The Ear
Basic concepts
Anatomy and physiology
Structurally, the ear has three parts (Fig. 1.1):

Fig. 1.1 Anatomy of the ear. For descriptive purposes the ear is divided into three parts: the external, the middle and the inner ear.
The external ear
The external ear includes the pinna, external auditory meatus and tympanic membrane. The outer third has a cartilage skeleton, and the rest is bony. Both are covered by skin. The skin on the outer part contains hair follicles and wax glands, but these elements are absent in the bony meatus. Canal skin migrates outwards from the deep meatus, but does not desquamate until it reaches the junction with the cartilaginous meatus. This normal mechanism may be disturbed by injudicious use of cotton buds.
The eardrum is the window of the middle ear and is divided into the pars tensa and pars flaccida. The main landmark on the drum is the malleus handle (Fig. 1.2).
The middle ear
The middle ear is an air-containing space connected to the nasopharynx via the Eustachian tube. It acts as an impedance matching device to transfer sound energy efficiently from air to a fluid medium in the cochlea (Fig. 1.3). The middle ear space, including the mastoid air cells, is closely related to the temporal lobe, cerebellum, jugular bulb and labyrinth of the inner ear. The space contains three ossicles (the malleus, incus and stapes) which transmit sound vibrations from the eardrum to the cochlea. The middle ear also contains two small muscles and is traversed by the facial nerve before it exits the skull.
The inner ear
The inner ear comprises a dense bony capsule containing a membranous labyrinth which forms the cochlea, vestibule and semicircular canals.
The membranous part is surrounded by fluid, called perilymph, and is sealed from the middle ear by the stapes footplate and round window membrane.
The membranous part itself contains fluid called endolymph. The cochlea contains the organ of hearing which is connected by the auditory nerve to the brainstem (Fig. 1.3).
The vestibule and semicircular canals form the peripheral balance organ. These have connections to the cerebellum and the eyes, and are important in the maintenance of posture and the ability to keep the eyes fixed when the head is moving.
Symptoms and signs
Symptoms
History taking in ear complaints should be brief but thorough. Table 1.1 provides a reference guide of the major points that should be covered. The otological symptoms are discussed in greater detail later in this section, but it is important to establish the predominant complaint and whether it affects one or both ears.
Table 1.1 Major points in history taking in patients with an otological complaint
Otological | Nasal |
Hearing loss – onset and rate of progression | Obstruction, discharge, etc. |
Otalgia | |
Otorrhoea | Drugs |
Tinnitus | Ototoxic agents (e.g. aminoglycosides) |
Imbalance | |
Family history | |
Noise exposure | Hearing loss |
Previous ear surgery |
Signs
Satisfactory examination cannot be undertaken without adequate lighting. Battery auriscopes with a fibre or glass ring light give a coaxial beam with bright uniform illumination. A pneumatic attachment tests the mobility of the eardrum (Fig. 1.4).

Fig. 1.4 Inserting the auriscope. The pinna is elevated upwards and backwards. The instrument should be gripped like a pencil.
The pinna should be examined for scars and signs of crusting or weeping. Before introducing the auriscope, the ear canal must be straightened by elevating the pinna upwards and backwards (Fig. 1.4). The condition of the ear canal should be noted before the eardrum is examined. If an adequate seal of the canal is achieved by the speculum, gentle pressure on the pneumatic bulb will move the eardrum if the middle ear contains air. This is helpful in distinguishing perforations from thin or translucent segments.
A complete examination also involves viewing the Eustachian tube orifice in the nasopharynx.
Clinical tests of hearing
A sympathetic approach is important to overcome embarrassment or denial with potential hearing problems. Whisper and voice tests are of little value unless performed in a quiet room with a sound pressure level meter placed near the patient. The following tests are more useful.
Tuning fork tests
Tuning fork tests distinguish between conductive and sensorineural hearing loss, but are of limited value in children. Two tests are usually employed using a 512 Hz fork. The fork is sounded by striking the tines against the patella or elbow.
Rinne test
The Rinne test compares air conduction (AC – hearing via ear canal and middle ear) with bone conduction (BC – direct transmission to the inner ear via the mastoid process). The examiner holds the fork by the ear canal and then places it on the mastoid process using gentle counterpressure with the other hand. The patient is asked which position of the fork sounds louder: in front of the ear or touching the mastoid (Fig. 1.5).

Fig. 1.5 Interpretation of tuning fork tests. These tests are invalidated if the ear canals are not free of wax debris.
Sound is normally heard better by air conduction than by bone conduction (Rinne-positive). Disease in the external or middle ear, producing a conductive deafness, will reverse the test result (Rinne-negative).
Weber test
The Weber test is more sensitive than the Rinne test. The tuning fork is placed on the forehead, in the midline, and sound waves are transmitted to both ears equally via the skull. A conductive deafness in one ear causes the sound to be heard on the same side. A sensorineural deafness causes the sound to be heard on the opposite side.
The interpretation of the tuning fork tests in relation to the type of hearing loss is shown in Figure 1.5. Avoid the false Rinne-negative by adequately masking the contralateral ear.
Audiometry, vestibulometry and radiology
Until the advent of audiometers, hearing was tested exclusively by the examiner’s voice and tuning forks. Modern hearing tests are performed in soundproofed rooms using high-precision electronic audiological equipment. All tests require cooperation from the patient. Those tests requiring patient response are termed subjective tests, while those not requiring patient response are termed objective.
Audiometry
Subjective tests
Pure tone audiograms are a standard means of recording hearing levels. Using headphones, each ear is tested individually for air conduction and, if necessary, bone conduction thresholds. The results are usually plotted as a graph. A result of 0 dB (decibels) is the average normal threshold for hearing in young adults (Fig. 1.6).

Fig. 1.6 A series of typical pure tone audiograms of the right ear. Hearing level (dBISO) is plotted on the vertical axis; frequency (Hz) is plotted on the horizontal axis. Air conduction (AC) signals are fed through headphones. Bone conduction (BC) signals are transmitted via a vibrator placed on the mastoid process.
Speech audiometry is a more sophisticated test. Phonetically balanced words are presented at different sound intensities and the number of correct answers is expressed as a percentage score. This is a useful test for evaluating hearing aids.
Objective tests
Impedance audiometry is an extremely useful test in the diagnosis of middle ear disease and some types of sensorineural hearing loss. By varying the pressure in the external ear canal, the compliance (i.e. mobility) of the eardrum may be calculated by the degree of sound reflected from a probe tone. This is very useful when screening for middle ear effusions, particularly in children, and for assessing Eustachian tube function (p. 7). It can also test the integrity of the middle ear mechanism and the auditory reflex arc (stapedius reflex).
Electric response audiometry (ERA) (Fig. 1.7) is another objective test. An evoked potential in the eighth nerve, brainstem or auditory cortex may be recorded using skin electrodes following acoustic stimulation of the cochlea. This principle is used to objectively assess hearing thresholds where the standard tests are not applicable, e.g. babies, disabled people and suspected malingerers.

Fig. 1.7 Evoked response audiometry. The response evoked by a sound stimulus can be recorded at a specific site along the auditory pathway, e.g. eighth nerve, brainstem or cortex.
Otoacoustic emissions testing is a useful screening test for neonatal sensorineural loss where the middle ear function is normal.
Hearing assessment in young children
From birth to about 6 months, the ‘gold standard’ method of testing is by electric response audiometry (see above). From 6 months to about 18 months, a child will turn to a noise, e.g. a rattle. This distraction test is performed by two observers and is a basic screening test performed on all children. From 2 years, various conditioning or cooperation tests are employed using free field noises, e.g. placing a peg in a basket after hearing the noise. It is not until the age of 3–4 years that headphones can be used to test each ear independently.
Vestibulometry
The vestibule has three parts: the utricle, the saccule and the semicircular canals (see Fig. 1.1, p. 2). Each vestibule tonically discharges information to the brain regarding head position, and linear and angular acceleration. This information is part of the general proprioceptive input (joint, tendon, skin and ocular inputs). Dysequilibrium may be the result of an abnormal input from any part of the proprioceptive sensors, or a dysfunction of the central nervous connection secondary to disease, e.g. ischaemia or demyelination.
Tests
The functional status of the peripheral vestibular system can be tested in a variety of ways. These include:
Positional test
From an erect sitting position on a couch, the patient lies flat with the head turned to one side and below horizontal (Fig. 1.8). The onset of any vertigo is noted and the eyes are observed for nystagmus. The feeling of movement and the nystagmus, if present, are allowed to settle before the patient sits upright. The manoeuvre is repeated with the head to the opposite side. This test may help to distinguish vertigo caused by peripheral (otological) as opposed to central pathologies.
Fistula test
If there is otoscopic evidence of middle ear disease in a patient with vertigo, this simple test may be applied.
A caloric effect is induced by either compressing the tragus or using an otoscope with a pneumatic bulb. A feeling of imbalance or vertigo, sometimes accompanied by nystagmus, indicates an abnormal communication between the middle ear and vestibular labyrinth (a positive sign).
Caloric test
Cold (30°C) or warm (44°C) water irrigation of the ear canal stimulates the labyrinth and will induce nystagmus in normal ears. Cold water produces nystagmus to the opposite side to that tested and warm the reverse. (Remember COWS – Cold Opposite, Warm Same – for direction of nystagmus.) This test indicates the presence or absence of function in a particular labyrinth. Air may be used in patients with perforation of the eardrums.
Rotation tests and electronystagmography
Rotational tests assess the vestibular response to angular acceleration by measuring nystagmus from surface electrodes around the ocular muscles. Various other tests of eye pivot, optical fixation and suppression of nystagmus may be recorded by electronystagmography. These investigations give information about central mechanisms and disorders of the vestibular nuclei in the brainstem (p. 20).
Radiology
Imaging of the temporal bone is now done with computed tomography (CT). Bone is black on magnetic resonance imaging (MRI), therefore MRI is used to image temporal bone. Plain radiographs only provide evidence of gross disease and their interpretation may be difficult. Clouding of mastoid air cells may be seen in acute mastoiditis. Diseases that produce significant bony erosion, e.g. carcinoma of the middle ear, may be shown on plain X-rays.
Modern CT scanning and MRI are now widely used to provide information on otitis media with complications, and in the diagnosis of acoustic neuromas (Figs 1.9 and 1.10). MRI is particularly useful in assessing the extent of vascular lesions such as glomus jugulare tumours, and in visualizing the acoustic nerve.

Fig. 1.9 Axial (a) and coronal (b) CT of the temporal bone. The patient has vertigo from a middle ear cholesteatoma eroding the left lateral semicircular canal (arrow). The mastoid air cell system is opaque.

Fig. 1.10 Large acoustic neuroma with early compression of the brainstem. The lesion is enhanced by injection of gadolinium contrast into a peripheral vein.
Audiometry, vestibulometry and radiology
Correctly performed pure tone audiograms are the most reliable method of assessing hearing thresholds.
Electric response audiometry may be required in assessing the thresholds in very young infants and others who are unable to respond to subjective audiometric tests.
Impedance audiometry is extremely useful in assessing the presence of middle ear effusions.
A patient with a positive fistula test in the presence of chronic ear disease requires urgent otological referral.
Hearing loss – general introduction and childhood aetiology
General introduction
A hearing loss, as mentioned previously, can be conductive, sensorineural or mixed. Any disease affecting the outer or middle ear will produce a conductive deafness. Sensorineural loss results from damage to the cochlea or eighth nerve. The degree of hearing loss can be quantified on an audiogram with the thresholds of hearing quoted in decibels (p. 4).
Table 1.2 lists the most common causes of hearing loss. Most of those leading to a conductive deafness will be evident from history, otoscopy, tuning fork tests and audiometry. However, the aetiology of sensorineural loss is frequently unclear. In these cases, specific points in the history should be determined. These points are listed in Table 1.3.
Table 1.2 Aetiology of hearing loss
Cause | Conductive hearing loss | Sensorineural hearing loss |
---|---|---|
Congenital | Atresia of ear, ossicular abnormalities | Prenatal: genetic, rubella |
Acquired | External: wax, otitis externa, foreign body | Perinatal: hypoxia, jaundice |
Middle ear: middle ear effusion, chronic otitis (cholesteatoma, perforated drum), otosclerosis, traumatic perforation of drum (ossicular disruption) | Trauma: noise, head injury, surgery | |
Inflammatory: chronic otitis, meningitis, measles, mumps, syphilis | ||
Degenerative: presbyacusis | ||
Ototoxicity: aminoglycosides, cytotoxics | ||
Neoplastic: acoustic neuroma | ||
Idiopathic: Ménière’s disease, sudden deafness |
Table 1.3 Points to cover in clinical history of a patient presenting with hearing loss
In general terms, a conductive hearing loss is amenable to surgery. However, a common feature of sensorineural deafness is loss of hair cells from the organ of Corti. Hair cells are not replaced, thus sensory deafness is usually permanent. Sensorineural losses often display predominantly high tone loss on audiometry as the hair cells responding to high frequencies are most susceptible to damage.
Hearing loss in children
Deafness is an impairment to communication at any age, but children born with a hearing loss have a major handicap in developing communication. Therefore, early detection and management are required for adequate speech and language development.
The incidence of severe sensorineural deafness is about 1 in 1000. Half of these children have a hereditary type of deafness (Fig. 1.11). The others have hearing losses resulting from acquired causes. Even mild degrees of hearing loss, either conductive or sensorineural, can impair learning ability.

Fig. 1.11 Waardenburg’s syndrome. This is a hereditary syndrome with sensorineural hearing loss. Other features include heterochromia iridian (different coloured irises), wide nasal bridge and a white forelock (not illustrated).
Childhood hearing loss should be suspected in certain groups of individuals (Table 1.4). Children falling into these risk categories should be referred to an audiological physician or otologist for audiometric assessment. This is often a multidisciplinary approach using teachers of the deaf and speech therapists in the same clinic. If a hearing loss can be overcome at an early age, particularly severe sensorineural losses, there is a greater chance the child can attend an ordinary school. Where a hereditary loss is confirmed, a geneticist may advise on risks to future children.
Table 1.4 The childhood groups at risk of suffering from hearing loss
History taking from the parents should concentrate on establishing the answers to specific questions, as well as making a general otological assessment (Table 1.5). Most hearing problems relate to middle ear disease. However, sensorineural deafness may coexist.
Table 1.5 History taking in childhood hearing loss
Children with a profound hearing loss should be fitted with an aid at the earliest possible opportunity after diagnosis. Great perseverance is needed with aiding, particularly in the first 2 years of life. Close observation by otologists, audiological physicians and teachers, with repeated assessments of hearing levels while aided, will give the best chance of normal development of speech and language.
Otitis media with effusion (glue ear)
Otitis media with effusion (OME) is the most common cause of acquired conductive hearing loss in children. The true incidence is unknown, but up to 60% of children in their first year may have middle ear effusions which are clinically asymptomatic. The peak clinical age group is 2–6 years, where about 30% of children suffer effusions. By the age of 11 the incidence has dropped to about 2%. There is a seasonal variation in the disease, associated with upper respiratory tract infections which are more common in October to March in the northern hemisphere.
The effusion in the middle ear may be serous, mucoid or thick (glue). The aetiology is usually Eustachian tube dysfunction, where normal ventilation of the middle ear is disturbed (Fig. 1.12). A diagnosis of chronic otitis media with effusion is made when fluid is present behind the eardrum for 12 weeks or more.

Fig. 1.12 Eustachian tube dysfunction resulting in defective middle ear ventilation. This can be due to a variety of causes and results in a middle ear effusion.
Clinical features
Children with OME usually present with hearing loss or recurrent otalgia. Children with a cleft palate or Down’s syndrome have a higher incidence of middle ear effusions. The otoscopic features of OME are characteristic (Fig. 1.13).

Fig. 1.13 Otoscopic appearance in otitis media with effusion (OME). The handle and short process of the malleus are brought into relief due to retraction of the eardrum. There is a slightly yellow appearance to the eardrum due to the middle ear effusion.
The hearing loss is conductive and may fluctuate down to as much as 40 dB. Tympanometry produces a flat trace, indicating an immobile drum (Fig. 1.14).
Treatment
There is as yet no effective long-term medical treatment for established OME. Short-term improvements with antibiotics are not sustained. Decongestant mixtures are ineffective. If the effusion persists, surgery may be required to restore hearing. Removal of the adenoids reduces the incidence of recurrent effusions. Myringotomy, aspiration of fluid and insertion of a ventilation tube (grommet) immediately restores the hearing (Fig. 1.15). Grommets may remain in the drum for up to 12 months before being extruded. After grommet extrusion some children require reinsertion due to recurrent or persisting middle ear effusions.

Fig. 1.15 Types of grommets (middle ear ventilation tubes). The designs are numerous in variety in an attempt to prevent too rapid an extrusion from the eardrum and to assist in insertion.
Following grommet extrusion, it is common to see tympanosclerosis (white patches) in the eardrum. This type of white patch does not impair hearing.
Chronic failure of the Eustachian tube to function normally results in persisting middle ear effusion and thinning of the tympanic membrane. The eardrum may collapse onto the ossicles, producing a retraction pocket. Long-term ventilation may be necessary to prevent progressive retraction from the low middle ear pressure and subsequent development of chronic suppurative otitis media with cholesteatoma.
Otorrhoea after grommets
Grommets may become infected, producing a mucoid discharge. This should be mopped away and anti-inflammatory drops instilled. Massaging the tragus will allow the drops to penetrate the grommet lumen. Antibiotic eardrops are not recommended except under specialist supervision. Oral antibiotics may also be necessary if the discharge follows an upper respiratory tract infection. Persistent otorrhoea will necessitate removal of the grommet.
Children with grommets should not be prevented from participating in swimming activities. Infection is uncommon and usually readily treated.
Hearing loss – general introduction and childhood aetiology
Childhood hearing loss needs early detection to maximize speech and language acquisition.
Screening at 7–8 months used to be mandatory. Test failure requires early referral.
Neonatal screening with otoacoustic emissions is now universal in the UK.
Middle ear effusions are common, and may be detected by pneumatic otoscopy.
OME may present with otalgia, or may be asymptomatic until hearing loss is suspected.
Insertion of grommets is required for persistent otitis media with effusion.
Otorrhoea due to infected grommets usually resolves with topical treatments.
Hearing loss – adult aetiology
The most common causes of hearing loss in adults are wax impaction and presbyacusis. However, there are a number of other diseases in which hearing loss is the primary complaint, although often with other associated otological symptoms.
Conductive hearing loss
The aetiology of adult conductive hearing loss may be due to pathology of the ear canal, the eardrum or the middle ear.
Ear canal
Wax production varies between individuals and races. Blind attempts to remove wax with cotton buds usually result in impaction. Wax may be properly removed by syringing the ear or with a blunt hook (p. 25). Preliminary softening can be achieved with sodium bicarbonate eardrops three times a day, or hydrogen peroxide. Rarely, excessive accumulations of desquamated skin and wax in the deepest part of the external meatus can expand and erode the ear canal. This is termed keratosis obturans, and an anaesthetic may be required to remove it.
The external canal may be narrowed by bony exostoses predisposing to keratin accumulation (Fig. 1.16). These exostoses often occur in swimmers and require no treatment unless they cause external otitis or hearing deficits.
Eardrum and middle ear
Perforations of the eardrum can occur from trauma and acute or chronic otitis media (Fig. 1.17). The degree of hearing loss depends on the site of the perforation and the extent of middle ear disease.

Fig. 1.17 A subtotal perforation of the left eardrum. The round window niche (RWN), the inudostapedial joint (ISJ) and promontory (P) are clearly visible.
Perforations from simple chronic otitis media where the mastoid is not diseased may be repaired by a tympanoplasty procedure using a graft (temporalis fascia). Ossicular discontinuity may also be treated surgically. Traumatic perforations, e.g. blow to the ear, invariably heal spontaneously if the ear is kept dry.
Adults may suffer with middle ear effusions, although less commonly than children. Investigations should rule out sinusitis, or nasopharyngeal tumours blocking the Eustachian tube (see Fig. 1.12, p. 7).
Otosclerosis is a disease where new bone growth occurs in the capsule of the inner ear. This may fix the footplate of the stapes. Hearing loss characteristically develops in the young adult and is usually conductive (p. 3), although the otoscopic appearance of the eardrum is normal. Pregnancy can accelerate the symptoms, suggesting a hormonal association with the disease. A family history is frequently elicited. Tinnitus may also be present.
Surgery for otosclerosis may restore normal hearing but also carries a small risk of total hearing loss. Use of a hearing aid has no complications, but is often refused (Fig. 1.18).
Sensorineural hearing loss
Presbyacusis (common)
Presbyacusis is a progressive loss of hair cells in the cochlea with age. Roughly 1% of cells are lost each year, and this affects the high-frequency part of the inner ear first (Fig. 1.19). It becomes clinically noticeable from the age of about 60–65 years. The degree of loss varies, as does the age of onset. Some patients with presbyacusis have recruitment (reduced dynamic range of hearing) which reduces effective amplification. The threshold for hearing and the uncomfortable level of sound are abnormally close (e.g. ‘Speak up, I can’t hear you … don’t shout so loud!’). Discrimination may also be affected (‘I hear you but can’t understand you’). There is no treatment to prevent this loss. When a significant social or work handicap is present, a hearing aid may be prescribed. This should be digital so that the pattern of amplification is tailored to the pattern of the individual’s hearing loss. Two hearing aids are better than one, because of binaural hearing.
Sudden (idiopathic) hearing loss (rare)
Cochlear failure may occur in a previously normal ear. The patient is suddenly aware of a blockage or rapid deterioration in hearing. Tinnitus or vertigo may be present. The aetiology is thought to be either a virus infection or vascular ischaemia. Treatment is largely empirical, and changes from decade to decade. Currently there is a great deal of interest in the role of steroids and antiviral agents. Preservation of high-frequency hearing on serial audiograms indicates a good prognosis.
Noise exposure (common)
Acoustic trauma occurs from sudden exposure (impact or blast), or from prolonged exposure, e.g. noise of heavy industrial machinery. Levels of 90 dB or greater require ear protection with properly fitted ear defenders. After exposure there may be a temporary threshold shift, perceived as ‘woolly hearing’ and associated with tinnitus. Continued noise exposure will lead to permanent threshold shifts, usually affecting the higher frequencies starting at 4 kHz.
Treatment is by avoidance or employing adequate ear protection in the form of ear defenders. An established hearing loss may benefit from a hearing aid. A system of compensation is available for occupational hearing loss.
Perilymph fistula (rare)
A rupture of the labyrinthine windows (round or oval) will result in leakage of perilymph fluid and a sensorineural type hearing loss. Mild features of imbalance or even frank vertigo may also occur. The rupture is usually preceded by an event that raises the intracranial pressure, e.g. straining to lift. It may also follow a stapedectomy operation where an iatrogenic fistula is sealed but the leak persists. The middle ear should be explored in cases where the hearing is deteriorating; otherwise, there is a risk of total hearing loss. The offending rupture is then sealed with a fat plug.
Inflammatory diseases (rare)
Measles, mumps, meningitis or syphilis may cause cochlear damage and can result in permanent sensorineural hearing loss. Chronic middle ear disease is also often associated with some degree of sensorineural loss.
Ototoxicity
The inner ear has many active metabolic processes which are susceptible to drugs. The cochlea or labyrinth may be affected in isolation or in combination, and this can result in hearing loss and symptoms of imbalance. Agents that are toxic to the renal system commonly affect the ear, e.g. systemic aminoglycosides and cytotoxic agents. Salicylates and quinine have reversible toxicity.
Acoustic tumours
Acoustic tumours are rare, but treatable, tumours of the vestibular element of the eighth cranial nerve. The most common presentation is a progressive unilateral hearing loss with tinnitus. MRI scanning with gadolinium is the investigation of choice and can demonstrate small tumours (Fig. 1.20). Current treatment options include serial scanning (for small tumours), surgical excision or stereotactic radiosurgery.
Non-organic hearing loss
Some patients are malingerers, either with a psychological problem or seeking benefits. In such cases the history and serial subjective audiometric tests do not match the clinical observations. Objective assessment obtained with electric response audiometry will unmask any difficult non-organic hearing loss.
Hearing loss – adult aetiology
Wax impaction and presbyacusis are the leading causes of hearing loss in adults.
Most causes of conductive hearing loss are identifiable on otoscopy.
Otitis media with effusion in adults is rare, so exclude neoplasia of the nasopharynx.
In otosclerosis the eardrum has a normal appearance.
A progressive unilateral sensorineural hearing loss should be fully investigated to exclude an acoustic neuroma.
Aids to hearing
Hearing loss is a major disability that can interfere with the social, work and educational spheres of a patient’s life. A 35 dB loss in the speech frequencies (500–2000 Hz) can result in major problems. Fortunately, the majority of sufferers may be helped by employing one or more of the remedies available (Table 1.6).
Electronic hearing aids
An electronic hearing aid consists of an earpiece, an amplifier and a microphone. There is a volume control, and many hearing aids are fitted with a ‘T’ setting that allows the use of electromagnetic induction waves to provide sound and cut out extraneous background noise.
A variety of aids is shown in Figure 1.21. The majority of patients will be fitted with a postauricular hearing aid which is relatively unobtrusive. However, severe hearing loss may only be assisted by body-worn (BW) aids. It is possible to incorporate the aid into a spectacle frame if desired. Miniaturized aids can also be worn in the ear or inserted into the ear canal.

Fig. 1.21 A selection of hearing aids. The patient’s hearing loss, manual dexterity and vanity will determine the precise aid that is recommended.
Fitting aids to both ears is preferable in most patients. It is vital to counsel the patient that discrimination may not necessarily be improved, but that amplification can provide benefit by better recognition of rhythms and phrases.
Problems with electronic hearing aids
To gain the maximum benefit from the aid, it is important to provide patients with training. It is a shock to many to learn that an aid cannot produce normal hearing. Patients with conductive hearing losses have better results with aids than those with sensorineural losses. This is due to the fact that many of the latter losses are associated with a phenomenon called ‘recruitment’, where loud sounds are heard exceptionally loudly so that the amplification from a hearing aid merely adds to the patient’s difficulties.
The common problems encountered with electronic aids are listed in Table 1.7. Probably the most frequent difficulty is with acoustic feedback. This produces the familiar high-pitched whistle and is particularly seen in patients who require high amplification, and in whom the ear mould allows sound to escape into the microphone. A similar event will occur if the mould is incorrectly inserted, as is frequently seen in elderly people suffering from arthritic joints.
Table 1.7 Common problems with electronic hearing aids
Problem | Cause |
---|---|
Feedback | Badly fitting ear mould |
Otorrhoea | Ear infection |
Allergy to mould | |
No sound | Dead battery |
Blocked tube |
A persistent otorrhoea may occur due to allergy to the mould. Alternative non-allergenic material can be employed. In some patients this manoeuvre is simply ineffective and, in others, continued insertion of a mould produces otitis externa or a discharge from a mastoid cavity. Such cases may benefit from a bone conducting aid worn as a headband with the microphone abutting firmly onto the mastoid. However, these are cosmetically unsightly.
More recent alternatives are bone conduction aids that are anchored in the temporal bone. The external stimulator sets the aid in vibration either across the intervening skin or by a direct percutaneous attachment facility (Fig. 1.22; Fig. 1.53, p. 24). Such aids do not suffer the feedback problems of conventional air conduction aids and also have the advantage of greatly reduced background noise.

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