132  Cortical Neuroplasticity in Hearing Loss
Anu Sharma, Hannah Glick
KEY POINTS
• Neuroplastic changes in hearing loss and deafness are
evident across the human lifespan.
• There are brief sensitive periods in early childhood
during which the central auditory pathways are
maximally plastic. Audiological intervention within these
critical windows may allow for optimal development of
the central auditory pathways, overcoming many
deleterious effects of auditory deprivation.
• Cross-modal reorganization is a form of compensatory
neuroplasticity, which occurs when deprivation in one
modality (e.g., auditory modality, as in hearing loss)
results in the repurposing of its cortical resources
by other modalities (e.g., vision, somatosensation).
Cross-modal reorganization is evident in children and
adults with congenital or acquired hearing loss ranging
from mild to profound in severity. Cross-modal
reorganization may explain some of the individual
variability affecting behavioral outcomes after
intervention.
• The noninvasive P1 cortical auditory evoked potential
(CAEP) biomarker can be used to objectively assess the
development and maturation of the central auditory
pathways in infants and children, helping to guide
clinical decision-making.
INTRODUCTION
Perhaps the most remarkable ability of the human brain is its
capacity for change. Neuroplasticity broadly refers to structural and
functional neuronal changes that take place across the lifespan.
Early in development, neuroplasticity serves as the catalyst for
the formation and refinement of the auditory pathways and the
establishment of neural networks. During childhood and into
adulthood, experience-related inputs (e.g., sensory inputs) drive
neuroplasticity, helping to facilitate language acquisition, learning,
and memory. Many pediatric otologic conditions are manifested
through cascading aberrations in neuroplasticity during develop-
ment. Many adult-onset otologic conditions occur as a result of
insult, injury, or age-related degradation. In either case, compensa-
tory changes in neuroplasticity may occur in an effort to adapt in
the face of auditory deprivation. In this chapter, we will review
the forces of neuroplasticity within the context of hearing loss
across the human lifespan, focusing on how neuroplasticity can
be used to guide clinical intervention and rehabilitation.
Typical development of the central auditory pathways is
dependent upon whether a child is receiving sufficient auditory
input. In the first part of this chapter, we review evidence of a
sensitive period for central auditory development, focusing primarily
on electroencephalography (EEG) evidence using the P1 cortical
auditory evoked potential (CAEP) biomarker in congenitally deaf
children receiving cochlear implants (CIs). We demonstrate how
audiological intervention may promote optimal brain and behavioral
1996
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outcomes if delivered within this sensitive period. In contrast, we
will describe how prolonged auditory deprivation beyond the
sensitive period may contribute to altered development of the
central auditory pathways. Using group and case-study evidence,
we demonstrate the clinical utility of the P1 CAEP biomarker in
making objective decisions about the clinical course of intervention
for special pediatric clinical populations including single-sided
deafness, auditory neuropathy spectrum disorder, cochlear nerve
deficiency, and multiple disabilities.
In the second part of this chapter, we describe new evidence
of cortical neuroplasticity in adult-onset, age-related hearing loss
(ARHL), including evidence of cross-modal neuroplasticity by
the visual and somatosensory systems and the recruitment of
additional brain regions (e.g., frontal cortex) for auditory processing
using high-density EEG and other neuroimaging methods. We
describe the growing body of research linking untreated ARHL
to long-term changes in neurocognitive function, and how
compensatory changes in neuroplasticity may contribute to
individual variability in behavioral outcomes.
Arguably one of the most successful neuroprosthetic devices
is the CI. In the coming decades, our knowledge of neuroplasticity
may lead to further advancement in auditory pharmacological,
technological, and therapeutic innovations for clinical populations
with hearing loss. Our goal should be to harness neuroplasticity
to direct more timely, targeted, and individualized intervention
and rehabilitation to clinical populations in otology.
NEUROPLASTICITY IN PEDIATRIC HEARING LOSS
Overview and Methodology for Studying
Neuroplasticity in Pediatric Hearing Loss
Pediatric hearing loss is a very prevalent chronic condition in
children, affecting 1 to 3 per 1000 children in the United States.1
Pediatric hearing loss may be congenital or acquired. Among
children, genetic forms of hearing loss account for more than
50% of cases, whereas in utero infections, meningitis, hyperbili-
rubinemia, ototoxic drug exposure, trauma, and other conditions
contribute to the remainder of nongenetic cases.2 Untreated hearing
loss during development may have long-lasting effects. For example,
pediatric hearing loss has been linked to receptive and expressive
delays in oral language acquisition, delays in educational achieve-
ment, behavioral and psychosocial problems, negative impacts on
quality of life, and a weighty economic burden from a societal
and socio-economic standpoint.3–5
Many forms of audiological intervention exist for the treatment
of pediatric hearing loss. Hearing aids and CIs are two of the
most common forms of intervention. CIs are used to treat deafness
while hearing aids are small electronic devices considered a treat-
ment option for lesser degrees of hearing loss. Hearing aids consist
of a microphone, amplifier, and receiver. Hearing aids amplify
and convert acoustic sound from the environment into digital
signals sent to the ear via the air conduction pathway, providing
enhanced audibility.6 A CI is a biomedical device consisting of an
internally implanted receiver/stimulator coupled to an external
processor. The CI bypasses the deficient or damaged portions of
the inner ear and provides direct electrical stimulation of the
auditory nerve, thus restoring hearing in more severe cases of
 CHAPTER 132  Cortical Neuroplasticity in Hearing Loss1996.e1

Abstract Keywords
132
The human brain demonstrates an exquisite capacity for neuro- Development
plasticity, capable of adapting to development, insult, injury, Sensitive period
age-related changes, and learning across the lifespan. As healthcare P1 cortical auditory evoked potentials (P1 CAEP)
providers, it would be useful for us to rely on the fundamental cortical visual evoked potentials (CVEP)
principles of neuroplasticity over the course of medical treatment cross-modal neuroplasticity
and recovery. This chapter reviews cortical neuroplasticity in cochlear implants
hearing loss across the age spectrum. We describe a brief sensitive auditory neuropathy spectrum disorder (ANSD)
period during early childhood when the central auditory system
is maximally plastic, in which audiological intervention may allow
for optimal outcomes. Offering evidence from congenital deafness,
auditory neuropathy spectrum disorder, single-sided deafness, and
children with multiple disabilities concomitant with hearing loss,
we describe the utility of the P1 cortical auditory evoked potential
(CAEP) in clinical decision-making. As a multidisciplinary profes-
sion, we are also just beginning to unearth the widespread effects
of adult-onset, age-related hearing loss on neuroplasticity, including
cross-modal reorganization by the visual and somatosensory
modalities and the recruitment of frontal cortex for auditory
processing, and the impact of these changes on speech perception,
cognitive, and behavioral outcomes. Further, we focus on how a
better understanding of neuroplasticity in the context of hearing
loss may lead to the development of clinically useful brain-based
tools (e.g., biomarkers). Such biomarkers may be useful in identify-
ing when a patient should receive intervention, what kind of
therapeutic intervention and/or rehabilitation plan is ideal, and
how well these interventions are working over time.

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more sensorineural hearing loss.6 These clinical interventions have
provided researchers with a natural framework in which they can
study the effects of auditory deprivation on the brain, and the
ability for these interventions to restore or reverse deprivation-
induced changes in neuroplasticity.
Many neuroimaging methods are used to study neuroplasticity
in hearing loss in humans: functional magnetic resonance imaging
(fMRI), functional near-infrared spectroscopy (fNIRs), positron
emission tomography (PET), magnetoencephalography (MEG),
and EEG, and each method has significant value. In this chapter,
we focus primarily on the utilization of EEG for several reasons.
First, EEG is not susceptible to the same types of acoustic artifact
during auditory experiments as other neuroimaging techniques,7–9
and is very compatible with clinical populations with CI. Second,
EEG provides essential millisecond-level temporal resolution
superior to other neuroimaging methods, providing detailed timing
information about neural processing along the auditory pathway.
And finally, EEG is noninvasive, inexpensive, and is relatively easy
to apply, making it feasible on both pediatric and adult populations
in a clinical setting. In addition to EEG recordings in humans,
we will discuss evidence from other neuroimaging methods (e.g.,
fMRI, PET) and near-field EEG recordings in animal models,
which provide us with more detailed spatial resolution about sensory
processing in specific brain regions.
Typical Development of the Central
Auditory Pathways
While the field of otology is primarily concerned with diagnosis
and treatment of disorders of the auditory system, it is useful to
first understand neuroplasticity of the central auditory system
under the conditions of typical development. During normal
development, the central auditory pathways are formed via a series
of intricate, sequenced, and time-dependent processes.10 Both
intrinsic neuroplasticity and extrinsic neuroplasticity play a role in
typical development of the central auditory pathways. Intrinsic
neuroplasticity refers to strictly regulated genetic, molecular, and
cellular processes that occur early in development. These intrinsic
processes help regulate neurogenesis (the creation of new neurons),
migration, differentiation, and synaptogenesis (the creation of new
synapses) in the developing auditory cortex. For instance, synap-
togenesis within auditory cortex begins in the fetal brain by the
27th week of gestation.11 Rapid myelination of axons in the auditory
cortex peaks within the first 3 months of life, then continues at a
slower rate into childhood.12 By 1 year after birth, all 6 layers of
the auditory cortex can be reliably differentiated.13
Extrinsic neuroplasticity refers to experience-driven forces (e.g.,
auditory input), which take place during development and across
the human lifespan. Over the first 4 to 12 years of life, auditory
stimulation guides the process of synaptic pruning, or refinement,
of the central auditory pathways.11,14 During this developmental
period, the age-old maxim in neuroscience, “neurons that fire
together wire together,” holds true.15 That is, synapses or neuronal
connections receiving repetitious and consistent auditory input
are strengthened, while unstimulated or underutilized connections
are eliminated.16–18 Repetitious and consistent auditory stimulation
also leads to the long-term potentiation (LTP) and long-term
depression (LDP) (strengthening or weakening, respectively) of
existing synapses, processes which are known to play a vital role
in learning and memory.19 In the developing auditory cortex, feed-
forward connections (e.g., thalamo-cortical connections)—which are
thought to be largely intrinsically regulated—develop first. Later
on, feed-back cortical connections (e.g., cortico-thalamic connec-
tions)—which are thought to be more extrinsically regulated—start
developing.20–25 In this sense, while a structural and rudimentary
neuronal framework is already in place by birth, the central auditory
pathways are continually refined through repetitious and consistent
auditory experience during infancy and childhood.
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CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 1997
Biomarkers of Central Auditory
132
Development in Children
The term biomarker is defined by the National Institutes of Health
as a “characteristic that is objectively measured and evaluated as
an indicator of normal biological processes, pathogenic processes,
or pharmacologic responses to a therapeutic intervention.”26 The
P1 CAEP biomarker is an EEG event-related potential (ERP)
recorded in response to an auditory stimulus. The P1 CAEP
biomarker reflects maturation in synaptic efficiency along the central
auditory pathways at the level of the primary auditory cortex (A1)
and the thalamus (Fig. 132.1A4). The P1 CAEP response is the
dominant response in infants and young children (see Fig. 132.1A1),
occurring at a latency of approximately 300 ms. As children age,
the P1 latency decreases dramatically at first and then gradually
(coinciding with the aforementioned intrinsically-regulated and
extrinsically-regulated developmental changes over the first few
years of life), until eventually reaching adult-like latency between
12 and 16 years of age.27–31
Our laboratory has established normative data for P1 CAEP
latency in typically developing, normal hearing children, from
infancy through adolescence,32–34 providing a basis by which we
can examine the effects of auditory disorders such as deafness
and hearing loss. Fig. 132.1A5 depicts P1 CAEP latencies in
individual normal hearing children as a function of age. The top
and bottom black lines in Fig. 132.1A5 represent the 5% and
95% confidence intervals for normal P1 CAEP latency, where
P1 latency values falling outside of the top black line indicate
significant delays in maturation of the central auditory pathways
with 95% confidence. Because P1 CAEP latency varies with age,
it can be used as a clinical biomarker of the maturation of the
auditory cortex. That is, by comparing P1 latencies in clinical
populations with hearing loss to these normative values, we can
determine whether the central auditory pathways are maturing at
an age-appropriate rate, or whether there are statistically significant
delays in typical maturation of these pathways. In many previous
studies, we have utilized the P1 CAEP biomarker to evaluate the
efficacy of intervention with hearing aids, to establish candidacy
for CI, and to monitor development of the central auditory
pathways.23–35
The morphology of the CAEP response can also be used as
an objective indicator of the maturational status of the central
auditory pathways. While the P1 response is the predominant
waveform component in the CAEP response in infants (see Fig.
132.1A1), as a child ages, extrinsic input to the auditory system
drives higher-level development of the central auditory pathways
and eventually the emergence of two later waveforms, the N1 and
P2 components, can be observed (see Fig. 132.1A2 and 132.1A3).
The N1 and P2 components are negative-going and positive-
going peaks in the CAEP waveform following the P1 response
in time.27,36–38 While the P1 response reflects cortical processing
at the primary auditory cortex (A1) and thalamus, the N1 and
P2 components reflect higher-level auditory cortical processing
at the level of secondary auditory cortex (A2), cortico-cortical
processing between areas of the auditory cortex, and feedback
(cortico-thalamic) processing between A2, A1, and the thalamus
(see Fig. 132.1A4).13,39
Our laboratory36,37 and other laboratories27,38 have systematically
examined the emergence of the N1 CAEP response under typical
development. For example, in a study by Campbell, Cardon, and
Sharma (2015),37 we evaluated the occurrence of the N1 CAEP
response in typically developing, normal hearing children at various
ages. Results from this study indicate that the N1 CAEP response
was present in approximately 57% and 71% in normal hearing
children between ages 3 to 6 years and ages 6 to 9 years, respectively.
In children 9 to 12 and 12 to 15 years of age, 100% of these
children exhibited present N1 CAEP responses.37 Thus, the
morphology of the CAEP response (e.g., presence or absence of
1998 PART VII  Otology, Neurotology, and Skull Base Surgery

Typical development in normal hearing children

1 P1 2 6 3 3
9 P1 P2
P2

Amplitude (µV)

Amplitude (µV)
Amplitude (µV)
6 3 N1 P1
3 0

0 0
N1
–3
–3 –3
–100 0 100 200 300 400 500 600 –100 0 100 200 300 400 500 600 –100 0 100 200 300 400 500 600
Time (ms) Time (ms) Time (ms)

4 5 300
P1 latency (ms) 250

200

150

P1 and N1 are 100

generated in the 50
auditory cortex Normal limits
0
0 2 4 6 8 10 12 14 16
A Age (years)

Development in deaf children

1 Unstimulated pathway 2 Partial maturation 3 Reorganized pathway

P1 3 of pathway 9
3
Amplitude (µV)

Amplitude (µV)

Amplitude (µV)
6
P1
Before implantation 0
3
0
0 –3
–3 –6
–100 0 100 200300 400 500 600 –100 0 100 200 300 400 500600 –100 0 100 200 300 400 500 600
Time (ms) Time (ms) Time (ms)
500
4
450
400
P1 Latency (ms)

350
300 Implant age (years)
250 0.5–1.5
1.5–2.5
200 2.5–3.5
3.5–4.5
150 4.5–5.5
5.5–6.5
100 6.5+
50 Normal limits
0
0 2 4 6 8 10 12 14 16 18 20
Chronological age (years)
P1 P1
5
6 P1 6 P2 7
Amplitude (µV)

3
Amplitude (µV)

Amplitude (µV)

3
3
After implantation 0 0 N1
0

–3 –3
–100 0 100 200 300 400 500 600 –100 0 100 200 300 400500 600 –100 0 100 200 300 400500 600
Time (ms) Time (ms) Time (ms)
8 9

Contralateral temporal activation Abnormal parieto-temporal cortical

B after early cochlear implantation activation after late cochlear implantation

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 CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 1999

Fig. 132.1  Development of the central auditory pathways in normal hearing children and in deaf children receiving cochlear implants.
The P1 cortical auditory evoked potential (P1 CAEP) is considered a clinical biomarker of the maturation of the auditory cortex. (A) Development 132
of the central auditory pathways in normal hearing children. During typical development, the morphology of the CAEP response changes with age.
(A1) The P1 CAEP response is the predominant component in infancy and early childhood. (A2, A3) Around preadolescence, the N1/P2 CAEP
components emerge. (A4) Source localization using high-density EEG indicates that the P1 reflects processing at the level of the primary auditory
cortex, while the N1/P2 responses reflect processing at higher-level auditory cortex. (A5) Rapid decreases in P1 CAEP latency are observed in
typical development over the first 2 years of life, followed by smaller latency decreases in adolescence. (B) Development of the central auditory
pathways in congenitally deaf children receiving cochlear implants. Morphological differences in CAEP morphology can be observed in deaf
children (n = 231) prior to receiving a cochlear implant (CI). (B1, B2) Young deaf children tend to exhibit abnormal CAEP morphology (a
“deprivation negativity”), reflecting an unstimulated auditory system (B1) or a delayed P1 CAEP response, suggesting that the auditory system has
received partial stimulation with hearing aids (B2). (B3) Older deaf children tend to exhibit abnormal polyphasic morphology, suggestive of a
reorganization of the central auditory pathways. (B5, B6, B7) While children who receive a CI early in development (<3.5 years) eventually develop
age-appropriate P1 latencies within 6 to 8 months of CI use (B5) and emergence of higher-level N1/P2 CAEP components in preadolescence,
similar to normal hearing children (B6), reflective of higher-levels of auditory processing. CI children who receive intervention late in development
(>7 years) exhibit significantly delayed P1 latencies and absent N1/P2 CAEP components even after years of implant use (B7). Source localization
using high-density EEG indicates differences in auditory cortical processing in early-implanted and late-implanted children. (B8, B9) Where
early-implanted children mostly exhibit expected activation of temporal (auditory) cortex contralateral to the implanted ear (B8) similar to normal
hearing children, late-implanted children show recruitment of atypical parietotemporal cortical regions, suggestive of cortical reorganization (B9).
Taken together, this data supports a brief sensitive period early in development, during which the central auditory pathways are maximally plastic
and CI may promote development of the central auditory pathways. (Adapted from Kral A, Sharma A: Developmental neuroplasticity after cochlear
implantation. Trends Neurosci 35(2):111–122, 2012.)

the N1 CAEP component) can be used to assess whether higher-

Age of Implantation
level auditory cortical maturation is occurring at a normal rate in
clinical populations with hearing loss. > 7 years n = 48
3.5–6.5 years n = 66
300 <3.5 years n = 131
A Brief Sensitive Period for Central Auditory
Development in Children
250
A sensitive period or critical period describes a developmental time
window in which there is peak neuroplasticity, a time during which
experience is vital for the neuronal circuitry to develop in a typical 200
P1 Latency (ms)

fashion. During these sensitive periods, changes in extrinsic input

may profoundly impact neurophysiological development, learning,
and the acquisition of particular skills. Documentation of a critical
period in vision was conducted via a series of famous visual experi-
ments by Nobel laureates Wiesel and Hubel,40–42 where long-term
monocular visual deprivation in developing deaf cats resulted in
abnormal development of ocular dominance columns within the
primary visual cortex. This led researchers to surmise that if visual
input is not restored within a brief sensitive period early in life,
then neuronal circuitries of the visual pathways do not develop
normally.
Using auditory evoked potentials (AEPs), researchers have
examined the effects of congenital deafness on central auditory
development.32,33,39,43–55 Inspired by the seminal research studies by
Wiesel and Hubel, our group has examined sensitive period within
the auditory modality in humans.33,52,53 For example, in a series of
studies by Sharma et al., P1 CAEP responses were recorded in
children with bilateral congenital deafness that received audiological
intervention with a CI at varying ages. P1 responses from these
children were then compared against 95% confidence intervals
for normal P1 CAEP latency developed from data in normal
hearing, typically developing children.33,52,53 Results from these
studies are depicted in Fig. 132.2. As can be seen, those children
who received a CI early in development (<age 3.5 years, indicated
by the red circles) exhibited normal P1 latencies, while children
receiving a CI late in development (>age 7 years, as indicated by
the green diamonds) exhibited delayed P1 latencies. Only about
half of children receiving a CI between 3.5 and 6.5 years (as
indicated by the blue triangles) exhibited normal P1 latencies
(see Fig. 132.2).
We have also examined individual developmental trajectories
in congenitally deaf CI children longitudinally using the P1 CAEP
150
100
50
Normal Limits
0
0 2 4 6 8 10 12 14 16
Age (years)
Fig. 132.2.  Auditory cortical development in deaf children
receiving a cochlear implant at different ages. P1 CAEP latencies
for deaf children receiving a cochlear implant (CI) at early (<3.5 years)
(red circles), middle (3.5–6.5 years) (blue triangles), and late (>7 years)
(green diamonds) ages plotted against normal limits (5% and 95%
confidence intervals) of normal P1 latency in typically developing,
normal hearing children. While majority of early-implanted CI children
show P1 latencies falling within the 95% confidence interval, majority
of late-implanted CI children exhibit delayed P1 latencies falling
outside of the 95% confidence interval. Children implanted between
age 3.5 and 6.5 years demonstrate highly variable responses, with
only about half of these children demonstrating normal P1 CAEP
latencies. Taken together, these data support a sensitive period of
approximately 3.5 years in which the central auditory pathways are
maximally plastic and audiological intervention may allow for age-
appropriate development of the central auditory pathways.

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2000 PART VII  Otology, Neurotology, and Skull Base Surgery

biomarker.53 Results from this study are indicated in Fig. 132.1B.
While early-implanted congenitally deaf children (receiving CI
<age 3.5 years) typically show delayed P1 latencies prior to
implantation (see Fig. 132.1B1), after implantation these children
exhibit rapid decrease in P1 latency over the first few months of
CI use (see Fig. 132.1B4), eventually developing P1 latencies falling
within the 95% confidence interval within 6 to 8 months of CI
use (see Fig. 132.1B5).53,56 In contrast, while late-implanted children
(receiving CI >age 7 years) do exhibit systematic decreases in P1
latency with CI use (see Fig. 132.1B4), these children continue
to show delayed P1 CAEP latencies even 7 to 10 years after
intervention (see Fig. 132.1B7).53
Interestingly, early-implanted children (receiving CI <age 3.5
years) also exhibit the emergence of the later N1/P2 CAEP
components with CI use (see Fig. 132.1B6) at a rate comparable
to typically developing, normal hearing children. In contrast,
late-implanted children (receiving CI >age 7 years) rarely develop
the later N1/P2 CAEP components.37,39 Lack of age-appropriate
development of these later CAEP components suggests atypical
maturation of higher-order auditory cortex, and these findings
are consistent with data from near-field EEG recordings in
congenitally deaf cats, in which late-implanted animals exhibit
delayed activation of supragranular cortical layers and reduced
synaptic electrical activity in infragranular cortical layers.57 Lack
of development this type of cortico-thalamic and cortico-cortical
circuitry is indicative of a functional decoupling between primary
cortex and secondary auditory cortex.57,58 Atypical development
of cortico-cortical connectivity may result in many downstream
effects on attention, working memory, and executive function.59
For example, in-vitro EEG studies in animal models of deafness
suggest that LTP in auditory cortex may be eliminated, indicating
that many vital synaptic neuronal connections necessary for the
development of auditory learning, and memory may not be instilled
if appropriate audiological intervention is not introduced within
a time-sensitive manner.60 In late-implanted children, there is
evidence the central auditory system may become reorganized.
In early-implanted CI children (<age 3.5 years), for example,
auditory stimulation using a speech stimulus elicits cortical activa-
tion patterns localized to temporal (auditory) cortex (see Fig.
132.1B8) similar to cortical activation patterns observed in normal
hearing children (see Fig. 132.1A4).61 In late-implanted CI children
(>age 7 years), the same type of auditory stimulation elicited cortical
activity localized to parietotemporal cortex (see Fig. 132.1B9).61
Absent N1/P2 CAEP responses and increased cortical activation
patterns in nontemporal regions to auditory stimulation may
indicate sensory reorganization of higher-order auditory cortical
regions in children with long durations of deafness who receive
audiological intervention in later childhood.
The aforementioned neurophysiological evidence coincides
with behavioral evidence of more optimal oral language outcomes
in early- compared to late-implanted CI children.62–71 For example,
early-implanted children (<age 2 to 3 years) demonstrate faster
rates of vocabulary growth, higher expressive language scores, and
higher performance levels on assessments of reading compared
to late-implanted children (>age 3 years).69,72–74 Taken together,
these data support the existence of a brief sensitive period (ideally
by age 1 year), in which audiological intervention has the greatest
potential to allow for age-appropriate development of the central
auditory pathways,50–53,56,75 and may successfully promote typical
development of oral listening and spoken language skills.
Clinical Utility of the P1 Cortical Auditory
Evoked Potential Biomarker to Monitor
Efficacy of Intervention With Hearing Aids
or Cochlear Implants
Whether assessing the efficacy of a chosen intervention method,
evaluating candidacy for hearing aids or CI, or monitoring the
development of the central auditory pathways in special pediatric
populations, the P1 CAEP biomarker is a valuable clinical tool
in assessing neuroplasticity and maturation of the central auditory
pathways in individual children. The P1 CAEP biomarker may
help monitor whether or not a chosen intervention method is
allowing for normal auditory cortical maturation.
Fig. 132.3 depicts P1 CAEP responses in a male child with
bilateral severe sensorineural hearing loss shortly after birth who
was fit with bilateral hearing aids at age 11 months.76 P1 CAEP
responses were recorded at the time of hearing aid fitting and at
subsequent intervals during hearing aid use to monitor the matura-
tion of the child’s central auditory pathways with hearing aids. As
can be seen in Fig. 132.3A, at hearing aid fitting the child showed

At HA Fitting
350
300
At HA Fitting
P1 Latency (ms)

250
2 μV 5 mo Post HA 200 5 mo Post HA
P1
150
18 mo Post HA
100
18 mo Post HA
50
0
0 1 2 3 4
A B Age (years)

Fig. 132.3  Clinical utility of the P1 cortical auditory evoked potential (P1 CAEP) biomarker in a child with
sensorineural hearing loss fit with hearing aids. This child was diagnosed with a bilateral severe sensorineural
hearing loss and fit with bilateral hearing aids (HA) at age 11 months. (A) While abnormal CAEP morphology
and a delayed P1 CAEP response were observed at HA fitting, within 5 months of HA use, developmentally
appropriate CAEP morphology was observed. (B) Continued monitoring at age 18 months post HA fitting
showed age-appropriate P1 CAEP latency, indicative of objective benefit from amplification. In this case, the
P1 CAEP biomarker helped monitor the efficacy of intervention with hearing aids in promoting age-appropriate
development of the central auditory pathways. (Adapted from Sharma A, Martin K, Roland P, Bauer, P, et al:
P1 latency as a biomarker for central auditory development in children with hearing impairment. J Am Acad
Audiol 16(8):564–573, 2005.)

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 CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 2001

abnormal CAEP morphology, marked by a large negativity preced-
ing the P1 CAEP response (called a “deprivation negativity”), and
a delayed P1 CAEP response falling outside of the 95% confidence
interval (see Fig. 132.3B), suggestive of a significantly under
stimulated auditory system.32,49 However, after 5 months of hearing
aid use, improvements in CAEP morphology, decreases in P1
latency, and increases in P1 amplitude are seen (see Fig. 132.3B),
with the child’s P1 response falling within normal limits for the
child’s age (see Fig. 132.3B). P1 CAEP latencies continued to
show age-appropriate development when the child was evaluated
at 18 months after hearing aid fitting. In this child, the P1 CAEP
biomarker provided valuable information regarding the efficacy
of intervention with hearing aids in promoting age-appropriate
development of the central auditory pathways.
Fig. 132.4 depicts P1 CAEP responses in a female child with
bilateral severe-profound sensorineural hearing loss over the clinical
course of intervention with hearing aids and CI.76 This child was
diagnosed at age 18 months and fit with bilateral hearing aids at
age 21 months. During hearing aid use, P1 responses were present
(see Fig. 132.4A) but occurred at a delayed latency for the child’s
age (see Fig. 132.4B), indicating that the hearing aids were providing
some, albeit insufficient auditory stimulation to allow for age-
appropriate development of the central auditory pathways. This
objective information was used in conjunction with the conventional
otologic and audiological test battery to determine candidacy for
CI, and the child received a CI at age 25 months. P1 CAEP
recordings after CI indicated rapid decrease in P1 CAEP latency
(see Fig. 132.4A), falling within the 95% confidence interval for
the child’s age within 3 months of CI experience and continuing
to show age-appropriate development when monitored at 12
months post-CI (see Fig. 132.4B). This case study highlights how
the P1 CAEP biomarker can be used in conjunction with the
conventional audiological and otologic test battery to evaluate
candidacy for CI, and to monitor development of the central
auditory pathways after intervention.
Clinical Utility of the P1 Cortical Auditory Evoked
132
Potential Biomarker in Auditory Neuropathy and
Children With Cochlear Nerve Deficiency
ANSD is an audiological disorder accounting for 5% to 15% of
children with sensorineural hearing loss, which may occur as a
result of dys-synchronous neuronal firing at the level of the inner
hair cells in the cochlear and/or the VIII nerve.77,78 ANSD poses
unique clinical challenges to physicians and audiologists, since
large within-patient and between-patient variability is common.
For example, pure tone audiological thresholds in ANSD may be
inconsistent with speech perception abilities, and behavioral
thresholds may fluctuate over time,79,80 making it difficult to rely
on behavioral thresholds alone when considering audiological
intervention. Furthermore, an absent or abnormal auditory
brainstem response (ABR) is a hallmark characteristic of ANSD,
so utilization of conventional electrophysiological techniques to
program hearing aids and CI for children with ANSD is quite
difficult. For all of these reasons, objective neurophysiological
measures at higher levels of the central auditory pathways (e.g.,
the P1 CAEP biomarker) have proven to be a good diagnostic
indicator in clinical cases of ANSD.81–83
Data from our laboratory indicate that the P1 CAEP biomarker
may reflect the degree of neural synchrony in children with ANSD84
and may provide an indicator of objective benefit with hearing
aids and CI after intervention.81–83 In one study, the majority of
ANSD children receiving a CI before age 2 years (slightly earlier
than the 3.5 year sensitive period described in congenital deaf-
ness) exhibited normal P1 CAEP latencies and better auditory
outcomes compared to ANSD children implanted after age 2
years, consistent with the notion of a brief sensitive period early
in life when the central auditory pathways are maximally plastic.81
In fact, CI in cases of ANSD may provide a more consistent,
robust electrical signal compared to hearing aids, yielding more
synchronous neuronal firing at the level of the auditory cortex.84

4 µV
1 mo Post HA 350
300
3 mo Post HA
1 mo Post HA 3 mo Post HA
P1 Latency (ms)

250
CI Hook Up CI Hook Up
200
3 mo Post CI
150
3 mo Post CI 100
50 12 mo Post CI
Normal Limits
12 mo Post CI 0
0 1 2 3 4
2 µV Age (years)

A B
Fig. 132.4  Clinical utility of the P1 cortical auditory evoked potential (P1 CAEP) biomarker in a child with
sensorineural hearing loss with a cochlear implant. This child was diagnosed with a severe-profound
sensorineural hearing loss at age 18 months and was fit with bilateral hearing aids (HA) at age 18 months.
(A, B) Longitudinal CAEP recordings at 1 month and 3 months post-HA fitting (A) indicate delayed P1 CAEP
responses (B), suggesting that the hearing aids were not providing adequate auditory input to allow for normal
development of the central auditory pathways. At 25 months of age, the child received a cochlear implant
(CI). (A) Longitudinal CAEP recordings at CI hook up, 3 months, and 12 months after CI indicate rapid
decrease in P1 latency, with P1 responses falling within the 95% confidence interval for the child’s age within
12 months of CI use (Fig. 132.4B). In this case, the P1 CAEP biomarker was used in conjunction with the
traditional audiological and otologic test battery in order to determine CI candidacy and to monitor the efficacy
of treatment after intervention with a CI. (Adapted from Sharma A, Martin K, Roland P, Bauer, P, et al: P1
latency as a biomarker for central auditory development in children with hearing impairment. J Am Acad
Audiol 16(8):564–573, 2005.)

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Further, previous studies in our laboratory indicate a significant
correlation between P1 CAEP latency and auditory skill develop-
ment (IT-MAIS), suggesting that biomarkers of the developmental
status of the central auditory system may be predictive of speech
perception outcomes81 and may provide valuable information
in the clinical management of ANSD children before and after
intervention.
Fig. 132.5 depicts P1 CAEP responses in a male child who
received a diagnosis of ANSD at age 3 months.83 The child exhibited
several high-risk factors for ANSD, including hyperbilirubinemia
requiring exchange transfusion and use of mechanical ventilation.
The child was fit with binaural hearing aids at age 4 months.
Binaural aided CAEP responses were recorded longitudinally over
time to monitor central auditory maturation with hearing aid use.
At both recording sessions during hearing aid use, no replicable
P1 CAEP response could be observed (see Fig. 132.5A top),
suggesting that the hearing aids were not providing adequate
quality or quantity input to promote age-appropriate development
of the central auditory pathways. These test results, in conjunction
with the audiological test battery, provided the family and medical
team with objective data, leading to a CI candidacy evaluation.
At age 21 months, the child received a CI in his left ear. Binaural
CAEP responses recorded after approximately 5 to 6 months of
left CI use showed rapid change in CAEP morphology, marked
by emergence of a robust and replicable P1 response (see Fig.
132.5A bottom) occurring at a latency falling within the 95%
confidence interval for the child’s age (see Fig. 132.5B). In this
case, close monitoring of this child’s neurophysiological develop-
ment helped the child’s medical team evaluate optimal time for
intervention with a CI.
The P1 CAEP biomarker has also proven to be a clinically
useful tool in the management of children with cochlear (VIII)
nerve deficiency, a disorder that has high levels of comorbidity
with ANSD.85,86 While a small (or hypoplastic) VIII nerve can
typically be identified via neuroimaging (e.g., MRI), structural
imaging cannot provide functional information about the viability
of the nerve for clinical intervention with a CI. In a study by
Roland et al. (2012),87 robust P1 CAEP responses were observed
in three out of four cases of children with cochlear nerve deficiency,
indicating at least partial viability of the aplastic VIII nerve in
these cases, useful in determination of CI candidacy.
Clinical Utility of the P1 Cortical Auditory
Evoked Potential Biomarker in Children
With Multiple Disabilities
Another application of the P1 CAEP biomarker is in children
with additional disabilities comorbid with hearing loss. Fortnum
and Davis (1997) reported presence of comorbidities in approxi-
mately 40% of cases of pediatric hearing loss.88 Common comorbid
conditions may include vision loss, motor disorders, cognitive
disabilities, neurodegenerative disorders, and speech and language
delays.88–90 Developmental disorders such as autism spectrum
disorder (ASD)91 are also highly comorbid with hearing loss.
Syndromic forms of hearing loss such as CHARGE syndrome, a
deletion of the CHD7 gene on chromosome 8 also contribute to
children with multiple disabilities and multiply complex needs.92
While children with multiple disabilities may benefit from interven-
tion with hearing aids or CI, these children may make slower
progress language development compared to children with hearing
loss without comorbid conditions who receive a CI,93,94 so setting
reasonable expectations and predicting outcomes following
intervention may be difficult. Further, assessment of candidacy
for children with multiple disabilities may be challenging when
behavioral data is inconsistent, incomplete, or unreliable. In such
scenarios, objective measurement of the developmental status of
the central auditory pathways using the P1 CAEP biomarker may
be recorded easily and without the need for sedation, providing
useful data to aid in clinical decision-making.
Fig. 132.6 depicts P1 CAEP data obtained in a female child with
CHARGE syndrome.95 This child was identified with hearing loss
during her newborn hearing screening and was diagnosed with a
bilateral moderate-severe sensorineural hearing loss at age 3 months.
This child presented with a cleft lip and palate, recurrent middle
ear infections during early childhood, and global developmental,
speech, and language delays. Despite well-fit amplification, this

Before CI (HA Use)

Before CI (HA Use)
NR
300
P1 Latency (ms)

250
4 µV
200
150
After CI After CI
100
50
Normal Limits
0
0 1 2 3
A B Age (years)

Fig. 132.5  Clinical utility of the P1 cortical auditory evoked potential (P1 CAEP) biomarker in a case of
auditory neuropathy. This child was diagnosed with bilateral auditory neuropathy at age 3 months and was
fit with hearing aids (HA) at age 4 months. (A) Longitudinal CAEP responses during HA use indicate absent
P1 CAEP responses, suggesting that the hearing aids were not providing adequate input to allow for normal
development of the central auditory pathways. At 21 months, the child received a cochlear implant (CI) for his
left ear. Within 5–6 months after CI use, a robust P1 CAEP response emerged (A) with P1 latency falling
within the 95% confidence interval for the child’s age, (B) indicating that intervention with CI helped promote
typical development of the central auditory pathways. In this case of auditory neuropathy, the P1 CAEP
biomarker helped to monitor central auditory maturation over the clinical course of intervention. (Adapted from
Cardon G, Campbell J, Sharma A. Plasticity in the developing auditory cortex: evidence from children with
sensorineural hearing loss and auditory neuropathy spectrum disorder. J Am Acad Audiol 23:396–411, 2012.)

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 CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 2003

P1
350 132
300
2 µV

P1 Latency (ms)
250
200 (HA Use)
150
100
50
Normal Limits
0
0 2 4 6 8 10
A B Age (years)

Fig. 132.6  Clinical utility of the P1 cortical auditory evoked potential (P1 CAEP) biomarker a case of
multiple disabilities. This child was born with CHARGE syndrome and was diagnosed with a moderate-
severe sensorineural hearing loss at age 3 months and fit with bilateral hearing aids (HA) at age 5 months.
The child was referred for CAEP testing at age 22 months by the child’s managing audiologist due to
inconsistent and unreliable behavioral aided test results, despite well-fit amplification using hearing aid
verification measures. A robust P1 CAEP response (A) occurring at a normal latency for the child’s age (B)
was observed in the binaural aided condition, indicating that the hearing aids were providing sufficient
auditory stimulation to allow for normal maturation of the central auditory pathways. In this case, the P1 CAEP
biomarker helped to monitor efficacy of intervention in the context of comorbid disabilities that prevent the
acquisition of reliable audiological and speech perception outcomes. (Adapted from Cardon G, Campbell J,
Sharma A: Plasticity in the developing auditory cortex: evidence from children with sensorineural hearing loss
and auditory neuropathy spectrum disorder. J Am Acad Audiol 23:396–411, 2012.)

child with CHARGE syndrome was referred for P1 CAEP testing
due to the fact that the child’s managing audiologist could not
obtain reliable aided behavioral data to demonstrate objective
benefit from amplification. Testing at age 1.91 years indicated a
robust and replicable binaural aided P1 CAEP response (see Fig.
132.6A) falling within the 95% confidence interval for the child’s
age (see Fig. 132.6B), indicating age-appropriate development of
the central auditory pathways. Despite unreliable behavioral data
regarding the child’s aided outcomes, normal P1 CAEP latencies
indicated age-appropriate development of the central auditory
pathways, consistent with well-fit amplification based on real-ear
verification measures. Overall, these cases highlight the clinical
utility of the P1 as an objective tool to complement the traditional
audiological and otologic test battery.
Cross-Modal Neuroplasticity in Hearing Loss:
Evidence From Pediatric Deafness
If auditory cortex does not receive sufficient auditory input and
higher-level auditory cortex does not develop normally, other
compensatory changes in neuroplasticity may occur. Compensatory
plasticity refers to changes in neuronal structure or function as a
result of atypical extrinsic input to the system, for example, as a
result of hearing loss or deafness. One form of compensatory
neuroplasticity is cross-modal neuroplasticity. Cross-modal neuro-
plasticity refers to the compensatory repurposing of cortical brain
regions deprived of sensory input by other sensory modalities.96
That is, in sensory deprivation (e.g., hearing loss or deafness),
brain regions typically used to process auditory information are
recruited by other sensory modalities. In deafness and hearing
loss, this means that lack of appropriate input to the auditory
cortex may induce repurposing of auditory cortical resources by
other senses (e.g., vision, somatosensation). For example, deaf cats
demonstrate increased responsivity to somatosensory, visual, and
multi-modal stimulation in secondary auditory cortex relative to
normal hearing controls,97 suggestive of cross-modal reorganization.
Bilateral, temporary de-activation of an area of auditory cortex
known as posterior auditory field (PAF) using super-cooling loops
mediates enhancement in visual localization in the periphery in
congenitally deaf cats, while temporary de-activation of a different
dorsal area of auditory cortex (DZ) mediates enhancement in
visual movement detection, indicating that deafness may induce
functional changes in cross-modal reorganization by vision in a
highly-specific manner.98
Cross-modal neuroplasticity by vision has been observed in deaf
CI children. For example, in a recent study by our laboratory, we
examined CVEPs in response to an apparent motion stimulus in a
group of CI children (n = 14) and a group of age-matched normal
hearing children (n = 41) using high-density 128-channel EEG,99
where the average age of implantation with the first CI was toward
the end of the sensitive period (average =3.12 years, SD = ±2.27
years) and the average age of implantation with the second CI
well after the sensitive period (average = 6.20 years, SD = ±3.45
years). Sentence-level speech perception in noise performance was
measured using the Bamford-Kowal-Bench Speech-in-noise test
(BKB-SIN). The BKB-SIN is a clinical test that provides a threshold
of the signal-to-noise ratio (difference in decibel hearing level [dB
HL] between the speech signal and the noise signal) required for
children to perceive 50% of words in a sentence, where a higher
score (threshold) indicates poorer auditory speech perception in
background noise.100 In this test, participants are presented with list
pairs of sentences in the context of 4-talker babble noise from a set
of 18 list pairs. Results from this study are shown in Fig. 132.7A.
EEG source analysis using current density source reconstruction
(CDR) was then computed to localize sources of cortical activity
in response to the visual stimulus. While visual stimulation in
the normal hearing children was localized to occipital (visual)
cortical regions (e.g., cerebellum, striate, extra striate) (see Fig.
132.7A1), visual stimulation in the CI children was localized to
occipital (visual) cortical regions and temporal (auditory) cortical
regions (inferior, middle, and superior temporal gyrus) (see Fig.
132.7A2), suggestive of cross-modal neuroplasticity. Further, earlier
CVEP latencies (considered a marker of cross-modal plasticity), as
observed in the CI children, were correlated with higher scores on
the BKB-SIN (poorer auditory speech perception in background
noise) (see Fig. 132.7B). Evidence of cross-modal reorganization by
vision has been similarly observed in PET imaging studies, whereby
CI children exhibit higher resting glucose metabolism rates over

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2004 PART VII  Otology, Neurotology, and Skull Base Surgery

Visual cross-modal neuroplasticity in CI children Cross-modal reorganization in individual CI children

1 2
Normal hearing children CI children Visual Somatosensory

N1 N1 Normal hearing child: 100% Normal hearing child: 100%

1 P2 4 N70

Good CI performer: 96% Good CI performer: 94%

Min Max 2 P2 5 N70
A F-Distribution

Correlation between visual cross-modal reorganization &

speech perception in CI children
20 r = –0.576
p < 0.05
15 Average CI performer: 67% Average CI performer: 76%
BKB-SIN socre

3 P2 6 N70
10

0
200 220 240 260 280 300 Min Max
B C F-distribution
N1 CVEP latency

Fig. 132.7  Cross-modal reorganization in cochlear implanted children. Fig. 132.7 (A) Current density
source reconstructions (CDRs) showing cortical localization patterns for the N1 cortical evoked potential
(CVEP) are depicted in a group of normal hearing children (n = 41) and a group of cochlear implanted (CI)
children (n = 14) in response to visual motion stimulus. The color scale (F-Distribution) indicates the likelihood
of cortical activity in a given location represented on an average magnetic resonance image (MRI) (sagittal
view). (A1, A2) While the normal children exhibit expected activation in occipital cortex typically associated
with visual motion processing (A1), the CI children exhibit additional recruitment of temporal cortex for the
higher-order CVEP components (A2), suggestive of cross-modal reorganization. (B) N1 CVEP latencies plotted
against speech perception scores on the BKB-SIN. The BKB-SIN is a clinical test providing a threshold of the
signal-to-noise ratio (difference in decibel hearing level [dB HL] between the speech signal and the noise
signal) required for children to perceive 50% of words in a sentence, where a higher score (threshold)
indicates poorer auditory speech perception in background noise. Earlier N1 CVEP latencies over the
temporal cortex are associated with poorer auditory speech perception in background noise. (C) CDRs
showing cortical localization patterns for the P2 CVEP in response to a visual motion stimulus and the N70
cortical somatosensory evoked potential (CSSEP) in response to a vibrotactile stimulus in six individual CI
children. Speech perception scores in quiet on the Consonant Nucleus Consonant (CNC), Mutli-syllabic
Lexical Neighborhood Test (MLNT), or Lexical Neighborhood Test (LNT), in terms of percent correct,
are indicated above the CDR images. While the normal hearing children and the two CI children good
performance outcomes (96% and 94% accuracy on clinical assessments of auditory speech perception)
exhibit cortical activity restricted to visual cortex for the processing of visual motion stimuli (C1, C2) and
cortical activity restricted to parietal cortex for the processing of vibrotactile stimuli (C4, C5), the two average
performing CI children (67% and 76% accuracy on clinical assessments of auditory speech perception) show
additional recruitment of temporal (auditory) cortex for visual processing (C3) and somatosensory processing
(C6), suggestive of cross-modal reorganization by the visual and somatosensory modalities. (Adapted from
Campbell J, Sharma A: Visual cross-modal reorganization in children with cochlear implants. PLoS ONE
11(1):e0147793, 2016; and Sharma A, Campbell, J, Cardon G: Developmental and cross-modal plasticity in
deafness: Evidence from the P1 and N1 event related potentials in cochlear implanted children. Int J Physiol
95(2):135–144, 2015.)

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auditory, frontal, and visual cortex, indicators of compensatory
changes in neuroplasticity.101–103
Cross-modal neuroplasticity by the somatosensory system has
also been documented in pediatric deafness using cortical somato-
sensory evoked potentials (CSSEP).37,104 In a study by Cardon
(2015), CSSEPs were recorded using 128-channel high-density
EEG in response to a 250 Hz vibrotactile stimulus delivered to
the index finger in a group of deaf children receiving their CI
toward the end of the sensitive period (average age at first implant
= 3.90 years, SD = ±4.03 years; average age at second implant =
7.33 years, SD = ±4.47 years) and in a group of age-matched
normal hearing children (n = 35, average age at test = 10.54 years,
SD = ±4.03 years).104 EEG source analysis using CDR was then
computed to localize sources of cortical activity in response to
the vibrotactile stimulus. While the group of normal hearing
children in this study exhibited cortical activity localized to brain
regions typically associated with vibrotactile processing in parietal
cortex (e.g., pre/post central gyrus), the group of CI children
exhibited cortical activity localized in parietal cortex and temporal
(auditory) cortex (e.g., inferior temporal gyrus, middle temporal
gyrus, superior temporal gyrus), suggestive of cross-modal
reorganization by the somatosensory modality. Somatosensory
cross-modal reorganization has similarly been observed in con-
genitally deaf adults.105–107
While the underlying mechanisms of cross-modal neuroplasticity
in hearing loss are debated in the field of neuroscience, on a
structural or anatomic level, cross-modal neuroplasticity may occur
via the unmasking or stabilization of silent, latent, or transient
neuronal inputs/connections; via the sprouting of new axons; via
an increase in intersensory connections via dendritic branching
or new synapse formation, or by some combination of the afore-
mentioned mechanisms.108 While the development of cortico-
thalamic and cortico-cortical pathways are just starting to develop
in early childhood, meaning these pathways may be just beginning
to stabilize, animal models indicate a strong inter-connectedness
between secondary sensory cortices even in normal hearing animals.
However, under the context of sensory deprivation (e.g., deafness
or hearing loss), certain neuronal connections within or between
modalities may become strengthened.97,109,110 Another hypothesis
is that cross-modal cortical neuroplasticity may reflect changes
in neuroplasticity at lower, subcortical levels,97 and there is some
evidence to support this at the level of the cochlear nucleus111 and
inferior colliculus112 in animal models of deafness.
Clinical Significance of Cross-Modal
Neuroplasticity in Pediatric Hearing Loss
Not all children who receive audiological intervention exhibit good
speech perception outcomes following CI. In hearing impaired
children, for example, it has been estimated that less than 50% of
variability in speech and language outcomes can be accounted for by
demographic factors alone (e.g., age of implantation),113 emphasizing
the large degree of heterogeneity and individual differences likely
influencing performance outcomes after audiological intervention.
Why do some children perform well with their devices, while other
children continue to struggle to make age-appropriate gains in
auditory performance? Individual differences in neuroplasticity,
including cross-modal reorganization, could contribute to individual
differences in performance outcomes. Fig. 132.7B highlights the
neurophysiological profile of six individual children in this way.37
Fig. 132.7B depicts EEG source localization using current density
source reconstructions (CDRs) for the P2 CVEP component in a
normal hearing child (age 10 years) (see Fig. 132.7C1), a pediatric
CI user (age 8 years) with excellent auditory speech perception
outcomes (96% on a clinical test of auditory speech perception in
quiet, the Lexical Neighborhood Test [LNT]) (see Fig. 132.7C2),
and a pediatric CI user (age 6 years) with average performance
outcomes (67% on a clinical test of auditory speech perception
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CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 2005
in quiet, the Multisyllabic Lexical Neighborhood Test [MLNT])
(see Fig. 132.7C3), in response to a visual motion stimulus using 132
128-channel high-density EEG described. While the normal hearing
child and CI recipient with excellent speech perception exhibit
expected activation of visual cortical regions typically associated
with visual motion processing (e.g., occipital gyrus, fusiform gyrus,
lingual gyrus) (see Fig. 132.7C1 and 132.7C2), the CI recipient with
average performance exhibits additional recruitment of auditory
cortical regions (e.g., middle and superior temporal gyrus) (see
Fig. 132.7C3), indicative of cross-modal neuroplasticity by vision.
Fig. 132.7B also depicts EEG source localization using CDRs
for the N70 CSSEP in three separate children in response to a
250 Hz vibrotactile stimulus applied to the right index finger using
high-density 128-channel EEG reported in Sharma et al. (2015)37: A
normal hearing child (age 7 years) (see Fig. 132.7C4), a pediatric CI
user (age 13 years) exhibiting excellent auditory speech perception
(94% on a clinical test of auditory speech perception in quiet, the
Consonant Nucleus Consonant [CNC]) (see Fig. 132.7C5), and a
pediatric CI user (age 15 years) exhibiting average performance
on an auditory unimodal test of speech perception (76% on the
CNC test) (see Fig. 132.7C6). While the normal hearing child
and pediatric CI recipient with excellent speech perception show
expected activation in cortical regions associated with somatosen-
sory processing (e.g., post-central gyrus) (see Figs. 132.7C4 and
132.7C5), the pediatric CI recipient with average auditory speech
perception exhibits additional recruitment of temporal processing
regions (e.g., superior temporal gyrus, transverse temporal gyrus)
(see Fig. 132.7C6), indicative of cross-modal neuroplasticity by
the somatosensory modality. While these data stem from single
subjects and should be interpreted cautiously, results provide some
preliminary evidence that underlying neurophysiological changes
in cross-modal plasticity may relate to functional outcomes fol-
lowing audiological intervention. With a better understanding of
cross-modal plasticity in the context of auditory deprivation and
the potential for audiological intervention to reverse these changes
in neuroplasticity, brain-based markers may help interventionists
individualize intervention, rehabilitation, and training programs
for individual patients with hearing loss receiving audiological
intervention with hearing aids or CI.
What functional purpose might cross-modal reorganization serve
within the context of speech perception for children with hearing
loss? Campbell and Sharma (2016)99 suggest that those children who
had more difficulty with auditory speech perception in background
noise also exhibited greater cross-modal reorganization. Under
certain communication contexts, particularly under ecologically valid
auditory-visual listening conditions, cross-modal neuroplasticity
may allow some children with hearing loss to compensate. For
example, several studies indicate that late-implanted CI children
are actually better lip readers than early-implanted CI children,
allowing them to maximize their use of visual (facial) cues.114 In
this same study, late-implanted CI children also exhibited higher
levels of auditory-visual integration compared with early-implanted
CI children. In this task, the two groups of CI children were asked
to repeat sentences presented in visual-only (lip-reading task) and
auditory-visual (auditory speech stimuli coupled with facial cues)
on speech perception tasks, and performance in the two conditions
were subtracted to obtain a score of functional reliance on visual
cues or auditory-visual integration.114 Similarly, other studies
indicate that CI children show enhanced auditory-visual integra-
tion abilities in multi-modal tasks of incongruous auditory stimuli
(e.g., McGurk Effect).115 In fact, even years after implantation, CI
children continue to exhibit gradual improvements in lip-reading
and auditory-visual integration abilities,116 suggesting that these
cross-modal changes may serve a functional purpose even after
audiological intervention.99 While less well-studied, somatosensory
cross-modal reorganization may also show functional significance.
For example, deaf listeners have been shown to rely more heavily
on vibrotactile inputs to differentiate same-sex speakers117 and in
2006 PART VII  Otology, Neurotology, and Skull Base Surgery
the differentiation of timbre between musical instruments.118 in
deaf listeners. In fact, several studies have documented enhanced
tactile discrimination in deaf children,119,120 and similar findings have
been observed in animal models of deafness.97,121–124 Dependence
on nonauditory sensory inputs may thus be a natural compensatory
mechanism, allowing children with hearing loss to compensate in
everyday multi-modal listening conditions.
A better understanding of changes in neuroplasticity in pediatric
hearing loss may lead to the development of more useful clinical
tools to predict and direct intervention to children with hearing
loss. For example, many audiological assessments (including tests to
evaluate CI candidacy) are assessed in an auditory-only condition,
despite the aforementioned studies that highlight how children
with hearing loss exhibit increased dependence on vision and/or
enhanced auditory-visual integration abilities. Thus, the develop-
ment of real-world, ecologically valid multi-modal (auditory-visual)
assessments may help clinicians make better predictions about the
potential for treatment success, or may help clinicians identify
which patients may be in need of more intensive aural rehabilita-
tion after treatment to maximize hearing aid or CI outcomes.125
Greater understanding of individual variability in cross-modal
neuroplasticity in clinical populations with hearing loss may also
help develop more targeted, individualized therapeutic plans for
pediatric patients. For instance, there still exists great debate over
communication approaches and modes for pediatric populations,
and many current therapeutic techniques lack evidence-based rigor.
In the future, objective clinical biomarkers of neuroplasticity may
help identify which therapy strategies might benefit individual
patients in reaching their highest potential with audiological
intervention.
Potential Audiological Intervention to Reverse
Cortical Cross-modal Neuroplasticity: Evidence
From Cochlear Implantation in a Pediatric Case
of Single-Sided Deafness
In a recently published case study of progressive pediatric single-
sided deafness in the right ear, we documented changes in central
auditory system neuroplasticity and cross-modal neuroplasticity
by vision and somatosensation before and after CI, to evaluate
the effects of intervention.126 SSD refers to unilateral severe-
profound sensorineural hearing loss in one ear and normal hearing
in the other ear. SSD occurs in less than 3% of children,127 with
higher incidence in adolescence128 and into adulthood. Among
pediatric SSD cases, the majority are congenital,129 due to structural
anomalies such as cochlear nerve deficiency or enlarged vestibular
aqueduct syndrome,130 but acquired causes, including congenital
cytomegalovirus (CMV),131 meningitis,132 and trauma,133 also
contribute. Unilateral hearing loss is a historically undertreated
audiological disorder134 and many children with unilateral hearing
loss continued to be late identified, despite a wealth of data citing
increased incidence of speech and language delays, educational
delays, and behavioral problems135–139 in these children. At present,
while there are very few large-scale studies evaluating the efficacy
of CI in SSD over conventional treatment options (e.g., conven-
tional hearing aid, contralateral routing of signal hearing systems,
bone conduction hearing devices), emerging data indicates that
CI may improve speech perception in background noise, decrease
tinnitus perception, and increase health-related quality of life in
some but not all SSD patients.139–146
In this child with progressive SSD in the right ear who received
a CI in her right ear at age 9.86 years, CAEPs, CVEPs, and CSSEPs
were recorded before and at subsequent intervals after CI using
128-channel, high-density EEG with speech, visual motion, and
vibrotactile stimuli, respectively. Behavioral correlates of speech
perception in noise and sound localization were also measured (see
Sharma et al. [2016]126 for details about stimuli and methodology
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used). Results from this case study are depicted in Fig. 132.8.
Prior to CI, the child’s CAEP response in her right SSD ear
showed immature morphology, marked by only a single P1 CAEP
component (see Fig. 132.8A1), whereas the left normal hearing
ear showed presence of age-appropriate morphology include a
P1, N1, and P2 response. Further, whereas monaural auditory
stimulation typically results in localization of cortical activity to both
temporal cortices (with stronger representation in the contralateral
temporal cortex to the ear stimulated), CAEP recordings obtained
by stimulating the right SSD ear show cortical activity localized
to temporal (auditory) cortex ipsilateral to the SSD ear, indicative
of abnormal auditory dominance patterns (see Fig. 132.8A5). This
finding is consistent with studies by Gordon and colleagues, in
which long durations of unilateral hearing experience during
development leads to atypical development of the central auditory
pathways.147–150 Further, as shown in Fig. 132.8B1, CDRs for the
P2 CVEP pre-CI shows auditory cortical activity localized to
occipital (visual) cortex in addition to temporal (auditory cortex),
suggestive of visual cross-modal reorganization. Similarly, as shown
in Fig. 132.8B3, localization of the P50 CSSEP occurred in parietal
(somatosensory) cortex and temporal (auditory), suggestive of cross-
modal reorganization by somatosensation. However, within 14
months of CI use, we observed a progressive decrease in P1 CAEP
latency after 3 months of CI use (see Fig. 132.8A2), the emergence
of the N1/P2 CAEP components within 8 to 14 months of CI use
(see Fig. 132.8A3 and 132.8A4), and a restoration of more typical
contralateral auditory dominance patterns when stimulating the
SSD ear (see Fig. 132.8A6), providing evidence that intervention
with CI helped promote more typical development of the central
auditory pathways, even after relatively late age of implantation (age
9.86 years). In this case study, rapid changes in CAEP morphology
were observed well after the typically described 3.5-year sensitive
period by Sharma et al. (2002a)32 in congenital bilaterally deaf
children, likely indicating that the progressive nature of the child’s
hearing loss and/or input from the child’s normal hearing ear
may have helped to preserve neuroplasticity. Further, within 27
months of CI use, we observed partial reversal in cross-modal
recruitment of the auditory cortex for visual motion processing (see
Fig. 132.8B2) and complete reversal in cross-modal recruitment
of auditory cortex for vibrotactile processing (see Fig. 132.8B4),
indicating that audiological intervention may help promote more
typical sensory processing patterns at the level of the auditory
cortex. Such dramatic changes in neuroplasticity observed in this
case study is supported by behavioral data, in which this SSD child
exhibited remarkable improvements in auditory speech perception
in background noise and auditory localization after CI.126 While
these data should be interpreted cautiously and a great deal of
future research is needed in this area, this case study highlights
the potential for neurophysiological biomarkers of brain plasticity
to help guide otologic intervention. The development of such
biomarkers may provide health care providers with data regarding
the efficacy of clinical interventions and to monitor neurophysi-
ological development over the clinical course of intervention and
rehabilitation in individual patients.
NEUROPLASTICITY IN ADULT-ONSET,
AGE-RELATED HEARING LOSS
ARHL, or presbycusis, is a significant public health issue.151–154
Hearing loss is one of the most common chronic disabilities facing
older adults.155 While hearing loss is nearly ubiquitous among the
oldest adults (approximately 80% of adults over age 80 years have
a clinically significant hearing impairment),156,157 epidemiological
evidence suggests that hearing loss starts relatively early in adult-
hood, affecting 34%, 53%, and 77% of adults in their 4th, 5th,
and 6th decades of life, respectively.158 Beyond the known
psychosocial consequences of untreated hearing loss including
elevated risk for social isolation and depression,159–161 several recent
 CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 2007

Central auditory maturation in pediatric SSD Cross-modal reorganization in pediatric SSD

132
before & after CI before and after CI
Visual
P1
1 Pre-CI 5 Pre-CI 1 Pre-CI 2 Post-CI
P1 P2 P2

P1
2 3 months post-CI

L R

Somatosensory
P1
3 8 months post-CI 6 Post-CI 3 Pre-CI 4 Post-CI

P2
P1 P50 P50

N1

P1
4 14 months post-CI
P2

N1
L R
Min Max Min Max
A F-distribution B F-distribution

Fig. 132.8  Central auditory maturation and cross-modal neuroplasticity in a pediatric case of right
single-sided deafness. The child had a progressive single-sided deafness (SSD) in her right ear and received
a cochlear implant (CI) at age 9.86 years. (A) Central auditory cortical maturation before and after cochlear
implantation. While immature cortical development marked by the presence of only a P1 cortical auditory
evoked potential (CAEP) component is observed when providing auditory stimulation to the child’s right SSD
ear (A1), longitudinal development of the CAEP response after CI indicates a decrease in P1 CAEP latency
after 3 months of CI use (A2), and development of age-appropriate N1/P2 components in the SSD when
assessed at 8 and 14 months post-CI (A3, A4). Further, current density source reconstructions (CDRs) for the
P1 CAEP recorded using high-density, 128-channel EEG indicates abnormal ipsilateral temporal (auditory)
cortical activity pre-CI (A5), which reverts to a more typical contralateral temporal (auditory) cortical dominance
pattern within 14-months of CI use (A6), suggesting objective benefit of CI use in promoting typical maturation
of the central auditory pathways. The color scale (F-Distribution) indicates the likelihood of cortical activity in a
given location represented on an average magnetic resonance image (MRI). (B) Cross-modal reorganization
before and after cochlear implantation. CDRs of the P2 cortical visual evoked potential (CVEP) and the P50
cortical somatosensory evoked potential (CSSEP) recorded in response to a visual motion stimulus and a
250 Hz vibrotactile stimulus, respectively, using high-density, 128-channel EEG before and after CI. The
color scale (F-Distribution) indicates the likelihood of cortical activity in a given location represented on an
average magnetic resonance image (MRI). While evidence of cross-modal reorganization by vision and
somatosensation is evident in this child pre-CI, marked by activation of the temporal (auditory) cortex in
addition to regions typically associated with visual and somatosensory processing (B1, B3), within 27 months
of CI use, partial reversal in cross-modal neuroplasticity by vision and complete reversal in cross-modal
neuroplasticity by somatosensation was observed (B2, B4), consistent with this child’s improvements in
auditory perception with her CI. (Adapted from Sharma A, Glick H, Campbell J, et al: Cortical plasticity and
reorganization in pediatric single-sided deafness pre- and post-cochlear implantation: a case study. Otol
Neurotol 37:e26–34, 2016.)

large-scale cohort studies have demonstrated a link between
untreated hearing loss and cognitive decline.162–164 For example,
in an 11-year follow-up period, the risk for acquiring all-cause
dementia increased from 1.89 to 4.94 as hearing loss progressed
from mild to severe, such that for each 25-decibel (dB) increase
in hearing loss, this equated to 7 years of cognitive aging.156,157
Despite this evidence, only a small proportion of adults with ARHL
seek treatment,165 usually about a decade after initial presentation
of hearing loss symptoms.
While there are many potential causal mechanisms underlying
the link between ARHL, both structural and functional brain
changes have been identified,166–168 suggesting that ARHL may be
linked to changes in neuroplasticity. Further, we are now begin-
ning to gain a greater understanding of the cognitive mechanisms
involved in ARHL that may be linked to cognitive decline, including
decreased cognitive spare capacity/cognitive reserve.153 In this next
section of the chapter, we describe neuroplasticity in adult-onset
hearing loss, including deafness and age-related, mild-moderate
hearing loss, describing changes in cross-modal neuroplasticity
and other compensatory changes in cortical resource allocation,
such as the recruitment of frontal cortex for auditory processing,
as it relates to clinical outcomes.

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2008 PART VII  Otology, Neurotology, and Skull Base Surgery

Cross-Modal Neuroplasticity in Auditory cortical neuroplasticity in ARHL

Adult-Onset Deafness 1 Normal hearing 2 ARHL
Cross-modal neuroplasticity of the auditory cortex by vision has
P2 P2
been reported in deaf adults using fNIRS,169,170 EEG,171–174 and
fMRI.175 For example, deaf adults show more extensive auditory
cortical activation for visual processing,176 earlier CVEP latencies
over auditory cortex,174 and increased CVEP amplitudes over
auditory cortex171 in EEG studies, indicative of cross-modal
reorganization by vision. Deaf adults also appear to exhibit recruit-
ment of auditory cortical regions for tactile processing,77,106 A
suggestive of cross-modal plasticity by somatosensation. Post-
lingually deaf adults with poorer auditory speech perception Visual cross-modal reorganization in ARHL
outcomes (lower performance on tests of auditory-speech perception 1 Normal hearing 2 ARHL
with their CI) exhibit more widespread cortical activation across
the scalp (including auditory cortical regions) for visual motion P2 P2
processing, whereas post-lingually deaf adults with higher levels
of auditory speech perception outcomes (higher performance on
tests of auditory speech perception with their CI) exhibit activation
patterns more restricted to the occipital lobe for processing visual
simuli.172 Together, these studies suggest that compensatory changes
in cross-modal plasticity may be correlated with the large variability B
in auditory performance outcomes observed in adult CI users,
and warrant further investigation. Somatosensory cross-modal reorganization in ARHL
However, “repurposing” of the auditory cortex for visual
processing may also help deaf adults to adapt in real-world, multi- 1 Normal hearing 2 ARHL
modal conditions. For example, deaf adults using oral language177,178 P100 P100
and deaf adults using sign language179 derive greater benefit from
visual cues (e.g., lip-reading) compared with normal hearing adults.
Cross-modal neuroplasticity by vision in deafness may also support
enhancements in auditory-visual integration abilities.180–184 For
example, deaf adults exhibit greater sensitivity to visual stimuli
(faces) over the right auditory cortex compared with non-face C Min Max
stimuli (houses) relative to normal hearing listeners,180,185 evidence F-distribution
that cross-modal recruitment of auditory cortex may be related
to enhanced face processing. Another study showed enhanced Fig. 132.9  Auditory, visual, and somatosensory cortical
auditory-visual integration for the McGurk Illusion in post-lingually neuroplasticity in early-stage, mild-moderate age-related hearing
deaf CI users relative to normal hearing listeners.180 The McGurk loss. Current density source reconstructions (CDRs) showing cortical
Illusion refers to special case of auditory-visual integration, in localization patterns for the P2 cortical auditory evoked potential
which two incongruous speech syllables (e.g., /ba/ and /ga/) are (CAEP) (A), the P2 cortical visual evoked potential (CVEP) (B), and the
presented simultaneously, one through the auditory modality and P100 cortical somatosensory evoked potential (CSSEP) (C) in a group
one through the visual modality (e.g., face articulation cues), leading of normal hearing adults and a group of adults with early-stage,
to a fused percept of these two signals (e.g., /da/). In this study, mild-moderate age-related hearing loss (ARHL) in response to a
cortical activation of the N170 CVEP component (a waveform speech stimulus, a visual motion stimulus, and a 250 Hz vibrotactile
component elicited by visual facial stimuli) localized to auditory stimulus, respectively. The color scale (F-Distribution) indicates the
cortex was significantly correlated with auditory-visual integration likelihood of cortical activity in a given location represented on an
abilities for the McGurk Effect in deaf CI adults, evidence that average magnetic resonance image (MRI) (sagittal view). While normal
cross-modal neuroplasticity by vision may help deaf adults adapt hearing adults show expected activation of temporal cortex, visual
in real-world communication settings when both auditory and cortex, and parietal cortex in response to auditory, visual, and
visual cues are available.180 somatosensory stimulation (A1, B1, C1), adults with ARHL exhibit
additional recruitment of frontal cortex for processing auditory stimuli
(A2), as well as recruitment of the temporal (auditory) cortex for
Cross-Modal Neuroplasticity in Early-Stage, processing visual motion stimuli (B2) and somatosensory stimuli
Age-Related Hearing Loss (C2) processing. Taken together, these data indicate evidence of
Recent studies from our laboratory indicate that cross-modal compensatory changes in auditory resource allocation and evidence
plasticity by vision and somatosensation is not just restricted to of visual and somatosensory cross-modal reorganization of the
deafness, but also occurs in early-stage, mild-moderate ARHL. auditory cortex. (Adapted from Campbell J, Sharma A: Compensatory
Fig. 132.9B and 132.9C show EEG source localization (CDRs) changes in cortical resource allocation in adults with hearing loss.
for CVEPs and CSSEPs in response to a visual motion stimulus Frontiers Systems Neurosci 7:71, 2013; Campbell J, Sharma A:
and a vibrotactile stimulus using high-density, 128-channel EEG Cross-modal reorganization in adults with early stage hearing
in a group of adults with normal hearing and a group of adults loss. PLoS ONE 9(2):e90594, 2014; and Cardon G, Sharma A:
with mild-moderate ARHL,187,188 many of whom were unaware Somatosensory cross-modal reorganization in adults with age-related,
that they had a hearing loss upon time of enrollment in the study. early-stage hearing loss. Frontiers 2018.)
Sentence-level speech perception in noise performance was also
measured using the Quick-SIN, a clinical test providing a threshold
of the signal-to-noise ratio (difference in dB HL between the speech
signal and the noise signal) required for adults to perceive 50%
of words in a sentence, where a higher score (threshold) indicates

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poorer auditory speech perception in background noise.189 While
cortical activity in response to the visual stimulus was localized
to occipital (visual) cortex in the normal hearing listeners (e.g.,
cerebellum, fusiform gyrus, lingual gyrus) for all CVEP components
(P1, N1, P2) (see Fig. 132.9B1), visual stimulation in the adults
with ARHL was localized to areas of occipital (visual) cortex, as
well as temporal (auditory) cortex (e.g., inferior temporal gyrus,
medial temporal gyrus, superior temporal gyrus) and frontal
cortex (e.g., inferior frontal gyrus) for the higher-order (N1
and P2 CVEP components) (see Fig. 132.9B2), suggestive of
cross-modal reorganization by vision.187 In this study, earlier N1
CVEP latencies, considered an indicator of visual cross-modal
plasticity, were significantly correlated with higher Quick-SIN
scores (poorer speech perception in background noise). Cross-
modal reorganization by somatosensation is also apparent in
mild-moderate ARHL. In a study by Cardon and Sharma (2018),188
vibrotactile stimulation elicited activation of cortical regions in
parietal (somatosensory) cortex in normal hearing adults (e.g.,
pre- and post-central gyrus, inferior parietal lobule, superior parietal
lobule) for all CSSEP components (P50, N70, P100, N140a,
N140b) (see Fig. 132.9C1), whereas adults with ARHL exhibited
localization of vibrotactile processing in somatosensory and auditory
cortical regions (e.g., superior, middle, inferior temporal gyrus)
(see Fig. 132.9C2), suggestive of cross-modal reorganization by
somatosensation.97,105,106,188,190,191
The results reported in Campbell and Sharma (2014) are similar
to the data reported in a recent EEG study by Stropahl and Debener
(2017).180 In this study, compared with normal hearing adults,
cross-modal reorganization of the auditory cortex by vision was
most pronounced in post-lingually deafened CI recipients, followed
by a lesser degree in adults with mild-moderate ARHL.180 Some
studies also indicate that adults with ARHL show increased
behavioral reliance on visual cues192 and enhanced auditory-visual
integration abilities.181–184 Taken together, these data suggest that
even mild auditory deprivation (as in early-stage ARHL) may
induce changes in cross-modal neuroplasticity in the auditory
cortex. Such changes in cortical neuroplasticity may occur in a
relatively short time course after hearing loss onset. For example,
a recent case study of an adult with sudden sensorineural hearing
loss indicates cross-modal reorganization of auditory cortex by
vision as early as 3 months after hearing loss onset.193 Similarly,
animal models indicate evidence of increased responsivity to
somatosensory inputs in the auditory cortex within 16 days after
deafness onset.97
Other changes in compensatory neuroplasticity may occur in
ARHL, including the recruitment of additional cortical networks
for auditory processing. For example, in the same group of adults
with mild-moderate ARHL reported in Campbell and Sharma
(2014),187 CAEPs were recorded using high-density, 128-channel
EEG in response to an auditory speech stimulus.186 Several key
findings emerged from this study. First, the hearing loss group
exhibited decreased activation over temporal (auditory) cortex
relative to normal hearing controls, consistent with MRI studies
in which ARHL has been associated with accelerated atrophy and
decreased volume of gray matter over the temporal lobes.194–196
Second, as shown in Fig. 132.9A, while CDRs for the CAEPs
indicate cortical activity localized to temporal (auditory) cortex
in the normal hearing adults, the hearing loss group showed
temporal (auditory) cortical activity and frontal cortex recruitment
(e.g., medial frontal gyrus, superior frontal gyrus) for auditory
processing. Increased frontal cortex recruitment has been seen in
normal hearing listeners under degraded acoustic listening condi-
tions and in older adults, some of whom showed signs of ARHL.195,197
It is postulated that these changes in cortical neurodynamics may
reflect increased listening effort and/or cognitive load in ARHL,
possibly leading to decreased cognitive spare capacity or reserve
downstream.168 It is also possible that the recruitment of these
additional networks may reflect changes in attention and/or changes
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CHAPTER 132  Cortical Neuroplasticity in Hearing Loss 2009
in the resting-state default mode network.198 While this type of
frontal cortex recruitment may help adults with ARHL to com- 132
pensate in the short-term, it is unknown whether these changes
in cortical neurodynamics relate to neurocognitive function,
including growing epidemiological evidence linking untreated
ARHL to all-cause dementia.156,157
Can Audiological Intervention Reverse
Cross-Modal Neuroplasticity in
Age-Related Hearing Loss?
Using methods described in previous studies,187 our group has
started to investigate whether audiological intervention with hearing
aids reverses compensatory changes in cross-modal neuroplasticity
by vision in individual patients with ARHL. Fig. 132.10A depicts
N1 CVEP source localization for an adult with normal sloping
to mild-moderate sensorineural hearing loss before and after
hearing aid fitting. As seen in Fig. 132.10A1, prior to hearing aid
fitting the visual stimulus elicited activation in occipital and cerebel-
lar regions typically associated with processing of visual motion
stimuli,49,187,199,200 in addition to activation of auditory (temporal)
cortex (e.g., inferior, middle, and superior temporal gyrus), sug-
gestive of visual cross-modal reorganization and consistent with
findings in Campbell and Sharma (2014).187 However, after hearing
aid fitting, we observed a reversal in cross-modal recruitment of
auditory areas by vision, such that the dominant activation was
observed in occipital and cerebellar regions (as expected for visual
motion processing) and only a small amount of residual auditory
(temporal) cortex activation could be seen (see Fig. 132.10A2).
Further, this patient demonstrated about a 20% reduction in
functional reliance on visual (facial) cues on an auditory-visual
speech perception test in background noise (the Arizona Auditory-
Visual Test (AzAv)125 and a four-point improvement on a test of
global cognitive status (the Montreal Cognitive Assessment
[MoCA])201 (see Fig. 132.10B), suggestive of objective behavioral
and neurocognitive benefits of amplification. While results come
from a single subject and should be interpreted with caution, this
case study and the pediatric SSD case study described in Fig.
132.8 demonstrate the potential for intervention with hearing
aids or CIs to reverse cross-modal neuroplasticity and restore
more typical cortical processing networks in some patients. There
exists a clear need for larger scale studies that systematically examine
the impact of intervention on cortical reorganization in clinical
populations with hearing loss, as it relates to speech perception
and cognitive outcomes.
Clinical Implications of Cross-Modal Plasticity in
Adult-Onset Hearing Loss
Compensatory changes in cross-modal neuroplasticity may be
one factor contributing to the wide variability in performance
outcomes in adults receiving audiological intervention with hearing
aids or CI.182 In CI adults, while the majority of users continue
to derive significant benefit from visual (facial) cues even after
intervention,182,202 studies show that behavioral gains in auditory
perception after intervention parallel decreases in visual cross-modal
reorganization.183 In a recent PET study by Strelnikov and col-
leagues (2013), the amount of brain activity over the auditory
cortex in adults prior to CI was negatively correlated with speech
perception recovery 6 months after CI, while the brain activity
over visual and frontal cortex prior to CI was positively correlated
with speech perception recovery 6 months after CI,203 suggesting
that cortical function prior to intervention might be a useful
predictor of auditory outcomes after intervention. Further, given
recent evidence that degradation in auditory function may induce
neural changes not detectible in conventional audiometric
testing,204,205 biomarkers of sensory cortical plasticity could be
useful in the identification of early brain-based changes before
2010 PART VII  Otology, Neurotology, and Skull Base Surgery
Visual cross-modal reorganization in ARHL
before & after hearing aid fitting
1 Before HA fitting 2 After HA fitting
Min
A increased speech perception relative to use of just a CI alone.
F-distribution
Behavioral performance in ARHL before &
after HA fitting
Assessment Pre-HA 30 days
fitting post-HA
fitting
Auditory only (A) 23.3% 54.4%
Auditory-visual (AV) 63.3% 74.5%
Benefit from vision (AV- 40.0% 20.1%
A)
Global gognitive score 26/30 30/30
(MoCA)
B intervention, or the clinical course of rehabilitation after interven-
Fig. 132.10  Visual cross-modal reorganization before and after
hearing aid fitting in an adult with age-related hearing loss.
Current density source reconstructions (CDRs) showing cortical
localization patterns for the N1 cortical visual evoked potential (CVEP)
in an adult with mild-moderate age-related hearing loss (ARHL)
before and after bilateral hearing aid (HA) fitting. The color scale
(F-Distribution) indicates the likelihood of cortical activity in a given
location represented on an average magnetic resonance image (MRI)
(sagittal view). (A1) Prior to HA fitting, visual motion stimuli elicited
activation in the occipital (visual) cortex and the temporal (auditory)
cortex, suggestive of cross-modal reorganization by vision. (A2) After
HA fitting, the adult shows a reduction in temporal (auditory) cortex
activation for visual processing, suggestive of partial reversal in
cross-modal reorganization by vision. The adult’s performance on the
Arizona Auditory-Visual Test (AzAv), a multi-modal auditory-visual
speech perception test in background noise, and the Montreal
Cognitive Assessment test (MoCA), a screening measure of mild
cognitive impairment and mild Alzheimer’s disease, was also
measured before and after hearing aid fitting. Performance in the
auditory-visual condition was subtracted from performance in the
auditory-only condition on the AzAv to evaluate the patient’s functional
benefit from visual cues. (B) Neurophysiological results are consistent
with behavioral results, in which the patient shows approximately a
20% decrease reliance on visual (facial) cues on the AzAv and a
4-point improvement in cognitive function on MoCA test.
they are detectible via the audiogram, helping medical professionals
identify the optimal time to fit hearing aids and chart a clinical
course of intervention with amplification for adults with ARHL.
Evidence of cross-modal neuroplasticity in adult-onset hearing
loss also has important implications on innovation in aural reha-
bilitation for adults. As it stands now, less than 10% adults with
hearing aids and CI receive tailored aural rehabilitation.206,207 Thus,
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future research should aim to systematically examine the efficacy of
different aural rehabilitation approaches in maximizing outcomes
following intervention. Another area where a better understanding
of neuroplasticity may be beneficial is in the development of phar-
macological interventions that could be coupled with audiological
intervention to maximize learning and performance outcomes.
Harnessing neuroplasticity through multi-modal inputs may also
prove beneficial in maximizing outcomes for clinical populations
with hearing loss. For example, while the use of tactile aids were
created prior to the invention of the CI,208 a recent study by Huang
et al. (2017) evaluated the feasibility of combining electro-acoustic
stimulation (EAS) in CI with simultaneous coupling of tactile
stimulation.209 Addition of this tactile stimulator (which delivered
Max fundamental frequency information in speech to the index finger)
SUMMARY
The primary themes outlined in this chapter are that auditory
deprivation may induce changes in neuroplasticity across the human
lifespan, and that these compensatory changes in neuroplasticity
may contribute to variability in performance outcomes following
audiological intervention. Studies of congenital deafness in animal
and human models highlight how timely audiological interventions
with hearing aids or CIs within developmentally sensitive periods
may overcome many deleterious effects of auditory deprivation
to allow for acquisition of age-appropriate auditory skills. Moreover,
clinicians and physicians can utilize clinical biomarkers of central
auditory maturation (e.g., P1 and N1 CAEP responses) in conjunc-
tion with the traditional audiologic and otologic test battery to
assess candidacy for pediatric intervention, the efficacy of a chosen
tion, particularly in complex pediatric cases of multiple disabilities,
auditory neuropathy, and cochlear nerve deficiency. Further, we
have described new research demonstrating the effects of pediatric
hearing loss on higher-order auditory cortical development, citing
evidence of visual and somatosensory cross-modal neuroplasticity
in congenitally deaf children receiving CI. Future research is needed
to understand the mechanisms underlying cross-modal neuro-
plasticity in pediatric hearing loss. Research in this domain may
lead to the development of better tools that can predict success
with intervention in individual patients, or to identify which patients
may require more intensive, tailored rehabilitation and training
programs to maximize success. Although we as a field are beginning
to unearth downstream effects of hearing loss on attention, working
memory, and executive function, future research is needed to
examine the relationship between these cognitive processes and
cross-modal neuroplasticity.
This chapter has also highlighted emerging documented changes
in cortical neuroplasticity in adult-onset, early-stage ARHL,
whereby decreased input to auditory cortex may result in compensa-
tory recruitment of frontal cortices for top-down modulation of
sensory processing and cross-modal recruitment of auditory cortex
by vision and somatosensation. Future research should focus on
examining changes in cortical neuroplasticity and cognition as a
function of severity of ARHL, duration of ARHL, as well as the
potential for amplification with hearing aids to restore more typical
cortical networks. Such data would contribute to our understanding
of the link between ARHL and incidence of all-cause dementia.
Ultimately, audiological intervention relies on the principles of
neuroplasticity, the ability for the brain to adapt to restored auditory
input. With a more solid understanding of the mechanisms of
neuroplasticity in hearing loss, this may help otologists to harness
neuroplasticity to optimize clinical outcomes in clinical populations
with hearing loss across the age spectrum.
  For a complete list of references, visit ExpertConsult.com.

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