Aetiology and clinical presentations of auditory processing disorders—a review

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  1. D-E Bamiou,
  2. F E Musiek,
  3. 50 Yard Luxon
  1. Department of Audiological Medicine, Great Ormond Street Infirmary, London WC1N 3JH, Great britain
  1. Dr Bamiou doriseva{at}ndirect.co.united kingdom of great britain and northern ireland

Abstract

Auditory processing disorders may have detrimental consequences on a child's life, if undiagnosed and untreated. We review causes of auditory processing disorders in order to raise clinical sensation. Auditory processing disorders may present against a background of neurological disease or developmental disorders, as well as in isolation. Clinicians need to exist aware of potential causes and implications of auditory processing disorders.

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Hearing is a complex process that orchestrates transduction of the acoustic stimulus into neural impulses by the ears, transmission of the neural impulses by the auditory nerves to the brain, and perceptual registration and cognitive elaboration of the acoustic signal past the brain as well as conscious perception of the audio. Hearing impairment(s) arising from pathology of the brain may have detrimental consequences on a child's life if untreated; even so, diagnostic and management strategies for these "central" hearing impairments in childhood are rarely implemented. These auditory deficits have been collectively termed "auditory processing disorders", in social club to incorporate in the term the interaction between peripheral and cardinal pathways.1

A rough prevalence approximate for auditory processing disorders (APD) in childhood is 7%.2 Despite the frequency of the trouble, a systematic arroyo to the diagnosis and rehabilitation of APD in children has just started emerging over the past xxx years, as a event of developments in bones sciences; emphasis has shifted from identification of the lesion that causes the disorder to identification of the dumb individual's difficulties and their appropriate remediation.three

Anatomy of the fundamental auditory nervous system

The primal auditory nervous system (CANS) extends from the cochlear nucleus in the brain stem to the auditory cortex. The superior olivary complex, lateral lemniscus and inferior colliculus, medial geniculate body, and reticular formation are important relay stations. The cortical and subcortical auditory areas mainly consist of Heschl'due south gyrus, the planum temporale (extending from the posterior attribute of Heschl's gyrus to the terminate of the Sylvian fissure), and the Sylvian crack with the insula.4 The cognitive hemispheres are continued by the corpus callosum. The CANS is characterised by an intrinsic "redundancy"—that is, an extensive interaction of its structures that is responsible for the resistance of the system to exhibit deficits on standard auditory testing in the presence of a lesion.4 In children, myelination and maturation continue until x–12 years of age.5 The young encephalon has an inherent ability for plasticity: the forebrain sensory representations may change in response to altered receptors, sensory environment, or apply and learning.6

Clinical presentation

Children with auditory processing disorders announced to be uncertain most what they hear, and may have difficulties listening in background noise, following oral instructions, and understanding rapid or degraded speech in the presence of normal peripheral hearing.one Symptoms may get apparent in the early school years or at a later academic stage of the kid's life, due to changes in the acoustic environment or to increased academic demands. In rare cases, these symptoms may be the showtime manifestation of a neurological disorder.vii Equally a consequence of the primary auditory difficulties, children with APDs may accept secondary characteristics of language, reading and spelling disorders, equally well every bit inattention and distractibility (tabular array 1)2; this profile requires careful consideration and diagnostic evaluation for differentiation from other mutual childhood developmental disorders.

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Table i

Deficits and resulting symptoms and behaviours which characterise APDs

Auditory processing disorders may issue from disruption of processes specific to audition, equally well as from more global deficits (for instance, memory or attention deficits) that accept a negative impact on the processing of auditory information.viii Irrespective of the causal mechanism, an APD may manifest as a deficit in sound localisation, bigotry, pattern recognition, temporal processing, and performance deficits when the auditory signal is degraded or embedded in competing audio-visual signals (table 1). These deficits take electrophysiological equally well equally behavioural correlates.8

Diagnosis

Central auditory testing clinically evaluates the integrity of the CANS and provides a "lesser up" sensory cognitive approach to learning and behavioural issues as well as an index to neuropathological constellations. Central auditory nervous system problems may be isolated or associated with more pervasive processes and atmospheric condition which closely interact with other sensorimotor modalities besides as "pinnacle downwards" cerebral functions. The diagnosis of APD thus requires a multidisciplinary approach with careful consideration of cognitive, retention, and linguistic parameters. Diagnosis relies on synthesis of information from history (medical, educational, developmental), behavioural and electrophysiological tests, besides as ancillary procedures such as neuroimaging, speech and language assessment, and psychological/cognitive assessment, afterward conscientious consideration of confounding factors.i

The testing battery (tabular array 2) includes:

  • Baseline audiometric assessment to exclude a peripheral hearing loss

  • Behavioural primal auditory tests. These tests may tap into more than than i auditory process, and fall into 3 main categories9: – monaural depression back-up: speech stimuli that are either degraded (due east.chiliad. in terms of frequency content), or embedded in competing signals (e.m. in noise or multispeaker babble) are presented to i ear, and the child is requested to identify the oral communication stimulus

  • dichotic/binaural interaction tests: stimuli are presented to both ears, and the task requires the child to attend to one ear only or to both at the same time

  • temporal tests, e.grand. sequencing tasks

  • Electrophysiological tests. These may include auditory encephalon stalk evoked responses and middle latency response, which are cardinal measures for auditory structures in the brain stem and in subcortical to cortical levels respectively; and late potentials, which may or may not exist affected by attending, such every bit the P300 or Mismatch Negativity (MMN).10

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Table 2

Testing battery for APDs

Classification

In terms of pathophysiological mechanisms, APD may exist classified as occurring in the presence of2: neurological conditions; delayed central nervous system maturation; or other developmental disorders.

NEUROLOGICAL CONDITIONS ASSOCIATED WITH APD

Few cases of APD in children have an underlying neurological deficit. Yet, an APD may occasionally exist the only or the presenting manifestation of a neurological disorder, highlighting the necessity for a high clinical index of suspicion and the value of neurological and developmental examination.

Tumours of the CANS

The concept of (central) APDs may be traced back to Bocca'due south audiological findings in adults with brain tumours that affect the auditory areas.9 Children with CANS tumours have similar ear deficits to adults,11 notwithstanding the young encephalon'south capacity for plasticity.half dozen In the presence of astringent neurological symptomatology, auditory difficulties may not be perceived equally a major symptom, even in the presence of grossly aberrant central auditory examination results.7 Conversely, APD may be the offset and just manifestation of a space occupying lesion,7and the auditory deficits may be mistaken for a learning inability. Advisable surgical and rehabilitational intervention may atomic number 82 to improvements in behavioural and electrophysiological findings,seven highlighting the young brain's potential for plasticity and the need for aggressive rehabilitation of the young patient after encephalon surgery.

Prematurity and depression birth weight

Preterm infants with low birth weight may endure from APD which significantly improves with time; however, by the age of 14 years some of these children will go on manifesting subtle auditory deficits, such as poor auditory memory span, in a significantly greater proportion than the normal birth weight population.12

Extrinsic harm to the brain

Bacterial meningitis is implicated equally a cause of auditory processing disorder, but the supporting evidence is inconclusive.xiii Single case reports also indicate thatherpes simplex encephalitis can be associated with central deafness in children—that is, key auditory system dysfunction that results in practically no useable hearing.7

Lyme disease, a tick borne infection acquired by the spirochete Borrelia burgdorferi, may have long term sequelae of auditory processing difficulties14 which may persist following treatment.

APD may be also be caused by caput trauma.fifteen Children who sustain closed caput injury may suffer from atrophy of the posterior corpus callosum, resulting in auditory hemispheric disconnection.15

Low level heavy metallic exposure in children may affect sites in the CANS. Blood mercury levels may correlate with auditory encephalon stalk response (ABR) delayed latencies,16 as well as with poorer primal auditory processing abilities.17 Similarly, prenatal exposure tocigarette smoke,18 alcohol,19 or postnatalanoxia 20 may also be implicated in college prevalence of APD.

Cerebrovascular disorders

The auditory deficit in stroke in childhood can be quite dramatic, with no behavioural response to sound despite the presence of normal otoacoustic emissions and ABR, as in the case of a iii year old child with Moyamoya illness.21

Metabolic disorders

Cortical deafness with auditory agnosia may exist a presenting feature of adrenoleucodystrophy; this symptom may temporarily answer to treatment.22 There are no systematic studies of APD in the presence of inborn errors of metabolism, although several of these atmospheric condition are known to affect central auditory structures with abnormal auditory evoked response potentials (run across, for case, Kaga and colleagues23). In view of new treatment possibilities, and of the brain's capacity for plasticity, such studies are urgently required.

Epilepsy

Central auditory impairment has been reported in clan with bihemispheric seizure disorder. Post-obit successful surgery to control the epilepsy,24 children may evidence comeback in measures of central auditory function, simply results are variable.

Landau–Kleffner syndrome is characterised by acquired aphasia and epileptic seizures, with onset in childhood.25 The major feature of the affliction is the inability to understand spoken language; this has in plow been interpreted equally reflecting an impairment of auditory phonological bigotry,26 a generalised auditory agnosia rather than a phonological decoding deficit,27 or a phonological deficit underlined by insensibility to loudness and a defect in temporal resolution.28 The length of electric status epilepticus in sleep has a stiff negative correlation with receptive besides as expressive language scores, highlighting the need for timely medical or surgical intervention.29

DELAYED MATURATION OF THE Cardinal AUDITORY PATHWAY

The man auditory system is fully developed at birth; yet,myelination continues for several years in the higher auditory pathways, as reflected in ABR and middle/late auditory potentials indices, which attain adult values around ii years of age and past 10–12 years of historic period respectively,ten too as in the improved behavioural performance with age in several behavioural primal auditory tests.9 Auditory deprivation may accept deleterious effects on the arrangement of the auditory pathway; thus maturation of some aspects of central auditory function may be limited by the onset and duration of theperiod of deafness prior to cochlear implantation.30 Similarly, auditory deprivation may underlie delayed maturation of the central auditory pathway in children who accept a history of gum ear, and who show significantly poorer performance in behavioural as well as prolonged ABR wave latencies31 than normal controls.

DEVELOPMENTAL ABNORMALITIES

Attention deficit hyperactivity disorder

The diagnosis of attention deficit hyperactivity disorder (ADHD) is made on the ground of reported symptoms of inattention, impulsivity, and hyperactivity that are developmentally inappropriate and which are observed in at least two different settings. In contrast, APD is diagnosed on the basis of history, audiometric behavioural and electrophysiological test findings, and ancillary procedures (see table3). Shortcomings arising from diagnostic methodologies and overlapping symptomatology of the two weather may account for the debate equally to whether APD and ADHD are a single32 or two singled-out but co-morbid developmental disorders.33 Clinicians can identify a reasonably exclusive set up of diagnostic behavioural characteristics for ADHD and APD.33 Even so, consistency does not ensure validity of the diagnosis, and APD and the predominantly inattentive subtype of attentional arrears disorder may yet be a single developmental disorder.33Neurophysiological studies have found smaller MMN amplitudes to auditory stimuli in children with ADHD,34 and this may underlie the presence of an auditory processing arrears; nevertheless, this is not a specific finding. In that location is a clear need to place electrophysiological indices that would permit a confident diagnosis of ADHD and/or APD in order to cull appropriate modes of treatment.

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Table iii

Behavioural signs of APD and ADHD, as ranked by clinicians in terms of frequency (high to depression) for each disorder

Dyslexia

At that place is still contend as to whether dyslexia is a specifically linguistic disorder35 or whether the underlining phonological deficit is caused by an auditory temporal processing deficit.36 ,37

Feature structural abnormalities of auditory areas in the brain have been reported in dyslexics.37-39 Behavioural studies take indicated that dyslexics suffer from temporal processing deficits which are differentially related to lexical and non-lexical reading strategies.40

There is abounding empirical support that an auditory processing deficit may underlie some forms of dyslexia; however, information technology needs to be clarified to what degree this temporal deficit affects other modalities such as vision, and whether other potential factors might contribute to dyslexia. We believe that dyslexics with listening behaviours strongly suggestive of an auditory deficit should be referred for detailed audiological evaluation and appropriate audiological rehabilitation.

Linguistic communication impairment

The issue of an auditory temporal processing arrears as opposed to a purely linguistic deficit being causal tospecific language damage (SLI) (developmental dysphasia) remains controversial. Specific linguistic communication impairment refers to language impairment that cannot be explained on the basis of neurological, cerebral, motor, or sensory deficits. However, this definition may exist inappropriate, as from the early 1970s, there is evidence to support the causal link of an auditory processing deficit to specific linguistic communication harm.41Neuropathological studies in developmental dysphasia have identified structural abnormalities of auditory areas of the brain.42Subsequent studies led to the hypothesis that the temporal processing deficit may as well touch other sensory modalities, but the auditory processing deficit seems to be of more crucial importance for the language damage.43 The strongest argument in favour of the auditory basis for SLI comes from remedial studies which found significantly greater improvement in auditory and language processing in children with SLI who received preparation with acoustically modified speech communication than in the command group who had been trained with natural speech.44

Learning disability

In some cases, learning disabled children may have key auditory deficits similar to those observed in adult patients with surgical section of the corpus callosum, indicating that the auditory deficits may exist due to disruption of interhemispheric processing of auditory information, possibly due to delayed myelination.v These children may also have longer latencies of the center latency response45 as well as diminished MMN to stimuli of specific rapid speech changes than normal children.46 Learning disabled children are a heterogeneous group; however, identification of underlying specific auditory deficits may indicate what remedial activity is appropriate.

Management

Management of APD (see table iv) consists of the following47:

  • Signal enhancement strategies which aim to amend the indicate to noise ratio, for example by minimising background dissonance or by using frequency modulated systems in the classroom.

  • Auditory preparation which makes use of the encephalon's plasticity and tin can be formal (past means of sophisticated equipment and strictly controlled stimuli) or informal. Formal auditory grooming may include: computerised commercial programs such as FastForWord (Scientific Learning Corporation, 1997; http://www.scilearn.com/) and Earobics (Cerebral Concepts, Inc., 1997; http://www.earobics.com/), which alter speech acoustics and adaptively speed up neural processing; or preparation in the audiology clinic with modified central auditory tasks. Breezy strategies can be applied at home or at school and include tasks such as vowel/consonant training, simple games such every bit "Simon", etc.

  • Linguistic and cerebral strategies which aim to increment employ of compensatory strategies.

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Table four

Management strategies forAPDs

APD management is not without controversy. Equally critics point out,48 these interventions are based on sure assumptions, including a bottom upwards (sensory to cognitive) model of the brain'southward processing of incoming speech signals, the assertion that auditory processing defects cause linguistic communication impairments, and the acceptance that targeting the auditory defect by a training program volition lead to improved linguistic communication. However, these assertions are still under fence. Despite this continuing debate on the exact relation of audition and language, in that location is a growing torso of evidence that APD management is beneficial.44 While further research is needed to clarify why and how this direction actually works, information technology is important to identify and to address these auditory processing deficits past advisable specific strategies.

Conclusion

Auditory processing disorders may be a feature of both neurological and developmental disorders. Even so, whereas APD appears to be well documented in relation to sure syndromes, in other disorders the quality of existing show is inconclusive and the relation of APD to the circumstantial disorder is poorly understood. Farther research into the interface between APD and neurological and developmental disorders is needed. Clear insight into the nature of the auditory processing arrears may take implications for appropriate management, in agreement with the trend to provide multimodal intervention for these disorders. Moreover, a detailed understanding of the structural and functional substrate of auditory processing disorders will enable phenotypic evaluation specifically for the purposes of genetic research.

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Royal College of Paediatrics and Child Health