the auditory nerve or to both. A sensorineural hearing loss may also be associated with lesions of the central auditory pathways.

The principles of acoustics outlined above can be applied to the vibrating system composed of the eardrum, ossicular chain and supporting ligaments. Since the actual middle ear is a complex mechanical system in which the mass, stiffness and friction are distributed throughout several structures and the values of these parameters poorly known, we can only do some qualitative reasoning rather than to obtain quantitative results. Nevertheless, the general principles can be used to predict the kinds of hearing impairment that would be expected on the basis of specified changes in the structures of the middle ear.

A conductive hearing loss may be detected and its severity measured with an audiogram. Because in a conductive hearing loss sound will be attenuated by malfunction of the sound-transmission system, an audiogram will show a loss in sensitivity at some or all test frequencies. Later, you will see how the audiogram can be used to differentiate between a conductive hearing loss and a sensorineural hearing loss.

Objective 6: Pathophysiology of the middle ear

Disorders of the middle ear and mastoid arise from maldevelopment, inflammatory and degenerative processes, trauma, or neoplastic disease. From the point of view of hearing, these disorders may result directly in a conductive hearing loss. Some of them (e.g., inflammation and neoplastic disease) can become serious medical problems if not treated, with involvement of the inner ear and systems beyond.

Congenital malformations of the middle ear

Congenital malformations are often related to malformations of the pinna and external ear canal. This is not surprising since both the external ear and a portion of the middle ear are derived from tissue of the first and second branchial arches. The conditions may be inherited or they may be acquired. In the latter category, for instance, thalidomide is known to be a potent teratogen that results in total or partial agenesis of the pinna, external canal, and middle ear.

Problems with the ossicles may include agenesis, atresia, fixation or discontinuity. Malleal and incudal fixation are most common. In some cases, a bony atresia plate, a malformation which may completely block the external ear canal, may fuse with an abnormal malleus which, in turn, may be associated with a fused incudomalleal joint (Figure IV-3). This malformation blocks most normal environmental sound being transmitted to the cochlea. The result is a conductive hearing loss. The stapes may also be malformed and immobile. Other structures in the area that may be anomalous include the facial nerve, middle ear muscles, blood vessels, bony partitions, and the oval and round windows.

Tympanicmembrane perforations


Fig. IV-4

Perforations of the tympanic membrane is a common serious ear injury that may result from a variety of causes including projectiles or probes (e.g. Q-tips, pencils, paper clips, etc.), concussion from an explosion or a blow to the ear, rapid pressure change (barotrauma), temporal bone fractures, and other miscellaneous causes. Perforations may include damage to the ossicles. Figure IV-4 are examples.

Hearing loss accompanying tympanic membrane perforation is conductive in nature. There may be two mechanisms at play that contribute to this hearing disorder. First, the normal structure, and hence action, of the tympanic membrane is altered. Sound pressure on either side of the tympanum is quickly equalized. The degree of conductive hearing loss is directly related to the size of the perforation. Second, sound waves that enter the middle ear space reach both the round and oval windows and do so nearly in phase. Recall that under normal conditions inward motion of the stapes footplate in the oval window results in an outward movement of the round window, and vice versa. A "leaky" tympanic membrane means that the normal "push-pull" action of these two membranes is, to some extent at least, circumvented and as a result the sound energy entering the inner ear is reduced.

Ossicular chain injuries

The various injurious mechanisms associated with the tympanic membrane apply to the ossicles as well, occasionally even without rupture to the membrane itself. Violent, closed-head injuries, especially if associated with a temporal bone fracture, are common causes of ossicular chain disruption. A major conductive hearing loss (30-60dB) may result which does not improve after tympanic membrane repair. The most common traumatic ossicular chain lesion is a incudostapedial joint dislocation with or without a fracture of the long process of the incus. However, just about any imaginable fracture or displacement can be found. Ossicular dislocation interrupts the normal transmission of sound energy from the tympanic membrane to the fluid of the middle ear. Hence, under these conditions the impedance matching mechanism, which alone overcomes the nearly 30 dB loss of energy when sound waves in air meet a fluid boundary, is lost. Coupled with the mechanisms surround a tear in the tympanic membrane (see above), the hearing loss is substantial and disabling.

Metabolic disease - otosclerosis

Otosclerosis is a common cause of hearing loss (Fig. IV-5). It is found in about 10% of the population, and is clinically significant in 10% of affected individuals. It is an osteodystrophy limited to the temporal bone, affecting primarily the otic capsule of the labyrinth. Otosclerosis usually results in fixation of the stapes in the oval window but may involve the cochlea and other parts of the labyrinth. Hence, the symptoms are confined to the auditory and vestibular systems. A conductive hearing loss is the usual outcome, but with cochlear involvement there may be a sensorineural component to the deafness and vertigo as well. The pathogenesis of the disease is not well understood. Early in the course of the disease there is increased mechanical stiffness of the ossicular chain due to a developing fixation of the stapes footplate in the oval window niche. Recall that a stiffness lesion of the middle ear tends to suppress the transmission of low-frequency sounds. This is reflected in the audiogram taken at this time as a low-frequency air-bone gap. Later, as the bone grows, there is added a mass component to the transmission system of the middle ear and a suppression of high tones. Thus, in advanced otosclerosis there is substantial conductive hearing loss at all frequencies usually tested .

Inflammatory processes in the middle ear - Otitis media

Inflammatory diseases of the middle ear are related and the occurrence of one often leads to the other. The progression of otitis media and the oft-accompanying processes of the mastoid, otomastoiditis is shown in the chart at right.

Otitis media evolves from the common cold, allergies, cigarette smoke exposure, or anything that can cause obstruction of the Eustachian tube. For instance, loss of ciliary action, hyperemic swelling, and increased production of mucus associated with an upper respiratory infection leads to temporary closing of the Eustachian tube and, as a result, negative pressure develops within the middle ear. This has two consequences: One involves pressure and pain as the result of distention of the tympanic membrane innervated by the trigeminal nerve. The other is a progressive conductive hearing loss due to added stiffness of the middle ear transmission mechanism. Because stiffness shifts the resonance point of this mechanical system toward high frequencies, sounds tend to lose their low frequency quality and take on a sharp "tinny" character not unlike that often experienced in high altitude flying. Otitis of this type usually subsides without further complication.

Negative pressure within the middle ear, if left unrelieved, will lead to fluid accumulation in the normally air-filled middle ear space (Figure IV-6). This condition is referred to as serous (or secretory) otitis media. As noted above, it may have predisposing factors including lymphatic engorgement, cleft palate, hypertrophic adenoids, allergic rhinitis, and neoplasms of the nasopharynx and, thus, may develop in the absence of infection. Again, the patient has a conductive hearing loss with a retracted immobile tympanic membrane. The middle ear is filled with an amber-colored serous transudate. The hearing loss is now further complicated by the presence of a fluid-air boundary at the tympanic membrane and mass-friction loading of the ossicles. The degree of hearing loss will vary depending on the amount and viscosity of the transudate, middle ear fibrosis, and tympanic membrane edema. It may be as low as 5-10 dB (and not too noticeable) to 40-50 dB (where it is disabling).

The disease can develop rapidly into an acute suppurative otitis media as organisms migrate to the middle ear from the nasopharynx. The fluid changes rapidly from serous to sero-sanguineous to sero-purulent and finally to the purulent stage. Hence, acute otitis media is a potentially serious disease.

Because of the relationships between the middle ear cavity and the mastoid pneumatic channels there is a wide range of possible complications that involve areas outside of the middle ear itself. An important one for our considerations is the labyrinth. Involvement here results in labyrinthitis and sensorineural hearing loss. A second important sequelae is acute mastoiditis. Here there is bony destruction and coalescence of mastoid cells. Pus under pressure results in venous stasis, local acidosis, and dissolution of calcium (halisteresis). The infection may break through the confines of the mastoid and lead to intracranial complications including facial paralysis, meningitis, brain abscesses, lateral sinus thrombophlebitis, and otitis hydrocephalus.

Chronic otitis media/cholesteatoma

Left untreated (or if unresponsive), Eustachian tube dysfunction may lead to chronic otitis media and cholesteatoma. Some lesions of chronic otitis media are reversible whereas others are not. In either case, the entire pneumatic system or any portion of the temporal bone and its constituent structures may be involved including the tympanic membrane, ossicles, labyrinth, facial nerve, mastoid cells, arteries, veins, and the bones of the middle and posterior fossae. Conductive hearing loss almost always accompanies this condition. Chronic negative pressure in the middle ear leads to a retraction of the tympanic membrane. The area of retracted tympanic membrane forms a closed pocket or cyst where epithelial debis from the lining of the tympanic membrane collects. This expanding collection of tympanic membrane debris erodes the ossicles, leading to a conductive hearing loss. It can also erode the bony labyrinth or bone of the cranial fossa.

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