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“The Kiss of Deaf”: A case study

Reiter, Levi A.

doi: 10.1097/01.HJ.0000327759.01969.cf
ARTICLE

You may have heard about this unusual case on national TV or read about it in your local paper. But here is the full story, with the audiologic details, of a mother whose ear was seriously damaged by a loving kiss from her 4-year-old daughter.

Levi A. Reiter, PhD, is Professor and Head of the Audiology Program at Hofstra University. He is also on the faculty of the Long Island AuD Consortium and maintains a clinical practice in diagnostic and rehabilitative audiology. Readers may contact Dr. Reiter at Department of Speech-Language-Hearing Sciences, Hofstra University, Hempstead, NY 11549, at ears@drreiter, or at www.drreiter.com.

A 49-year-old mother, surprised by an unexpected and forceful kiss into her external auditory meatus (EAM) from her 4-year-old daughter, suffered consequences reminiscent of, but more serious than, acoustic shock injury (ASI) or even acoustic trauma (AT). Following the insult to the EAM, the patient reported having lost all hearing in that ear. Follow-up evaluations that week and 1 year later revealed persistent sensorineural hearing loss in the lower frequencies of the affected ear, among other symptoms. A routine hearing exam taken before the kiss revealed that her hearing had been normal bilaterally.

Acoustic shock injury or ASI has been defined as a symptom complex “…arising from exposure to an abrupt, intense, and unanticipated acoustic stimulus…”1 ASI is different from acoustic trauma (AT), in which the cochlea may be damaged directly by a sudden impulsive signal of approximately 140 dB SPL. In contrast, ASI may result from signals as soft as 82 dB SPL.2

The key stimulus in ASI seems to be the suddenness, or unexpected nature of the acoustic signal, rather than its damaging intensity. A moderately intense sound that comes without warning presumably elicits an acoustic startle reflex, which includes contraction of the tensor tympani muscle as well as skeletal muscles about the aural area.3 The symptoms of ASI include ear pain, tinnitus, hyperacusis, aural fullness, hollow feeling in the ear, and ear flutter, as well as numbness, tingling, and twitching of the face near the affected ear.2 But because of the moderate intensity of the eliciting sound, hearing loss is rarely a symptom of ASI.

The patient in the present case study reported symptoms similar to those associated with ASI, but with some unusual additional symptoms, including unilateral sensorineural hearing loss and stapedial reflex paralysis. The patient was a female, 49 years of age at the time of the incident. Six months earlier she had received a routine, semi-annual cerumen check up and audiometric evaluation at an ENT office. At that time her hearing in both ears was found to be within normal limits (WNL), with hearing thresholds ranging from 10 to 20 dB HL from 500 to 8000 Hz (250 Hz was not tested). The patient was reported to be in good health in general, and had no history of tinnitus, vertigo, or other ear-related difficulties. Unfortunately, immittance data were not available.

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THE INCIDENT

As reported, the incident occurred while the patient and her 4-year-old daughter sat together on the living room floor watching television. The child suddenly placed a vigorous kiss on mom's left ear while hugging and pulling her down. Unfortunately, the kiss landed directly on the aperture of the EAM, causing considerable negative pressure to be applied to the EAM and tympanic membrane (TM).

Reportedly, the suction resulted in immediate and complete loss of hearing in the woman's left ear. This profound effect was short-lived, and was followed several hours later by a more moderate loss of hearing, as well as dysacusis, screeching tinnitus, a hypersensitivity to all external auditory stimuli, and continuous unprovoked facial muscle spasms about the ear.

One week after the mishap, the woman received another hearing evaluation in the same ENT office. By this time, the initial hearing loss was reported to have improved further, the tinnitus had changed from a loud screech to a soft rushing sound, and the muscle spasms had become less frequent. However, the hypersensitivity to sound remained unchanged.

The post-incident audiograms revealed a low-frequency sensorineural hearing loss of 35 dB HL at 500 and 1000 Hz, rising to 15 dB HL at 2000 and 4000 Hz. SRTs were within 5 dB of the pure-tone average at 500, 1000, and 2000 Hz for each ear. The patient's speech-recognition scores (SRS) at 40 dB SL were 100% for the normal right ear, but only 76% for the impaired left ear.

Immittance testing revealed two normal Type A tympanograms. Ipsilateral acoustic reflexes were elicited at normal levels for the right ear at 500, 1000, 2000, and 4000 Hz. Ipsilateral reflexes could not be elicited at any level in the left ear. Contralateral acoustic reflexes were not tested.

Because of the unilateral nature of the hearing loss and the asymmetrical SRS, both ABR and DPOAE measurements were conducted. ABR results were WNL. The DPOAE findings were WNL from 1500 to 5000 Hz in the right ear, but spotty in the left, with acceptable emissions absent at 2000 and 5000 Hz.

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ONE YEAR LATER

Approximately a year after the ear-damaging kiss, the patient referred herself to the author's office for a follow-up evaluation and possible diagnosis.

Over the course of the year preceding the follow-up evaluation, her symptomatology developed as follows: The “rushing” tinnitus occurred now only in quiet settings; distortion was reduced in severity; hypersensitivity remained unchanged; and muscle spasms were no longer spontaneous, but occurred only in reaction to loud sounds. For example, after the patient attended a family wedding, she reported that the muscle spasms around her ear and neck persisted for several days before subsiding.

A new symptom also emerged: the perception of something like a flag or banner waving within the middle ear space when the patient turned her head from side to side.

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FOLLOW-UP EVALUATION

The patient was evaluated via pure-tone and speech audiometry, ABLB, immittance testing, acoustic reflexes (both ipsilateral and contralateral), and DPOAEs. The results were as follows:

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Audiometric data

Audiometric data were obtained using the Beltone 2000 audiometer. Hearing thresholds were WNL in the right ear, ranging from 5 to 15 dB HL from 500 to 4000 Hz. Thresholds in the left ear continued to show a low-frequency SNHL of 30 to 35 dB HL from 250 to 1000 Hz, recovering to 10 dB HL from 2000 to 4000 Hz.

As expected, SRTs were consistent with the pure-tone thresholds, and speech-recognition scores obtained at 40 dB SL using the NU6 were now 100% in both ears.

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DPOAE testing

DPOAEs were measured at 1500, 2000, 3000, 4000, 5000, and 6000 Hz, using the Maico EroScan. DPOAEs were present at all test frequencies in both ears.

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Recruitment testing

To objectify the patient's report of hypersensitivity to loud sounds in the impaired (left) ear, a direct measure of loudness growth was administered using the ABLB method proposed by Hood.4 A 1000-Hz pure tone was presented alternately to both ears. The tone to the normal (right) ear was fixed in intensity, while the tone to the impaired ear was varied in intensity until the patient judged it as being as loud as that in the normal ear. The tone in the normal ear was fixed at each of the following levels: threshold (5 dB HL), 35, 55, 75, and 95 dB HL. Figure 1 depicts the patient's loudness balance at each level.

Figure 1

Figure 1

Observing the so-called “laddergram,”5 one can see two noteworthy phenomena. One is that the full measure of loudness obtained in the normal ear by raising tone intensity from 5 to 95 dB HL was experienced by the impaired ear when tone intensity was raised from 35 to 80 dB HL. That is, the 45-dB increment produced in the impaired left ear was perceived as being as loud as a 90-dB increase in the normal right ear. This represents objective evidence of an abnormally accelerated loudness growth rate in the patient's impaired ear. This is consistent with the patient's report of heightened sensitivity to increases in sound intensity.

The second effect is evident when one observes the last two balance levels on the laddergram. That is, as we view the balance levels from threshold to 75 dB HL, we note that the impaired ear's loudness perception eventually catches up to that of the normal ear. However, at the highest balance level, we see that presenting a 1000-Hz tone at 80 dB HL to the impaired ear has the sensory impact of presenting a far more aversive tone of 95 dB HL. The latter phenomenon suggests the presence of hyperacusis.

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Magnetic Resonance Imaging (MRI)

The MRI was entirely normal, ruling out any retrocochlear pathologies.

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Immittance and acoustic reflexes

Immittance results were obtained with the GSI 33 Middle Ear Analyzer, and a 226-Hz probe tone. Tympanograms were entirely WNL in both ears (see Figure 2).

Figure 2

Figure 2

Acoustic reflexes were assessed both ipsilaterally and contralaterally. When the probe was inserted into the unimpaired ear, acoustic reflexes were elicited at normal levels for each frequency tested, both ipsilaterally (when the eliciting stimulus was presented to the probe ear) and contralaterally (when the eliciting stimulus was presented to the opposite ear). In contrast, when the probe was inserted into the impaired ear, no acoustic reflex could be elicited at any level for any frequency presented to either the ipsilateral, probe ear, or contralateral ear.

Such a finding is normally thought to indicate paralysis of the stapedius muscle via a lesion to the seventh cranial nerve. However, in this case, a thorough clinical otolaryngological examination revealed seventh cranial nerve function to be normal. In addition, a CT scan of the left temporal bone ruled out any possible temporal bone anomalies. In the present case, paralysis of the stapedial reflex was secondary to powerful suction applied to the TM, making it more likely that the paralytic lesion was to a damaged stapedial muscle or tendon.

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DISCUSSION

The results of the evaluation indicate that a possibly permanent ear injury was sustained by the recipient of a strong kiss on the aperture of the left EAM. The injury consisted of a mild (35-dB HL), low-frequency, sensorineural hearing loss, accompanied by a cluster of symptoms somewhat similar to those found in ASI. These are: tinnitus, dysacusis, aural area muscle spasms, and hyperacusis. In ASI, however, the sequelae are ascribed to an acoustic startle reaction to a moderately intense, unexpected sound, leading to persistent spasms in the tensor tympani muscle. Therefore, permanent sensorineural hearing loss is rarely symptomatic of ASI, and stapedial reflex paralysis never is.

This study supports the notion of a causal relationship between a forceful kiss on the aperture of the EAM and damage to certain identifiable auditory structures, specifically to the cochlear outer hair cells and to the musculature involving the stapedial reflex. Outer hair cell damage was indicated by sensorineural hearing loss in the left ear and hyper-recruitment findings on the ABLB exam. Damage to stapedial musculature was evidenced by a paralytic acoustic reflex pattern without seventh cranial nerve dysfunction. That is, the left-ear reflex could not be elicited by either ipsilateral or contralateral stimulation, whereas the right-ear reflex could be elicited by both.

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CONCLUSION AND IMPLICATIONS

The results of this case study show that a kiss applied to the aperture of the EAM can cause a persistent collection of aversive symptoms in and about the peripheral auditory system. Eighteen months after the initial insult to the ear, the patient continued to suffer from sensorineural hearing impairment, tinnitus, hyperacusis, muscle spasms around the external ear, paralysis of the acoustic reflex, and a sensation of middle ear flutter upon head movement.

While some of these symptoms are common to ASI—stemming from a person's startle reaction to a surprising noise—the present findings of acoustic-reflex paralysis and sensorineural hearing impairment are more likely to have been induced directly by the intense suction applied to the TM by the kiss. One can speculate that the kiss-induced suction pulled the TM laterally to the point of damaging the stapedial musculature mediating the acoustic middle ear reflex, and resulting in its paralysis. Had the negative EAM pressure disrupted the ossicular chain rather than its musculature, a conductive hearing loss would have obtained, as well as Type Ad tympanograms. Neither was the case.

A disrupted stapedial musculature may also account for the perception of middle ear flutter upon moving the head from side to side.

The importance of the findings in this case study is self evident and should be publicized widely. This report does not represent an isolated case; the damaging effects of forceful kisses to the ear have been observed before.6 The TM and its associated structures are as delicate as they are vital to one's sense of hearing. Permanent sensorineural hearing loss, tinnitus, hyperacusis, and aural muscle spasms can result from negative pressure applied directly to the TM by kissing on the pinna at the aperture of the EAM. In addition, the potential loss of the acoustic reflex can make the inner ear more vulnerable to the damaging effects of excessive noise exposure that a functioning reflex would normally attenuate. This has been amply demonstrated in cases of Bell's Palsy.7

Ear-kissing is generally thought of as an act of affection between adults. But young children also eagerly kiss the ears of their baby siblings and parents the ears of their new arrivals. Google has 1289 entries under “ear-kissing,” and even Shakespeare uses the term in King Lear.8 As the present case study reveals, ear-kissing can also have a negative side. If applied with force directly to the EAM, even a loving kiss can permanently injure the auditory mechanisms.

In her articles at Audiology Online, Carolyn Smaka named this syndrome “REKS” (Reiter's Ear Kiss Syndrome). Indeed, a misdirected kiss on the ear “wrecks” the ear of the recipient.

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REFERENCES

1. McFerran DJ, Baguley DM: Acoustic shock. J Laryngol Otol 2007;121:301–305.
2. Milhinch JC: Acoustic shock injury: Real or imaginary? At www.audiologyonline, 2002.
3. Patuzzi R, Milhinch J, Doyle L: Acute aural trauma in telephone headset and handset users. Presentation at the Neuro-otological Society of Australia Annual Conference, Melbourne, 2000.
4. Hood JD: Basic audiological requirements in neuro-otology. J Laryngol Otol 1969;83:695–711.
5. Jerger J: Hearing tests in otologic diagnosis. Asha 1962;4:139–145.
6. Ross M: Personal communication, 2008.
7. Zakrisson JE, Borg E: Stapedial reflex and auditory fatigue. Audiology 1974;13:231–235.
8. Shakespeare W: King Lear. Act II, Scene I. Gloucester's Castle.
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