The human middle ear, showing the tensor tympani tendon (yellow) and stapedius tendon (red). The muscles themselves are recessed in bone. According to the intralabyrinthine pressure theory, activation of the tensor tympani muscle pulls the malleus and ear drum inwards and pushes the stapes into the oval window, protecting the cochlea by raising the pressure of fluids inside. It is suggested that the pressure controls the gain of the cochlear amplifier. Modified from [80] and used with permission. The intralabyrinthine pressure (ILP) theory of middle ear muscle action dates from the 19 th century, and, although simple and elegant, it was never widely accepted. By the middle of the 20 th century it was totally dismissed. The theory proposes that contraction of the middle ear mus- cles causes the stapes to press inwards on the cochlea’s flu- id contents, raising their pressure. In this paper, the pres- sure is taken to be a key parameter which controls the gain of the cochlear amplifier via its action on outer hair cells – sensing cells which, importantly, are in continuous hy- draulic connection with the cochlear fluids. It is this ac- tion which rapidly, silently, and with minimum observable movement, protects the cochlea’s supersensitive detectors. In the 1880s, Gellé developed a theory of why action of the stapes should produce lower hearing acuity [16,17]. He had observed that pressure applied to the ear canal led 

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Context 1

... human middle ear is an intricate arrangement of mem- branes, bones, muscles, and ligaments ( Figure 1). The de- vice functions as a mechanical transformer helping to bring the acoustic impedance of air closer to the impedance of the cochlear fluids [1]. The middle ear has been closely studied since audiology began, but even now its functions are not fully understood [2], not least because the ear can respond to acoustic motions of subatomic dimensions. At hearing threshold, the eardrum moves of the order of picometres [3]. Understanding how such minute move- ments are transmitted through a delicate system of bones and joints stretches experimental apparatus to its limits. This synthesis paper concerns itself with one particular as- pect of the middle ear, and that is the function of the middle ear muscles, the two smallest skeletal muscles in the human body: the tensor tympani attached to the malleus, and the stapedius, only 1 mm long, attached to the stapes (Figure 1). Years of research have made it plain that the muscles are in- volved in attenuating loud sounds [4–7], so that the delicate sensing elements in the cochlea are not overloaded or dam- aged. The question addressed here is, how is this achieved? The standard answer is that when the middle ear muscles contract, they stiffen up the joints and ligaments, partic- ularly the annular ligament surrounding the stapes, caus- ing an increase in mechanical impedance and hence re- ducing sound transmission to the cochlea [8–11]. But as Békésy noted, there is only about a 5% alteration in im- pedance when the muscles contract (p. 72) and he could not find any physiologically important change (p. 203). Our knowledge has since expanded [4–7], but the gener- al picture remains the same – the middle ear muscles ap- pear to provide only a minor degree of protection against loud sounds. Most animal-based studies find a change in impedance of around 5–10 dB [12,13], while human stud- ies show an effect of only 1–2 dB over the range 0.06–11 kHz [14,15]. Changes in cochlear potentials are some- what larger and more variable, and are discussed in the next section. This paper questions the idea that the pur- pose of the strategically placed middle ear muscles, with their complex anatomy and physiology, is to cause a mi- nor change in sound transmission. Instead, this paper sets out what seems to be a much more effective mechanism: when the muscles contract they create a fast control sig- nal in the cochlear fluids – hydraulic pressure. to a loss in hearing sensitivity, and he proposed that the stapes in a similar way produced a “pressions centripètes” in the labyrinth which caused a reduction in cochlear sensitivity. Figure 2 illustrates the mechanism: contrac- tion of the tensor tympani draws the whole middle ear system inwards and presses the stapes into the oval win- dow. According to Borg [11], the labyrinthine pressure- regulation theory can be traced back to Politzer in 1861, who noted that electrical stimulation of middle ear mus- cles led to changes in middle-ear pressure and, presum- ably, to changes in labyrinthine pressure. Similarly, Borg also notes that Lucae in 1866 proposed that contraction of the tensor tympani affected low frequency hearing via labyrinthine pressure, and this was taken up and promot- ed by Zimmerman in the early 1900s who claimed that pressure somehow controlled the vibration of the basilar membrane fibres. What happened to Gellé’s theory? Borg mentions [11] that Kato in 1913 was the first to discredit the hypothesis by observing no displacement of the round window mem- brane during tensor tympani contractions. Of course, the displacements involved are minute (micrometres or less), and with the instruments available at the time Kato failed to see an effect. Today, that motion has indeed been seen [18]. However, it was probably Békésy’s traveling wave the- ory [8] that eventually caused the ILP theory to be dis- carded, for the mechanics of the passive traveling wave do not depend on static pressure. According to the traveling wave theory, the pressure difference across the partition is the effective stimulus, and static pressure is not important. For most of the 20 th century, the cochlea was considered a passive transducer, and there was no conception of active mechanics that might be sensitive to pressure. Nowadays, the situation is different, and the cochlea is seen as an active transducer [19]. Although the traveling wave theory remains at the core of cochlear mechanics, there is now room for additional active processes. It is now possible to consider that the outer hair cells, responsible for the activity, could be affected by static pressure. This proposed sensitivity to static pressure is a logical counter- part to a recent speculation that outer hair cells are pres- sure sensors and respond to the fast pressure wave sig- nal [20,21]. Extending the idea, the proposal is that outer hair cells respond to static (d.c.) pressure as well as alter- nating (a.c.) pressure. In the version of the ILP theory put forward here, the d.c. pressure is the factor controlling the gain of the cochle- ar amplifier, which is part of a positive feedback loop in- volving the outer hair cells, which themselves are respon- sive to a.c. pressure. Simply put, pressure acts to squeeze the compressible outer hair cells. In the following, the ILP theory is reexamined and the arguments for it are as- sessed. The conclusion is that the arguments common- ly raised against the ILP theory are not decisive. The ILP theory has the potential to unify much audiological un- derstanding and deserves renewed attention. There is a paradox surrounding middle ear sound con- duction, and it begins with Békésy. In his monumental work [8] he took a freshly excised ear from a cadaver and covered its round window with a hollow rubber tube that led to the ear of a living observer (himself). When sound was applied to the ear ...

Context 2

... human middle ear is an intricate arrangement of mem- branes, bones, muscles, and ligaments ( Figure 1). The de- vice functions as a mechanical transformer helping to bring the acoustic impedance of air closer to the impedance of the cochlear fluids [1]. The middle ear has been closely studied since audiology began, but even now its functions are not fully understood [2], not least because the ear can respond to acoustic motions of subatomic dimensions. At hearing threshold, the eardrum moves of the order of picometres [3]. Understanding how such minute move- ments are transmitted through a delicate system of bones and joints stretches experimental apparatus to its limits. This synthesis paper concerns itself with one particular as- pect of the middle ear, and that is the function of the middle ear muscles, the two smallest skeletal muscles in the human body: the tensor tympani attached to the malleus, and the stapedius, only 1 mm long, attached to the stapes (Figure 1). Years of research have made it plain that the muscles are in- volved in attenuating loud sounds [4–7], so that the delicate sensing elements in the cochlea are not overloaded or dam- aged. The question addressed here is, how is this achieved? The standard answer is that when the middle ear muscles contract, they stiffen up the joints and ligaments, partic- ularly the annular ligament surrounding the stapes, caus- ing an increase in mechanical impedance and hence re- ducing sound transmission to the cochlea [8–11]. But as Békésy noted, there is only about a 5% alteration in im- pedance when the muscles contract (p. 72) and he could not find any physiologically important change (p. 203). Our knowledge has since expanded [4–7], but the gener- al picture remains the same – the middle ear muscles ap- pear to provide only a minor degree of protection against loud sounds. Most animal-based studies find a change in impedance of around 5–10 dB [12,13], while human stud- ies show an effect of only 1–2 dB over the range 0.06–11 kHz [14,15]. Changes in cochlear potentials are some- what larger and more variable, and are discussed in the next section. This paper questions the idea that the pur- pose of the strategically placed middle ear muscles, with their complex anatomy and physiology, is to cause a mi- nor change in sound transmission. Instead, this paper sets out what seems to be a much more effective mechanism: when the muscles contract they create a fast control sig- nal in the cochlear fluids – hydraulic pressure. to a loss in hearing sensitivity, and he proposed that the stapes in a similar way produced a “pressions centripètes” in the labyrinth which caused a reduction in cochlear sensitivity. Figure 2 illustrates the mechanism: contrac- tion of the tensor tympani draws the whole middle ear system inwards and presses the stapes into the oval win- dow. According to Borg [11], the labyrinthine pressure- regulation theory can be traced back to Politzer in 1861, who noted that electrical stimulation of middle ear mus- cles led to changes in middle-ear pressure and, presum- ably, to changes in labyrinthine pressure. Similarly, Borg also notes that Lucae in 1866 proposed that contraction of the tensor tympani affected low frequency hearing via labyrinthine pressure, and this was taken up and promot- ed by Zimmerman in the early 1900s who claimed that pressure somehow controlled the vibration of the basilar membrane fibres. What happened to Gellé’s theory? Borg mentions [11] that Kato in 1913 was the first to discredit the hypothesis by observing no displacement of the round window mem- brane during tensor tympani contractions. Of course, the displacements involved are minute (micrometres or less), and with the instruments available at the time Kato failed to see an effect. Today, that motion has indeed been seen [18]. However, it was probably Békésy’s traveling wave the- ory [8] that eventually caused the ILP theory to be dis- carded, for the mechanics of the passive traveling wave do not depend on static pressure. According to the traveling wave theory, the pressure difference across the partition is the effective stimulus, and static pressure is not important. For most of the 20 th century, the cochlea was considered a passive transducer, and there was no conception of active mechanics that might be sensitive to pressure. Nowadays, the situation is different, and the cochlea is seen as an active transducer [19]. Although the traveling wave theory remains at the core of cochlear mechanics, there is now room for additional active processes. It is now possible to consider that the outer hair cells, responsible for the activity, could be affected by static pressure. This proposed sensitivity to static pressure is a logical counter- part to a recent speculation that outer hair cells are pres- sure sensors and respond to the fast pressure wave sig- nal [20,21]. Extending the idea, the proposal is that outer hair cells respond to static (d.c.) pressure as well as alter- nating (a.c.) pressure. In the version of the ILP theory put forward ...