Preservation of Auditory P300-Like Potentials in Cortical
Deafness
Marianna Cavinato1*, Jessica Rigon1, Chiara Volpato1, Carlo Semenza1,2, Francesco Piccione1
1 San Camillo Foundation, Institute of Care and Research, Venice, Italy, 2 Department of Neuroscience, University of Padova, Padova, Italy

Abstract
The phenomenon of blindsight has been largely studied and refers to residual abilities of blind patients without an
acknowledged visual awareness. Similarly, ‘‘deaf hearing’’ might represent a further example of dissociation between
detection and perception of sounds. Here we report the rare case of a patient with a persistent and complete cortical
deafness caused by damage to the bilateral temporo-parietal lobes who occasionally showed unexpected reactions to
environmental sounds despite she denied hearing. We applied for the first time electrophysiological techniques to better
understand auditory processing and perceptual awareness of the patient. While auditory brainstem responses were within
normal limits, no middle- and long-latency waveforms could be identified. However, event-related potentials showed
conflicting results. While the Mismatch Negativity could not be evoked, robust P3-like waveforms were surprisingly found in
the latency range of 600–700 ms. The generation of P3-like potentials, despite extensive destruction of the auditory cortex,
might imply the integrity of independent circuits necessary to process auditory stimuli even in the absence of
consciousness of sound. Our results support the reverse hierarchy theory that asserts that the higher levels of the hierarchy
are immediately available for perception, while low-level information requires more specific conditions. The accurate
characterization in terms of anatomy and neurophysiology of the auditory lesions might facilitate understanding of the
neural substrates involved in deaf-hearing.
Citation: Cavinato M, Rigon J, Volpato C, Semenza C, Piccione F (2012) Preservation of Auditory P300-Like Potentials in Cortical Deafness. PLoS ONE 7(1): e29909.
doi:10.1371/journal.pone.0029909
Editor: Lawrence M. Ward, University of British Columbia, Canada
Received June 6, 2011; Accepted December 7, 2011; Published January 17, 2012
Copyright: ß 2012 Cavinato et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The authors have no support or funding to report.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: marianna.cavinato@ospedalesancamillo.net

related potentials (ERPs) to assess auditory processing and perceptual
awareness. Generally, auditory potentials are characterized by a
time-resolution on the order of milliseconds and can therefore
provide temporal correlates of the stages of information processing
between stimulus and response. AEPs reflect the activation of
auditory nerve and central auditory pathways up to the primary
auditory cortex [8]. Differently, ERP recordings represent a valuable
method to provide quantitative information about the perception
and higher order processing of acoustic stimuli [9,10].
On the basis of these assumptions, the present study should
provide a procedure by which electrophysiological methods can be
used to study auditory unawareness or deaf-hearing.

Introduction
Extensive bilateral lesions of the primary auditory cortex can
produce a complete loss of hearing, known as cortical deafness.
Bitemporal damage required to produce this deficit is rare and is
most frequently caused by ischemic cerebrovascular accident [1,2].
There is a relatively limited research on this condition, likely
because cortical deafness is typically transient and rapidly resolves
in more selective hearing disorders, such as auditory agnosia or
word deafness [3]. In some isolated cases, however, cortical
deafness may be permanent [4].
Generally, cortical deafness is characterized by the complete
disruption of central auditory processing, despite intact peripheral
auditory function [2]. However, from the limited literature available,
several authors have described the presence of residual auditory
behaviors in completely deaf patients [2,5,6]. Relatives reported
occasional unexpected reactions of patients to environmental sounds
despite they denied hearing. This phenomenon has been likened to
blindsight, referring to residual visual abilities of individuals without
acknowledged awareness [7]. Similarly, ‘‘deaf-hearing’’ seems to
imply a dissociation between detection and perception of sounds.
In the present report, we had the opportunity to study a patient
with severe persistent cortical deafness caused by two consecutive
strokes. The lesions extended into both Heschl’s gyri, insulae and
superior temporal gyri. Surprisingly, the patient showed some
reactions to unexpected sounds, despite the lack of any startle
response to loud noises. We adopted an electrophysiological
approach involving auditory evoked potentials (AEPs) and event
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Methods
Ethics statement
The present study was approved by the Research Ethics
Committee (REC) of the Scientific Foundation ‘‘San Camillo’’
and was compliant with the declaration of Helsinki guidelines.
Written informed consent to publication for case details was
obtained from the patient and the healthy volunteers that
participated in the study.

Case report
CDB, a 55-year-old, right-handed female with previously
normal hearing was admitted to our Neurorehabilitation Unit
for two consecutive strokes. The first ischemic attack occurred in
December 2007 and involved the territories of the middle cerebral
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P300 Potentials in Cortical Deafness

artery of the right hemisphere. A week later, a second infarction
affected the areas of the middle artery of the left side of the brain.
On admission, the patient was alert and oriented in space and
time, but often appeared agitated and perplexed. Neurologic
examination showed no sensorimotor deficits, but she complained
a complete loss of hearing. Her speech was characterized by a
severe dysarthria; she was unable to respond to verbal questions or
environmental sounds and startle response to loud noises could not
be detected. She could understand and execute complex written
instructions and recognize and use gestures for communication.
Writing was performed hesitantly with much persuasion and
showed graphemic errors and agrammatism. The T1-weighted
MRI scan showed bilateral lesions of the superior temporal gyrus
and its subregions (planum polare, Heschl gyrus, planum
temporale), the inferior parietal lobe and angular gyri and the
insular cortex. On the right, the lesion extended into the inferior
frontal gyrus.
During the first year in our Neurorehabilitation Unit, CDB
showed consistent evidence of cortical deafness. Language
functions were measured with the Aachen aphasia test (AAT)
[11] and revealed that the patient could not understand speech,
repeat words and write to dictation. She could recognize and
name pictures and match written words with objects. She showed
a good visual-spatial memory and the Weigl’s test revealed normal
executive functions. She presented with buccofacial and constructional apraxia. There were, however, no signs of ideomotor
apraxia.
The patient mood progressively improved. She appeared to
become aware of her deafness and was distressed by this. The
agitation that the patient showed a few days after the lesion,
tended to resolve gradually. Occasionally, her relatives reported
that she unconsciously manifested some startle reactions with
blinking and head-turning in the direction of unexpected sounds.
In two-year follow up we did not find improvements in the
clinical features of the patient. She complained complete loss of
hearing and she could only communicate through reading and
writing. Three years after stroke, CDB showed substantially
unchanged clinical and neuropsychological features, confirming a
persistent cortical deafness. However, sporadic startle responses
were reported.
The MRI scan confirmed the extensive area of infarction in the
territory of the bilateral middle cerebral artery. MRI sections of
the lesion are shown in Fig. 1. In addition, we compared the voxelbased structural data of the patient with the T1-weighted MRI
scans of ten age-matched healthy controls. We used an automated
technique of statistical parametric mapping (SPM) to the analysis
of gray matter (GM) to detect functional abnormalities that were
not accounted for by either visible or unsuspected structural
abnormalities. At the corrected threshold of p,0.05, the SPMbased morphometric comparison revealed that the patient had a
decrease of GM distribution in the bilateral caudate nucleus and
the pulvinar thalamus, in addition to the lesional areas delineated
with traditional MRI [12]. We planned to perform a functional
magnetic resonance (fMRI), but the patient refused the procedure.

Figure 1. T1-weighted MRI scans of the patient. Consecutive
sequences of axial T1-weighted MRI scan of the patient’s brain three
years after her strokes (right hemisphere is on the left side of the
picture). Hypodense lesion massively extends from the bilateral superior
temporal gyrus toward the transverse temporal gyrus, the pulvinar,
thalamus and insula and the middle temporal gyrus. The right
hemisphere was further damaged in the lentiform nucleus, the
postcentral gyrus, the inferior frontal gyrus and the inferior parietal
lobe.
doi:10.1371/journal.pone.0029909.g001

The audiological examination was completed with the auditory
brainstem responses (ABRs) and further tests of the central
auditory system: middle and long latency auditory evoked
potentials (MLAEPs and LLAEPs, respectively). ABRs include
short-latency potentials and are associated with the eighth nerve,
cochlear nucleus, superior olive, and midbrain. They occur in the
first 10 ms following stimulus onset. MLAEPs represent the
earliest cortical response to acoustic stimulus and cover the 10–
80 ms latency range, including Na, Pa, Nb and Pb components.
Finally, N1, P2, and N2 components of LLAEPs occur between 80
and 200 ms after sound onset and are related to auditory system
on primary and secondary cortical areas involved in the central
auditory process.
Auditory responses were recorded with the patient rested on a
bed in an acoustically shielded room. 1-kHz tone bursts were
presented monaurally at a frequency of 10 Hz with alternating
polarity (condensation and rarefaction clicks). The acoustic
stimulus was applied monaurally via TDH-49 earphones. The
estimation of auditory threshold was traced by the wave V
detection which can be used as a robust indicator that the central
nervous system detected an auditory stimulus [14]. The patient
exhibited large and reproducible waves V at an intensity of
100 dB. Thus, we adopted the same stimulation intensity to evoke
auditory responses. The contralateral ear was masked by 40 dB
white noise in all trials. Recordings were derived from the vertex
(Cz), referenced to the earlobes (A1 and A2). At least two runs,
consisting of 2000 click presentations each, were obtained for all
auditory evoked potentials. ABRs were set as follows: 10 ms
epochs, bandpass filtering of 150–3000 Hz. Middle-latency
response variables were: 80 ms epochs using band-pass of 5–

Audiological testing
Audiological examination comprised pure tone audiometry and
auditory evoked potentials.
Standard pure-tone air and bone conduction threshold
audiometry tested for peripheral hearing impairment using tones
of different frequencies with increasing sound pressure intensity,
according to the guidelines recommended by the British Society of
Audiology [13].
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P3 was measured relative to the pre-stimulus baseline and was
defined as the largest positive component occurring after the N1P2-N2 complex, within a latency window between 300 and
700 ms after a deviant stimulus was detected.
Auditory oddball ERP signals of the patient were compared
with those of ten healthy controls matched for age and gender to
gain insight into underlying mechanisms of P3 in cortical deafness.
Healthy controls were submitted to the same data collection and
analysis conditions as the patient. Topographic maps of P3
distribution were constructed using grand-average voltage information from all scalp electrodes.
Within and between group analysis was performed by the
modified t-test described by Crawford and Howell (1998) [15].
Statistical analysis was restricted to P3 findings in terms of peak
amplitude at central midline electrodes (Fz, Cz, and Pz), as well as
overall brain electrical activity mapping when P3 component
exhibited largest amplitude in both groups. Statistical significance
was accepted when p,0.05.

1000 Hz. Late auditory potentials were analysed in 500 ms epochs
and band-pass of 0.5–30 Hz.
All auditory signals were inspected visually. All visual analyses
were revised by one investigator aware of the patient but blinded
to the patient’s age and further clinical data. Auditory recordings
classified as distorted or insufficient for interpretation were
excluded. Individual waveforms were included in a grand average
providing a better estimate of peak amplitudes and latencies.

Event-related potentials (ERPs)
In addition to audiological tests, the later, more cognitive stages
of auditory processing were examined in an auditory oddball
experiment.
Electroencephalogram (EEG) was recorded from a 32 channel
electrode cap, according to the extended 10–20 method of
electrode application, referred to linked earlobes with a forehead
ground. Additional electrodes were placed below the right eye and
at the outer canthus, for bipolar recordings or the electroocular
activity (EOG). Stimuli were presented monaurally at 90 dB. Two
sinusoid tones of 1000 and 2000 Hz served as frequent and rare
tones, respectively. Probability of rare tones was 20% and
probability of occurrence of frequent tones was 80%. The
interstimulus interval was 1.0–1.3 sec. The experimental session
was subdivided into four blocks consisting of 100 stimuli each,
separated by 1-min breaks. Data were recorded with a band-pass
of 0.15 to 70 Hz and digitized at 1000 Hz (NeuroScan Amplifier,
Compumedics Neuroscan) for later off-line analysis. EEG data
analysis was performed using EEGLAB 9.0.4, an open source
Matlab toolbox. A notch filter was used to eliminate the
frequencies centred on 50 Hz. The EEG data were segmented
in epochs of 1200 ms including 200 ms pre-stimulus baseline,
time-locked to the beginning of the stimulus presentation. Epochs
including EEG excursions exceeding 690 mV were rejected. After
averaging, a further digital low-pass filter at 30 Hz was applied.
For assessment of the MMN, we computed the increase in the
negativity of the evoked potential in response to the deviants as
compared with the response to the standards occurring within a
100–300 ms time window.

Results
Audiological testing
Pure tone air and bone conduction audiometry indicated a
complete sensorineural hearing loss bilaterally. The patient had no
response at output limits of audiometry (110 decibels, dB) in the
frequency range of 250–8000 Hz.
Figure 2 shows the grand-averaged waveforms of auditory
evoked potentials for the two runs of stimulation. Brainstem
auditory potentials of either ear evoked essentially normal
responses suggesting the integrity of the auditory nerves and
pathways up to the inferior colliculi of both sides.
Conversely, middle latency auditory responses (Na, Pa, Nb and
Pb) and long latency potentials with N1, P2 and N2 could not be
identified reliably.

Event-related potentials (ERPs)
The Mismatch Negativity could not be recorded in response to
deviant stimuli. However, robust positive peaks in the latency

Figure 2. Grand-averaged auditory evoked potentials to sound onsets. Auditory brainstem responses (ABRs; top), middle-latency auditory
evoked potentials (MLAEPs; middle), and long-latency auditory evoked potentials (LLAEPs; bottom) recorded by routine clinical protocols in the
patient with cortical deafness (left) and in the control group (right). Note the integrity of brainstem auditory responses and the absence of bilateral
middle- and long-latency evoked potentials, characterizing cortical deafness.
doi:10.1371/journal.pone.0029909.g002

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range of 650–700 ms were clearly seen following the right ear
stimulation (Fig. 3B). Contralateral responses were abolished.
Statistical comparison between patient and controls revealed
significant differences in P3 scalp distribution. In the within-group
analysis, the control group showed a significantly larger right
centro-parietal P3 in response to left ear stimulation (p = 0.0001),
and a bilateral centro-temporal dominance in response to right ear
stimulation (p = 0.01) (Fig. 3A). Differently, the patient exhibited
the largest amplitude of P3 at the left posterior and central areas
after right ear stimulation (p = 0.0001; p = 0.0001) (Fig. 3B). No P3
could be recorded in response to left ear stimuli. Finally, the
between-group analysis showed a significantly lower P3 amplitude
over the right fronto-temporal and central regions of the patient
compared to controls (p = 0.0001; p = 0.008, respectively).

and the surrounding region of the superior temporal gyrus and the
frontal and parietal operculum [16,17]. Thus, in our patient the
extent of the brain damage and the absence of MLAEP waves
provide evidence of a cortical origin of the mid-latency potentials.
Concerning the long-latency auditory potentials, recent neuroimaging data have suggested that abnormalities in the P1, N1 and
P2 components reflect lesions extended into the multi-modal areas
of the inferior parietal lobule. This area appears to exert a critical
modulatory influence over LLAEP generators outside of the
superior temporal plane [18]. The absence of LLAEPs in our
patient does not necessarily reflect a damage to primary auditory
cortex, but also a damage to adjacent posterior areas.
Finally, we recorded two main components of ERPs: the
Mismatch Negativity and the P3. Although we supposed to
observe an absence of endogenous potentials, we found some
unexpected results.
MMN could not be recorded in response to deviant sounds.
Generally, the MMN appears in response to changes in sound
stimulation and is known to reflect a relatively automatic
comparison of incoming sounds to auditory cortex sensorymemory representations of the preceding repetitive stimuli [19].
Some authors have suggested that these representations might be
explained by the transient adaptation of feature-specific neurons
within the anterior and posterior parts of the primary auditory
cortex that regulate the access to the conscious perception of sound
[20,21]. In fact, numerous brain imaging studies on preattentive
auditory deviance detection have demonstrated an initial contribution of the primary auditory cortex followed by the activation of
the posterior superior temporal gyrus and the lateral planum
temporale. These areas might be involved in the withdrawal of the
details of the acoustic change [22,23]. Through the connections of
the arcuate and superior longitudinal fascicle, the superior
temporal gyrus is in communication with the inferior frontal
gyrus. The activation of this region of the mid-ventrolateral
prefrontal cortex might indicate a higher cognitive processing
related to the judgement of sufficient novelty of auditory stimulus
to require attentional resources [24]. The brain damage of CDB
extended to the primary auditory cortex, the superior temporal
gyrus, planum temporale and inferior frontal gyrus and could
hamper sounds to access consciousness.

Discussion
In the present study, we reported the rare case of a patient with
persistent cortical deafness. This disorder is characterized by
bilateral temporo-parietal lesions involving the primary auditory
areas and their radiations and implies the complete absence of
auditory afferent input at the cortical level. In contrast, several
authors have presented evidence of residual capacity of the
damaged auditory system to process acoustic stimuli [2,5,6].
The goal of the present study was, therefore, a systematic
examination of several levels of auditory function using auditory
evoked potentials in the attempt to better evaluate the dissociation
between perception and higher order processing of acoustic
information.
Cortical deafness is generally associated with a damage of
central auditory functions, in spite of normal peripheral hearing.
Accordingly, our patient showed normal ABRs, expression of the
integrity of the inner ear and cochlear nerve, as well as the
auditory pathways within the brainstem. However, middle-latency
responses were consistently absent to both right and left ear
stimulation. The neural origin of MLAEPs is still a subject of
controversy. Although some authors support the hypothesis of a
subcortical involvement in the potential generation, it is generally
assumed that MLAEPs arise from the medial geniculate and the
supratemporal plane comprising the primary auditory area (A1),

Figure 3. Grand-averaged event related potentials (ERPs) elicited by classic oddball at electrode Cz. Grand-averaged ERP waveforms at
electrode Cz and thirty-one channel ERP topographical maps recorded in the patient (B) and controls (A). The latency is referred at the time point at
which the positive peak between 300 and 700 ms latency is maximum at Cz electrode site. ERP waveform from the patient revealed a significantly
higher P3 at the left posterior and central sites in response to right stimulation. No P3 could be recorded after left ear stimuli.
doi:10.1371/journal.pone.0029909.g003

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P300 Potentials in Cortical Deafness

In contrast with the absence of the MMN, a reliable positive
peak at 660 ms could be clearly detected in response to right ear
stimulation. Because of its morphology and topographic distribution, we inferred that such late waveform could represent a P3-like
potential.
P3 offers a covert and indirect measure of attentional resource
allocation that represents an index of change detection [25]. P3 is
related to the activity of associative cortical areas and is sensitive to
complex processes around recalled information, stimulus significance, recognized auditory information and memory context
updating [26,27]. The sources of P3 are believed to be located in
heteromodal areas of the fronto-parietal cortex and their
activation might reflect an attention switch to an environmental
change encoded by the cerebral process generating the MMN
[28,29]. The bilateral supramarginal gyrus, frontal operculum and
insula seem to be mainly involved in the network for saliency
detection in auditory modality [30]. However, some authors have
demonstrated an asymmetrical cortical activation of P3 by using
unilateral auditory stimulation. Among others, Gilmore and
colleagues (2009) argued that in normal condition the right
hemisphere is more prominently engaged during working memory
and updating processes underlying P3 [31]. Accordingly, our
healthy controls exhibited a right lateralized potential in response
to left ear stimulation, and a bilateral distribution of ERPs to right
ear stimulation. This denotes a more marked right side activation
of P3 wave (Fig. 3A). In contrast, the patient showed robust P3-like
components over the left posterior areas and a significantly lower
distribution of the potentials over the right fronto-temporal and
central areas in response to right ear stimulation. The left ear
stimulation could not evoke any detectable responses. (Fig. 3B).
Depth recordings and lesion studies have implicated the frontal,
temporal and inferior parietal lobes in the generation of the
auditory P3 [32]. The interaction of these structures seems to play
a key role in the auditory perceptual awareness, and the right
hemisphere seems to be mainly engaged during working memory
updating processes [31,33]. Thus, the marked right fronto-parietal
dysfunction of our patient, in particular the damage of the right
inferior frontal gyrus and the inferior parietal lobe, might partially
explain the dissociation between detection and perception of
sounds. Several authors have demonstrated that ERPs can be
elicited even when stimuli are presented outside conscious
awareness [34,35]. Bernat et al. (2001) offer evidence that
subliminal stimuli can evoke consistent P3 waves. They speculated
that P3 could represent a link between unconscious and conscious
awareness in the context updating processes [35]. In our patient
the generation of P3-like potentials implied that deviant stimuli
were selectively processed bypassing networks involved in
conscious perception. Schönwiesner et al. (2007) and Pandya
(1995) hypothesized that association areas in and adjacent to the
auditory parabelt might form an independent circuit from
thalamo-cortical projections in the auditory system [26,36]. These
alternate pathways could be preserved in our patient and
responsible for the generation of P3-like potentials.
In addition, the lack of awareness of auditory stimuli might be
further aggravated by the bilateral functional abnormalities of the
pulvinar. In fact, the auditory association area seems to be
preferentially related to the pulvinar complex [36]. The thalamic

pulvinar nucleus plays an important role in the coupling of sensory
and attentional functions. As demonstrated by Hugdahl et al.
(1991), a lesion of this structure might imply an auditory neglect
that further affected the conscious awareness of sounds of CDB
[37].
As a final consideration, our findings seem to be in contrast with
the hypothesis of a hierarchical information processing of auditory
stimuli. A large body of physiological and functional data suggests
that processing of auditory information is implemented in a
hierarchical manner [38]. Lower levels are considered responsible
for extracting basic spectro-temporal features of the auditory
signal. Higher cortical areas are involved in a higher level of
information processing, such as abstraction, perception, reasoning,
and learning. They are characterized by at least four different,
hierarchically organized processing levels, each containing several
segregated sub-regions: the primary areas that receive their input
from the thalamus; surrounding lateral and medial ‘‘belt’’ areas,
that receive input from primary areas; a parabelt area on the
dorsal plane of the superior temporal gyrus; and higher-level areas
in the superior temporal sulcus and the frontal lobe. From that, the
higher level integrative functions evolved from and are dependent
on the integrity of lower-level structures. In other words, simple
processing operations are necessary prerequisites for more
complex operations [39,40].
Our results are rather compatible with a growing body of
literature demonstrating another line of thought, based on the
reverse hierarchy theory (RHT) [41]. The reverse hierarchy
theory provides a representational hierarchy to describe the
interaction between sensory input and top–down processes to
guide plasticity in primary sensory areas [42–44]. RHT asserts
that neural circuits mediating a certain percept can be modified
starting at the highest representational level and progressing to
lower-levels in search of more refined high resolution information
to optimize perception. RHT may be a plausible explanation for
top–down influences on cortical levels of sensory processing [45].
This might further clarify the presence of higher order auditory
cortical responses, even when more automatic components are
lacking.
In conclusion, the paradoxical partial preservation of P3-like
potentials in a patient with persistent cortical deafness suggests the
integrity of independent neural circuits necessary to process
auditory stimuli even in the absence of conscious awareness.
Furthermore, electrophysiological techniques combined with
functional neuroimaging could be of primary importance in
demonstrating the activation of neural substrates underlying deafhearing.

Acknowledgments
The authors gratefully acknowledge the very helpful discussions with Drs
Luciano Foscolo, Annalena Venneri and Luca Ghezzo.

Author Contributions
Conceived and designed the experiments: MC. Performed the experiments: MC JR. Analyzed the data: MC CV. Contributed reagents/
materials/analysis tools: MC. Wrote the paper: MC CV CS FP.

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January 2012 | Volume 7 | Issue 1 | e29909