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Case Study of a 5-Year-Old Boy with Unilateral Hearing Loss

Jan 15, 2015 | Pediatric Care | 0 |

Case Study | Pediatrics | January 2015 Hearing Review

A reminder of what our tests really say about the auditory system..

By Michael Zagarella, AuD

How many times have I heard— and said myself—that the OAE is not a hearing test? How many times have I thought to myself that, just because a child passes their newborn hearing screening test, it does not mean they have normal hearing? This case brought those two statements front and center.

A 5-year-old boy was referred to me for a hearing test because he did not pass a kindergarten screening test in his right ear. His parents reported that he said “Huh?” frequently, and more recently they noticed him turning his head when spoken to. He had passed his newborn hearing screening, and he had experienced a few ear infections that responded well to antibiotics. The parents mentioned a maternal aunt who is “nearly totally deaf” and wears binaural hearing aids.

Initial Test Results

Otoscopic examination showed a clear ear canal and a normal-appearing tympanic membrane on the right side. The left ear canal contained non-occluding wax.

Tympanograms were within normal limits bilaterally. Unfortunately, otoacoustic emissions (OAE) testing could not be completed because of an equipment malfunction.

Behavioral testing with SRTs was taken, and I typically start with the right ear. The child seemed bright and cooperative enough for routine testing. I obtained no response until 80 dB.

I switched to the left ear and he responded appropriately. This prompted me to walk into the test booth and check the equipment and wires; everything was plugged in and looked normal. I tried SRTs again with the same results, even reversing the earphones. Same results. When the behavioral tests were completed, the results indicated normal hearing in his left ear and a profound hearing loss in his right ear.

The child’s parents were informed of these results, and we scheduled him to return for a retest in order to confirm these findings.

Follow-up Test

One week later, the boy returned for a follow-up test. The otoscopic exam was the same: RE = normal; LE = non-occluding wax.

Tympanograms were within normal limits. I added acoustic reflexes, which were normal in his left ear (80-90 dB), and questionable in his right ear (105-115 dB).

DPOAEs were present in both ears. The right ear was reduced in amplitude compared with the left, but not what I would expect to see with a profound hearing loss (Figure 1).

I repeated the behavioral tests with the same results that I obtained the first time (Figure 2). Bone conduction scores were not obtained at this time because I felt I was reaching the limits of a 5-year-old, and the tympanograms were normal on two occasions.

Recommendation to Parents

After completing the tests, I explained auditory dyssynchrony to the parents, and told them that this is what their son appeared to have. Since they were people with resources, I advised them to make an appointment at Johns Hopkins to have this diagnosis confirmed by ABR.

Johns Hopkins Results

The initial appointment at Johns Hopkins was at the ENT clinic. According to the report from the parents, the physician reviewed my test results and said it was unlikely that they were valid. She suggested they repeat the entire test battery before proceeding with an ABR. All peripheral tests were repeated with exactly the same results that I had obtained. The ABR was scheduled and performed, yielding:

“Findings are consistent with normal hearing sensitivity in the left ear and a neural hearing loss in the right ear consistent with auditory dyssynchrony (auditory neuropathy). The normal hearing in the left ear is adequate for speech and language development at this time.”

Additional Follow-up

The boy’s mother was not completely satisfied with the diagnosis or explanation. After she arrived home and mulled things over, she called Johns Hopkins and asked if they could do an MRI. The ENT assured her that it probably would not show anything, but if it would allay her concerns (and since they had good insurance coverage), they would schedule the MRI.

Further reading: Vestibular Assessment in Infant Cochlear Implant Candidates

Figure 1. DPOAEs of 5-year-old boy.

Findings of MRI. Evaluation of the right inner ear structures demonstrated absence of the right cochlear nerve. The vestibular nerve is present but is small in caliber. The internal auditory canal is somewhat small in diameter. There is atresia versus severe stenosis of the cochlear nerve canal. The right modiolus is thickened. The cochlea has the normal amount of turns, and the vestibule semicircular canals appear normal.

The left inner ear structures, cranial nerves VII and VIII complex, and internal auditory canal are normal. Additional normal findings were also presented regarding sinuses, etc.

Key finding: The results were consistent with atresia versus severe stenosis of the right cochlear nerve canal and cochlear nerve and deficiency described above.

The Value of Relearning in Everyday Clinical Practice

Figure 2. Follow-up behavioral test of 5-year-old boy.

According to the MRI, the cochlea on the right side is normal—which would explain the present DPOAE results. The cochlear branch of the VIIIth Cranial Nerve is completely absent, which would explain the absent ABR result and the profound hearing loss by behavioral testing.

This case has certainly caused me to re-evaluate what I think and say about my test findings. How many times have I heard—and said myself!—that the OAE is not a hearing test? How many times have I thought to myself that, just because a child passes their newborn hear- ing screening test, it does not mean that they have normal hearing?

This case has surely brought those two statements front and center. In addition, what about auditory neuropathy? In about 40 years of testing, I had never seen a case that I was convinced was AN. Naturally, I was somewhat skeptical about this disorder: Is it real, or does it reside in the realm of the Yeti. (Personal note to Dr Chuck Berlin: I truly don’t doubt you, but I do like to see things for myself!)

Finally, this case only reinforces my trust in “mother’s intuition” and the value of deferring to the sensible requests of parents. If she had not felt uneasy about what she had been told at one of the most prestigious clinics in the country, the actual source of this problem would not have been discovered.

So what? Does any of this really make a difference? The bottom line is we have a 5-year-old boy with a unilateral profound hearing loss. How important is it that we know why he has that loss? From a purely clinical standpoint, I think that it is poignant because it brings home the importance of understanding what our tests really say about the hearing mechanism and auditory system (ie, is working or not working?).

And although it may not make a large difference in the boy’s current treatment plan, I do know that the boy’s mother is grateful for understanding the reason for her son’s hearing loss and that it’s at least possible the boy may benefit from this knowledge in the future.

Michael Zagarella, AuD, is an audiologist at RESA 8 Audiology Clinic in Martinsburg, WVa.

Correspondence can be addressed to HR or or Dr Zagarella at: [email protected]

Citation for this article: Zagarella M. Case study of a 5-year-old boy with unilateral hearing loss. Hearing Review . 2015;22(1):30-33.

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Noise Induced Hearing Loss: A Case Study from a Speech-Language Pathologist’s Perspective

Submitted: 14 September 2020 Reviewed: 01 February 2021 Published: 24 February 2021

DOI: 10.5772/intechopen.96332

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Hearing loss is very common in the United States and the most widespread disability in the U.S. Hearing loss is the third most chronic health condition in the U.S. Noise induced hearing loss (NIHL) results from damaging external noise. This injury leads to temporarily or permanently affecting sensitive inner ear structures (e.g., cochlea, organ of Corti, and hair cells). NIHL can result from a single high-level noise exposure or repeated exposures to excessively loud noises [i.e., typically 85 dBA or greater, (A weighted decibel)]. Damage to the inner ear can also result from aging (i.e., presbycusis). This case study documents the hearing loss of an otherwise healthy 21-year-old, male individual and his progressive moderate-to-severe sensorineural hearing loss over a period of 41 years. His history will be reported along with his perspective as a speech-language pathologist and speech scientist. The individual with hearing loss has adapted to wearing hearing aids over the last five years. Issues that have occurred affecting comprehension along with compensatory strategies that assisted listening and comprehension will be discussed.

Noise induced hearing loss
presbycusis
sensorineural hearing loss
compensatory strategies

Author Information

Alejandro brice *.

University of South Florida, Tampa, FL, USA

*Address all correspondence to: [email protected]

1. Introduction

Hearing loss is very common in the United States. It is the third most chronic health condition in the U.S. [ 1 ]. A common cause of hearing loss is noise induced hearing loss (NIHL). NIHL results from damaging external noise, typically short high intensity noise. Loud sounds overstimulate delicate cells, leading to the permanent injury or death of cochlear hair cells. The hair cells cannot regenerate and there is no current cure for cochlear hair cell restoration. Therefore, once the hair cells die, the hearing loss become permanent.

NIHL injury leads to temporarily or permanently affecting sensitive inner ear structures (e.g., cochlea, organ of Corti, and hair cells). NIHL can result from a single high-level noise exposure or repeated exposures to excessively loud noises [i.e., typically 85 dBA or greater, (A weighted decibel)]. Noise induced hearing loss (NIHL) is one of the primary causes for chronic hearing loss. In the United States, NIHL from occupational noise ranges from 16–24% [ 2 ]. Up to 7% of noise induced loss in Australia has been found to arise from occupational noise [ 3 ]. Zhou, Shi, Zhou, Hu, and Zhang [ 4 ] reported that the prevalence of NIHL in Hungary was 21.3%, with 30.2% was related to high frequency NIHL. Thus, NIHL occurs with regularity in many world societies.

NIHL can result from occupational noises and/or non-occupational noise (e.g., gun blast or loud music). A characteristic of NIHL is the classic V notch occurring around 4,000 Hz. The surrounding frequencies must be at minimum 10 Hz or less than the hearing level at 4,000 Hz [ 5 ]. Noise exposure hearing loss is likely to become permanent six months after noise exposure has ceased [ 4 ].

Cutietta, Klich, Royse, and Rainbolt [ 5 ] found that high school band teachers displayed greater degrees of hearing loss than non-music teachers. Hearing loss incidence among professional musicians has been found to be very high, i.e., musicians had 3.51 fold increase rate of NIHL than non-musicians [ 6 ]. Other high-risk professions included aviation related professionals, i.e., incidence among aviators was found to be higher for certain U.S. military branches than others. Sensorineural hearing loss (SNHL) was greater for those in the U.S. Army and Air Force than the Navy or Marines [ 7 ].

1.1 Other causes of hearing loss

Nishad, Gangadhara, Mithun, and Sequeira [ 8 ] found that 30.7% of newborn babies screened for otoacoustic emission (OAE) and brain stem-evoked response audiometry (BERA) were high risk for hearing loss. Of the babies tested for high risk, 3.6% showed left ear hearing loss; 5.2% showed right ear hearing loss; while, 6.8% showed bilateral hearing loss. Consequently, congenital hearing loss and noise induced hearing loss (NIHL) are both contributors to hearing loss world-wide. Other etiological causes of hearing loss may include head injuries. Sports accidents, work related traumas, and road accidents are among the leading causes of head trauma.

1.2 Head trauma and hearing loss

Since, the case study participant (AB) experienced repeated chronic traumatic encephalopathies (CTEs) via karate for a period of years, TBI and CTEs will be reviewed. Other types of injuries may result from sports injuries (i.e., traumatic brain injuries, repeated chronic traumatic encephalopathies). Many contact sports involve CTEs with its participants (e.g., karate, football, wrestling, basketball, etc.). Some non-contact sports may also involve head traumas, such as cycling.

It has been noted that auditory issues following mild traumatic brain injury (TBI) are common [ 9 ]. Hoover et al., [ 9 ] examined speech in noise comprehension following mild traumatic brain injury (MTBI). Measures included monaural word (WIN) tasks, sentence (QuickSIN) tasks, and binaural spatial release task. The MTBI and non-MTBI participants were matched on pure-tone thresholds, thus, measuring speech in background noise. Results indicated that a high number of individuals with MTBI experienced difficulties with speech-in-noise. Speech-in- noise difficulties were related to auditory and non-auditory factors. Spatial separation was found to be related to working memory and peripheral auditory factors.

Traumatic brain injuries and head traumas arising from concussions or repeated sub-concussive impacts have been shown to be intertwined much deeper than what was previously thought [ 10 ]. While, NIHL affects the cochlea, sub-concussive impacts affect how the brain perceives sound [ 9 ] and affects the brain’s ability to comprehend speech and sustain one’s auditory attention to task [ 10 , 11 ]. AB’s sub-concussive impacts over the period of six years may have had a more lasting impact on auditory processing [ 10 ], difficulties with speech in noise [ 9 ], and/or sustaining listening abilities over time [ 11 ] than the noise induced hearing loss.

Concussions can result in auditory processing deficits without noted hearing loss [ 11 ]. Children and adolescents who have sustained a concussion were compared to a control group (non-concussive orthopedic injuries). Thompson et al. [ 11 ] found that the children with concussion had difficulties with speech in noise and with sustaining attention on cognitively taxing auditory tasks. These auditory difficulties are compounded with the existing MTBIs.

Fluctuating hearing loss is most likely to occur within the first year of the trauma [ 3 ]. Reports of head trauma and SNHL have been minimal [ 10 ]. Studies investigating trauma and hearing loss have mostly looked at immediate and short-term effects and have not investigated long term and chronic effects. There is no consensus regarding the endpoint for sensorineural hearing loss, cognitive and language difficulties after head trauma [ 10 ]. However, it appears that 90% of individuals who suffered a TBI do not experience further deterioration of hearing following the trauma [ 10 ]. Further research into auditory processing, attention, speech-in-noise processing, and other cognitive and language difficulties following a TBI are still warranted.

1.3 Hearing loss and cognitive loss

The most common cognitive loss disorder that affects memory and disruption of executive functioning (planning, organizing, sequencing, abstracting) that also interferes with activities of daily living (ADLs) is Alzheimer’s dementia (AD) [ 12 ]. According to Livingston et al. and the 2017 Lancet Commission on Dementia Prevention [ 13 ], hearing impairment is one of nine modifiable risk factors associated with dementia. The other eight factors include hypertension, smoking, obesity, depression, physical inactivity, diabetes, low social contact (i.e., limiting conversation and mental processing of sounds), and less education. The National Institutes of Health (NIH) identifies social isolation (which can be perpetuated by a hearing loss) and hearing loss as a potentially modified dementia risk factor [ 14 ]. According to the 2017 Lancet Commission model [ 15 ] and their “new model of life-course risk factors”; hearing loss contributes the highest risk factor associated with dementia.

Hearing loss may contribute to dementia via social isolation and reduced opportunities for communication. However, hearing loss has been directly associated with neurodegeneration and cortical thinning in otherwise cognitively normal adults. Ha et al. [ 15 ]. They found that right ear hearing loss was associated with right superior temporal and left dorsolateral frontal areas. Neurodegeneration precedes dementia. Griffiths et al. [ 16 ] propose an important interaction occurs between auditory and cognitive processing in the medial temporal lobe and later dementia pathology.

Nadhimi and Llano [ 17 ] have found that hearing loss in animals produced cognitive decline. Specifically, Nadhimi and Llano stated that, “The data suggest that noise-exposure produces a toxic milieu in the hippocampus consisting of a spike in glucocorticoid levels, elevations of mediators of oxidative stress and excitotoxicity, which as a consequence induce cessation of neurogenesis, synaptic loss and tau hyper-phosphorylation” (p. 1). Acute noise exposure has also been shown to have detrimental effects on hippocampal physiology, particularly neurogenesis. Individuals with hearing loss may consequently experience dementia in later life. Further study in this area is needed.

1.4 Age related hearing loss

Age related hearing loss (ARHL, presbycusis) is a progressive and chronic impairment, that is often bilateral [ 17 ]. The prevalence of ARHL increases with age. ARHL, in and of itself, can lead to decreased health care. In addition, noise induced hearing loss (NIHL) and age-related hearing loss (ARHL) increase hearing thresholds over time [ 18 ]. Noise exposure creates a higher, combined burden on hearing loss. Grobler et al. [ 19 ] suggest that this combined hearing burden increases even if exposure to the excessive noise has stopped.

ARHL, in and of itself, leads to mild hearing loss in individuals over 60 years of age and moderate hearing loss in individuals over 72 years of age [ 20 ]. ARHL is a prevalent and chronic condition for individuals over 65 years of age. No international classification system takes into account frequencies above 4 kHz for ARHL [ 20 ]. ARHL accounts for 42% of hearing impairment for individuals from 60–69 years of age. This progressively increases until 85–90 years of age, at which time ARHL accounts for 100% of hearing loss issues [ 20 ].

2. Case study (AB)

This is a case study of a cognitively normal, male adult (AB) with a noise induced hearing loss (NIHL) from a young age (documented at 21 years of age). AB is a fluent Spanish-English speaker. Initial diagnoses pointed to two possible etiologies leading to sensorineural hearing loss: (a) a singular incident of shooting a loud firearm without ear protection; and/or (b) repeated sub-concussive impacts from karate over a period of six years (1973–1979) (diagnostic conversation with audiologist after an evaluation, Dr. Barbara Packer-Muti, 1992). Initial diagnosis at 21 years of age indicated a NIHL, bilateral, V notch hearing loss beginning at 1 K and progressing through 8 K. See Table 1 which illustrates the hearing loss with audiograms obtained for following ages of 21, 34, 42, 49, 45, and 57 years of age.

Patient’s audiograms over time.

AB’s hearing has deteriorated over time. It is difficult to ascertain his loss over 4 kHz completely to ARHL [ 19 ]. However, his losses over time are most likely due to the combined factors of ARHL and NIHL [ 19 ]. Consistently, his worse frequencies are in the 4 KHz to 8 KHz. His bilateral loss is more severe in his right ear; however, the left ear also shows significant loss in these same frequencies and with severity. AB at the time of the last evaluation was 57 years of age. Evidence of age related hearing loss is apparent across frequencies from 25o Hz to 4 kHz. AB’s hearing loss has progressed due to NIHL and age related hearing loss (ARHL) as illustrated by Figure 1 . Figure 1 shows contrasting audiograms obtained at 21 and 57 years of age.

Contrasting Audiograms Obtained at 21 and 57 Years of Age.

2.1 Career as a speech-language pathologist

AB had been a practicing speech-language pathologist for 32 years when the last audiogram was obtained. He started as a school-based speech-language pathologist, worked later in private practice, and then as a university faculty. AB’s research for the past 20 years has been in the area of speech perception, phonetics, and phonology. AB is a native Spanish speaker and has spoken English since 5 years of age and for over 52 years at the time of the last hearing evaluation in 2015.

AB has worked in a university environment (university faculty) for 30 years in speech-language pathology. His research after 10 years shifted towards phonology, phonetics, speech perception, and word identification among bilingual populations with and without disabilities/disorders. AB has been a member of his professional organization for over 30 years (i.e., the American Speech-Language-Hearing Association, ASHA). AB’s research has focused on issues of transference or interference between two languages in the areas of phonetics (study of sounds), phonology (study of how sounds form words), semantics (words and word relationships), syntax (sentence structure) and pragmatics (how language is used in social interaction) related to speech-language pathology and cognition. His clinical expertise relates to the appropriate assessment and treatment of Spanish-English speaking students and clients in the United States. Clinically, AB has worked with toddler, pre-school age children, school age children and adolescents, adults in acute care, adults in rehabilitation care, children and adults in home health care settings, and children and adults in out-patient care. AB has supervised graduate students in clinical settings. AB has worked with other professionals including audiologists, medical doctors, physical and occupational therapists, teachers, psychologists, counselors, parents, and family members. This clinical knowledge has facilitated AB’s own self-care hearing rehabilitation.

2.2 Speech intelligibility

Hearing deficits impacted AB’s hearing, perception, and identification of certain sounds in both Spanish and English. Sounds that have been affected have included high frequency sounds such as /p, t, k, g, h, f, s, ʃ, tʃ, θ, ð/. These sounds range from 500 Hz to 8 kHz and more specifically in the 2 to 4 kHz range.

Factors influencing speech intelligibility include loudness, distance from the speaker, pitch, unique features of consonants and vowels, and noise in the environment [ 21 ]. Sound levels (loudness) vary according to the speaker’s intensity as measured in decibels (dB). The difference between speaking and shouting may vary only by 20 dB [ 21 ]. The distance from the speaker will also affect the sound’s intensity. Hence, a speaker at 1 meter may produce an utterance at 55 dB, however, at 5 meters it will be heard at 45 dB [ 21 ]. Each speaker’s complex speech tone (pitch) or fundamental frequency (f0) lies in the range of 100–150 Hz for men; approximately 180–250 Hz for women; and, around 300 Hz for children (exact averages vary by researchers; however, the general trends are consistent). Consonants in English speech are above 500 Hz. The energy from vowels diminishes rapidly above 1 kHz. It is not possible to increase the sound levels of consonants as one can with vowels; hence, some aspects of speech cannot be changed with increased intensity or volume. With regard to speech frequencies, most speech sounds occur around 2 kHz with the range of sounds occurring from 125 Hz to 8 kHz [ 21 ].

Difficulty with perception of sounds initially occurred when AB was in his forties and later progressed as his hearing thresholds increased. When in quiet environments, AB was able to function and adequately perform his research duties and engage in most conversations with no noise or minimal noise. However, as his hearing loss increased, in research, AB relied on the perceptual judgments of others in ascertaining sound discrimination and differentiation (i.e., use of graduate students with normal hearing). Use of amplification for discriminating participant responses and the ability to play-back responses were helpful.

Conversationally, AB was able to engage in conversation in quiet and in minimal noise without difficulties. AB’s ability to discriminate sounds in noise became increasingly more difficult. Conversation in noisy environments were not possible. AB relied on visual cues, repetition, and understanding of topics to assist understanding. These strategies did not alleviate or generally improve understanding. AB’s spouse tired of having to repeat herself and others tired of AB’s miscommunications due to his hearing loss.

In his 50’s AB experienced more hearing loss difficulties in both professional and conversational environments. AB relied more on graduate assistants in his research environment for auditory discrimination of sounds. AB continued to use previously recorded speech stimuli that was created for his experiments, thus, not needing to create new stimuli (which would require intact hearing, speech perception, and speech discrimination abilities). AB discontinued child phonology studies which involve extensive sound discrimination. Hence, AB’s research was constricted by his hearing loss.

Conversationally, AB in his 50s withdrew more and had difficulty hearing and understanding others. Use of subtitles with movies became a regular feature. He consistently asked for conversation to be repeated. Even after several repetitions he still would not grasp the entire intent or message. He engaged more in attempts to read lips and to use word cues in the messages to guess at unclear words. AB’s frustration with communication increased as well as those around him.

2.3 Rehabilitation

Rehabilitation began when AB conceded to using amplification (i.e., hearing aids) when he was in his late 50’s. AB first attempted to make use of local government services in an attempt to obtain hearing aids (i.e., Health and Human Services). This attempt was not successful. Although, AB was ready to purchase hearing aids individually, the cost for bilateral, behind-the-ear (BTE) aids were prohibitive.

AB and his wife attended an international conference for speech-language pathologists and audiologists. It was at this conference that colleagues informed AB that the same hearing aids sold and used in the U.S. could be obtained for one half of the cost. AB’s hearing was tested when he was 57 and it was at this time that he purchased his first pair of behind-the-ear (BTE) hearing aids. Over the course of five years AB continued to use his BTE aids until the point where he wears the aids 100% of the time.

AB continues to use compensatory strategies to conserve existing hearing, to make use of amplification and existing technology, and modifies his environment to enhance listening skills. Hearing conservation strategies include: (a) education about hearing; (b) reducing exposure to loud noise; (c) using hearing protection in noisy environments; (d) using hearing amplification; and, (e) participating in routine hearing evaluations [ 22 ]. AB has studied hearing loss through his professional affiliation as a speech-language pathologist. AB uses hearing protection in extremely noisy environments (i.e., ear plugs or head phones). AB wears his hearing aids regularly, makes use of closed captioning when available, and smartphone use. His hearing aids are smartphone capable; thus, AB is able to adjust different listening levels within the app program. Conversationally, AB adjusts his distance to speakers (i.e., moves closer when appropriate); AB maintains eye contact and looks at the speaker to increase visual and vocal cues; AB attunes more to key words in deciphering ambiguous words; and, AB can adjust his hearing aids via his smartphone to better hear in noisy environments.

3. Conclusion

Noise induced hearing loss is a common disorder that has many health consequences [ 1 , 2 , 3 , 4 ]. NIHL has many health consequences ranging from auditory processing deficits, attention and cognitive loss to social isolation. Traumatic brain injury, hearing loss, and auditory processing deficits are interwoven. Individuals who experience TBI or CTEs will most likely experience trouble with speech in noise, trouble with taxing auditory tasks, and trouble overall with speech processing. Age related hearing loss (ARHL) affects most individuals after 60 years of age. A non-hearing-impaired individual at 60 years of age will experience a mild hearing loss. If a person experiences noise induced hearing loss at an early age; then combined with ARHL, the effects can be compounded.

AB’s speech in noise difficulties, resulting from his noise induced hearing loss (NIHL), were reduced through the use of hearing aids, use of aural rehabilitation strategies of paying attention to the speaker’s lips, limiting loud and noisy environments, and practicing proper hearing conservation. Strategies to address AB’s age related hearing loss (ARHL) consisted of wearing his hearing aids, noise conservation strategies, and scheduling regular audiological exams. It should be noted that some ARHL and NIHL strategies overlapping occurred.

AB is an adult male, currently 63 years of age. He was identified as having a noise induced hearing loss (NIHL) at 21 years of age. Over the course of 36 years, AB has documented his hearing loss with six hearing evaluations. AB’s loss is a bilateral, sensorineural, and a high frequency sloping loss. AB currently wears hearing aids and practices hearing conservation. His work is minimally impacted by his hearing loss since he began wearing his hearing aids five years ago. AB is able to engage more fully in activities of daily living, i.e., conversations with others. Hearing obstacles include difficulty with high frequency speech sounds, listening in noisy environments, and maintaining strict hearing conservation.

While, noise induced hearing loss is a chronic condition with no means for improvement; hearing conservation strategies become of utmost importance. Conservation strategies include education about hearing, reducing exposure to loud noise, use of hearing protection, use of hearing amplification and making sure that continual hearing evaluations occur.

Conflict of interest

The author declares no conflict of interest. The author has no financial interest, direct or indirect, in the subject matter or materials discussed in the manuscript.

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Open access
Published: 30 March 2023

Etiological analysis of patients with sudden sensorineural hearing loss: a prospective case–control study

Wen Xie 1 ,
Niki Karpeta 2 , 3 ,
Busheng Tong 4 ,
Jiali Liu 1 ,
Haisen Peng 1 ,
Chunhua Li 1 ,
Sten Hellstrom 2 , 3 ,
Yuehui Liu 1 &
Maoli Duan 2 , 3

Scientific Reports volume 13 , Article number: 5221 ( 2023 ) Cite this article

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Neurological disorders
Risk factors

Sudden sensorineural hearing loss (SSNHL) is a multifactorial emergency disease. Until now, the etiology of SSNHL is still unknown. Previous studies regarding the etiology of SSNHL are clinical studies depending on clinical data collection and analysis. Due to the insufficient sample size or various selective bias in clinical studies, the results of these studies may be inaccurate. This prospective case–control study aimed at exploring the possible etiology and risk factors of SSNHL. We enrolled 255 SSNHL patients and 255 sex-, age- and residence-matched non-SSNHL subjects in the control group. Our study shows that there was no significant difference in the prevalence of comorbidities including hypertension and diabetes, as well as the incidence of smoking and drinking habits between the case and control groups (P > 0.05). In addition, the peripheral blood white blood cell count, neutrophil count, platelet-to-lymphocyte ratio (PLR) and fibrinogen level of the case group were significantly higher than those in the control group (P < 0.05). These findings suggest smoking, drinking, hypertension and diabetes may not be related to the onset of SSNHL. However, hypercoagulable state and inner ear vascular microthrombosis related to an elevated fibrinogen level might be the risk factors of the disease. In addition, inflammation play an important role of SSNHL onset.

Trial Registration : Chinese Clinical Trial Registry. Registration number: ChiCTR2100048991.

Analysis of Clinical and Laboratory Findings of Idiopathic Sudden Sensorineural Hearing Loss

Wen Xie, Qingqing Dai, … Maoli Duan

Association between atherosclerosis, hearing recovery, and hearing in the healthy ear in idiopathic sudden sensorineural hearing loss: a retrospective chart analysis

Nobuyoshi Tsuzuki, Koichiro Wasano, … Hiroyuki Ozawa

Severe sudden sensorineural hearing loss related to risk of stroke and atherosclerosis

Nobuyoshi Tsuzuki, Koichiro Wasano, … Kaoru Ogawa

Introduction

Sudden sensorineural hearing loss (SSNHL) is a multifactorial emergency disease. Until now, the etiology of SSNHL is still unknown, resulting in the lack of specific treatment targeting for its etiology. Previous studies reported that microarteriosclerosis, microthrombosis, infection and immune factors may be the pathogenesis of SSNHL 1 , 2 . Some risk factors and diseases which may directly or indirectly lead to the cochlear hair cells damage and the ultrastructural changes can result in SSNHL.

The risk factors associated to SSNHL include psychological factors and living habits, such as depression, smoking and drinking 3 , 4 . The impairment of auditory recognition function in patients with depression may be related to the occurrence of SSNHL 4 . Smoking and drinking may lead to inner ear arteriosclerosis and microthrombus formation, which will affect the inner ear blood supply and thus cause SSNHL. On the other hand, no such association was found by some previous reports. For example, Nakashima et al. found that smoking and drinking habits had no significantly increase the risk of SSNHL 5 , in particular smoking did not seem to be a causative factor of SSNHL 6 , 7 .

In addition to lifestyle, other comorbidities, such as hypertension, diabetes and hyperlipidemia may also be risk factors of SSNHL. These findings are supported by some case–control studies, which showed that SSNHL patients had a higher likelihood of these diseases than non-SSNHL controls 2 , 5 , 8 , 9 , 10 . These finding has been supported by a large sample size case–control study, including 514 patients with SSNHL and 2570 controls 11 . Moreover, SSNHL patients with these cardiovascular risk factors had a worse prognosis 2 . The pathogenesis of SSNHL caused by hypertension, diabetes and hyperlipidemia is that these diseases tend to cause internal auditory arteriosclerosis and microthrombosis, resulting in the disturbance of inner ear microcirculation and degeneration and necrosis of hair cells. In addition, these diseases may lead to ultrastructural changes, lipid deposition and metabolic abnormalities of inner ear hair cells. Although evidence showing these comorbidities as potential risk factors for SSNHL has been demonstrated in many studies, some studies show different results. For example, Berjis et al. 12 found that compared with controls, SSNHL patients had a similar prevalence of hypertension and diabetes as healthy subjects. Rudack et al. 13 found that hypercholesterolemia was not a major risk factor for SSNHL in their case control study. Until now, there is no study of a large number of cases to evaluate whether patients with hypertension, diabetes and hyperlipidemia do indeed have an increased incidence of SSNHL.

The test results of SSNHL patients also provide clues for the etiology of SSNHL. Many previous studies have shown that, compared with healthy individuals of control groups, some laboratory test results of SSNHL patients were abnormal. These laboratory findings include changes in the coagulation system (such as increased plasma levels of fibrinogen, antithrombin and factor VIII, and deficiency of protein C or protein S), parameters of hemorheology (increased blood and plasma viscosity, erythrocyte aggregation index and erythrocyte filtration index), biomarkers of vascular endothelial cell function (decreased brachial artery flow mediated dilation, expression of endothelial progenitor cells and circulating adhesion molecules), oxidative stress response (increased oxygen free radicals), homocysteine and folate levels, inflammatory indexes [such as leukocyte count, neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR)] and autoimmune biomarkers (such as circulating immune complex, antinuclear antibody and complement 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 .

Although the possible etiology of SSNHL has been widely studied, its exact etiology is still unable to be confirmed. One obstacle for SSNHL etiological study is that it is difficulty to establish an animal model simulating SSNHL. Therefore, most studies of SSNHL are clinical studies depending on clinical data collection and analysis. Due to the insufficient sample size or various selective bias in clinical studies, the results of these studies may be inaccurate. In order to explore the possible etiology of SSNHL, we conducted a prospective case–control study, which included 255 SSNHL patients and 255 non-SSNHL patients matched by gender, age and residence. We investigate the possible etiology of SSNHL by comparing the comorbidity occurrence and laboratory test results of the SSNHL patients with control subjects.

Materials and method

This prospective study included 255 SSNHL patients and 255 controls consecutively hospitalized between June 2021 and December 2021 in the Second Affiliated Hospital of Nanchang University, a provincial tertiary referral hospital in southeast China. All the 255 SSNHL patients with complete medical record data were recruited in this study. The control groups were randomly selected from the non-SSNHL subjects consecutively hospitalized in our department at the same period. Each patient of the case group and control group was matched for age, sex, income, and the region where they lived.

Inclusion criteria

Case group inclusion criteria were as follows: patients suffered from SSNHL and the diagnostic criteria were based on the latest guidelines revised by the American Academy of Otolaryngology-Head and Neck Surgery in 2019. That is, patients had abrupt sensorineural hearing loss of more than 30 dB in three contiguous frequencies within 72 hours 22 . The control group consisted of 255 non-SSNHL patients, including 84 patients with epiglottic cyst, 122 patients with vocal cord polyp, 44 patients with deviated nasal septum and 5 patients with nasal vestibular cysts.

Exclusion criteria

Exclusion criteria of case group included following: patients with normal hearing or with hearing loss due to other causes, such as otitis media, Meniere's disease, otosclerosis, congenital deafness, presbycusis, vestibular schwannoma and inner ear malformation. Cases with insufficient medical data were also excluded.

The control group excluded criteria were as follows: patients with sudden sensorineural hearing impairment.

All patients in the case group and the control group combined with other diseases, which cause abnormal serum white blood cells, platelet counts and fibrinogen level, such as acute and chronic infectious diseases, bleeding and hematological diseases and malignant tumor.

The study was done in accordance with the ethical principles and approved by the Second Affiliated Hospital of Nanchang University Institutional Review Board. Written, informed consent was obtained from all patients and/or their guardians.

Test procedure

All patients underwent detailed clinical interview. Clinical data, demographic information, past medical history and personal history were obtained. All patients underwent routine physical examination, general otorhinolaryngological examination, nervous system physical examination, audiological examination and laboratory tests. Magnetic resonance imaging (MRI) was conducted in all SSNHL patients. The flow gram of this study is shown in Fig. 1 .

Flow diagram of the study.

Hearing evaluation

All patients’ hearing was evaluated with pure tone audiogram and tympanometry. All hearing tests were carried out by the same audiologist. Air and bone conduction were assessed at frequencies of 250 Hz, 500 Hz, 1 kHz, 2 kHz, 4 kHz, and 8 kHz. Pure tone average (PTA) was calculated as the mean of air conduction thresholds at 0.5, 1, 2, and 4 kHz 23 . The hearing loss levels were categorized into 5 grades: mild (26–40 dB HL), moderate (41–55 dB HL), moderate to severe (56–70 dB HL), severe (71–90 dB HL), and profound (> 90 dB HL) 24 . Audiogram patterns were classified into 5 types: ascending (the average threshold of 0.25–0.50 kHz was 20 dB higher than that of 4–8 kHz), descending (the average threshold of 4–8 kHz was 20 dB higher than that of 0.25–0.50 kHz), flat (all frequencies present similar thresholds and hearing threshold was below 80 dB HL), profound (all frequencies show similar threshold and hearing threshold was over 80 dB HL), and concave or convex type (average hearing degree of the mid-tone frequency was 20 dB higher than low and high frequencies) 25 .

Hematological evaluation and comorbidities

Hematological tests were carried out in all patients. In addition to routine blood tests and biochemical tests, the parameters analyzed in this study were fasting blood sugar, hemostasis determinations, and lipid profile. The reference values which were defined normal in our laboratory are listed in Table 1 .

Comorbidities including hypertension and diabetes mellitus were also assessed. Hypertension was defined as blood pressure ≥ 140/90 mmHg 26 or previous physician-diagnosed hypertension. DM was diagnosed according to the consensus of the expert committee on the diagnosis and classification of diabetes mellitus 27 , or diagnosed by internists and were treated with antidiabetic medications.

Statistical analysis

Categorical data were shown as percentages and compared using Chi square test. Fisher exact test was used when expected counts in Chi square test were insufficient. Ranked data conforming to normal distribution and homogeneity of variance were assessed through Student’s T test, and Mann–Whitney 2-sample test was used for data which were not normally distributed. To evaluate the risk factors of SSNHL, odds ratio (or) and 95% confidence interval (95% CI) was calculated by univariate and multivariate logistic regression analysis. All analyses were conducted using SPSS version 25 for Windows. All statistical tests were 2-sided, and statistically significant levels were set at 0.05 (P < 0.05).

Ethical approval

This study was approved by the Second Affiliated Hospital of Nanchang University Institutional Review Board. (reference number IIT-O-2021-002).

Clinical characteristics, comorbidities and laboratory test results

Table 2 shows the clinical characteristics, comorbidities and laboratory test results of the two groups of patients. The average age of the patients in both groups was 46 years (range 12–83 years). Of the 255 patients in each group, 124 were males (48.6%) and 131 were females (51.4%). In the case group, SSNHL affected unilateral ear in 245 patients, and bilateral ears in 10 patients. Of the 245 unilateral ears, there were 116 affected left ears and 129 right ears. The duration from onset to treatment ranged from 1 to 30 days, with an average of 8.07 days. Regarding the degree of hearing loss in 265 ears of 255 patients, the most common one is profound (26.4%) and mild hearing loss (26.4%), followed by severe hearing loss (18.5%) and moderate to severe hearing loss (16.6%), moderate hearing loss was relatively rare (12.1%) (Fig. 2 ). Regarding audiogram shape, as depicted in Fig. 3 , flat type hearing loss occurred in 131 ears (49.4%), pronounced hearing loss affected 75 ears (28.3%), followed by ascending (11.7%) and descending type (10.6%). The prevalence of comorbidity in the two groups was shown in Fig. 4 . In the case group, 53 patients (20.8%) had comorbidities with hypertension, and 20 patients (7.8%) suffered from diabetes. In the control group there were 45 cases (17.6%) with hypertension and 13 cases with diabetes mellitus (5.1%). There was no significant difference in the incidence of comorbidity between the two groups (P > 0.05).

The numbers of affected ears in different hearing lever group.

The numbers of affected ears in different audiogram type group.

The numbers of subjects with comorbidities in the case and control groups.

The personal history of smoking and drinking habits in the two groups are shown in Fig. 5 . In the case group, 28 patients (11%) had smoking habits and 21 patients (8.2%) had drinking habits. The percentage of subjects with smoking and drinking habits were 7.8% and 5.1%, respectively in the control group. There was no significant difference in the proportion of subjects with smoking and drinking history between the two groups (P > 0.05).

The numbers of subjects with smoking and drinking habits in the case and control groups.

The laboratory examination results showed that there was no significant difference in peripheral blood lymphocyte count, platelet count, platelet-to-lymphocyte ratio (PLR), cholesterol, triglyceride, high-density lipoprotein and low-density lipoprotein levels of the patients between the two groups (P > 0.05). In contrast, the peripheral blood leukocyte count, neutrophil count, NLR and fibrinogen levels of the patients in case group were significantly higher than those in control group (P < 0.05).

All 255 SSNHL patients’ MRI of ear had normal results. Regarding brain MRI results, 137 patients’ results were normal, but old slight ischemia was visualized in 118 patients, and 4 of them had mild brain atrophy. The 4 latter patients were over 70 years old.

Clinical characteristics, comorbidities, laboratory test and hearing results of SSNHL patients with different genders

We investigated the difference in terms of clinical characteristics, comorbidities, laboratory test and hearing results of male and female patients (Table 3 ). There was a significant difference in prevalence of hypertension and diabetes, proportions of patients with smoking and drinking habits, peripheral blood lymphocyte count, platelet count, PLR, fibrinogen, cholesterol, triglyceride and high-density lipoprotein between the male and female SSNHL patients (P < 0.05). Notably, the prevalence of hypertension in female patients was higher than in male patients, whereas the diabetes prevalence was lower in female patients. Additionally, almost all patients with smoking or drinking habits were males.

Analysis of possible risk factors of SSNHL

Univariate and multivariate logistic regression analysis were used to evaluate the strength of association between hypothesized risk factors and the likelihood of SSNHL (Tables 4 , 5 ). The results showed that hypertension, diabetes and hyperlipidemia, and smoking or drinking habits were not be associated with SSNHL.

The results of our prospective case–control study on sudden sensorineural hearing loss neither showed any significant relation to comorbidities by hypertension or diabetes or hyperlipidemia nor to living habits as smoking and drinking habits. This is in agreement with previous studies conducted by Nakashima et al. 5 and Mosnier et al. 6 but contrasts to other studies by Passamonti 28 and Lin et al. 3 , of which the latter was a systematic review and meta-analysis study. Lin et al. reported that smoking was risk factor of SSNHL, but this finding was discordant with the result of systematic review and meta-analysis conducted by Saba et al. 29 . The size of the cohort and the population-based data set in various studies could account for the controversial results. Another reason of this discrepancy regarding our study is that there was low proportion of smoking and drinking patients in both the case and control groups in our study, which may result in no significant difference in statistical values although there is a somewhat higher incidence in the case group than control group.

Our study did not show that significant difference exists in the prevalence of hypertension, diabetes and hyperlipidemia between SSNHL patients and controls. Furthermore, the difference in OR value is not statistically significant between the patients of the two groups, suggesting that hypertension, diabetes and hyperlipidemia is not related to the onset of SSNHL. Our previous retrospective study also supports this conclusion, which found that the prevalence of hypertension and diabetes in SSNHL patients was not higher than in the local population 30 . Hyperlipidemia, as a risk factor of SSNHL, has been reported by two systematic review and Meta-Analysis 29 , 31 . Regarding the prevalence of hypertension and diabetes in SSNHL patients, he results of these two studies are inconsistent. Saba et al. found SSNHL patients had high risk of hypertension and diabetes 29 , but Simões et al. reached different conclusion after pooled analysis of adjusted ORs 31 . Our finding is also inconsistent with that of previous studies 2 , 5 , 8 , 9 and except differences in sample size and population one possible explanation of this discordant result could be that the enrolled subjects in our control group were non-SSNHL patients rather than healthy people.

As mentioned before, vascular factors and thrombosis may be an important cause of SSNHL, and the increase of blood viscosity and hypercoagulable state of blood may contribute to microthrombosis. In agreement with previous studies 32 , 33 , our study showed that the serum fibrinogen level of SSNHL patients was higher than that of the controls. Moreover, another case–control study obtained similar results, but there was no significant difference in the levels of triglycerides, low-density lipoprotein and high-density lipoprotein between SSNHL patients and controls 13 . Although most studies have confirmed that hyperfibrinogenaemia may lead to SSNHL, previous works conducted by Passamonti et al. did not support this hypothesis 28 . His study enrolled 118 SSNHL patients and 415 controls and found that the levels of serum VIII and homocysteine increased, and antithrombin protein C decreased in SSNHL patients, but no significant difference existed in fibrinogen level between subjects in the two groups. In our study, we found that hyperfibrinogenaemia may be a risk factor for SSNHL, due to a mechanism that an elevated fibrinogen level may increase the risk of microthrombosis. As we all know, plasma viscosity mainly depends on the amount of fibrinogen, which is the most abundant plasma protein. It is an indicator of hypercoagulability and hypofibrinolysis, and is the premise for thrombosis. The fibrinogen content in SSNHL patients is higher than that in controls, suggesting that hypercoagulability is more common in SSNHL patients. This in line with the Chinese guidelines for the diagnosis and treatment of SSNHL revised in 2015 that pointed out that a disturbed inner ear embolism or thrombosis may be the pathogenesis of profound SSNHL 25 . Most SSNHL patients referred to our hospital which suffered from severe to profound hearing loss, also had an elevated fibrinogen level which supports this hypothesis.

In addition to regulate coagulation, fibrinogen is a product and potent driver of inflammation. On one hand, higher plasma fibrinogen can be caused by acute inflammation, in which inflammatory cytokines can stimulate increased hepatic expression of fibrinogen. On the other hand, fibrinogen are key functional factors in mediating inflammatory response. Firstly, fibrinogen can promote leukocyte to migrate out of the vascular system by acting as a bridging molecule to promote intercellular adhesion, as it is a ligand for many cell surface receptors expressed by leukocytes endothelial cells and other types of cells 34 . Secondly, fibrinogen can profoundly change leukocyte function by changing cell movement, phagocytosis, NF-B–mediated transcription, production of chemokines and cytokines degranulation 35 , 36 , 37 , 38 . Collectively, the elevated plasma fibrinogen among SSNHL patients indicate that SSNHL is both an inflammation-driven coagulation disease and coagulation-driven inflammation disease.

Another important finding in our study to confirm the role of inflammation in SSNHL is that the peripheral blood leukocyte count, neutrophil count and NLR of patients in the case group are higher than those of the control group. This is in accordance with other case–control studies. Thus, Seo et al. 18 revealed that the NLR and PLR of SSNHL patients were higher than those of the control group. In addition, they found that the NLR of the unrecovered patients was significantly higher than the recovered patients. Therefore, they concluded that NLR was a reliable predictor for the prognosis of SSNHL. Similar results have also been reported by Ulu et al. 39 , Qiao et al. 40 and Masuda et al. 41 . They found that the NLR and PLR of the case group were higher than those of the control group. Additionally, Ulu documented that the systemic immune inflammation index of the case group was also higher among SSNHL patients. The results of a meta-analysis also supported this finding and also showed that NLR is a prognostic biomarker of SSNHL 42 . It is widely accepted that that peripheral leukocyte count is an indicator of inflammatory reaction and elevated NLR reflects the active inflammatory activities as well. These findings suggest that inflammation is involved in the pathogenesis of SSNHL. Previous studies have also demonstrated that NLR is a marker of other peripheral vascular afflictions than atherosclerosis and arterial thrombosis, such as acute coronary syndrome, heart failure and end-stage renal disease. Some scholars believed that the increase of these inflammatory indicators will support the theory that systemic stress activates inflammatory reaction, resulting in endothelial function damage, which leads to atherosclerosis and ischemic events of inner ear. This process is characterized by the increase of NLR and PLR 18 . Patients with higher values of inflammatory indexes also had a poor prognosis, indicating that patients with severe endothelial cell damage had worse treatment effects 18 , 40 , 41 . This finding also confirms the effectiveness of glucocorticoids in SSNHL treatment by inhibiting inflammatory response, which is also unanimously supported by SSNHL treatment guidelines in various countries.

Our finding is in agreement with those of previous studies reporting that inner ear microcirculation disorder, arteriosclerosis, arterial thrombosis or embolism and immune factors may be the main causes of SSNHL. However, the etiology of most SSNHL patients is still unclear, further studies will be needed to explore the etiology of SSNHL.

Strengths and limitations of this study

The primary strength of our study is that it is a prospective case–control study with a large sample size. In addition to analyzing the possible risk factors of SSNHL. Moreover, we explored the clinical characteristics, comorbidities, laboratory test results and imaging examination results of SSNHL patients. We investigated the difference in terms of clinical characteristics, comorbidities, laboratory test and hearing results of male and female patients. which can provide useful information for the readers in the field.

This study had some limitations. Firstly, the subjects enrolled in control group enrolled were non-SSNHL patients instead of healthy individuals, which may affect the accuracy of the study results. Secondly, there may existed some self-report bias regarding the personal history collection process, since participants may conceal their smoking or drinking habits due to people’s negative attitude towards these living habits in China. We found that the self-reported proportion of patients with smoking and drinking was very low both in case and control group.

Conclusions

Our prospective case–control study on SSNHL did not demonstrate any comorbidities with hypertension, diabetes or hyperlipidemia. Neither could any relation to living habits like drinking and smoking be shown.

Interestingly our study demonstrated an increased level of serum fibrinogen among SSNHL patients which suggests that a hypercoagulable state and an inner ear vascular microthrombosis might be the risk factors of the disease. This is also supported by the fact that the elevated peripheral blood white blood cell count, neutrophil count, and NLR in SSNHL indicate that inflammation plays an important role of SSNHL onset.

Data availability

After publication of the primary and secondary analyses detailed in the individual deidentified patient data, including a data dictionary, will be made available via our data sharing website indefinitely (web site link: https://mrhuajian.github.io/index.html ) or from the corresponding author on reasonable request.

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Acknowledgements

We thank the assistance provided by Xiong Wenping for collecting the participant data for this study. We thank all participants for their contributions.

Open access funding provided by Karolinska Institute. This study was funded by the Science and Technology Department of Jiangxi Province Programme (project No 20202BBGL73017), but the Science and Technology Department of Jiangxi Province had no role in the design, conduct, analysis, interpretation, or writing up of the results.

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Wen Xie, Jiali Liu, Haisen Peng, Chunhua Li & Yuehui Liu

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Niki Karpeta, Sten Hellstrom & Maoli Duan

Department of Otolaryngology Head and Neck and Audiology and Neurotology, Karolinska University Hospital, 171 76, Stockholm, Sweden

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W.X., Y.L. and M.D. designed the study. W.X., J.L., H.P. and C.L. collected the data. N.K. and B.T. analysed the data. W.X. wrote the first draft of the manuscript. S.H. and M.D. revised the manuscript. Y.L. and M.D. are equal contributors to this work and designated as co-corresponding authors.

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Xie, W., Karpeta, N., Tong, B. et al. Etiological analysis of patients with sudden sensorineural hearing loss: a prospective case–control study. Sci Rep 13 , 5221 (2023). https://doi.org/10.1038/s41598-023-32085-7

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DOI : https://doi.org/10.1038/s41598-023-32085-7

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Case studies of adults with central auditory processing disorder: Shifting the spotlight!

Chyrisse heine.

1 Department of Community and Clinical Allied Health, College of Science, Health and Engineering, La Trobe University, Melbourne, VIC, Australia

Michelle Slone

2 The School of Psychological Sciences, Faculty of Social Sciences, Tel Aviv University, Tel Aviv, Israel

Vast literature exists detailing the identification and management of central auditory processing disorder in children: however, less information is available regarding central auditory processing disorder in the adult population. This study aimed to document the diagnostic and management procedure for adults presenting at a multidisciplinary clinic due to concerns regarding their listening and central auditory processing skills. This retrospective study was a case file audit of two adults (a male, aged 37 years and a female, aged 44 years) who presented at a multidisciplinary (audiology and speech pathology) clinic for a hearing and central auditory processing evaluation. Both participants completed a case history questionnaire and were then interviewed with results being documented in their file. Participants were evaluated by a dually qualified audiologist-speech pathologist on a battery of peripheral hearing tests (including pure-tone threshold audiometry, immittance measures and speech tests), central auditory processing assessments (including monaural low redundancy, dichotic listening and temporal processing tests) and evaluation of short-term auditory memory skills. Participants were self-referred, never having been assessed previously for central auditory processing disorder, yet had perceived heightened difficulty with processing information; having conversations (particularly in noisy work or social environments) and remembering information, resulting in a range of psychosocial responses. Following diagnosis of central auditory processing disorder, participants undertook an individualized short-term aural rehabilitation program as dictated by their needs and preferences. Post-program participants perceived better ability to listen and process information even in adverse listening conditions. They reported that their newly learned skills improved their work abilities and social participation leading to positive outcomes. Medical and other allied health professionals should consider the possibility of presentation of central auditory processing disorder in adulthood and make appropriate referrals for central auditory processing testing to facilitate diagnosis and appropriate intervention. Aural rehabilitation should be considered for adults newly diagnosed with central auditory processing disorder.

Introduction

Central auditory processes (CAP) are the auditory mechanisms responsible for sound localization and lateralization, auditory discrimination, auditory pattern recognition, temporal aspects of audition (including temporal resolution, temporal masking, temporal integration and temporal ordering) and auditory performance with competing or degraded acoustic signals. 1 Accordingly, deficits in any of these functions lead to inadequate processing of auditory information. Central auditory processing disorder (CAPD) is a deficit in the processing of auditory-presented information despite usually normal pure-tone hearing thresholds.

CAPD is a topical area frequently discussed in reference to children and less frequently discussed in relation to adults, particularly in regard to assessment, diagnosis, treatment and management. CAPD in children is characterized by listening and/or processing difficulties, usually with no other medical conditions such as stroke, traumatic brain injury or temporal lobe tumors. Among children, behavioral characteristics associated with CAPD include difficulty comprehending speech in competing or reverberant environments, frequent requests for repetition of information, misunderstanding messages, inconsistent or inappropriate responses, delays in response to oral communication, difficulty following complex auditory directions, difficulty with sound localization, inattentiveness and distractibility and literacy difficulties. 1 Furthermore, children suspected of suffering from CAPD are often reported as being intolerant to loud noise, are frequently distracted by background noise and have difficulty following instructions. 2 These symptoms are not exclusive to CAPD and diagnostic audiological testing is undertaken to confirm the diagnosis of CAPD.

According to the American Academy of Audiology (AAA) 3 and the European Perspective on Auditory Processing Disorder, 4 the behavioral manifestations and symptoms reported and/or observed during interviewing or observation of patients (both children and adults) suspected of having CAPD may include difficulty with understanding speech in competing background noise or reverberant environments, localizing to sound sources, hearing on the phone, following rapid speech, following directions, detecting subtle changes in prosody, learning a foreign language or novel speech materials, maintaining attention, musical ability, literacy and learning. Further behavioral manifestations include seeking visual or facial cues to aid understanding, frequently requesting repetition or rephrasing, responding inconsistently or inadequately, having hyperacusis and being easily distracted.

Research on test performance in young and middle-aged adults is surprisingly less common than the literature on children, especially since many original tests of central auditory processing were developed based on adult samples, for example, the pitch and duration pattern tests developed by Musiek. 5 , 6 Since the pure-tone audiogram provides no information about CAP, specific CAP tests should be used to provide diagnostic and rehabilitative information. 7 Neijenhuis 8 evaluated and developed a test battery for use with adult populations and concluded that, although more research is needed to refine test batteries for use on specific populations, the developed battery is of clinical value.

In general, adult-based research has identified CAPD as a “hidden hearing loss” characterized by difficulty with listening or recognizing speech in the presence of noise despite normal pure-tone thresholds. 9 The association between CAP (particularly temporal processing) and literacy deficits in adults has also been explored. Hari and Kiesila 10 evaluated 10 dyslexic adults and 20 control subjects using a series of binaural clicks, with an auditory processing deficit defined as difficulty processing rapid sound sequences. Results suggested that dyslexic adults displayed difficulty processing rapid sound sequences, which was manifested as a significant delay in their conscious auditory perceptions and continued throughout their lifetime. Ahissar et al. 11 also investigated the association between CAP abilities and reading skills. In this study, 102 adults were assessed on a battery of psychoacoustic measures and standard measures of reading and spelling. Results suggested that an association exists between CAP skills and reading. In particular, poor readers had difficulty with tasks that required spectral distinctions, such as frequency discrimination.

CAPD may occur subsequent to or comorbid with other primary conditions, for example, after stroke, 12 following traumatic brain injury 13 or comorbid with cognitive deficits such as Alzheimer’s disease. 14 To distinguish between multiple conditions with similar symptoms, a comprehensive, multidisciplinary assessment is required. 15

In aging adults, difficulty associated with listening in compromised environments, such as situations in which there is background noise, is commonly associated with peripheral hearing loss but may also be reflective of CAPD in this population. 16 In particular, aging adults experience difficulty with speech perception (particularly speech-in-noise) and discrimination. 17 , 18 In a sample of 2015 adults aged 55 years and older, Golding 19 concluded that the detection of CAP abnormality for average older adults increased with age (binaural abnormality was detected in 27.3% of participants aged 64 years and lower; 44.3% of participant aged 65–74 years and 69.0% of participants aged 75 years and above), with men more likely to have a higher number of abnormal CAP test outcomes than women. The probability of demonstrating CAP abnormality increased with accompanying cognitive decline or increased hearing impairment. According to Atcherson et al., 20 structural and functional central nervous system changes occur with advancing age and contribute to the processing of auditory information but are also influenced by hearing loss and cognitive decline. Cognitive aging research highlights that aging is associated with reduced sensory and mental processing speed and a reduction in cognitive skills (reduced working memory and attention), which affects listening. 21 Furthermore, in a study examining central aspects of perception (temporal resolution and speech recognition in noise) and the role of attention (gap detection) in a group of 18 adults diagnosed with mild cognitive impairment and age-matched controls, Iliadou et al. 22 found that the group with mild cognitive impairment performed significantly poorer than the control group on the speech recognition in noise task as well as the gap detection task (particularly in the right ear which although must be interpreted with caution, may be linked to a left hemisphere auditory processing deficit). These authors further concluded that auditory temporal processing tests might be useful in the early diagnosis of mild cognitive impairment.

In regard to management, Whitelaw 23 exposed the myth that since there is no cure for CAPD in adults, there is no value in assessing their CAP skills or in providing adults with management. Whitelaw 23 further highlights that the auditory system remains plastic for a long period of time and that offering intervention to adults with CAPD is viable. While numerous child-focused management approaches have been developed, only few have been trialed on adults, despite the notion that most people with CAPD will potentially live with these disorders throughout their lives. 24 , 25

According to Bellis et al., 26 auditory interventions aim at improving auditory deficits identified by valid tests of auditory function in a targeted, deficit-specific manner. Bellis 27 suggested the inclusion of environmental modifications, remediation activities and compensatory strategies in remediation interventions. Both bottom-up and top-down interventions have commonly been used in the management of CAPD which may be particularly applicable if CAPD is viewed as a spectrum disorder. 28 More specifically, interventions described in the CAPD literature have included the use of assistive listening devices (e.g., frequency modulated or remote microphone listening systems as used by Koohi et al. 12 with stroke patients with CAPD), phonemic training program, 29 dichotic interaural intensity difference training, 30 metalinguistic approaches 31 or computer programs such as Earobics (by Compu.Ed.), 32 LACE, 33 ARIA, 34 BrainHQ exercises (e.g., results of the IMPACT study 35 found that using Brain HQ exercises for 40 h led to an average increase in auditory processing speed of 135%) and the ReadMyQuips Speech Comprehension Training System (developed by Levitt, 36 who found that following the use of this program, individuals with mild to moderate hearing loss were able to improve their speech comprehension by around 30%). Some of these intervention examples have primarily been used with children who have CAPD, with only few programs (e.g., LACE) specifically containing materials applicable to adults. It is thus important to investigate the assessment and management of young adults who present for the first time in adulthood with symptoms suggestive of CAPD.

The aim of this retrospective study was to document the diagnostic outcomes and management process for two adults presenting at a multidisciplinary audiology and speech pathology clinic due to concerns regarding their listening and CAP abilities.

Case section

This retrospective study was a case file audit of two adults (Cases A and B) who presented at a multidisciplinary (audiology and speech pathology) clinic for a hearing and CAP evaluation. These adults (out of a total of four adults with CAPD seen in a 6-month period) were specifically selected for this audit, since they both participated in intervention post diagnosis of CAPD. One participant was 37-year-old man, working in an administration office servicing international students. The other participant was a 44-year-old woman and was the owner of a retail shop in a busy shopping precinct that attracts local and international shoppers. Both participants lived (with their respective partners) in metropolitan Melbourne and were English speaking. They both provided written informed consent allowing their information to be used for research purposes as long as anonymity was upheld.

The following procedure was followed for the diagnostic evaluation:

Participants completed a short, generic questionnaire that enquired about their demographic information, referral information (referrer and concern leading to the referral), work history, education, medical history and family history of hearing, CAP or learning difficulty. The final part of the questionnaire covered 10 questions devoted to hearing, listening and communication. Nine questions required a rating on a 3-point Likert-type scale (1 = no difficulty; 2 = some difficulty and 3 = lots of difficulty), while one question was an open-ended question enquiring about the top three situations that participants perceived as the most difficult and which were important for them to improve.
Participants were interviewed and further details regarding their completed case history form and social-communication functioning were discussed and results were documented.
Participants were evaluated by a dually qualified audiologist-speech pathologist using the following test battery:
Peripheral hearing tests (including pure-tone threshold audiometry, immittance measures and speech audiometry using the AB word list developed by the National Acoustic Laboratory).
CAP assessment—the test battery was derived in accordance with AAA 3 and specific tests were selected for use with these participants. Tests were as follows: monaural low-redundancy speech tests to evaluate auditory figure-ground, discrimination and auditory closure ((1) Speech-in-noise test using the AB word list with monaural speech noise and (2) The Time compressed Speech Test), 37 dichotic listening tests to evaluate binaural integration ((1) the Macquarie Staggered Spondaic Word Test 29 , 38 and (2) Dichotic Digits Test 5 ) and test of temporal patterning to evaluate auditory patterning and sequencing (Pitch Pattern Test 6 , 39 ). All stimuli were presented at suprathreshold level at 60 dBHL. A diagnosis of CAPD was made on the basis of ‒2SD on any one test or ‒1SD on two or more tests. 1
Short-term auditory memory (STAM) testing using the digits forwards and backwards (working memory) subtests of the Test of Memory and Learning. 40 Working memory is the ability to follow, retain and integrate auditory-presented information and is a primary component of speech perception. 41 Hence a measure of working memory was included in the test battery.

Comparison between pure-tone hearing threshold tests, middle ear functioning and CAP test performance against normative data led to a diagnosis of CAPD.

Following diagnosis, the following intervention procedure was adopted.

Adults participated in 60-min individualized intervention sessions over consecutive weeks (Adult A participated in two sessions and Adult B participated in four sessions). Management sessions were individualized to suit each participant’s preferences and determined by factors such as restricted time off work and financial constraints rather than dictated by the clinician as to how many sessions they should attend. The intervention sessions were client-centered and tailored to individual client’s needs. 42 Post-program results were obtained via interview and documented in their file.

Analysis of participant’s case histories and interviews ( Table 1 ) revealed that both participants were self-referred, never having been assessed previously for CAP due to their essentially non-eventful school and work career. Participants both had recently perceived heightened difficulty with processing information; having conversations (particularly in noisy work or social environments) and remembering information. Participants reported that these difficulties had resulted in a range of psychosocial responses (including low confidence and depression), leading them to talk to their General Physician and seek a CAP assessment. For further details refer Table 1 .

Case history and interview information.

Case A reported a significant case history (when younger) of ear problems (detached earlobe), for which he sought medical attention (ear surgery) and additionally reported a positive history of noise exposure (gun fire when he was in the military at age 18 for 2 years). Case B did not report any history of ear problems. For both participants, no congenital abnormalities were reported and no further significant medical history was experienced. In regard to psychological status, both participants reported decreased psychological well-being including responses such as depression, embarrassment, anxiety and lack of confidence. Case A reported frequently feeling fatigued and experienced headaches.

These negative reactions were reinforced by participants’ self-reports. Results of the “Hearing Difficulty” sections of the case history suggested similar results for both participants, in that, neither had difficulty in quiet conditions, hearing family members, hearing the phone ringing from another room or hearing environmental sounds such as a car horn. Both participants reported some difficulty with hearing strangers speak and lots of difficulty with listening in noisy conditions and in group situations. In addition, Case A reported some difficulty with meetings while Case B reported a lot of difficulty with meetings and using the telephone. The three situations Case A identified as the most difficult and the most important for improvement included; participating in group activities, communication and listening effectively at work and being able to participate at a party or social activity. The three situations Case B identified as the most difficult and the most important for improvement included: hearing on the phone, controlling a noisy workplace so that listening and communication is easier and understanding accents.

On pure-tone audiometric testing, it was evident that Case A had normal hearing in the right ear (Pure-Tone Average of 5 dB) until 8000 Hz with a mild high-frequency dip at 8000 Hz (possibly attributed to previous noise exposure). Case A had normal hearing in the left ear (pure-tone average of 5 dB). Case B had normal hearing bilaterally (pure-tone average of 20 dB right ear and 15 dB left ear). Both participants had normal middle-ear functioning bilaterally on acoustic immittance testing and high accuracy on speech discrimination testing in quiet conditions (Case A = 94% right ear and 97% left ear; Case B = 97% accuracy bilaterally). On CAP and STAM testing, some difficulties were identified. See Table 2 for participant’s test profiles.

Diagnostic test results, intervention targets and post-training outcomes.

WNL; within normal limits; TCST: Time Compressed Speech Test; MSSW: Macquarie Synthetic Sentence Test; DDT: Dichotic Digits Test; STAM: short-term auditory memory; TOMAL: Test of Memory and Learning; DF: digits forwards; DB: digits backwards.

As can be seen from Table 2 , both participants experienced difficulty with speech processing in conditions with low redundancy (Time Compressed Speech), dichotic listening and STAM. Case B also experienced difficulty with speech-in-noise (auditory figure-ground).

In regard to intervention, in addition to the one-on-one session with the dually qualified audiologist-speech pathologist, guidance materials were provided suggesting home and work strategies for promoting effective listening and communication, acoustic noise control, use of technology (e.g., a recording pen or voice to text teletext) and STAM. Participants were cooperative and motivated to participate in all intervention activities. In particular, intervention focused on the following: speech discrimination, auditory figure-ground (for case B only), auditory closure, dichotic listening, STAM strategy training and conversational management. More specifically, the management program consisted of exercises to improve listening, such as the landmark auditory tracking technique according to De Filippo and Scott; 43 using speech stimuli in the presence of either or both four talker babble background noise and/or reverberant modified babble noise presented binaurally, speech discrimination training (repetition of syllables and minimal pairs) as per Sloan’s technique; 44 exercises targeting auditory closure as per Heine; 45 dichotic listening (using the Dichotic Interaural Intensity Difference training procedure) as per Musiek et al. 46 as well as targeting directed attention using speech stimuli monaurally and four talker babble background noise in the opposite ear; STAM training using strategies such as repetition, chunking, association, visualization and mnemonic training as per Baddeley, 47 McNamara and Scott 48 and Bell; 49 and communication training, which is frequently used with adults with hearing loss or dual sensory loss. 50 Communication training included strategies to address environmental, speaker–listener variables and the content of the conversation. For example, developing a listener difficulty hierarchy and problem solving of how each step of the hierarchy could be managed using communication training techniques. The Listening now! program 45 covers many of the above areas and was used as a resource. For further details refer Table 2 .

In post-training interviews, both participants reported significant improvements in deficit areas post-intervention. Case A made changes to his home and work environment (e.g., using topic maintenance and communication repair strategies at home, and introducing the use of headphones to control noise and acoustic modifications for noise control at work) and enrolled at University to pursue a higher degree. This participant also reported less fatigue, greatly improved communication skills (use of clarification strategies to repair conversational breakdown) and communication confidence, particularly at work. Case A also reported better directed attention to speakers and less distraction when multiple speakers were speaking. Case B reported having improved conversational and STAM skills (necessary for ordering stock in her retail shop and serving customers) and better speech discrimination and listening skills in general (including when there was high background noise). Case B made acoustical changes in her work environment (made a quiet listening corner using her retail stock as a barrier), structured more off-site meetings in quiet conditions, sought out a quieter environment for telephone conversations, introduced the use of teletext, used earplugs to control noise, proactively took rest breaks when fatigued and used communication strategies more effectively (e.g., she used assertive listening strategies, ensured topic maintenance, increased her use of clarification requests and asked for specific clarification when a conversation broke down). In addition, Case B reported increased self-esteem manifested as improved confidence at work.

The present compilation of case studies presents important evidence for CAP difficulties experienced by young adults. Interestingly, the two adults in this study only sought help for their listening and CAP difficulties in adulthood. Possible explanations for this late referral and subsequent diagnosis may be that 20–30 years ago, CAPD was not topical and diagnostic, and rehabilitation services were not as readily available, particularly in the absence of a peripheral hearing loss. Limited knowledge of CAPD may have restricted identification and referral for assessment. It is also plausible that these adults showed mild symptoms of listening and processing difficulty as children and were not overly debilitated and thus professional assistance was only sought when their listening difficulties, work environment and emotional state exacerbated. Research has shown that educators are the primary referrers for CAP assessments, while self-referral or families refer less often. 51 Since the participants in this study were no longer in an educational setting, it is possible that their difficulties were subtle (not due to noticeable peripheral hearing loss for example) and may not have been easily identified by themselves or their family.

The positive value of questionnaires has been identified by Bamiou et al. 52 and by us, the “Hearing Difficulty” questionnaire substantiated information obtained via the case history, allowed for measurement of participant’s perceived hearing, listening and communication difficulty and allowed for identification of participant’s perceived area of deficit requiring change (goals for intervention).

Both participants in this study were diagnosed with CAPD. However, they did not have the identical auditory test profile or difficulty with all the CAP assessments in the test battery. The importance of identification of sub-skills under the CAPD category is that a client-focused approach is necessary to address each individual’s strengths and weaknesses and to plan intervention goals that are specific to each individual’s needs.

In regard to each participant’s aural rehabilitation management program, a client-centered approach was used. A client-centered approach “actively involves the client in every decision concerning treatment” including consideration of the client’s expressed social and psychological needs. 42 Based on the participant’s descriptions of their work and home environment, as well as consideration of their CAP difficulties, simulations were set up (e.g., if high background noise was a distracter, a noise recording was used). Auditory training was thus conducted in as realistic a manner as possible. Both participants showed improvements in their listening, communication, STAM and general CAP abilities following participation in their individualized aural rehabilitation program. These adults’ participation in the auditory program highlights the notion that successful rehabilitation should be based on careful diagnosis of impairment and disability, identification of individual needs, setting specific goals and supporting self-management.

Hearing loss is associated with disability and psychological distress. 53 Furthermore, hearing loss is related to maladaptive communication strategies, self-perceptions of poor social skills and reduced self-esteem and, as a result, deterioration in quality of life. One of the findings of a study of the psychological profile and social behavior of young hearing-impaired working adults showed a higher level of psychological distress among the hearing-impaired group than among the control group, which was reflected mainly in the symptom domains of anxiety, depression, phobic anxiety, interpersonal sensitivity and hostility. 54 This association may be true for people with CAPD.

The participants in this study had reduced social activities, experienced increased relational problems with family and friends and suffered emotional difficulties at work. It is conceivable that these participants may have been discouraged from exposure to socially challenging situations, resulting in isolation, depression and irritability which, in a vicious cycle, lead to poorer social-communication performance.

The participants in this case study were able to implement helpful, learned strategies into their home, work and social environments. They reported experiencing improved confidence and self-esteem following intervention, which resulted in positive feelings of well-being and overall improved quality of life. Positive well-being has implications for physical, mental and social health and is associated with better health outcomes and ultimately reduced healthcare burden. 55

The adults presented in this case study were diagnosed with CAPD based on their results of an audiological (including CAP) diagnostic test battery. A client-centered approach to management was adopted and included face-to-face training and home and work practice. Participants responded well to the auditory-based interventions and reported significant improvements in their symptoms and accompanying difficulties.

CAPD is traditionally and usually identified in childhood, and it is questionable whether these individuals missed diagnosis during childhood or whether the difficulties appeared only in later life. Nonetheless, the study presents evidence for the presence of CAPD in adults, although, surprisingly first diagnosed in adulthood.

CAPD may be comorbid with other disorders or difficulties. However, the adults’ positive responses to the auditory-based interventions used in their management plan confirm the influence of the disorder on a variety of work and social functions. Participants-reported improvement post intervention suggest that young and middle-aged adults are not too old to be tested for CAPD and can benefit from an aural rehabilitation program targeting their CAP, listening and associated skills. Further research investigating CAPD in adults is essential so that adults can improve their well-being and quality of life. These case studies highlight that adults with CAPD are an under-diagnosed segment of the population. Medical and other allied health professionals should be alerted to the possibility of presentation of CAPD in adulthood in order to make appropriate referrals for CAP testing to facilitate diagnosis and appropriate intervention.

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ethical approval: Ethical approval to report this case series was obtained from La Trobe University Human Ethics Committee (approval number/id: HEC18134)*.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

Informed consent: Written informed consent was obtained from the patient(s) for their anonymized information to be published in this article.

Environmental Medicine: Integrating a Missing Element into Medical Education (1995)

Chapter: case study 52: behavioral and audiologic manifestations of noise-induced hearing loss, behavioral and audiological manifestations of noise-induced hearing loss.

Sufficiently intense sounds have the potential of disrupting all parts of the peripheral and central auditory system. Noise can have direct mechanical effects on the middle ear, such as ossicular and discontinuity, tympanic membrane perforation, or fistula of the oval window, and on cochlear structures. The outer hair cells are particularly vulnerable to the effects of excessive noise exposure, followed in vulnerability by the inner hair cells. The cochlea, once damaged, cannot be repaired; the subsequent loss of sensory cells and neural changes produces an auditory pathology that represents the morphologic substrate for the loss of hearing threshold, referred to as a noise-induced sensorineural hearing loss, or simply a noise-induced hearing loss (NIHL). A similar set of cochlear changes can be induced by lower levels of noise that continuously stress the metabolic processes of the cochlea. While these changes may initially produce a temporary loss of threshold, with repeated exposures they may lead to permanent changes.

Hearing loss resulting from noise exposure can be separated into three distinct categories: acoustic trauma, temporary threshold shift (TTS), and permanent threshold shift (PTS). A single, relatively intense noise exposure is referred to as an acoustic trauma and is usually followed by tinnitus and a change in hearing threshold. While hearing may improve slightly over time, if the exposure is sufficiently intense a PTS will result. One or both ears may be involved. Those who experience an acoustic trauma may also suffer from tympanic membrane perforation(s) and disarticulated or fractured ossicles. Such middle-ear disorders are more likely to appear, if at all, once the peak noise exposure level exceeds approximately 160 dB SPL. In general, however, any acute sound exposure that causes any of the following symptoms represents a hazard to the auditory system and could result in an acute acoustic trauma: immediate pain, a tickling sensation in the ears often occurring if the SPL exceeds approximately 120 dB, vertigo, tinnitus, hearing loss, or reduced communication skills.

Lower levels of noise (<85 dB[A]) are potentially hazardous and may result in an NIHL if, following exposure, there is a transient shift in the threshold of hearing that recovers gradually (a TTS). While the onset of hearing loss in acute acoustic trauma is instantaneous, the onset and progression of NIHL is far more insidious since it accumulates, usually unnoticed, over a period of many years of exposure to noise on a daily basis. During the initial stages of NIHL, the temporary hearing loss recovers within a few hours or days following removal from the noise. However, if the exposure to this noise is repeated often enough, the hearing loss may not recover completely (that is, permanent sensorineural hearing impairment will begin).

The following is a typical case history of an history individual with permanent NIHL:

A 48-year-old man had chief complaints of constant, high-pitched tinnitus and progressive hearing loss in both ears over the previous 2 years. He reported some difficulty hearing in quiet surroundings but noticed marked difficulty understanding speech in noisy environments. He did not report any previous serious illnesses, accidents, atypical drug use, or problems with his ears. For the past 8 years, he had worked in a noisy textile mill, where he said that he “occasionally” wore hearing protective devices. The patient had not been exposed to other hazardous noises off the job, such as gunfire or motorbikes.

The diagnosis of NIHL comes under the domain of the audiologist, whose primary responsibility is the identification and measurement of hearing loss and the rehabilitation of those with hearing impairment. By measuring auditory thresholds in decibels (relative to a normal hearing level or 0 dB HL) for pure tones as a function of frequency, an audiogram (a frequency-intensity graph) is generated. Hearing level (HL) is a term used to designate an individual’s hearing threshold at a given test frequency, referenced to an audiometric zero level. The audiogram will help answer the following questions: (1) Is there evidence of hearing loss? (2) If so, what is the severity of the loss? (3) What is the nature of the loss (conductive, sensorineural, or mixed)? and (4) Can the use of a hearing aid(s) benefit the hearing-impaired individual? A typical normal audiogram and an audiogram from an individual with an NIHL are shown in Fig. 16–5.

Hearing loss induced by most industrial noise characteristically produces a bilateral symmetrical loss that is progressive in nature so long as the individual is continuously exposed to hazardous noise levels (Fig. 16–5). In the initial stages of development, the loss usually occurs at frequencies lying between 3,000 and 6,000 Hz. The maximum loss is usually centered at 4,000 Hz. The audiometric configuration, therefore, is characterized by a downward slope with greater loss in the high-frequency region (3,000–6,000 Hz) than in the low- and mid-frequency regions (250–2,000 Hz). As the NIHL accumulates following further exposure, the 4,000-Hz loss increases in magnitude and the adjacent (higher and lower) frequencies also become increasingly affected. The progressive nature of NIHL may eventually result in a moderate to severe impairment across most of the usable hearing frequency range (250–8000 Hz) unless preventive measures are taken to reduce the degree of hazard imposed by the noise.

Although the diagnosis of a permanent NIHL may be indicated by the audiometric configuration of the hearing loss (the 4,000-Hz notch), it would be premature to make a definitive diagnosis unless additional factors are considered, such as: (1) What is the duration, type, and time-weighted average of the individual’s noise exposure? (2) What is the individual’s hearing both before and after exposure? (3) What is the age and general health of the individual? (4) Are there any other disorders that may result in

Fig. 16–5 . An example of a typical audiogram from a normal individual (dashed lines) and an individual with a bilateral sensorineural hearing loss resulting from excessive noise exposure. Note the maximum loss at 4,000 Hz and the spread of loss to the lower frequencies.

hearing impairment (such as middle-ear disorders, congenital factors, Meniere’s disease, an eighth cranial nerve lesion, ototoxicity, and presbycusis)? Consideration of these questions provides important information as to whether the cause and degree of impairment can be solely attributable to noise exposure. Two major diagnostic problems are distinguishing NIHL from hearing loss associated with presbycusis or ototoxic agents and determining the degree of impairment attributed to the aging process. A reported history of tinnitus or “muffled” hearing occurring immediately after any noise exposure or after leaving the work environment and a characteristic 4,000-Hz notch on the audiogram strongly suggest an occupational NIHL hearing loss. Complaints of vertigo are also common.

People usually do not report any difficulty in hearing until a hearing loss of more than 25 dB HL occurs at a frequency at or below 4,000 Hz. Difficulty in hearing the high-frequency sounds of speech (such as s, f, k, t, and sh) may provide the only clue to the individual of an NIHL. Performance on speech intelligibility tasks varies considerably depending on the magnitude of the loss and the affected frequencies. If the hearing loss is confined to frequencies above 3,000 Hz, speech intelligibility measured in quiet surroundings is usually within normal limits. As the frequencies below 3,000 Hz become involved, intelligibility decreases in relation to the degree of impairment. Given that approximately 95 percent of the frequency components in speech lie between 300 and 3,000 Hz, it should not be surprising to find a deterioration in speech intelligibility performance once the NIHL extends into this range of frequencies. Also, individuals with sensorineural hearing loss, due either to noise exposure or other factors, usually have greater difficulty understanding speech against a competing background noise environment than in a quiet environment. This common complaint may be minor if the hearing loss is restricted to frequencies at or above 3,000 Hz but may present market difficulty for those with losses below 3,000 Hz. Since the usual pattern of progressive NIHL is one in which the speech frequencies are affected last, it is important to identify NIHL during its initial stages to help prevent future deterioration of hearing sensitivity and speech discrimination abilities.

Occupational health nurses and physicians involved in assessing and monitoring hearing status in hearing conservation programs should refer the worker to an audiologist if a significant change in hearing level (≥10 dB at any frequency in either ear) is observed after the worker has had a minimum of 48 hours to recover from environmental noise exposure. Audiological management of the individual with NIHL may include the use of hearing aids, aural rehabilitation, and assistive listening devices to help improve some of the communication dysfunction experienced in certain listening situation. What, if any, strategies are implemented depends largely on the severity of the communication handicap produced by the noise exposure and the listening needs of the individual.

People are increasingly concerned about potential environmental health hazards and often ask their physicians questions such as: "Is the tap water safe to drink?" "Is it safe to live near power lines?" Unfortunately, physicians often lack the information and training related to environmental health risks needed to answer such questions. This book discusses six competency based learning objectives for all medical school students, discusses the relevance of environmental health to specific courses and clerkships, and demonstrates how to integrate environmental health into the curriculum through published case studies, some of which are included in one of the book's three appendices. Also included is a guide on where to obtain additional information for treatment, referral, and follow-up for diseases with possible environmental and/or occupational origins.

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Case Study of a 5-Year-Old Boy with Unilateral Hearing Loss
Figure 2. Follow-up behavioral test of 5-year-old boy. According to the MRI, the cochlea on the right side is normal—which would explain the present DPOAE results. The cochlear branch of the VIIIth Cranial Nerve is completely absent, which would explain the absent ABR result and the profound hearing loss by behavioral testing.
Experience of sudden sensorineural hearing loss ...
A woman in her 30s was referred to an otolaryngologist with an acute onset of aural fullness, noise sensitivity, unilateral sudden onset hearing loss, vertigo and tinnitus. She had a confirmed COVID-19 infection 5 weeks prior. A pure tone audiogram confirmed sensorineural hearing loss. MRI identified an empty sella of the pituitary gland and without an obvious cause for hearing loss. Oral ...
Immediate Treatment of Sudden Sensorineural Hearing Loss: A Case Study
The purpose of this case study is to support best practices in treating sudden sensorineural hearing loss (SSNHL), particularly the importance of immediate audiological evaluation and treatment of suspected SSNH to ensure an optimal outcome. SSNHL is most commonly defined as a hearing loss of 30 dB or greater at three consecutive frequencies ...
Noise Induced Hearing Loss: A Case Study from a Speech-Language
This case study documents the hearing loss of an otherwise healthy 21-year-old, male individual and his progressive moderate-to-severe sensorineural hearing loss over a period of 41 years. His history will be reported along with his perspective as a speech-language pathologist and speech scientist. The individual with hearing loss has adapted ...
All Audiology Case Studies
An interprofessional practice (IPP) team worked together to assess hearing loss and language skills in a 2-year-old child. The team recommended a cochlear implant and a plan of therapy for language development and listening skills. As a result, the child's expressive vocabulary began showing steady growth. Download Full Case Study & Rubric
The Hearing Journal
Clinical Case Studies. Creator: The Hearing Journal. Updated: 9/16/2022. Contains: 111 items. Read and diagnose these intriguing case studies that come with exclusive patient videos.
From Clinic to Classroom: Helping Families of Children With Hearing
Helping families help themselves: a case study. When family members of children with hearing loss express concerns about school-related issues to the clinic-based audiologist, we want to respond in a supportive manner, without overstepping our role. The tendency may be to jump in and try to solve the problem for the family.
Sudden irreversible hearing loss post COVID-19
Sudden onset sensorineural hearing loss (SSNHL) is frequently seen by otolaryngologists. The exact pathophysiology of the disease is still unknown, with the most likely causative factor being following a viral infection. Immediate steroids are the best treatment to improve prognosis. Despite a plethora of papers in the literature describing SSNHL, there are only a few reported cases of hearing ...
Etiological analysis of patients with sudden sensorineural hearing loss
The results of our prospective case-control study on sudden sensorineural hearing loss neither showed any significant relation to comorbidities by hypertension or diabetes or hyperlipidemia nor ...
Bilateral Sudden Mixed Hearing Loss: Case Study
This study presents a case of a patient with sudden hearing loss of a mixed type in both ears. Case report: A 45-year-old man came to our center for consultation because he had had no improvement in hearing after therapy in another clinic. In our clinic the patient was treated for 2 weeks. During each of his visits to our center, a battery of ...
A 67-Year-Old Woman with Sudden Hearing Loss Associated with SARS-CoV-2
Case Report: A 67-year-old woman with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as confirmed by reverse transcription-polymerase chain reaction (RT-PCR) testing from nasopharyngeal and oropharyngeal swabs, was examined. She experienced sudden hearing loss in her right ear and disabling tinnitus.
Guidelines for Writing an Audiology Case Study : The Hearing Journal
An audiologist for 30 years, his research emphasizes epidemiology, hearing loss prevention, and hearing protection measures. Dr. Hall is an audiologist with over 40 years of clinical, teaching, research, and administrative experience. He is a professor of audiology at Salus University and the University of Hawaii. ... Case studies provide ...
BILATERAL SUDDEN MIXED HEARING LOSS: CASE STUDY
email: [email protected]; Phone: +48 22 35 60 359. Abstr act. Background: is study presents a case of a patient with sudden hearing loss of a mixed type in both ears. Case report: A 45-year-old ...
A Hospital based study on sudden sensorineural Hearing Loss: It's
Hence the current study was conducted to explore the prevalence & characteristics of sudden sensorineural hearing loss. This study has significant importance as its finding may be helpful for researchers to conduct in depth research in the field with different objectives. ... No significant association (p=0.32) of vertigo was noted with no case ...
Case studies of adults with central auditory processing disorder
This retrospective study was a case file audit of two adults (a male, aged 37 years and a female, aged 44 years) who presented at a multidisciplinary (audiology and speech pathology) clinic for a hearing and central auditory processing evaluation. ... Hearing loss is associated with disability and psychological distress. 53 Furthermore, hearing ...
Full article: Key findings about hearing loss in the working-life: a
Hearing impairment without HL (e.g. only tinnitus, hyperacusis), multiple disabilities (e.g. deaf-blindness, reported dual-sensory loss), deafness involving sign language, mixed target groups if also mixed in the results section, prevalence studies of HL in the general work force, risk factors for HL in the general work force, systematic ...
CASE STUDY INVESTIGATION
A 10-year-old female presented to the audiology department at a large pediatric hospital. She recently failed a hearing screening in both ears at her pediatrician's office. The patient reported she was unable to hear. She stated that sounds were muffled and she was unable to understand when spoken to. The audiologist attempted to converse ...
Case Study: Team Helps Child with Hearing Loss Develop Language ...
Download Full Case Study & Rubric. An interprofessional practice (IPP) team worked together to assess hearing loss and language skills in a 2-year-old child. The team recommended a cochlear implant and a plan of therapy for language development and listening skills. As a result, the child's expressive vocabulary began showing steady growth.
Symptom: Mild Asymmetric Hearing Loss : The Hearing Journal
Clinical Consultation. Symptom: Mild Asymmetric Hearing Loss. Djalilian,, Hamid R. MD. Author Information. Dr. Djalilian is the director of neurotology and skull base surgery and a professor of otolaryngology and biomedical engineering at the University of California, Irvine. The Hearing Journal: January 2018 - Volume 71 - Issue 1 - p 30,32,33.
CASE STUDY INVESTIGATION
In addition to the symptoms stated earlier, DK also has an infrequent history of a beeping tone in her ears and fullness, and denied a history of hearing loss and visual impairment. There is a family history of dizziness (paternal grandmother) and migraines (mother and aunt).
Case Study 52: Behavioral and Audiologic Manifestations of Noise
Case Study 52: Behavioral and Audiologic Manifestations of Noise-Induced Hearing Loss 868-871; Case Study 53: Reproductive and Developmental Hazards 872-892; Case Study 54: Childhood Asthma and Indoor Enviromental Risk Factors 893-903; Case Study 55: Populations at Risk From Particulate Air Pollution - United States, 1992 904-908
Sudden Hearing Loss Following a Traumatic Head Injury: A Case Study
This is a case study of a 40-year-old male with a sudden profound sensorineural hearing loss experienced secondary to a skull fracture incurred during a violent assault. Following the acute phase of his medical care, the patient received long-term multidisciplinary rehabilitative care in two states that included audiologic, psychologic, and ...
PDF CASE STUDY Bilateral Hearing Loss Deﬁned as Due to Bone Damage and/or
ear due to bone damage; began wearing a hearing aid at that time. Note: diagnosis made by an MD based on assessment with a "machine" in the of-ﬁce. At age 11, diagnosed with partial hearing loss in her left ear due to nerve damage. CASE STUDY Bilateral Hearing Loss Deﬁned as Due to Bone Damage and/or Nerve Damage Proved Reversible
The Stigma Of Hearing Aids: Hearing Loss Report
People with hearing loss may avoid hearing aids for a number of reasons, including cost, skepticism of hearing devices and mistrust of audiologists, says Lindsey Banks, Au.D., a Florida-based ...

Case Study of a 5-Year-Old Boy with Unilateral Hearing Loss

Case Study | Pediatrics | January 2015 Hearing Review

Initial Test Results

Follow-up Test

Recommendation to Parents

Johns Hopkins Results

Additional Follow-up

The Value of Relearning in Everyday Clinical Practice

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Author Information

1. Introduction

1.1 Other causes of hearing loss

1.2 Head trauma and hearing loss

1.3 Hearing loss and cognitive loss

1.4 Age related hearing loss

2. Case study (AB)

2.1 Career as a speech-language pathologist

2.2 Speech intelligibility

2.3 Rehabilitation

3. Conclusion

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Etiological analysis of patients with sudden sensorineural hearing loss: a prospective case–control study

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Case studies of adults with central auditory processing disorder: Shifting the spotlight!

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Environmental Medicine: Integrating a Missing Element into Medical Education (1995)

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