Journal of Communication Disorders 40 (2007) 295–304

Auditory processing disorders:

Acquisition and treatment
David R. Moore
MRC Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK
Received 1 March 2007; accepted 1 March 2007

Abstract

Auditory processing disorder (APD) describes a mixed and poorly understood listening problem
characterised by poor speech perception, especially in challenging environments. APD may include
an inherited component, and this may be major, but studies reviewed here of children with long-term
otitis media with effusion (OME) provide strong evidence for changes in auditory processing
acquired through altered experience (deprivation) and brain plasticity. Whether inherited or acquired,
it is suggested that APD may be reversed by active learning. Training tunes both bottom-up and top-
down neural mechanisms, some that are specific to the trained stimulus and some that reflect more
generalised arousal. APD and its treatment therefore provide examples of brain plasticity working
either in a negative or in a positive way to modulate listening.
Learning outcomes: (1) Readers will be able to discuss APD in the context of inheritance and
experience. (2) Readers will be able to explain how OME has been shown to alter auditory
processing. (3) Readers will be able to list examples of good and bad brain plasticity. (4) Readers
will be able to explain what auditory learning is, list some of its properties, and provide examples of
its application in therapy for communication disorders.
# 2007 Elsevier Inc. All rights reserved.

1. Introduction

Brain development and pathology are primarily determined by inheritance, but there is
abundant evidence that environmental factors influence both the development and
maintenance of the brain (Sanes, Reh, & Harris, 2005), a process often referred to as
plasticity. Auditory deprivation and auditory learning produce two contrasting examples of
brain plasticity, leading to impaired and improved performance, respectively. In this brief

0021-9924/$ – see front matter # 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.jcomdis.2007.03.005
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overview, I consider evidence that APD can be caused by auditory deprivation and that
recovery from APD occurs normally through, and can be accelerated by, auditory learning.

2. Auditory processing disorder

APD has been defined (ASHA, 2005; BSA, 2005) as a disorder in the recognition,
discrimination, ordering, grouping and localization of sounds, with both organizations
emphasizing the processing of non-speech sounds. The etiology of APD is complex and
heterogeneous (Moore, 2006). It remains unclear, for example, the extent to which central
and peripheral factors contribute to the widespread group of symptoms that can be given
the label APD. It is now well established that outer hair cell pathology can lead to both
spectral and temporal processing deficits (Oxenham & Bacon, 2003). Those particular
deficits are nevertheless often considered to be the hallmark of APD, and their alleged brain
origin is belied by the fact that many still refer to APD as ‘central’ (C)APD. If we assume,
however, that peripheral dysfunction is not the primary cause of APD, as suggested by
clinical screening procedures, there are many central candidates for the disorder. Not least
of these is the abundance of descending pathways, both those wholly within the cerebral
cortex and long distance connections, deriving from the core auditory cortex, that reach
directly to all levels of the central auditory system (Winer & Lee, 2007) and that are now
known to influence profoundly the activity of most, perhaps all neurons in the core,
ascending auditory system (Palmer et al., 2006).
APD has been closely associated with the more well defined, if not more well
understood, language processing problems of dyslexia (specific reading disorder, SRD)
and specific language impairment (SLI). It is clear that a higher than expected proportion of
individuals diagnosed with SLI and SRD on the basis of language and reading tests also
perform poorly on psychoacoustic measures of non-speech detection and discrimination,
including auditory backward masking (Wright, Buonomano, Mahncke, & Merzenich,
1997) and pure tone frequency discrimination (McArthur & Bishop, 2004).

3. Auditory deprivation

Because of its close relationship to hearing loss and language problems, which are
known to receive a strong genetic influence, APD is likely to include an inherited
component. Recent work on the genetics of SLI provides evidence of separate genes
involved in various underlying aspects of language (Bishop, Adams, & Norbury, 2006), and
genetic analysis methods that may be applicable to APD (Newbury, Bishop, & Monaco,
2005). However, these studies suggest an environmental origin for at least one aspect of
APD (tone sequencing, Bishop & Tallal, 2002), thus raising the possibility that APD may
be more acquired than inherited.
The most direct evidence for the existence of APD comes from cases of naturally-
occurring auditory deprivation: children with long-term otitis media with effusion (OME).
In two papers published within months of each other in 1991, Pillsbury, Grose, and Hall and
Moore, Hutchings, and Meyer showed that children attending clinics for treatment of
 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304 297

Fig. 1. Effect of OME on auditory processing. (A) Prevalence of OME in the first 6 years in a pseudo-random
(self-selected) sample of typically developing children in Oxford, UK. The data show the mean annual prevalence
of OME (determined by monthly tympanometry), divided into quartiles by overall (6 year) OME prevalence.
Children in the highest quartile (4) had OME in either or both ears for 50% of the first 5 years of life. (B) Binaural
MLD in 6–7 year old children as a function of the total prevalence of OME in the first 5 years. Data show the mean
(SEM) in each quartile of OME experience. Also shown are the data for adult listeners with unknown OME
experience. Children only in the highest OME prevalence group had reduced MLD, but all children had immature
MLD (modified from Hogan & Moore, 2003).

chronic OME had poor binaural hearing in the form of reduced binaural unmasking.
Crucially, the impairment was present when the ears were effusion free and
audiometrically normal, demonstrating that the impairment had a central origin.
Subsequent research, including a prospectively studied group of children whose
lifetime history of OME was documented (Fig. 1, Hogan & Moore, 2003), confirmed
those original findings. In addition, it has confirmed earlier findings that binaural
unmasking is immature in children as old as 7–8 years who have a history of low OME
incidence. Based on this index of listening, auditory processing would not be as good as in
adults in these typically developing older children, and would be further impaired in those
who had a lot of OME.
Fortunately, the influence of OME on binaural hearing and, it appears, on other forms of
listening contributing to normal speech perception declines with age. This is attributable to
at least two factors. One is that the prevalence of OME peaks in the second year of life, then
declines steadily over the next few years, with a more dramatic decline after the fifth year
(Fig. 1, Hogan & Moore, 2003). The other is that the sequelae of OME appear to be
reversible, and thus also decline with age. Hall’s group has shown this most clearly in a
group of children who received treatment for chronic OME and were then tested regularly
for binaural unmasking over more than 4 years (Hall, Grose, & Pillsbury, 1995). The
binaural hearing deficit originally found in these children gradually declined so that, by
about 2–3 years after treatment, they were statistically indistinguishable from a control
group of children. The most likely interpretation of this result is that, just as the binaural
hearing in these children was impaired through learning of inappropriate cues during the
period of auditory deprivation, when that deprivation was permanently removed the
children relearned normal cues. We thus see here two contrasting examples of brain
plasticity, serving initially to impair and then to improve listening.
298 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304

Recent research has been directed towards testing this interpretation experimentally,
mainly in adult listeners who have various forms of devices placed in one ear, selectively to
remove some of the localization cues (Hofman, Van Riswick, & Van Opstal, 1998). Just as
found in the ‘natural’ experiment of OME, those listeners made mistakes in sound
localization tasks when the devices were first inserted, but improved their performance
over the following days and weeks. Current evidence suggests the improved performance is
accelerated by active auditory training—by having the listeners perform sound localization
tasks during the ‘recovery’ period.
Coming back to OME, it appears (Roberts et al., 2004) that the long controversy about
whether chronic OME does or does not produce language problems may be resolved by a
model based on the above arguments and two experimental observations: First, that
children only from socially deprived backgrounds tend to have longer term language
problems. Second, that only the most persistent OME results in poor auditory processing. If
we assume that children from deprived backgrounds experience reduced communicative
opportunities, itself a form of deprivation, this may be additive to the deprivation produced
by the OME, resulting in auditory brain plasticity and language problems only in this
doubly deprived group.

4. Auditory learning

APD, whether or not caused by OME, is likely to benefit from auditory learning. Active
auditory learning is simply an improvement in performance of listening tasks with practice
or ‘training’. For example, it has been known for many years that repetition of auditory tone
detection results in improved performance and that the improvement is likely due to both
sensory and non-sensory (e.g. motivation) factors (Zwislocki, Maire, Feldman, & Rubin,
1958). Moreover, auditory learning can be very rapid (Hawkey, Amitay, & Moore, 2004)
and perceptual learning in general is long lasting—one visual learning task persisted for
more than 6 months after just 15 min training (Jones & Holding, 1975). Finally, it seems
that the perception of virtually every type of sound can be improved by training.
Two major issues we have recently been addressing are how to optimise training, in
terms of task difficulty, and the extent to which training transfers to untrained tasks. Task
difficulty relates to the efficiency of learning (Fig. 2, Amitay, Irwin, Hawkey, Cowan, &
Moore, 2006a). We started with the hypothesis that a training task could be either too easy
or too difficult to promote optimal learning. While we confirmed that an easy task, on
which a listener performed at 100% correct, promoted less learning than more difficult
tasks, a surprising result was that a training task could not be too difficult. Thus, an optimal
training task should keep the listener performing at a challenging level, while ensuring that
motivation is retained. Prolonged training may be enhanced through the use of computer
games that are both fun to play and highly portable. These games can be played in
community-based settings, such as schools and home (see below), and on devices that may
include PDAs and cell phones.
Transfer of training to untrained stimuli can be extensive (Fig. 2), and may be cross-
modal, although the greatest transfer occurs for stimuli that are closest to the trained
stimulus. These results indicate that top-down, attention mechanisms contribute to training
 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304 299

Fig. 2. Auditory learning (frequency discrimination, FD) produced by various sorts of training. (A) Experimental
design. A short demonstration of the task (3 interval, ‘odd-one-out’) was followed by an FD threshold assessment
(pre-training probe). This was followed by four training blocks of one of 10 different tasks (as in ‘B’), a mid-
training probe, four more training blocks, and a final post-training probe. The only difference between the groups
was the content of their training blocks. (B) Overall learning effect size (mean  95% CI) in the different training
groups: Adaptive (tracking 50, 75 or 95% threshold levels), Constant (frequency of deviant re: 1 kHz standard),
Control (no training, Tetris–visual computer game without sound, Passive–unattended tones plus Tetris), and
Transfer (train at 4 kHz, test at 1 kHz). Asterisks show (corrected) significant learning. FD in listeners improved
on all trained tasks, including an impossibly difficult one (0 Hz) and one (Tetris) that didn’t involve any sounds
during training (modified from Amitay et al., 2006a; Amitay, Irwin, & Moore, 2006b).

at least as much as bottom-up refinement of sensory processing. The attention mechanisms

contributing to training are both general and task-specific. For transfer of training, it is
probably these attention influences that are of greatest importance. For the management of
listening problems, and specifically for speech-in-noise, it would seem to follow that
adaptive training using speech materials closely resembling those encountered in the
listener’s personal environment are likely to be the most effective. These materials would
activate stimulus specific top-down and bottom-up brain circuits, as well as promoting
general arousal.

5. Training listening and language

With these principles of auditory learning, and underlying brain processing in mind, I
consider here in more detail the design and effectiveness of therapeutic training. Several
studies have reported improvements in listening and literacy skills following adaptive
auditory training using a variety of exercises. These reports have varied from training
restricted to simple, non-verbal auditory-visual sequence matching (Kujala et al., 2001),
while others (Merzenich et al., 1996; Tallal, 2004), have used highly multi-faceted training
300 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304

regimes (Fast ForWord) on large samples of children in community settings. Based on the
preceding discussion, these latter designs are generally to be preferred, in the absence of
evidence showing that non-linguistic training is as effective as linguistic training for
improving language-based skills.
Another design issue concerning the choice of stimuli is based on the theory of language
impairments. Fast ForWord was developed on the premise that an APD, consisting of a
specific auditory temporal processing deficit, underlies language problems. However,
several studies designed to test this hypothesis have found a more generalised auditory
processing deficit in dyslexia (Amitay, Ben-Yehudah, Banai, & Ahissar, 2003) and SLI
(Wright et al., 1997). In fact, pure tone frequency discrimination (FD), a measure of
spectral processing, appears to be a more sensitive marker of an APD in these groups than
measures of temporal processing. Preliminary analysis of data from large samples of
typically developing children performing a large battery of tests (Ferguson, Riley, Cowan,
Hind, & Moore, 2006; Hind, 2006) shows that FD is also the task that children appear to
have particular difficulty with.
The generalised nature of the processing problems in poorly performing children, raises
the possibility that APD is actually a problem primarily with top-down processing, rather
than the stimulus-specific deficit that may be assumed. For the design of training, these
considerations suggest two contrasting possibilities—either that the training should aim to
address a wide range of behavioural change (the model adopted by Fast ForWord) or that
training on any of a number of specific tasks will work just as well, since the same top-
down controls are used in each task. In either case, the training should be adaptive in order
to keep it at a level where the task remains difficult (Fig. 2). While this may present
problems in terms of task engagement, especially for children, one of the great benefits in
the use of digital devices is that they can be portable and may be used for short intervals at
any time of the day, thus promoting training.
We have recently shown (Moore, Rosenberg, & Coleman, 2005) that a single
adaptive training exercise, phoneme discrimination, can improve listening and
phonological awareness in typically developing 8–9 year old children (Fig. 3). Using
an arcade-style computer game (‘Phonomena’; see www.mindweavers.com), 12
different phoneme contrasts, and 6 h of training over 4 weeks in a school classroom
setting, we found a 2.3 year age-equivalent increase in a composite phonological
awareness score using the Phonological Assessment Battery, PhAB (Frederickson,
Frith, & Reason, 1997). Training benefit was maintained for at least 5 weeks post-
training. A control, age-matched group did not improve performance on the PhAB
following participation in the regular curriculum over the same period. The dramatic
changes in such a broadly-based measure of phonological awareness tends to support
the second hypothesis proposed above; that training on just one dimension (in this case,
phonemes) could work as well as a more broadly-based set of exercises. A note of
caution needs to be expressed, however. It isn’t yet clear whether the dramatic, broadly-
based performance improvements in this study are dependent on the use of complex
auditory stimuli like phonemes, or on the variety of phonemes presented. One of our
current research goals is to explore this association further in the hope of providing
more definitive answers to our broader questions about what should be trained and how
that training should be delivered.
 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304 301

Fig. 3. (A) Phonological awareness as measured by the Phonological assessment battery (performance measured
in UK standardized age units) in 8–10 year old children. All children were tested before and after 6 h (over 4
weeks) of ‘Training’ (3I-2A, ‘XAB’ adaptive presentation schedule tracking 70% threshold) on a phoneme
discrimination task (‘Phonomena,’ MindWeavers Ltd.), or participation in regular classes (‘Control’). The Trained
group were retested 5–6 weeks later without additional training. Trained children achieved and maintained
dramatically improved phonological awareness as a result of their training. (B) Phoneme discrimination scores
during training for all individual children who completed at least five repetitions of each of the indicated phoneme
contrasts. The bold line shows that, overall, there was a small, significant amount of training (modified from Moore
et al., 2005).

One unexpected aspect of this study was that, despite the clear improvement in a
broadly-based outcome measure (Fig. 3), discrimination of the trained phonemes did not
improve markedly. While our previous, unpublished work has shown that the
discrimination of individual phonemes can readily be trained in both children and adults,
their relative failure to do so in this study tends to support the ‘top-down’ hypothesis. It
could be that engaging actively with the stimuli, even without marked sensory learning, is
sufficient to activate attention and/or linguistic circuits involved in phonological awareness
and other cognitive processes.
It is, finally, important not to lose touch with the unmanaged time course of APD. If this
and other learning problems remain untreated, to what extent will the ‘passive’ exposure to
sounds experienced in everyday life result in brain plasticity? There are examples of
passive recovery following neurological infarcts and the recovery from the effects of OME
without specific intervention has already been discussed. While such passive recovery
leads to ‘catch up’ for many auditory processing and other tasks, a process leading some to
argue that APD may be a form of ‘developmental delay’, there does seem little doubt that
active auditory learning should be able to effect a more rapid and more complete recovery.

Appendix A. Continuing education

1. Which one of the following is evidence that APD is caused by central pathology
a. Poor auditory temporal processing
b. Poor spectral processing
c. Disordered binaural interaction
d. Normal audiograms
e. None of the above
302 D.R. Moore / Journal of Communication Disorders 40 (2007) 295–304

2. Is APD likely to be
a. Inherited only
b. Acquired only
c. Both inherited and acquired
d. Due to a single gene mutation
e. Mainly caused by OME
3. Auditory learning
a. Is an example of instrumental learning
b. Only occurs for some processing tasks
c. Receives bottom-up and top down influences
d. Is mainly due to sharpening of auditory frequency filters
e. Can be best induced by training on easy tasks
4. Transfer of learning can
a. Occur between senses
b. Be complete with sufficient training
c. Does not occur during phoneme discrimination training
d. Account fully for improved phonological awareness
e. Decrease performance of unlearned tasks
5. Passive auditory learning
a. Describes the effects of adaptive training
b. Does not affect binaural processing following OME
c. Prevents active learning
d. Has long-term effectiveness in treating language and listening disorders
e. Is more efficient than active learning

Appendix B. Selected internet-accessible resources

http://www.mindweavers.co.uk: MindWeavers’ software apply world leading neu-
roscience to harness the dynamism of the human brain. They intelligently and selectively
stimulate and train the brain to help individuals attain, sustain and retain their true potential
from early childhood to later-life. Using sophisticated technology from cutting edge
research at Oxford University, they cleverly adapt in response to the performance of the
user - ‘‘Software as clever as you are’’.

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