FAQs from the Audiology Committee | IALP : International Association of Communication Sciences and Disorders (IALP) FAQs from the Audiology Committee – IALP : International Association of Communication Sciences and Disorders (IALP)

FAQs from the Audiology Committee

1. How important are hearing disorders globally?

Hearing loss as Global Burden according to the World Health Organization

(The following text passages stem from several publications of the WHO and related groups as indicated in the reference list. [1-3])

Hearing loss is one of the most common disabilities in the world and is often referred to as the hidden disability. Hearing impairment is the 2nd or 3rd most common chronic non-life-threatening disorder in the world. The World Health Organization (WHO) estimated that in the year 2005 there were 278 million people in the world with disabling hearing impairment; of these the loss began in childhood in 68 million people, and in adulthood in 210 million people. A further 364 million people are estimated to have a mild hearing loss (see Table 1).

Two thirds of the burden of hearing impairment is in developing countries. The global production of hearing aids is less than one tenth of the need. Current annual production of hearing aids provides approximately 33% of those needed in high-income countries, but less than 3% of those needed in low and middle-income countries. 88% of the produced hearing aids are distributed in North America, Europe, Japan, Australia, and New Zealand.

Since 2001, the WHO has included adult-onset hearing loss in the tables of the global burden of disease in the World Health Report. The causes of the global burden of disease are compared according to the percentage of total Disability Adjusted Life Years (DALYs) in the world that each cause contributes to. DALYs are a measure of the years of healthy life lost (YLL) due to premature death together with the years lived with disability (YLD); hence this method takes much more account of the burden of chronic conditions, including disability, than with previous indicators that focused only on death rates. In the global burden of disease, adult-onset hearing loss ranked 12th in the year 2005, coming after perinatal conditions, lower respiratory infections, HIV/AIDS, depression, heart disease, diarrhoea, stroke, road accidents, tuberculosis, malaria, chronic lung disease in that order of ranking. If one excludes YLL and focuses on disability alone and using the assessment of years lived with disability, adult-onset hearing loss ranks third at 4.8% of total YLD (after depressive disorders and other unintentional injuries which rank first and second with 12.1% and 4.8% of the total).

Thus hearing loss imposes a huge social and economic burden on society so the prevention of hearing impairment by governments and other organizations would be an excellent investment.

Particularly in children, hearing loss constitutes a serious obstacle to their optimal hearing, language, cognitive, social, emotional, school and professional development. Zero point five to 5 out of 1000 neonates and infants have congenital or early childhood onset persistent hearing loss (in most reports prevalence data is given for 2-3/1000 neonates, but is often higher in developing or threshold countries).

If a hearing impairment is not treated properly during the first months of life (critical period of central auditory pathway development), the benefit of therapy is limited. Therefore, early hearing loss detection and intervention (EHDI) is vitally important for children with a permanent childhood hearing loss and will help them enjoy equal opportunities in society alongside all other children.

Benefits of EHDI programs have been frequently demonstrated. Successful newborn and infant hearing screening programs have been implemented in many countries.

Return to overview

2. How is the human ear built and how does hearing work?

Hearing is one of the five senses. Every source of sound produces vibrations that cause sound waves in air (or any other medium). These are funneled into the ear through the auditory canal to reach the eardrum, making it vibrate. These vibrations travel through delicate ossicles in the middle ear which redirect the vibrations to the inner ear. There, hair cells convert them into an electrical signal that is sent to the brain. The brain perceives this as sound: music, a voice, a door closing, etc. Sounds that are too loud can cause the hair cells in the inner ear to become overloaded and die. The longer the exposure and/or the more the noise increases, the more hair cells will die. As the number of hair cells decrease, so does the ability to hear. Dead hair cells cannot be brought back to life, which means that this damage is irreversible.

The human hearing system is divided into a peripheral and a central part. The peripheral part of the ear contains the outer ear (pinna, ear canal and surface of ear drum) the middle ear (tympanic cavity with malleus, incus and stapes), the inner ear (cochlea, vestibule and semi-circular canals) and the acoustic nerve (pars cochlearis as part of nervus vestibulocochlearis) (Figure 1).

The central part of the ear consists of the central auditory system (different processing stages of the brainstem, mesencephalon, and diencephalon) as well as the cortical and subcortical auditory structures. The anatomical border between the peripheral and central part of the ear is the entrance point of the auditory nerve into the brain stem. Functionally, the peripheral part of the ear ends in the centers of the brain stem.

Figure 1: The human ear

Outer ear

Figure 2: the outer ear

The outer ear (Figure 2) is the most external portion of the ear. It includes the pinna (also called auricle), the ear canal, and the very most superficial layer of the ear drum (also called the tympanic membrane). In humans and almost all vertebrates, the only visible portion of the ear is the outer ear. Although the word “ear” may properly refer to the pinna (the flesh covered cartilage appendage on either side of the head), this portion of the ear is not vital for hearing. The outer ear does help retrieve sound (and imposes filtering), but the ear canal is very important. Unless the canal is open, hearing will be dampened. Ear wax (cerumen) is produced by glands in the skin of the outer portion of the ear canal. This outer ear canal skin is applied to cartilage; the thinner skin of the deep canal lies on the bone of the skull. Only the thicker cerumen-producing ear canal skin has hairs. The outer ear ends at the most superficial layer of the tympanic membrane. The tympanic membrane is commonly called the ear drum. The pinna helps direct sound through the ear canal to the tympanic membrane.

Middle ear

Figure 3: The middle ear

The middle ear (Figure 3) consists of several air-filled cavities behind the ear drum (tympanic membrane) that are ventilated through the eustachian tube (tuba auditiva). The tympanic cavity includes the three ear bones or ossicles called the malleus (hammer), incus (anvil), and stapes (stirrup).

The malleus has a long process (the manubrium, or handle) that is attached to the mobile portion of the eardrum. The incus is the bridge between the malleus and stapes. The stapes is the smallest named bone in the human body. The three bones are arranged so that movement (evoked by sound waves) of the tympanic membrane causes movement of the malleus, which causes movement of the incus, which causes movement of the stapes. When the stapes footplate pushes on the oval window, it causes movement of fluid within the cochlea (a portion of the inner ear).

Inner ear

Figure 4: The inner ear

The inner (Figure 4) ear lies in a small system of hollows (labyrinthus osseus) within the petrous part of the temporal bone. It includes both the organ of hearing (the cochlea) and a sense organ that is attuned to the effects of both gravity and motion (labyrinth or vestibular apparatus).

The cochlea is 30 mm to 35 mm long and is spiraled two and a half times. In a lateral view three fluid filled spaces that are lying upon each other are visible, the vestibular canal (scala vestibuli), the middle canal (scala media), and the tympanic canal (scala tympani).

The balance and the hearing part of the inner ear are similarly built. Both are filled with a fluid (endolymph) and have hair cells. The hair cells are cylindrical and are named after the 30 to 150 hair-like processes at the apical part of the cell (stereocilia). Cochlear hair cells come in two anatomically and functionally distinct types: three rows of outer (acoustical pre-amplifiers which transduce the mechanical movement of the basilar membrane by their property to actively contract themselves) and one row of inner hair cells (sound to nerve signal).

The eighth cranial nerve (vestibulocochlear nerve) comes from the brain stem to enter the inner ear. When sound strikes the ear drum, the movement is transferred to the footplate of the stapes, which presses into one of the fluid-filled spaces of the cochlea. The fluid inside this duct is moved, producing a travelling wave of the basilar membrane which separates the scala media from the scala tympani and carries the hair cells of the organ of corti within the middle canal. The moved hair cells stimulate the fibers of the auditory nerve which sends auditory information to the brain.

Central auditory system

Figure 5: The auditory pathway

The sound information travels down the vestibulocochlear nerve (VIIIth cranial nerve of which the auditory nerve is a part), through intermediate stations such as the cochlear nuclei and superior olivary complex of the brainstem and the inferior colliculus of the midbrain, being further processed at each waypoint. The information eventually reaches the thalamus, and from there it is relayed to the cortex. In the human brain, the primary auditory cortex is located in the temporal lobe (Figure 5).

Return to overview

3. How are hearing disorders classified?

Hearing disorders can be classified according to different criteria, e.g. to localization, cause, and degree.

Return to overview

Classification of hearing impairments according to their degree

Ahearing loss can be slight/mild, moderate, severe, or profound including total deafness (Table 1).

Table 1: Grades of hearing impairment (in: [1])

Return to overview

Classification of hearing impairments according to their causes

Hearing impairments can be caused by organic impairments of the ear, the auditory pathway, or the auditory brain structures. Disturbances of the central transportation and processing of auditory information at the various levels of the auditory brain result in central auditory processing disorders. Here, the peripheral hearing may function normally.

A hearing loss might be hereditary or acquired. In case of a hereditary hearing loss, about 20% of the heredity is autosomal dominant, 75% autosomal recessive, and 1-2% x-chromosomal. Acquired hearing impairments in babies may be caused pre-, peri-, or postnatal, for instance, by virus infections contracted from the mother, prematurity, or a critical respiratory status after birth. Later acquired hearing impairments might be due to meningitis, middle ear infections, virus infections, sudden hearing loss, traumata, occupational, or leisure noise. With increasing life expectancy the number of age-related peripheral and central hearing disorders increases.

Return to overview

Classification of hearing impairments according to their kind and localization

Over the years a range of definitions of different types of hearing impairment has been proposed. However, overlapping, unclear or absent definitions have resulted in some confusion in the past. Clear definitions, adapted to the current state of scientific knowledge, are necessary for educational purposes, both for diagnosis and for optimal habilitative or rehabilitative management, and can also contribute to the patient´s acceptance of their condition. Therefore, this overview focuses on a classification of hearing disorders and definitions relevant to clinical diagnosis as proposed in a recent article, published in the Folia Phoniatrica et Logopaedica, the scientific journal of the IALP [4]. In the context of impairment and disability, the World Health Organization’s “International classification of functioning, disability and health” is the most useful source [5].

Hearing impairments can, for example, be classified into sensorineural hearing loss caused by damage to the inner ear or the auditory nerve or conductive hearing loss caused by a blockage or reduction of sound waves passing through the outer or middle ear. Also a combination of the two types is possible. Both types may negatively affect language development, educational and professional success and social relationships. This fosters the importance of an early identification.

Conductive hearing loss

Disturbed conduction of the sound via air from the outer and/or the middle ear to the inner ear. Here, the acoustic impedance (resistance) increases and may lead to a better sound conduction via bone of the skull than the (normal) air conduction via the sound transportation apparatus of outer and middle ears. Hence, the diagnosis of a conductive hearing loss is delineated by a comparison of air-conduction and bone-conduction sound sensation thresholds with more detailed information coming from ear microscopy, otoadmittance (impedance) measures, and high resolution CT and MRT scans.

Sensorineural hearing loss

Impairment of the auditory system either at the level of the inner ear (outer hair cells and/or inner hair cells à “sensory hearing loss”) or in the auditory nerve and/or central auditory system = “neural hearing loss”.

The great majority (about 98%) of human sensorineural hearing loss is caused by abnormalities in the hair cells in the cochlea. This kind of hearing loss is often associated with recruitment, i.e. a phenomenon where the active properties of the hair cells are disturbed resulting in a steeper slope of the perceived loudness than normal when sound level increases (sound is perceived as getting too loud too fast with increasing sound level) and in a kind of “fuzzy” hearing due to stimulation of additional frequency regions in the inner ear adjacent to the mainly stimulated ones.

Outer hair cell lesions are generally related to the motility of the outer hair cells which is essential for fine frequency tuning. Therefore, the term “cochlear motor lesions” should be applied when a sensory hearing loss is restricted to damage of the outer hair cells only.

The Weber test, in which a tuning fork is touched to the midline of the forehead, localizes to the normal or better ear in people with this condition. The Rinne test, which tests air conduction versus bone conduction, is positive (normal), because both bone and air conduction is reduced equally.

There are also unusual sensorineural hearing impairments that involve the vestibulocochlear nerve or the auditory portions of the brain. In the rarest of these sorts of hearing loss, only the auditory centers of the brain are affected. In this situation of central hearing loss, sounds may be heard at normal thresholds, but the quality of the sound perceived is so poor that speech can not be understood.

Most sensorineural hearing loss is due to poor hair cell function. The hair cells may be abnormal at birth, or damaged during the lifetime of an individual. There are both external causes of damage, like noise trauma and infection, and intrinsic abnormalities, like deafness genes.

Sensorineural hearing loss may also result from abnormalities of the VIII cranial nerve.

Sensorineural hearing loss that results from abnormalities of the central auditory system in the brain is called Central Hearing Impairment. Since the auditory pathways cross back and forth on both sides of the brain, total deafness from a central cause is unusual.

This type of hearing loss can also be caused by prolonged exposure to very loud noise, for example, wearing headphones full blast for a few hours.

Retrocochlear hearing impairment

Lesion in the auditory pathway after leaving the cochlea but before entering the brainstem [5]. Test batteries to separate cochlear and retrocochlear disorders comprise measures of otoacoustic emissions, recruitment, intensity discrimination, abnormal adaptation and speech recognition. The term was largely discarded with the introduction of high resolution CT and MRI imaging, and three-dimensional reconstruction of the auditory structures and should not be used anymore.

Auditory Neuropathy, King Kopetzky Syndrome, Central Auditory Disorders

Over the past twenty years, a number of new terms have been introduced for a number of different reasons. Such reasons include the development of improved diagnostic techniques, the clarification of previously obscure disease entities and the desire to integrate diagnostic concepts with educational and rehabilitative approaches. Terms applied include (Central) Auditory Processing Disorders, Auditory Neuropathy and King Kopetzky Syndrome (Obscure Auditory Dysfunction). There is much overlap between these conditions, which are summarized in Figure 6, and also between them and their earlier definitions.

Figure 6: Recent diagnostic classifications of King Kopetzky Syndrome (KKS), Auditory Neuropathy (AN), and Central Auditory Processing Disorder (CAPD) [in: 1]

The term (Central) Auditory Processing Disorder – (C)APD – has been subject to different definitions, in particular in the USA and theUnited Kingdom[7-9]. A recent definition in the Handbook of (Central) Auditory Processing Disorders [10] is shown in Table 2.

The rationale behind the term (C)APD is not completely clear (related to two competing schools of thought). In addition, the existing definitions of (C)APD are somewhat restrictive. Such restricted definitions may be useful from the standpoint of audiometric tests, but have less value from a clinical diagnostic standpoint.

Table 2 also gives definitions of King Kopetzky Syndrome [12] and of Auditory Neuropathy [13].

Table 2: Recent definitions of (C)APD, King Kopetzky Syndrome and Auditory Neuropathy

Type of Auditory Disorder Definition

(Central) Auditory Processing Disorder

A deficit in neural processing of auditory stimuli that is not due to higher order language, cognitive or related factors, yet (C)APD may lead to or be associated with difficulties in higher order language, learning, cognitive and communication functions.
King Kopetzky Syndrome (Obscure Auditory Dysfunction) Perceived auditory disability or disabilities in association with an essentially normal pure tone audiogram. The condition could be regarded as primarily a psychogenic (auditory stress) disorder, and in many cases is associated with a subclinical cochlear disorder.
Auditory Neuropathy A set of auditory disorders with poor speech recognition arising in the inner hair cells, in the cochlear nerve or in the synaptic connection between them, which share the following diagnostic findings: combination of normal otoacoustic emissions (TEOAEs) and/or cochlear microphonics with absent or severely abnormal click-evoked auditory brainstem responses (ABRs) at high stimulus levels.

Auditory Neuropathy (also named “Auditory dys-synchrony” or “Auditory Synaptopathy”) can involve dysfunction from the inner hair cells to the lower brainstem resulting in poor speech recognition and abnormal auditory brainstem responses to sound stimuli. Its impact and management will depend very much on whether the lesion is located in the inner hair cells and their synapses with the cochlear nerve, or more centrally.

The vast majority of lesions affecting the inner hair cells and their synapses with the cochlear nerve dendrites arise from alleles of the Otoferlin gene (DFNB9). Hence, the term “Auditory Synaptopathy” should be used for lesions arising in the synapses between the inner hair cells and the dendrites of the cochlear nerve and “Cochlear Sensory Lesion” for disorders arising specifically in the inner hair cells. This term could be considered to differentiate such lesions from the true “Auditory Neuropathy”, which should be reserved for lesions of the somata and axons of the cochlear nerve and the cochlear nuclei.

King Kopetzky Syndrome (also named Obscure Auditory Dysfunction)

Group of “medically unexplained diseases” comprising difficulty in hearing speech in noise, poor speech recognition but with a normal pure tone audiogram. Its basis is assumed to be psychological or linguistic, while generally including minimal auditory dysfunction. Sensitized tests of hearing may demonstrate minor pathology in many parts of the auditory system, most commonly in the cochlea, but sometimes in the central auditory system. The King Kopetzky syndrome can cover disorders in any part of the auditory system from the cochlea to the auditory cortex, as well as psychological disorder.

Central Auditory Disorders

Central auditory dysfunction is generally regarded as beginning in the cochlear nuclei and extending to all higher levels in the auditory pathway.

Current audiological definitions of central auditory disorders are often too limited, excluding a range of related conditions. They generally exclude patients with any associated conditions which are very likely, given the nature of lesions affecting the brain. At the same time it is, anatomically, an all-embracing condition including lesions in most parts of the central auditory pathways and so has little value from a diagnostic and functional standpoint. Thus, from an aetiological standpoint, central auditory disorders may be subclassified into:

(1) Central auditory processing disorders (CAPDs) which are further subdivided here:

[a] CAPDs without any cognitive deficit, without a peripheral hearing disorder and without any hearing disorders due to demonstrable brain lesions or states of altered consciousness. This can be regarded as the (C)APDs according to recent definitions including the definition from American Speech-Language-Hearing association (ASHA) at http://www.asha.org/docs/html/TR1996-00241.html

[b] CAPDs associated with cerebral deficits such as cognitive deficits involving memory and attention, neurodegenerative alterations, demonstrable brain lesions or states of altered consciousness but without peripheral hearing disorders

[c] CAPDs associated with peripheral hearing disorders but without cerebral deficits

[d] CAPDs associated with both peripheral hearing disorders and cerebral deficits

(2) Central auditory disorders due to demonstrable brain lesions (see Table 3)

[a] Central deafness mostly due to extended (bilateral) temporal lesions

[b] Moderate central auditory deficits due to circumscribed lesions in the auditory cortex or in the acoustic radiation

[c] Central auditory disorders due to neurodegenerative diseases

[d] Central auditory disorders associated with aphasia or other central speech/language disorders

(3) Other abnormal central auditory activities

Certain forms of tinnitus

Abnormal central auditory processing during states of altered consciousness such as autistic disorders, schizophrenia and coma [21-23].

Table 3: Central auditory disorders due to demonstrable brain lesions (definitions of these conditions are shown in the glossary)

Type Sub-categories Examples
2.1 Central deafness mostly due to extended (bilateral) temporal lesions
Auditory agnosia (cortical deafness)

Perceptual form of the auditory agnosia

Developmental auditory agnosia

Non-verbal agnosia, environmental sound agnosia

Verbal agnosia


2.2. Moderate central auditory deficits due to circumscribed lesions in the auditory cortex or in the acoustic radiation
Disturbed perception of contralaterally presented stimuli (unilateral lesions)


Audiogenic memory disturbances

2.3. Central auditory disorders due to neurodegenerative diseases Multiple sclerosis, Alzheimer´s disease
2.4. Central auditory disorders associated with aphasia or other central speech/language disorders Wernicke´s aphasia, transcortical aphasia, global aphasia, disconnection syndrome

Glossary of Central Auditory Disorders due to demonstrable brain lesions:

Amusia: a particular type of auditory agnosia, inability to recognize and enjoy music

Auditory agnosia (cortical deafness): inability to interpret (recognize) sounds but relatively normal pure tone hearing on audiometry

Developmental auditory agnosia: a congenital form of amusia with deficits in the perception of music (tone deafness, tune deafness)

Hemianacusia: heavily disturbed or no hearing on the contralateral ear due to unilateral temporal or callosal lesions

Non-verbal agnosia (environmental sound agnosia): selective difficulty in recognizing and identifying nonverbal or environmental sound

Perceptual form of the auditory agnosia: sound cannot be interpreted although detected; mostly due to bilateral or left-hemispheric lesions of the temporal cortex, but also to subcortical lesions, e.g., to the capsula interna or to the insula

Verbal agnosia: only perception of spoken language is disturbed but speech production, reading, and spelling are normal.

With regards to Central Auditory Processing Disorders, Baran and Musiek [24] have suggested a division, on the basis of functional effects, into low brainstem, high brainstem, auditory cortex and interhemispheric pathways. These and other current recommendations are summarized in Figure 7. For CAPDs, not only the “pure” (C)APDs should be considered, but also their combinations with other cerebral deficits and with peripheral hearing disorders, which should be specified.

The definition of Central Auditory Disorders must take into consideration the fact that many conditions exist other than “pure” CAPDs and that auditory disorders due to demonstrable brain lesions and other abnormal central auditory activities constitute a considerable proportion of Central Auditory Disorders [25]. Thus, for example, we may refer to an “Auditory cortical disorder associated with amusia” or “Auditory cortical disorder associated with tinnitus”. Sometimes, hearing deficits are the first or only manifestations of central pathological processes such as ischemia. If a hearing disturbance does not fit with pure tone audiogram, differentiated tests of central auditory functions are recommended [26].

Figure 7: Proposed terminology of hearing disorders (Note: Disorders resulting in King Kopetzky syndrome may occur in any part of the auditory system from the cochlea to the cortex.)

Return to overview

4. Diseases which specifically affect hearing and their treatment

Disorders of the outer ear


Malformations of the auricle and the ear canal, often combined with malformations of the middle ear, can occur. Malformations can be observed in 1 out of 20.000 newborns. Only one or both ears may be affected. Causes for malformations can be congenital dispositions or exogenous factors, such as thalidomide, a rubella infection during pregnancy, syndroms, or radioactivity. Smaller malformations such as auricular appendages do not lead to hearing dysfunctions. More pronounced malformations such as rudiments or a total lack of the auricle can be accompanied by an atresia.

Malfunctions of the outer ear can also be acquired due to trauma, surgery or inflammation.

These malformations lead to a conductive hearing loss.


With bilateral malformation of the outer and middle ear a BAHA (bone anchored hearing aid) or a middle ear prosthesis such as Vibrant Soundbridge should be supplied. Constructive surgeries of one ear or both ears may start approximately one year before school enrollment.

Inflammation of the outer ear canal (otitis externa)

Inflammation of the outer ear canal only induce conductive hearing loss due to swelling or blocking of the ear canal. Infections are mostly caused by the penetration of bacteria through small fissures or cracks of the ear canal. Often such inflammation is the consequence of manipulations of the ear canal using cotton swabs or hair pins, but also bathing. Furthermore, mycoses with dirty-white or blackish covering can occur.


Cleaning of the ear canal and treatment with local disinfecting, antibiotic or antifungal (sometimes corticoids) salves or ear drops.

Foreign body in the ear canal and earwax

Earwax (cerumen) or objects can lead to minor sound conduction problems, but are easily removable.

Disorders of the middle ear


see outer ear disorders


Injuries caused by a direct hit to the ear or hitting the water surface can lead to perforation of the ear drum. These go along with mild conductive hearing loss (10 – 20 dB). These injuries spontaneously close up again or are “splinted” by surgery.

Injuries evoked by foreign bodies such as cotton swabs or twigs can lead to dislocations or fractures of the ossicles. The resulting more severe dysfunctions of sound conduction have to be corrected through surgery.

Middle ear ventilation problems

The predominant part of hearing impairments during childhood are induced by middle ear ventilation problems. They are due to a swelling of the mucous membrane in the aperture of the eustachian tube or in the complete tube so that no sufficient pressurization is warranted. Pharyngeal tonsils (adenoids), cleft lips, allergic reactions, sinustis (inflammation of the paranasal sinuses), nasopharyngeal carcinoma, and impaired nasal breathing can lead to middle ear ventilation problems. As a result the air located in the middle ear gets reabsorbed and due to filtration fluids are sucked from surrounding tissue into the middle ear (transudate). In case of a sustained closure exudate is formed, a fluid that manifests in a middle ear infusion. With persistent tube ventilation impairment a tenacious secretion (mucotympanon) is produced leading to so-called glue ear.


Conservative measures like treatment of infections or allergic reactions have to be considered. If these measures fail during childhood, adenoids must be removed (adenoidectomy). Often a concurrent paracentesis (puncture of tympanic membrane) and drainage of the secretion is necessary. In case of a mucotympanon a tympanostomy is the action of choice.

Serous otitis media

If the eustachian tube becomes blocked by swelling or congestion in the nose and throat, by swelling of the mucous membrane in the middle ear, or by swelling of the mucous membrane of the eustachian tube itself, the air pressure in the middle ear cannot equalize properly. A negative pressure develops, and if the obstruction is prolonged, fluid may be drawn into the air space of the middle ear from the mucosa. This may occur with a cold or flu virus and is a common cause of ear infections in children (serous otitis media).


Serous otitis media may resolve without treatment or may require a parecentesis with or without placement of tubes in the tympanic membrane.

Acute/Chronic otitis media

If the eustachian tube blockage persists, chronic changes in the tissue of the middle ear begin to occur. First, the mucous secretions become thicker, and therefore less likely to drain. Then, the membranes themselves begin to thicken and become inflamed. The defense mechanisms of the eustachian tube and middle ear become compromised and bacteria normally present in the nose may enter the middle ear and cause a painful condition called acute otitis media.


This responds to antibiotic treatment, but may require placement of tubes.

The negative pressure in the middle ear or alternating periods of negative, normal and positive pressure may deform the eardrum. In the long term, the eardrum may become severely distorted, thinned, or even perforated. These changes may cause conductive hearing loss and a sensation of pressure. When there is a hole in the eardrum, the natural protection of the middle ear from the environment is lost. Water and bacteria entering the middle ear from the ear canal can cause inflammation and infection. Drainage from the ear is a sign of a perforation.

Inflammation and infection in time can cause erosion of the ossicles and the walls of the middle and inner ear. The patient may experience hearing loss, imbalance, or weakness of facial movement on the affected side. In rare instances, the infection may extend deeper into the head, causing meningitis or brain abscess.

Surgery (tympanoplasty) to reconstruct the eardrum and/or the small bones of the middle ear (ossicles) is the therapy of choice. Additionally or alternatively (if surgery is not sucessful), hearing aids may be necessary.


A cholesteatoma, or skin cyst, is essentially skin in the wrong place. Epidermal skin from the ear canal or outside surface of the eardrum, like that on the back of the hand, does not belong in the middle ear. If it is trapped by a deformed eardrum or migrates through a perforation, it tends to grow out of control and can cause significant damage to the structures of the middle ear and mastoid.


Surgery in one or two steps is the action of choice. The risks of surgical removal are generally less than the risk associated with leaving the cholesteatoma in situ.


Otosclerosis is an abnormal, microscopic growth of bone in the walls of the inner ear which causes the stapes bone (stirrup) to become frozen in place or “fixed”. Normally the stapes, the smallest bone in the body, vibrates freely to allow the transmission of sound into the inner ear. When it becomes fixed to the surrounding bone, it prevents sound waves from reaching the inner ear fluids and hearing is impaired.


No medication has proven to be effective in the treatment of otosclerosis. Although a hearing aid can be worn successfully by most patients, natural hearing is preferred. Surgery (stapedectomy) has been found to be the most effective method of improving hearing loss caused by otosclerosis.

Disorders of the inner ear

Sudden Sensorineural Hearing Loss (SSHL)

Sudden Sensorineural Hearing Loss (SSHL), or sudden deafness, is a rapid loss of hearing. SSHL can happen to a person all at once or over a period of up to 3 days. It should be considered a medical emergency. A SSHL is diagnosed by conducting a hearing test (pure tone audiometry) if a sudden loss of at least 30 decibels in three connected frequencies is measured. Hearing loss affects only one ear in 9 out of 10 people who experience SSHL. Many people notice it when they wake up in the morning. Others first notice it when they try to use the imapired ear, such as when they make a phone call. Still others notice a loud, alarming “pop” just before their hearing disappears. People with SSHL often experience dizziness or a ringing in their ears (tinnitus), or both. Some patients recover completely without medical intervention, often within the first 3 days. This is called a spontaneous recovery. Others get better slowly over a 1 or 2 week period. Although a good to excellent recovery is likely, 15 percent of those with SSHL experience a hearing loss that gets worse over time. Though there are more than 100 possible causes of sudden deafness, it is rare for a specific cause to be precisely identified. Only 10 to 15 percent of patients with SSHL know what caused their loss. Normally, diagnosis is based on the patient’s medical history. Possible causes include the following: Infectious diseases, trauma, such as a head injury, neoplasms such as acoustic neuroma, immunologic diseases such as Cogan’s syndrome, toxic causes, such as snake bites, ototoxic drugs, circulatory problems, neurological causes such as multiple sclerosis, and other disorders such as Ménière’s disease.


The most common therapy for SSHL, especially in cases with an unknown cause, is treatment with steroids. Steroids are used to treat many different disorders and usually work to reduce inflammation, decrease swelling, and help the body fight illness. Steroid treatment helps some SSHL patients who also have conditions that affect the immune system, which is the body’s defense against disease. Other common methods that may help patients are infusions increasing blood flow or oxygenation or hyperbaric oxygen therapy.

Acoustic trauma

Acoustic trauma is an injury to the hearing mechanisms in the inner ear due to very loud noise.

Acoustic trauma is a common cause of sensory hearing loss. Damage to the hearing mechanisms within the inner ear may be caused by an explosion near the ear, gunshots, long-term exposure to loud noises (such as loud music or machinery), fireworks etc. The hearing loss may be permanent in the affected ear. Ear protection may prevent the hearing loss from getting worse.


The hearing loss may not be treatable. The goal of treatment is to protect the ear from further damage. A hearing aid may help you communicate.

Ototoxic hearning loss

Ototoxicity is damage to the ear (oto-), specifically the cochlea or auditory nerve and sometimes the vestibular system, by a toxin. It is commonly medication-induced; ototoxic drugs include antibiotics such as the aminoglycoside gentamicin, loop diuretics such as furosemide, and platinum-based chemotherapy agents such as cisplatin. It can result in sensorineural hearing loss, dysequilibrium, or both. Either may be reversible and temporary, or irreversible and permanent.


No specific treatment is available, but immediate withdrawal of the drug may be warranted in cases where the consequences of doing so are less severe than the consequences of the ototoxicity. Hearing aids or cochlea implants are appropriate therapies of an ototoxic hearing loss.

Ménière’s disease

Ménière’s disease is a clinical syndrome that consists of four symptoms:

1. Episodes of severe, incapacitating vertigo lasting on the order of several minutes to a few hours (usually 30 minutes to 8 hours or so). The vertigo is usually a sensation of spinning, but can also be a feeling of being pushed or pulled (pulsion). In rare forms of Ménière’s disease, patients experience sudden “drop-attacks”, which cause them to fall suddenly to the ground without warning and without loss of consciousness (the so-called otolithic crisis of Tumarkin). These attacks last only for a few seconds, but because of their unpredictability and severity are potentially the most devastating amongst all forms of Ménière’s disease.

2. Fluctuating, slowly progressive hearing loss. The hearing loss is of a “sensorineural” type, arising in the inner ear. The hearing classically will worsen during a vertigo attack, and may improve after resolution of the acute symptoms. Typically, mainly low frequencies are affected.

3. Episodic tinnitus (abnormal perception of sound in the ear; usually a roaring, buzzing or ringing). There is frequently a baseline tinnitus in the ear, but this typically worsens temporarily with a vertigo attack.

4. Aural fullness: A sensation of plugging or clogging in the ear that worsens when a vertigo attack begins.

The root cause of Ménière’s disease is unknown, though the symptoms are thought to be produced by an increase in the fluid pressure in the inner ear, i.e., by “endolymphatic hydrops”. In all likelihood, a variety of insults to the ear can lead to endolymphatic hydrops as their common final pathway, thereby producing symptoms akin to those of Ménière’s disease. When the inciting cause of hydropic symptoms is identified, then the proper descriptor is Ménière’s syndrome or delayed endolymphatic hydrops. When the symptoms develop spontaneously, with no identifiable cause, it is termed Ménière’s disease.


Because Ménière’s cannot be cured, treatments focus more on treating and preventing symptoms.

Several environmental and dietary changes (low-sodium diet) are thought to reduce the frequency or severity of symptom outbreaks. Treatments aimed at lowering the pressure within the inner ear include antihistamines, anticholinergics, steroids, and diuretics. To manage attacks, patients may be advised to take antiemetic drugs, antivertigo drugs or antihistamines.

If symptoms do not improve with conservative treatment, surgery is considered. Permanent surgical destruction of the balance part of the affected ear can be performed for severe cases if only one ear is affected. This can be achieved through a chemical labyrithectomiy, in which a drug (such as gentamicin) that “kills” the vestibular apparatus is injected into the middle ear.

Surgery to decompress the endolyphatic sac has shown to be effective for temporary relief from symptoms. Most patients see a decrease in vertigo occurrence, while their hearing may be unaffected.

Destructive surgeries involve removing entire functionality of most, if not all, of the affected ear. The inner ear itself can be surgically removed via labyrinthectomy. Hearing is always completely lost in the affected ear with this operation. Alternatively, surgeons can cut the nerve to the balance portion of the inner ear in a vestibular neurectomy where hearing is often mostly preserved.

Age-related hearing loss (Presbycusis)

Presbycusis, or age-related hearing loss, is the cumulative effect of aging on hearing. It is defined as a progressive bilateral symmetrical age-related sensorineural hearing loss. The hearing loss is most marked at higher frequencies. Presbycusis is usually a sensorineural hearing disorder, possibly associated with a central auditory dysfunction. It is most commonly caused by gradual changes in the inner ear. The cumulative effects of aging, repeated exposure to daily traffic sounds or construction work, noisy environment, equipment that produces noise, and loud music can cause sensorineural hearing loss. Sensorineural hearing loss is most often due to a loss of hair cells (sensory receptors in the inner ear). This can occur as a result of hereditary factors as well as aging, various health conditions, and side effects of some medicines (aspirin and certain antibiotics). Presbycusis may be caused by changes in the blood supply to the ear because of heart disease, high blood pressure, vascular (pertaining to blood vessels) conditions caused by diabetes, or other circulatory problems. The loss may be mild, moderate, or severe.


There are several strategies to treat people with presbycusis. Hearing aids are recommended for the most individuals. Assistive listening devices can provide further improvement in hearing ability in certain situations. One example of such a device is the built-in telephone amplifier. Another example is the FM system, which make sounds clearer, with or without a hearing aid, by delivering sound waves like a radio. Training in speechreading (using visual cues to determine what is being spoken) can help those with presbycusis to understand better what is being said in conversations or presentations.

Tinnitus aurium

Tinnitus is the perception of sound within the human ear in the absence of corresponding external sound. Tinnitus is not a disease, but a symptom resulting from a range of underlying causes that can include: ear infections, foreign objects or wax in the ear, nose allergies that prevent (or induce) fluid drain and cause wax build-up. Tinnitus can also be caused by natural hearing impairment (as in aging), as a side effect of some medications, and as a side effect of genetic (congenital) hearing loss or noise-induced hearing loss. Every deprivation from sound must be regarded as a potential source of tinnitus. In many cases tinnitus must be regarded a central disregulation in the auditory system.


There are many approaches for the treatment of tinnitus. If a metabolic, drug, infectious, or inflammatory cause is identified, specific treatment can be initiated. This may include changing or eliminating medications, managing elevated blood sugars, and treatment with antibiotics, antivirals, and/or anti-inflammatories. If a tumor is found it may be treated with surgery or radiation, or it may be simply monitored.

If none of the named factors can be identified, the adequate treatment comprises acoustic measures such as hearing aid, masker or noiser, and psychologic intervention such as tinnitus retraining therapy. In cases of cervical spine involvement, physiotherapeutic treatment may be the way to succeed.

Return to overview

Central Auditory Processing Disorders (CAPDs)

According to the definition of the American Speech and Hearing Association [27] (C)APDs can be regarded as ’…deficits observed in one or more of the central auditory processes responsible for generating the auditory evoked potentials and the following behaviors:

sound localization and lateralization
auditory discrimination
auditory pattern recognition
temporal aspects of audition, including
– temporal resolution (i.e. detection of changes in frequency, amplitude, and duration of auditory stimuli, and detection of time intervals between auditory stimuli)

– temporal masking (i.e. obscuring of signals by pre- or post-stimulatory presentation of masker)

– temporal integration (i.e. summation of power over durations less than 200-400 msec)

– temporal ordering (i.e. detection of sequence of sound over time)

auditory performance with competing acoustic signals
auditory performance with degraded acoustic signals.’

CAPDs may either occur isolated as bottom-up processes or combined with other disturbances (memory, attention, storage functions) as top-down-processes. They may have negative impact on listening, communication, academic success, and job performance.

For auditory processing, the following features can be distinguished: auditory localization, selection, separation, temporal resolution, pattern analysis, and differentiation. Auditory perception rather includes auditory identification, analysis, completion, awareness, and sequencing.

Children with CAPD are mostly characterized by one or more of the following symptoms: conspicuously reduced speech perception in noise; poor speech perception if more than one person is talking; low interest, attention, or short perseverance if somebody reads to them or tells stories; poor sound localization in everyday life; inconstant auditory reactions already as baby; responding to verbal requests with questions; inadequate reactions on verbal requests; frequent misunderstandings of verbal requests; conspicuous insensitivity to sound stimuli and/or increased sensitivity to loud or shrill sounds. They may confuse similarly sounding words, have problems in learning or memorizing rhymes, song texts or poems, have memory problems in everyday situations with multiple requests, have problems with rhythm while clapping during rhymes or songs and suffer from reading and spelling difficulties while other school achievements are average. Furthermore, they can be distracted easily by other stimuli (visual or auditive ones). These symptoms might be associated with dyslexia later in development.

Adults with CAPD especially face difficulties regarding noise and sound localization and in situations with speech perception in noise, in particular in speech noise when several speakers talk simultaneously [27].

There are several risk factors for being affected by CAPD: family history of dyslexia; developmental language delay or impairments, in particular specific language impairment; other hearing impairments; pre-, peri-, and postnatal risk factors for developmental disorders; long lasting conductive hearing loss during the sensitive phases of maturation of the auditory pathway during baby age and early childhood.

Universally accepted diagnostic criteria for CAPDs are lacking. Test batteries must meet accepted psychophysical and scientific standards and must be appropriate to the individual (e.g., regarding age and cognitive abilities). The diagnosis of CAPDs requires a multidisciplinary approach and is based on a synthesis of information from history (medical, educational, developmental), behavioural and electrophysiological test procedures, as well as ancillary procedures such as neuroimaging, speech and language assessment and psychological/cognitive assessment. Furthermore, its diagnosis requires careful consideration of cognitive, memory and linguistic parameters and potentially confounding factors. Hence, cognitive abilities, attention, and working memory need to be tested.


Acoustic treatment of rooms

This intervention aims at reducing noise levels and reverberation times by several means, e.g., by adding carpets, curtains, and doors to the room or by putting seals on doors and windows to reduce the effect of outside noise. Moreover, noise absorbent partitions or screens can be installed within the room. Also covering hard reflective surfaces with absorptive material such as cork can improve reverberation time.

Hearing Devices

Soundfield and personal frequency modulated (FM) amplification systems are technical interventions regarding hearing deficits. These are wireless devices that receive distant auditory input, amplify and transmit the signal to the ear of the listener. A microphone worn by the speaker and connected to a transmitter picks up the speech signal of the speaker and converts this to an electrical signal, which is transmitted via FM band waves to the receiver. These systems help counteract the problem of distance between teacher and student, as loss of critical speech elements is overcome since the distance travelled by the speech signals is reduced, while masking of the speech signals by ambient noise is minimized and overall audibility is increased.


Regarding CAPD, several interventions based on auditory training are available. (1) The test-driven approach aims at choosing training tasks according to test findings. (2) The profile-driven approach classifies the patient into one of several CAPD subtypes while training tasks are chosen according to this classification.

More generally, one intervention for affected children might be that the speaker (e.g., the teacher) tries to speak as clearly and slowly as possible to the child. Key points of the message should be emphasized, e.g., by altering the pace of the speech. Messages should be short, and if not understood, they should be repeated or rephrased. This requires the speaker to frequently check for the patient’s understanding. Also, very generally, auditory training should be administered systematically with gradually increasing difficulty.

Auditory training can be conducted formally or informally: for the formal form, which is predominantly a bottom-up process, training is administered rigorously in a control setting. Acoustically controlled stimuli are used and specific auditory processes are directly exercised. For the informal form, which is predominantly a top-down process, training is administered at home or in school. Multiple auditory processes are trained using predominantly language stimuli. Features of this training are vowel training, localization of sounds, discrimination of words and listening to stories or songs while detecting sounds or words [28].

Return to overview


1 World Health Organization: Primary ear and hearing care training resource advanced level. Geneva, World Health Organization, 2006.

2 World Health Organization: Neonatal and infant hearing screening. Current issues and guiding principles for action. Outcome of a WHO Informal consultation held at WHO Headquarters, Geneva, Switzerland, 09-10 November, 2009. Geneva, World Health Organization, in press.

3 World Health Organization/WWHearing: Affordable hearing aids – a stepwise framework. WHO/WWHearing fifth workshop on the provision of hearing aids and services for developing countries. Geneva, World Health Organization, 2007.

4 Neumann K, Stephens D: Definitions of types of hearing impairment – a discussion paper. Folia Phoniatrica et Logopaedica, in press.

5 World Health Organization: International classification of functioning, disability and health – ICF. Geneva, World Health Organization, 2001.

6 Martin MC, Summers IR: Dictionary of Hearing. London, Whurr,1999.

7 Jerger J, Musiek F: Report of the consensus conference on the diagnosis of auditory processing disorders in school-aged children. J Am Acad Audiol 2000;11:467-474.

8 British Society of Audiology: Working definition of APD. 2004;http://www.thebsa.org.uk/apd/Home.htm#working%20def (Consulted 060709)

9 American Speech-Language-Hearing Association: (Central) Auditory Processing Disorders [Technical Report]. 2005;http://www.asha.org/docs/html/TR2005-00043.html (Consulted 060709)

10 Chermak GD, Musiek FE (eds): Handbook of (Central) Auditory Processing Disorder. San Diego, Plural, 2007.

11 Moore BCJ. Cochlear Hearing Loss: Physiological, Psychological and Technical Aspects. 2nd ed. Chichester, Wiley, 2007.

11 Hinchcliffe R: King-Kopetzky syndrome: an auditory stress disorder? Journal of Audiological Medicine 1992;1:89-98.

12 Starr A, Picton TW, Sininger Y, Hood LJ, Berlin CI. Auditory neuropathy. Brain 1996;119;741-753.

13 Saunders GH, Haggard MP: The clinical assessment of obscure auditory dysfunction. Ear Hear 1989;10:200-208.

14 Stephens SDG, Rendell RJ. Auditory disability with normal hearing. Quaderni di Audiologia 1988;4:233-238.

15 Pryce H, Wainwright D: Help-seeking for medically unexplained hearing difficulties: A qualitative study. International Journal of Therapy and Rehabilitation 2008;15:1-7.

16 Zhao F, Stephens D: Subcategories of patients with King-Kopetzky syndrome. Br J Audiol 2000;34:241-256.

17 Rance G. Auditory neuropathy/dys-synchrony and its perceptual consequences. Trends amplif 2005;9:1-43.

18 Moser T, Strenzke N, Meyer A, Lesinski-Schiedat A, Lenarz T, Beutner D, Foerst A, Lang-Roth R, von Wedel H, Walger M, Gross M, Keilmann A, Limberger A, Steffens T, Strutz J: Diagnosis and therapy of auditory synaptopathy/neuropathy. HNO 2006;54:833-839.

19 Loundon N, Marcolla A, Roux I, Rouillon I, Denoyelle F, Feldmann D, Marlin S, Garabedian EN. Auditory neuropathy or endocochlear hearing loss? Otol Neurotol 2005;26:748-754.

20 Griffiths TD: Central auditory pathologies. Br Med Bull 2002a;63:107-120.

21 Griffiths TD: Central auditory processing disorders. Curr Opin Neurol 2002b;15:31-33.

22 Neumann K, Rübsamen R: Central auditory disorders in adults with brain lesions [Zentrale Hörstörungen bei hirngeschädigten Erwachsenen] (Bookchapter written in German); in: Jochims S (ed) Musiktherapie in der Neurologie/Neurorehabilitation Erwachsener. Weltweite Konzepte, Forschung und Praxis. Bad Honnef, Hippocampus, 2005, pp 43-82.

23 Baran JA, Musiek F: Central auditory disorders; in Luxon L, Furman JM, Martini A, Stephens D. (eds): Textbook of Audiological Medicine: Clinical Aspects of Hearing and Balance. London, Martin Dunitz, 2003, pp 495-511.

24 Marshall L: Auditory processing in aging listeners. J Speech Hear Disord 1981;46:226-240.

25 Bamiou DE, Liasis A, Boyd S, Cohen M, Raglan E: Central auditory processing disorder as the presenting manifestation of subtle brain pathology. Audiology 2000;39:168-172.

26 Chermak GD, Hall JW, Baran JA, Sloan C, Musiek FE: Diagnosis and management of CAPD and ADHD. Singular Publishing Group, San Diego, CA, 1997.

27 Bamiou DE: Auditory processing disorders. Definitions, aetiology and differential diagnosis. Proceedings of the First International Composium on Central Auditory Processing Disorders (CAPD). Cairo, March 15-18, 2009; http://ialp.info/joomla/index.php?/Selected-papers-of-CAPD-Comps.html (Consulted 300709)

28 Chermak GD: Intervention for (C)APD Treatment and Management. Proceedings of the First International Composium on Central Auditory Processing Disorders (CAPD). Cairo, March 15-18, 2009; http://ialp.info/joomla/index.php?/Selected-papers-of-CAPD-Comps.html (Consulted 300709)

5. Worldwide links to information on hearing disorders and impairments:

Where can I find help?

Please select your nationality from the list below. You will then be referred to national organizations which provide answers to this question.

Great Britain
New Zealand
South Africa
The Netherlands
The United States of America

Return to overview

Pan American Society of Audiology:


Return to overview


Better Hearing Australia (Victoria) Inc:


Audiological Society of Australia:


Hearing Aid Audiometrist Society of Australia:


Return to overview


Österreichische Gesellschaft für Hals-, Nasen- und Ohrenheilkunde, Kopf- und Halschirurgie:


Berufsverband Logopädie Austria:


Österreichische Gesellschaft für Sprachheilpädagogik:


Return to overview


Organizations of therapist

National Union of Audiologists:


Union Professionelle des Logopèdes Francophones:


Vlaamse Vereniging voor Logopedisten:


Return to overview


Organizations for therapists

Associaçao Brasileira De Foniatria E Audiologia:

Endereço: R Dra Neyde a Sollitto, 435-2 Andar Sala 40. Bairro: Vila

Clementino, Sao Paulo

Return to overview


Canadian Association of Speech-Language Pathologists and Audiologists – Association Canadienne des Orthophonistes et Audiologistes (CASPLA-ACOA):


Hearing Aid Society of Nova Scotia:


Return to overview


China, Hong Kong, SAR Society of Audiology:


Speech Language Hearing Association of the Republic of China:


Hearing the Future:


Return to overview


Nordiska audiologiska sällskapet:


Audiologopædisk Forening (ALF):


Foreningen af Universitetsuddannede Audiologopæder:


Dansk Selskap for Logopaedi og Foniatri (DSLF):


Return to overview

European Community

European Federation of Audiology Societies:


Comité Permanent de Liaison des Orthophonistes / Logopèdes de l’Union Européenne (CPLOL)

CPLOL promotes the harmonization of professional education profiles, ethical standards and practices across the European Union and organizes public discussion forums and similar events.


Return to overview


Nordic Audiological Society:


Finnish Audiological Society:


Return to overview


Société Française d’Audiologie:


Fédération Nationale des Orthophonistes:


L’ Institut Bruckhof:


Return to overview


Deutsche Gesellschaft für Audiologie (German Audiology Society): http://www.dga-ev.com/

Deutsche Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie:


Arbeitsgemeinschaft Deutschsprachiger Audiologen und Neurootologen:


Fachverband Deutscher Hörgeräteakustiker e.V.:


Deutscher Berufsverband für Logopädie e.V.:


Deutsche Tinnitus-Liga e.V.:


Return to overview

Great Britain

British Society of Audiology:


British Association of Audiovestibular Physicians:


British Association of Paediatricians in Audiology (BAPA):


British Association of Educational Audiologists:


British Society of Hearing Aid Audiologists:


British Tinnitus Association:


Return to overview


Nordic Audiological Society:


Icelandic Audiological Society:

Heyrnar – og talmeinastoo Islands

Haaleitisbraut 1

105 Reykjavik


Phone: 35+ 45 8138 55

Fax: 35+ 45 6800 55

Return to overview


Indian Speech Language and Hearing Association:



Return to overview


Irish Society of Audiology:


Irish Society of Hearing Aid Audiologists:


Return to overview


The Israeli Speech Hearing and Language Association:

עמוד הבית

Return to overview


Italian Society of Audiology:


Federazione Logopedisti Italiani


Associazione Italiana Tecnici Audiometristi:


Return to overview


Japan Audiological Society:


Japanese Association of Speech-Language-Hearing Therapists (JAS):
JunKatsuki-Nakamura, PhD
Kaga Yawata Onsen Hospital
Ishikawa, ken 923-8551


Return to overview


Malaysian Association of Speech Language and Hearing (MASH)


Return to overview

New Zealand

New Zealand Audiological Society:


The Hearing Association of New Zealand:


New Zealand Tinnitus Association:


Return to overview


Norsk Logopedlag:


Nordic Audiological Society:


Return to overview


Associação Portuguesa de Audiologistas:


Return to overview


Russian Society of Audiology:


Association of Phoniatricians and Speech Therapists:
Prof. Yuris Vasilenko, M.D.
Proesd 5. cor 9
12501 Moscow 2nd Botkinski, Russia

Return to overview

South Africa

South African Speech Language Hearing Association:


The South African Society of Hearing Aid Acousticians


Return to overview


Asociación Española de Audiología:


Asociación de Diplomados Universitarios en Logopedia:


Return to overview


Nordic Audiological Society:


Swedish Society of Audiology (Svenska Audiologiska Sällskapet):


Svensk Förening för Foniatri och Logopedi (SFFL):


Return to overview

Taiwan, China

The Speech-Language-Hearing Association of the Republic of China


Return to overview

The Netherlands

Nederlandse Vereniging voor Audiologie:


Nederlandse Vereniging voor Logopedie en Foniatrie (NVLF)
Steinhagenseweg 2b, Postbus 75, 3440 AB WOERDEN

Dutch Association of Voice, Speech and Language Pathology (NVSST)
Prof. H.K. Schutte
ENT Clinic
University Hospital, P.O. Box 30.001
NL-9700 RB Groningen, Netherland


Return to overview

The United States of America

American Academy of Audiology:


American Auditory Society:


American Speech-Language-Hearing Association (ASHA).

ASHA is the primary certification and professional association for speech-language-pathologists in the United States. ASHA represents over 100,000 speech-language pathologists:


Association for Research in Otolaryngology:


Michigan Hearing Society:


Oregon Hearing Society:


Georgia Society of Hearing Professionals:


Washington Hearing Society:


Iowa Hearing Association:


Missouri Hearing Society:


Nebraska Hearing Society:


Florida Society of Hearing Healthcare Professionals:


The Colorado Hearing Aid Society:


Hearing Aid Association of Kentucky:


Texas Hearing Aid Association:


Alabama Society for Hearing Healthcare Providers:


American Hearing Aid Associates:


American Tinnitus Association (ATA):


California Speech-Language-Hearing Association:


Illinois Speech-Language-Hearing Association:


Missisippi Speech-Language-Hearing Association:


Texas Speech-Language-Hearing Association:


Wisconsin Speech-Language-Hearing Association:


Return to overview.

Important links

European Federation of Audiology Societies:


Hearing International:


International Hearing Society:


International Society of Audiology:


WHO: Project Prevention of deafness and hearing impairment


Return to overview