10/6/23, 9:00 AM Hearing Loss - ClinicalKey

CLINICAL OVERVIEW

Hearing Loss
Ferri, Fred F., MD
Publicado January 1, 2022.

Basic Information
• The normal ear can detect sound frequencies ranging between 20 and 20,000 Hz; the upper range drops off fairly rapidly with
advancing age. The ear is most sensitive between 500 and 4000 Hz, which roughly corresponds to the frequency range most
important for understanding speech. The hearing level in this range has several practical implications in terms of the degree
of handicap and the potential for useful correction with amplification. A 30- to 40-dB hearing level in the speech range would
impair normal conversation, whereas an 80-dB hearing level would make everyday auditory communication almost
impossible (the social definition of deafness). 1 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-
B9780323755702011127#fur1)

• Disabling hearing loss is defined by the World Health Organization as greater than 40 dB in the better hearing ear in adults
and greater than 30 dB in the better hearing ear in children.

• Sudden sensorineural hearing loss (SSNHL) is defined as the idiopathic loss of hearing of 30 dB over at least three test
frequencies occurring over a period of less than 3 days.

Epidemiology & Demographics

• About 5% of the world population suffers from disabling hearing loss.
• The prevalence of disabling hearing loss is twice as high in poorer countries compared with richer countries.

• The prevalence increases with every age decade, and it is higher in men than in women across all age decades.

• Age-related hearing loss (ARHL) is the second leading cause of years living with disability (YLD) behind depression and is a
larger nonfatal burden than alcohol use, osteoarthritis, and schizophrenia.

• Over the last generation, the ARHL population has grown at a rate 1.6 times that of U.S. population growth, with 36 million
Americans self-reporting hearing impairment.

• By the year 2030, at least 21 million Americans older than 65 yr are projected to have a hearing impairment.

• ARHL prevalence ranges from 30% to 47% among persons older than 65 yr, doubling with each age decade, so that nearly two
thirds of persons 70 yr of age and older and 80% of persons older than 85 yr having an ARHL that affects their
communication ability. 2 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#fur2)

• The peak incidence of SSNHL occurs in the fifth or sixth decade of life with an equal distribution between the sexes. The
overall incidence ranges from 5 to 20 per 100,000 people per year. Severity ranges from difficulty with conversation to
complete hearing loss.

Etiology & Risk Factors

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• Each acoustic nerve is composed of two divisions with separate courses and functions: Hearing and balance. The cochlear
nerve, one of the two divisions, transmits auditory impulses from each inner ear to the superior temporal gyri of both
cerebral hemispheres. This bilateral cortical representation of sound explains the observation that damage to an ear or only
its acoustic nerve may cause deafness in that ear, but the patient will still hear sounds and speech because they pass through
the other ear’s acoustic nerve.

• Hearing loss associated with older age, presbycusis (Greek, presbys, old man; acusis, hearing) affects about 25% of people
older than 65 yr. It typically begins with loss of high frequencies and eventually progresses to involve all frequencies. A
hallmark of ARHL is neuronal loss in the periphery. The neuronal changes that tend to affect processing of speech sounds
include the following: (1) Disrupted neural synchrony, which is associated with reduced amplitude of the action potential; (2)
decreased neural inhibition; (3) longer neural recovery time; (4) a decrease in the number of neurons in the auditory nuclei; (5)
changes in synapses between inner hair cells and the auditory nerve; and (6) age-related changes in the level of inhibitory
neurotransmitters.

• Age-related increased activity of cerumen glands in the cartilaginous portion, physical obstruction due to a hearing aid,
frequent use of cotton-tipped swabs, or production of drier and less viscous cerumen contribute to the excessive
accumulation of wax. Accumulation of excessive cerumen (cerumen impaction) is present in approximately one third of older
adults, with estimates ranging from 19% to 65%.

• The causes of SSNHL are as follows: idiopathic causes (71%), infectious disease (12.8%), otologic disease (4.7%), trauma (2.4%),
vascular or hematologic causes (2.8%), neoplastic causes (2.3%), and other causes (2.2%).

• Acoustic nerve injury may result from ototoxic medications, such as aspirin or streptomycin, skull fractures’ severing the
nerve, or cerebellopontine angle tumors, particularly acoustic neuromas, which may be associated with neurofibromatosis.

• In utero rubella infections or kernicterus commonly cause syndromes involving mental retardation and deafness.

Risk Models & Risk Scores

• ARHL is a multifactorial condition with a number of modifiable and nonmodifiable risk factors. Nonmodifiable factors
include increasing age, genetic predisposition, race (decreased risk in African Americans), and gender (males, increased risk).
Modifiable risk factors include environmental exposure (e.g., noise, ototoxicity), smoking, and multiple health comorbidities,
including cerebrovascular disease, cardiovascular disease (CVD), and diabetes.

• Cognitive decline increases the risk for hearing impairment, and kidney disease, metabolic conditions such as lupus, thyroid
dysfunction, and head trauma are also medical conditions associated with hearing loss. Data from the Health ABC Study, a
population-based prospective cohort study, has revealed that history of smoking is associated with poorer high-frequency
hearing levels in men. Similarly, data from the NHANES cross-sectional survey has confirmed that heavy smoking increases
the odds of hearing loss nearly twofold. Exposure to loud noise accelerates ARHL, and noise exposure and history of CVD
appear to have a synergistic effect, elevating hearing threshold levels. 3 (https://www-clinicalkey-
es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#fur3)

• CVD risk factors, including higher levels of triglycerides and poorer resting heart rate, are related to poorer hearing. This
association is likely linked to the fact that an insufficient cochlear blood supply can disrupt the chemical balance of the fluids
within the inner ear, influencing the activity of the hair cells and activation of the auditory nerve. Similarly, a history of
diabetes mellitus is linked to poorer hearing sensitivity, most likely due to the effect on the cochlear vascular system, with a
prevalence higher among persons with diabetes as compared to those without.

• Social isolation has been linked to hearing impairment.

Pathophysiology 1 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#fur1)
• Conductive hearing loss results from lesions involving the external or middle ear. It is typically characterized by an
approximately equal loss of hearing at all frequencies and by well-preserved speech discrimination once the threshold for
hearing is exceeded. Patients with conductive hearing loss can hear speech in a noisy background better than in a quiet
background because they can understand loud speech as well as anyone.

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• Sensorineural hearing loss results from lesions of the cochlea or auditory division of the eighth cranial nerve, or both. With
sensorineural hearing loss, the hearing levels for different frequencies are usually unequal, typically resulting in better
hearing for low- than for high-frequency tones. Patients with sensorineural hearing loss often have difficulty in hearing
speech that is mixed with background noise and may be annoyed by loud speech. Three important manifestations of
sensorineural lesions are diplacusis, recruitment, and tone decay. Diplacusis and recruitment are common with cochlear
lesions; tone decay usually accompanies eighth nerve involvement.

• Central hearing disorders result from lesions of the central auditory pathways. As a rule, patients with central lesions do not
have impaired hearing for pure tones, and they can understand speech as long as it is clearly spoken in a quiet environment.
If the listener’s task is made more difficult with the introduction of background noise or competing messages, performance
deteriorates more markedly in patients with central lesions than in normal subjects.

Diagnosis
• The history, examination, and audiometry usually provide the key differential features for identifying common causes of
hearing loss (Fig. E1 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#f0010)).

• Physical examination includes a thorough inspection of the external canal and TM integrity. The Weber test for hearing and
the Rinne test may help in distinguishing conductive versus sensorineural deficits. A comprehensive neurologic examination
including cranial nerve and cerebellar testing may localize brain stem involvement.

FIG. E1
Evaluation of hearing loss. BAER, brain stem auditory evoked response; C-P, cerebellopontine.

From Goldman L, Schafer AI: Goldman-Cecil medicine, ed 26, Philadelphia, 2019, Elsevier.

Staging or Classification
• Hearing loss is classified based on anatomic deficit as conductive, sensorineural, or mixed.

• Hearing loss is quantified based on the decibels hearing level (dB HL):

1. Mild: dB HL 26 to 40

2. Moderate: dB HL 41 to 60

3. Severe: dB HL 61 to 80
4. Profound: dB HL >80
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History & Physical Examination

• Initial screening for hearing loss can be done with self-assessment questionnaires. Their positive and negative predictive
values range from 60% to 80%. 4 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-
B9780323755702011127#fur4)

• In the office setting, initial examination should include finger rub 6 inches from the patient’s ear and whisper test while
standing 2 feet behind the patient.

• Handheld audiometers or smartphone audiometers can be used to confirm the hearing loss.

• If hearing loss is identified, use of Weber and Rinne tests can further identify the hearing loss as conductive or sensorineural.

Laboratory Tests
Routine laboratory evaluation is indicated only when suspecting a systemic illness contributing to the hearing loss.

Imaging Studies
An MRI with gadolinium of the brain is the study of choice for sudden hearing loss and when suspecting an acoustic neuroma.

Diagnostic Procedures
• Pure tone testing is the cornerstone of most auditory examinations. Pure tones at selected frequencies are presented through
either earphones (air conduction) or a vibrator pressed against the mastoid portion of the temporal bone (bone conduction),
and the minimal level that the subject can hear (threshold) is determined for each frequency. Two speech tests are routinely
used. The speech reception threshold is the intensity at which the patient can correctly repeat 50% of the words presented.
The speech reception threshold is a test of hearing sensitivity for speech and should reflect the hearing level for pure tones in
the speech range. The speech discrimination test is a measure of the patient’s ability to understand speech when it is
presented at a level that is easily heard. In patients with eighth nerve lesions, speech discrimination scores can be severely
reduced, even when pure tone thresholds are normal or nearly normal; by comparison, in patients with cochlear lesions,
discrimination tends to be proportional to the magnitude of hearing loss.

• Brain stem auditory evoked responses can be recorded from scalp electrodes at 0 to 10 msec (early), 10 to 50 msec (middle),
and 50 to 500 msec (late) following a click (a high-frequency stimulus). The early potentials reflect electrical activity at the
cochlea, eighth cranial nerve, and brain stem; the later potentials reflect cortical activity. Computer averaging of the responses
to 1000 to 2000 clicks separates the evoked potential from background noise. Early evoked responses may be used to estimate
the magnitude of hearing loss and to differentiate among cochlea, eighth nerve, and brain stem lesions.

Other Diagnostic Tools

When individuals feign deafness, neurologists may attempt to startle them with a loud sound or watch for an auditory-ocular
reflex (involuntarily looking toward a noise). Neurologists wishing to confirm a diagnosis of psychogenic hearing loss may order
brain stem auditory evoked response (BAER) testing. Audiometry is advisable in children with autism symptoms, cerebral palsy,
intellectual disability, speech impediments, and poor school performance, as well as those suspected of having a psychogenic
hearing impairment.

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Treatment 5 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#fur5)

Approach to Treatment (Table E1 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-

B9780323755702011127#t0010))

• The first step in evaluating hearing complaints is to ascertain the location and extent of the hearing loss.

• The history must include details about the timing of hearing loss, laterality, previous episodes, associated symptoms (tinnitus,
vertigo, or pain), preceding events (diving, plane rides, trauma), potential placement of a foreign body, environmental noise
exposure, and potential ototoxic drugs.

• Tuning fork tests provide the best clues to distinguish between conductive and sensorineural hearing loss.

1. The Weber test compares the two ears with each other (Fig. E2 (https://www-clinicalkey-
es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#f0015)). A vibrating fork is placed midline on the
top of the head. The patient is asked which ear hears the vibrations better. If the fork is heard louder in one ear, either
that ear has a conductive deficit or the other ear has a neural deficit (Table E2 (https://www-clinicalkey-
es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#t0015)).

2. The Rinne test evaluates each ear independently (Fig. E2 (https://www-clinicalkey-

es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#f0015)). Normally, air conduction is more
sensitive than bone conduction, and one should be able to hear a vibrating fork longer through the air than through
bone. The handle of a vibrating fork is placed on the mastoid process of the side being evaluated. The vibrating end is
then held near the ear canal. Normally functioning ears hear the air conduction louder and longer than the bone
conduction. Perception of sound better through bone conduction indicates a conductive deficit. Lack of hearing either
bone or air conduction points to sensorineural hearing loss (Table E2 (https://www-clinicalkey-
es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#t0015)).

TABLE E1
Lesions That Cause Hearing Loss
From Adams JG: Emergency medicine: clinical essentials, ed 2, Philadelphia, 2013, Elsevier.

Description of Pathology Onset/Course Actions or Treatment Prognosis

Conductive Lesion
Foreign body Mass in external canal Acute onset associated or not Removal. Evaluate for infection. Excellent
blocks sound with pain, drainage, or odor Evaluate for TM perforation
conduction
Otitis externa Edema and detritus Rapid onset. Pain, edema, Aural toilet to remove debris. Topical (± Excellent if treated
obstruct external canal swelling. Drainage, odor often oral) antibiotics. Evaluate for appropriately
present necrotizing otitis
Exostosis Bony growths obstruct Slow insidious onset. No pain or Evaluate for infection. Reassure patient. Good
canal. Often seen with drainage unless causes complete Refer to ENT
prolonged exposure to obstruction
cold water (divers)

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Description of Pathology Onset/Course Actions or Treatment Prognosis

Tympanosclerosis TM scarring from Slow onset following perforations, ENT referral. Reassurance Variable
perforations or trauma, or infections
infections. Decreased
mobility impairs sound
conduction
Perforated TM Disruption of TM Acute onset. May follow direct Treat infectious causes. Counsel on Good
integrity results in trauma or sudden barotrauma. importance of keeping water out of ear
impaired transmission May have sudden relief from pain canal. ENT referral
of sound to ossicle if caused by otitis media
Sterile effusion Fluid in middle ear Often following flight, diving, or Decongestants. Evaluate for infection. Excellent
(barotrauma) dampens conduction URI. Bubbles can cause Follow-up
through ossicles intermittent pain
Acute otitis media Pus (or fluid) in middle Acute to subacute onset, often Antibiotics (unless viral cause Excellent if treated
ear dampens conduction following URI. Often associated suspected), decongestants, pain control appropriately
through ossicles with pain ± fever
Cholesteatoma Trapped stratified Slow onset. Often history of ENT referral Variable. May destroy
squamous epithelial previous perforations or chronic ossicles or erode into
mass in middle ear. infections surrounding
Interferes with ossicle structures
conduction
Glomus tumor Vascular tumor occupies Slow onset. May be associated ENT referral Variable
middle ear space. with rushing pulsatile sensation
Interferes with ossicle
conduction
Cancer Squamous cell most Slow onset. Often noticed first by ENT referral. Evaluate for secondary Variable
common. Obstructs others. Painless unless occlusion infection
external canal causes otitis externa
Sensorineural Lesion
Perilymph fistula Disruption of round or Sudden onset of hearing loss Complete bed rest. Elevate head of bed Variable
(inner ear oval window allows often with tinnitus and vertigo. and avoid increases in CSF pressure.
barotrauma) leakage of perilymph Frequently follows straining or Severe symptoms or noncompliance
into middle ear abrupt change in pressure. may require hospitalization. ENT
Turning in direction of fistula consultation for possible oval or round
exacerbates symptoms window patch
Viral cochleitis Cochlear inflammation. Rapid onset. Often following URI Steroids often used (no good data) Variable
Often following URI
Presbycusis Age-related hearing loss. Slow onset. Usually symmetric. Hearing aid may help with both Variable
May be related to High frequencies most affected. hearing loss and tinnitus
previous chronic noise Tinnitus may occur
exposure
Acoustic neuroma Benign schwannoma of Slow onset. Usually unilateral. May require surgical excision if Variable
8th cranial nerve May exhibit tinnitus, vertigo. May symptoms debilitating
exhibit facial hyperesthesias or
twitching
Ototoxic agents Direct toxicity to inner Variable onset. High frequency Stop use of offending agent Variable. Hearing loss
ear structures most affected. Exposure to at time of stopping
ototoxic drugs. May have offending agent is
associated tinnitus usually permanent
Multiple sclerosis Multiple demyelinating Often other associated neurologic Standard multiple sclerosis treatment Variable
lesions interfere with findings. May wax and wane (steroids, cytotoxic agents)
nerve conduction
Stroke/CVA Focal ischemic lesion of Sudden onset. Often associated Treat CVA risk factors (ASA, Variable
auditory nerve or with other neurologic deficits anticoagulants, glycemic control, BP
auditory cortex control)
Meningitis Infection enters inner Follows clinical picture of Treat infection. Steroids may limit Variable
ear through CNS- meningitis inflammation and damage
perilymph connection.
Damages organ of Corti
Meniere disease Abnormal homeostasis Episodic spells of vertigo. Reduce salt, caffeine, nicotine Variable
(endolymphatic of inner ear fluids Associated sensation of fullness, (vasoconstrictors) intake. Consider
hydrops) (clinical diagnosis; tinnitus, and SNHL or auditory diuretics, antihistamines,
definitive diagnosis distortion. Low-frequency ranges anticholinergics. ENT referral
made histologically) most affected

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Description of Pathology Onset/Course Actions or Treatment Prognosis

Chronic noise Direct mechanical Slow onset. Usually high Prevention measures (earplugs). Stop Usually permanent
exposure damage to cochlear frequency most affected exposure
structures and hair cells
Skull trauma Interruption of cranial Sudden onset after trauma ENT consultation for possible surgical Variable: Ossicle
nerve VIII, ossicle repair disruption has better
disruption, or shearing prognosis than nerve
effects on organ of Corti or organ of Corti
damage
Autoimmune causes Vascular or neuronal Bilateral asymmetric SNHL. May Outpatient autoimmune evaluation. Variable
inflammatory changes be fluctuating or progressive. Steroids and cytotoxic agents may slow
Often other systemic progression
autoimmune findings
ASA, Acetylsalicylic acid; BP, blood pressure; CNS, central nervous system; CSF, cerebrospinal fluid; CVA, cerebrovascular accident; ENT, ear, nose, and throat; SNHL,
sensorineural hearing loss; TM, tympanic membrane; URI, upper respiratory infection.

FIG. E2
The Weber test compares hearing in the two ears with each other.

A vibrating tuning fork is held midline against the patient’s forehead (A). The patient is asked whether one ear hears the fork
more loudly. Unequal perception of sound indicates a conductive deficit in the loud ear or a neural deficit in the quiet ear. The
Rinne test compares air and bone conduction in each ear independently. A vibrating tuning fork is held against the mastoid
process (bone conduction; (B) until the vibrations can no longer be heard. The still-vibrating tip is then moved near the canal
opening to see whether the patient can still hear the vibration through air conduction (C). Longer or louder hearing through air
conduction is normal. Longer or louder hearing through bone conduction indicates a conductive hearing deficit.

From Adams JG: Emergency medicine: clinical essentials, ed 2, Philadelphia, 2013, Elsevier.

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TABLE E2
Interpretation of the Weber and Rinne Tests
From Adams JG: Emergency medicine: clinical essentials, ed 2, Philadelphia, 2013, Elsevier.

Weber without Weber Lateralizes Right Weber Lateralizes Left

Lateralization
Rinne both ears: AC > Normal S/N loss in the left ear S/N loss in the right ear
BC
Rinne left ear: BC > – Combined loss: conduction and S/N loss in the Conduction loss in the left ear
AC left ear
Rinne right ear: BC > – Conduction loss in the right ear Combined loss: conduction and S/N loss in the
AC right ear
AC, Air conduction; BC, bone conduction; S/N, sensorineural.

First-Line Treatment
• Cerumen impaction is one of the leading causes of temporary hearing loss. Removal of cerumen impaction by manual
extraction, irrigation, or use of cerumenolytics should be performed and repeat hearing testing should be performed before
further evaluation of hearing loss.

• Hearing aids improve the audibility of the sounds of speech in a wide range of settings while also preserving comfort and
sound quality for persons with hearing loss. They do not restore hearing to normal but do reduce speech understanding
difficulties, especially in a noisy setting, in a large and reverberant room, and they make communication less effortful for the
person with hearing loss and his or her communication partners. Directional and remote microphone technology and the
ability to control the hearing aid using smartphone software are innovations that have affected functionality and end user
experience.

• Surgically implanted devices consist of an internally placed receiver-stimulator connected to an electrode array coiled within
the cochlea of the inner ear, which delivers the unique electrical representation of each speech sound to the auditory nerve.

• Older adults with single-sided deafness (unilateral severe to profound hearing loss) may benefit from a surgically implanted,
contralateral, bone-anchored hearing aid (BAHA), wherein sound is delivered into the skull via sound vibration. The sound
vibrations transfer sound from the bad ear side to the good ear side through the skull.

• Middle ear implants (MEIs) are a relatively new class of technology available for partial restoration of hearing for those with
moderate to severe sensorineural hearing loss. Unlike cochlear implants, the success of an MEI rests on the health of the
cochlea; the amplified vibratory signal is delivered to the inner ear via a normally functioning middle ear structure. They are
similar to cochlear implants in that the internal processor is surgically attached to the skull behind the ear, and an external
processor delivers sound to the internal processor.

• Hearing-assisted technology (HAT): Designed to be used as a complement to or in lieu of hearing aids, HAT enhances or
helps maintain the functional communication capacities of the hearing-impaired person by enhancing the level of the signal
relative to the noise. By making the signal louder, HAT is akin to binoculars for the ears. In essence, placing a microphone
close to the talker’s mouth catches the desired speech before it travels across the room, loses energy, and becomes degraded
by noise and reverberation, preserving the intensity level and clarity of the speech. HAT improves the reception of face to face,
small- and large-group communication, enhances reception of media, and facilitates understanding of telecommunication
devices. HAT is effective in a variety of settings, including home, work, private practice, theater, and hospital. In addition to
setting specific uses, HAT can be classified according to portability; it can be personal or private, portable versus stationary, or
hard-wired rather than wireless. 6 (https://www-clinicalkey-es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-
B9780323755702011127#fur6)

Pharmacologic Therapy

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• Consider herpes zoster oticus if there is otalgia or vesicles are seen on the pinna or in the canal. If tuning fork testing is
consistent with SSNHL, the patient is commenced empirically on oral prednisolone 1 mg/kg up to 60 mg daily (for 7 days
then reducing over a week) and urgent audiogram and ENT follow-up planned for the same or following day. Intratympanic
steroids may be used by ENT if there are contraindications to oral steroids.

Complications
Hearing impairments no matter what their cause may also lead to misdiagnoses of apathy or dementia.

Referral
• Referral to an audiologist for hearing testing is indicated in patients with significant hearing loss. Otolaryngology
consultation may also be needed for further evaluation of associated vertigo, conductive hearing loss, fluctuating hearing loss,
and failure of hearing aids to be useful.

• Urgent referral to an otolaryngologist is warranted for SSNHL or hearing loss associated with trauma. 7 (https://www-clinicalkey-
es.pbidi.unam.mx:2443/#!/content/derived_clinical_overview/76-s2.0-B9780323755702011127#fur7)

Prevention
• Prevention of noise-induced hearing loss at work and leisure activities with use of hearing protections is the most effective
way to prevent hearing loss.

• Prompt treatment of ear infections, avoidance of ototoxic medications, and limiting head trauma constitute other preventive
measures.

References
1. Baloh R.W., Jen J.C.: Hearing and equilibrium. In Goldman L., Shafer AI. (eds): 2019. Elsevier, Philadelphia

2. Lin F., Niparko J., Ferrucci L.: Hearing loss prevalence in the United States. JAMA Intern Med 2011; 171: pp. 1851-1853.

3. Yamasoba, Lin F., Someya S., et al.: Current concepts in age-related hearing loss: epidemiology and mechanistic pathways. Hear Res 2013; 303:
pp. 30-38. 23422312 (pmid:23422312).

4. Helzner E., Patel A., Pratt S., et al.: Hearing sensitivity in older adults: associations with cardiovascular risk factors in the health, aging and
body composition study. J Am Geriatr Soc 2011; 59: pp. 972-979. 21649629 (pmid:21649629).

5. Morrissey T, Lissoway J: Ear emergencies. In Adams JG (eds): Emergency medicine, clinical essentials., ed 2 2013. Elsevier, Philadelphia

6. Compton C.: Wireless systems for hearing aids. http://hearinghealthmatters.org/waynesworld/2013/2566

(http://hearinghealthmatters.org/waynesworld/2013/2566).

7. Nieman C.L., Oh E.S.: In the clinic: hearing loss. Ann Intern Med, ICC 2020; pp. 81-96.

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