Case Report: Diagnostic Indicators of a Contracted Tensor Tympani Muscle

Abstract

The tensor tympani muscle (TTM) is a long-striated muscle that originates in a bony canal superior to the cartilaginous section of the Eustachian tube. The tendon of the muscle emerges laterally from the opening of the canal, courses through the middle ear cavity, and attaches at the neck of the manubrium. Contraction of the TTM draws the manubrium of the malleus medially, resulting in an inward displacement of the tympanic membrane (TM) and increased middle ear pressure. TTM contraction has been shown to occur simultaneously with the contraction of the tensor veli palatini muscle (TVPM).1,2 The TVPM assists with swallowing and is considered the primary dilator of the Eustachian tube (ET).3 Both the TTM and TVPM are innervated by the mandibular division of the trigeminal nerve and share continuous muscle fibers.4,5Figure 1: (A) Jerger Type A tympanograms obtained with the TTM at rest, which yielded a normal tracing, bilaterally. (B) A tympanogram obtained during extended TTM contraction, which resulted in a tracing with a reduced peak compliance for both ears. (C, left Column) A tympanogram performed following the Toynbee maneuver resulted in negative peak pressure. (C, right Column) Following TM contraction, a second tympanogram was obtained which revealed a return to relative ambient peak pressure.Figure 2: (A) Repetitive TM contractions were recorded over a 15-second window. Each deflection contained four distinct stages: (1) a reduction in compliance (downward tracing) with TTM contraction, (2) an increase in compliance (upward tracing) with the relaxation of the TTM, (3) a further increase or spike in compliance (upward tracing) above baseline, and (4) a near return to baseline compliance (leveling of the tracing). The brief upward spike in compliance above baseline (arrow) is consistent with the breakage of the ET seal. (B) TTM contraction resulted in upward deflections with negative pressure applied to the EAC. The superimposed dotted line highlights the change in baseline compliance between TTM contractions. This appears to reflect a flow of air bolus through the ET with repeated TTM contraction. (C) Extended TTM contraction over a 15-second window.Figure 3: Right ear pure-tone air- and bone-conduction thresholds were obtained with the TTM in a relaxed state (gray) and contracted (red). TTM contraction resulted in mild low-frequency hearing loss.The TTM has been implicated in numerous conditions including middle ear myoclonus, palatal tremor, and Meniere’s disease; albeit its presumed role in these pathologies is speculative.6–8 A previous report theorized that TTM injury may lead to continuous, tonic TTM contraction with secondary otologic symptoms that include tinnitus, aural fullness, vertigo, and otalgia.9 The principal clinical tool that is used for the assessment of TTM contraction is immittance audiometry. TTM contraction has been shown to produce distinct tympanometric findings such as low static compliance and tracings that change direction when negative pressure is applied to the external auditory canal (EAC).10 A comprehensive audiological test battery, including immittance audiometry, was performed on an adult male who presented with voluntary TTM contraction. The purpose of this report is to demonstrate the potential diagnostic indicators associated with TTM contraction. CASE PRESENTATION A 33-year-old male described his ability to manipulate his ear muscles and elicit “clicking” and low-frequency “rumbling” sounds. He explained that he was able to alter his middle ear pressure by ear-muscle contraction. To determine the audiometric and tympanometric effects of the reported muscle contraction, an audiological evaluation was administered in the clinic. An otoscopic inspection was conducted using a handheld otoscope while the ear muscles were relaxed and then contracted. For the right ear, probe-tube measurements were -obtained using the Verifit 2 by Audioscan. The instrument was set to manual control using an A-weighted filter. A probe tip was placed within 5 millimeters of the TM and he signaled when the ear muscle was contracted (https://bit.ly/48PKNJH). Middle ear immittance audiometry was conducted bilaterally using a GSI Tympstar Pro clinical tympanometer (Grason-Stadler, Eden Prairie, MN) with a 226 Hz probe tone. Tympanograms were obtained with the ear muscle in a relaxed state (Figure 1A) and during an extended muscle contraction (Figure 1B). The subject was asked to perform a Toynbee maneuver by pinching his nostrils and swallowing, which was followed by a tympanogram in the right ear (Figure 1C). To ensure the absence of any underlying throat or jaw movement, he was asked to immediately contract his right ear muscle while being observed visually and tympanometrically (Figure 1C). A right-ear modified-decay test was conducted without the use of a probe tone and insertion of the contralateral probe. During a cycle of rapid ear-muscle conditions (contracted and relaxed) for 15 seconds in ambient air pressure (Figure 2A), and with negative EAC pressure (Figure 2B), modified acoustic decay testing was administered. This test was followed by extended contraction of the ear muscle (Figure 2C). Pure-tone audiometric threshold testing from 250-8000 Hz was conducted with a GSI AudioStar Pro (Grason-Stadler, Eden Prairie, MN) in a certified11 acoustic test room. Hearing thresholds were first obtained with the muscle in a relaxed state and then contracted (Figure 3). Before each threshold measure, hand signals were used to indicate when the ear muscle was contracted. Various elements of the test battery were administered monaurally to avoid muscle fatigue. DISCUSSION The purpose of this case study was to investigate an individual’s self-described ability to voluntarily contract his TTM muscle. Tympanic membrane movement during TTM contraction could not be visualized with the use of a handheld otoscope although reports have described visible TM movement during volitional TTM contraction under varying magnifications.10,12,13 A short-duration objective tinnitus was confirmed with the use of a probe-microphone. Clicking tinnitus has been reported to occur during the opening of the Eustachian tube and may be caused by sudden disruption of the lumen’s mucosa film.14,15 The low-frequency rumbling sound that was reportedly present during TTM contraction may be linked to several sources including muscle contraction noise or an increase in internal cochlea hydraulic pressure from medial stapes movement within the oval window. Irrespective of its source, tinnitus may function as a masker and, together with increased stiffening of the tympano-ossicular system, may be responsible for the mild low-frequency hearing loss observed during voluntary TTM contraction. During tympanometry, evidence of middle ear ventilation that corresponded to TTM activity was observed in three instances: Tympanograms obtained following the Toynbee maneuver demonstrated a shift from negative middle ear pressure to near ambient middle ear pressure with contraction of the TTM. This finding indicates air bolus flowed through the Eustachian tube with contraction of the TTM. Modified acoustic decay demonstrated an increase in middle ear compliance above baseline following each contraction of the TTM. This points to a short-term spike in compliance following TTM contraction due to an enlarged middle volume caused by a breakage of the Eustachian tube seal. Repeated contraction of the TTM during modified decay testing with negative pressure applied to the EAC resulted in a gradual reduction in middle ear compliance over baseline. The steady change in compliance with repeated TTM contraction appears to be consistent with the pumping of an air bolus into the middle ear and a widening pressure gradient between the middle ear and the EAC. To our knowledge, middle ear ventilation after voluntary TTM contraction has not been previously reported. Although novel, this is not surprising given the close relationship between the TTM, and the primary dilator of the Eustachian tube, the TVPM. Both muscles are innervated by the mandibular section of the trigeminal nerve, co-contract, and share a localized muscular connection. The mechanism for which the TTM may aid the TVPM in opening the Eustachian tube may be examined using Boyle’s law, which suggests that volume and pressure are inversely proportional within a closed system. Under normal conditions, the Eustachian tube is closed, and the middle ear represents an enclosed air space. As such, even subtle inward movement of TM with TTM contraction could produce a sudden drop in middle ear volume with a corresponding rise in middle ear pressure. Middle ear overpressure from voluntary TTM contraction may exert pressure on the Eustachian tube seal and assist the TVPM in opening the Eustachian tube. This way, the middle ear may be viewed as containing a pump mechanism that facilitates middle ear ventilation. In cases where tinnitus is reported, it would be prudent for clinicians to inquire about TTM dysfunction and seek a patient description of that tinnitus sensation. A patient might report low-frequency subjective tinnitus as well as clicking tinnitus that might be audible in a quiet room or detectable using a probe microphone. A practical TTM test battery may include pure-tone air- and bone-conduction audiometry from 125 to 8,000 Hz, in addition to otoscopy, tympanometry, and acoustic decay testing without an acoustic stimulus. CONCLUSION We present a case that is consistent with previous reports in the literature yet provides new clinical insight regarding voluntary TTM contraction. A unique observation was that TTM contraction appeared correlated with the flow of air bolus through the Eustachian tube. Volitional TTM contraction resulted in both an objective clicking tinnitus as well as a subject tinnitus in the form of a rumbling sound, mild low-frequency hearing loss, and a tympanogram with low static peak compliance. Other indicators of TTM contraction included high amplitude compliance changes during modified acoustic decay testing and an inversion in the direction of the tympanometric tracing when negative pressure was applied to the EAC. Knowledge of these diagnostic findings may assist clinicians in identifying abnormal TTM activity in patients with suspected otologic pathologies, such as tinnitus.