Disorders of Peripheral and Central Auditory Processing
Handbook of Clinical Neurophysiology, Vol. 10
G.G. Celesia (Vol. Ed.)
# 2013 Elsevier B.V. All rights reserved
CHAPTER 23
Auditory agnosias
Ayse P. Saygin* and Luke E. Miller
Department of Cognitive Science, MC 0515, University of California, San Diego, La Jolla,
CA 92093-0515, USA
23.1. Introduction
The goal of this chapter is to review the research on audi-
tory agnosias, the impaired capacity to recognize sounds,
despite adequate hearing. Throughout the review, we
aim to link neuropsychological findings to theories of
auditory processing in humans and functional neuroanat-
omy of cortical auditory areas in the brain.
Auditory agnosia can affect the processing of ver-
bal (speech) or nonverbal (environmental) sounds.
Cortical disorders affecting sound processing are not
limited to agnosias and include amusia and “auditory
neglect” or sound localization impairments (Clarke
and Thiran, 2004; Pavani et al., 2004; Peretz et al.,
2009); but these aspects of auditory processing are
covered in other chapters in this volume.
The concepts of functional specialization, localiza-
tion, and modularity have long been a part of discourse
in neurology and neuropsychology (Broca, 1863;
Lashley, 1950; Fodor, 1983; Elman et al., 1996). Mul-
tiple lines of evidence (neuroanatomy, connectivity,
imaging, and lesion studies) indicate that the superior
temporal cortex is crucial for higher-level auditory
processing in humans (see other chapters in this volume
for earlier stages of processing). There are several audi-
tory areas in the primate brain outside of A1 in the supe-
rior temporal region. Combining new neuroimaging
studies with comparative neuroanatomy, the functional
neuroanatomy of cortical auditory areas in the human
brain is becoming better understood (Galaburda and
Pandya, 1983; Rauschecker, 1998; Kaas et al., 1999;
Dick et al., 2004; Lomber and Malhotra, 2008;
*
Correspondence to: Dr. A.P. Saygin, Department of Cogni-
tive Science, MC 0515, University of California, San Diego,
9500 Gilman Drive, La Jolla, CA 92093-0515, USA.
E-mail: saygin@cogsci.ucsd.edu;
Web: http://www.sayginlab.org
449
Rauschecker and Scott, 2009). Human neuroimaging
studies have shown differential (though not necessarily
selective) response patterns in temporal cortex to differ-
ent types of sound such as speech sounds, voices,
or environmental sounds (Price et al., 1996, 2005; Belin
et al., 2000; Binder et al., 2000; Scott et al., 2000; Wise
et al., 2001; Zatorre and Belin, 2001; Davis and
Johnsrude, 2003; Dick et al., 2004; Lewis et al., 2004;
Vigneau et al., 2006; Whalen et al., 2006; Campbell,
2008; Leech and Saygin, 2011). However, whether acti-
vation differentials arise due to sound category effects,
perceptual differences in the stimuli, and in case of lin-
guistic sounds, phoneme processing, lexical access, or
semantic retrieval is not always clear. It is likely that
a combination of these factors is at play and such effects
can be difficult to distinguish with neuroimaging.
The idea that the brain has specialized regions for
processing specific kinds of information has been
more prominent in vision research (e.g., brain areas
that specialize in motion or color processing have been
reported (Zeki and Bartels, 1998). The extent to which
cortical specialization for sound processing is localized,
modular, or domain specific (e.g., verbal vs. nonverbal)
is under debate (Saygin et al., 2003, 2004; Romanski,
2004; Bates et al., 2005; Dick et al., 2005; Justus and
Hutsler, 2005; Thierry and Price, 2006; Pernet et al.,
2007; Chartrand et al., 2008; Staeren et al., 2009; Cum-
mings and Ceponiene, 2010; Goll et al., 2010b; Leech
and Saygin, 2011). The auditory cortex of the primate
brain is much smaller than the visual cortex and has
fewer distinct, well-characterized areas (Van Essen
and Gallant, 1994). These factors make it difficult to
use lesion sites of neuropsychological patients to draw
conclusions about functional localization in the audi-
tory domain. More generally, lesions in humans are
rarely as small and focal as in experimental animals.
Lesions also have indirect effects on the functioning
of other areas. Often, little is known about the patients’
450
functional neuroanatomy before the lesion and their
variability in post-lesion functional reorganization
and recovery. These factors combined make it difficult
to use neuropsychological data to reach conclusions
about localization claims. Recent computational
approaches to lesion mapping with large groups of
patients is one way to acquire more precise information
about localization of functions (Bates et al., 2003b).
However, it is also possible to use data from patient
research to shed light on functional associations and
dissociations. Thus, even though fine localization of
functions is difficult with neuropsychological studies
of the auditory system, patient studies are still invalu-
able in evaluating claims of domain specificity and
modularity (Dick et al., 2004, 2005).
In this review we discuss aspects of auditory agno-
sias in relation to neuropsychological theories of
functional specialization, domain specificity, and mod-
ularity in higher-level auditory processing. For both
verbal and nonverbal auditory agnosia, we consider
the selectivity of patients’ impairments, and associa-
tions and dissociations in the literature. In particular,
since the early days of neurology, there have been
speculation and empirical evidence supporting an inti-
mate relationship between language processing and
other domains. Finkelnburg (1870) proposed an under-
lying factor, sometimes called asymbolia, may be com-
mon to both the language impairments that patients
with aphasia exhibit, and deficits in nonverbal domains
(Finkelnburg, 1870; Duffy and Liles, 1979). Hughlings
Jackson (1878) had also observed a high incidence of
nonverbal impairments in aphasic patients and posited
that aphasics may be “lame in thinking”. Despite such a
long history of evidence to the contrary, aphasia was at
times presented as a deficit restricted to the linguistic
domain. In modern cognitive neuroscience and
neuropsychology, there is ever-increasing evidence that
language may best be viewed as an embodied system,
interwoven with sensory, motor and nonlinguistic cogni-
tive processes (Barsalou, 1999; Dick et al., 2005;
Meteyard et al., 2010; Saygin et al., 2010b). This
view is consistent with a link between aphasia and
impairments in non-linguistic tasks that share neuro-
computational resources. Although such effects were
most commonly discussed in the realm of gesture, action
and pantomime processing (Duffy and Duffy, 1981;
Varney, 1982; Wang and Goodglass, 1992; Saygin
et al., 2004; Saygin, 2007), there are also relevant find-
ings in the auditory modality that we will present in this
review. Thus we situate auditory agnosias in the broader
discussion on localization, modularity and domain spec-
ificity in human perception and cognition.
A.P. SAYGIN AND L.E. MILLER
23.2. Auditory agnosias
Auditory agnosia is a rare neurological disorder char-
acterized by a relatively isolated deficit in auditory
comprehension despite normal hearing. Much of the
literature on auditory agnosia consists of case studies
(Spreen et al., 1965; Albert et al., 1972; Miceli, 1982;
Rosati et al., 1982; Vignolo, 1982; Lechevalier et al.,
1984; Motomura et al., 1986; Lambert et al., 1989;
Eustache et al., 1990; Kazui et al., 1990; Pasquier
et al., 1991; Engelien et al., 1995; Griffiths et al.,
1999; Taniwaki et al., 2000), including a few on children
(Hattiangadi et al., 2005). The associated lesions are not
particularly consistent and have included unilateral right
(Spreen et al., 1965; Haguenauer et al., 1979; Vignolo,
1982; Eustache et al., 1990; Fujii et al., 1990), unilateral
left (Vignolo, 1982; Haguenauer et al., 1979; Eustache
et al., 1990; Pasquier et al., 1991; Clarke et al., 2000)
and bilateral cortical lesions (Albert et al., 1972;
Haguenauer et al., 1979; Rosati et al., 1982; Vignolo,
1982; Lechevalier et al., 1984; Motomura et al., 1986;
Mendez and Geehan, 1988; Engelien et al., 1995; Kaga
et al., 2000). Subcortical lesions have also been reported
(Kazui et al., 1990). Experimental studies with larger
groups of patients have been more informative regarding
lesion sites associated with auditory deficits (Varney and
Damasio, 1986; Schnider et al., 1994; Saygin et al.,
2003) and will be discussed in more detail below.
Auditory agnosia is a rare condition, certainly not
as widely reported or investigated as visual agnosia.
There are several reasons for the relatively low prev-
alence of auditory agnosia. Auditory pathways tend
not to be affected often by stroke due to redundancies
in blood supply. The auditory system also features
redundancies at the cortical level, with strong bilateral
representation (Hausler and Levine, 2000). This is not
to say auditory processing is not affected following
stroke, but that the literature on auditory agnosia
focuses on a small number of patients with pro-
nounced deficits. In fact, subtler but significant defi-
cits in sound processing are not infrequent following
stroke if detailed psychoacoustic or electrophysiolog-
ical testing is carried out (Schnider et al., 1994; Saygin
et al., 2003, 2010a).
When auditory agnosia affects only verbal material
it is often called word deafness (WD); when the deficit
is in recognizing nonverbal sounds such as environ-
mental sounds (Ballas, 1993), it is often termed non-
verbal auditory agnosia. We will follow this
nomenclature, although one main point we make is
that dissociations between verbal and nonverbal
domains are the exception rather than the norm.
CENTRAL DISORDERS OF AUDITORY PROCESSING
23.2.1. Nonverbal auditory agnosia
23.2.1.1. Clinical features and lesion sites
Auditory agnosia restricted to nonverbal material is a
very rare phenomenon usually associated with bilat-
eral (Spreen et al., 1965; Albert et al., 1972; Kazui
et al., 1990) and rarely with unilateral left (Saygin
et al., 2010a) or right hemisphere (Fujii et al., 1990)
lesions. Studies with groups of patients and lesion-
symptom mapping have shown that temporal cortex
lesions are associated with nonverbal sound
processing deficits (Schnider et al., 1994; Saygin
et al., 2003).
Two forms of auditory agnosia have been pro-
posed: perceptual-discriminative, with patients failing
to identify whether two consecutive sounds are
identical, and associative-semantic, with patients
being impaired at audio-visual matching or naming.
Bilateral lesions appear to be implicated in severe
discriminative disorders (Albert et al., 1972; Rosati
et al., 1982; Vignolo, 1982; Lechevalier et al., 1984;
Motomura et al., 1986; Mendez and Geehan, 1988;
Kazui et al., 1990; Taniwaki et al., 2000). Unilateral
right hemisphere lesions can lead to normal associa-
tion with impaired discrimination (Vignolo, 1982;
Eustache et al., 1990), deficient association with nor-
mal discrimination (Spreen et al., 1965), or deficient
association and deficient discrimination (Fujii et al.,
1990). Unilateral left hemisphere lesions have been
linked to deficient association (Saygin et al., 2003)
and normal discrimination (Vignolo, 1982), though
in most studies with this sample, discrimination was
not tested on left hemisphere injured patients due to
a focus on language processing (Varney, 1980; Varney
and Damasio, 1986; Saygin et al., 2003). Some of the
inconsistencies in these findings may be due in part to
the heterogeneity of the tests used in the literature (for
review see Vignolo, 1982; Griffiths et al., 1999;
Clarke et al., 2000; Griffiths, 2002; Saygin et al.,
2003, 2010a; Goll et al., 2010b).
23.2.1.2. Specificity, associations, and dissociations
In the 1960s, Vignolo, Spinnler and Faglioni reported
disturbances of environmental sound recognition fol-
lowing unilateral hemispheric damage in a group of
patients (Spinnler and Vignolo, 1966; Faglioni et al.,
1969). They noted that right hemisphere-damaged
(RHD) patients tended to perform significantly worse
than controls on perceptual tests involving environ-
mental sounds, while left hemisphere-damaged
(LHD) patients performed significantly worse on asso-
ciative or semantic tests. In 1980, Varney used
451
environmental sounds to examine both verbal and
nonverbal comprehension deficits in the same aphasic
patients and found that impairments in environmental
sound recognition were seen only in subjects with
impaired verbal comprehension, and that aphasic
patients with intact verbal comprehension also per-
formed well on sound recognition. There were some
patients who were impaired in verbal comprehension,
but not in sound recognition. More recently, Schnider
et al. (1994) observed that both LHD and RHD
patients performed significantly worse than a group
of normal controls on an environmental sound recog-
nition test. They found no significant differences in the
performance of the two patient groups; however, the
pattern of errors appeared to differ over groups:
LHD patients made more semantically based errors,
while RHD patients and control subjects made almost
exclusively acoustic errors. For all patients, accuracy
in recognizing environmental sounds correlated with
language comprehension as measured by the Western
Aphasia Battery (Kertesz, 1979). Lesion–behavior
correlations showed that LHD patients with impaired
environmental sound recognition tended to have dam-
age to the posterior superior temporal gyrus (pSTG)
and the inferior parietal lobe.
Although these studies supported a link between
aphasia and nonverbal auditory agnosia, none had
attempted a precise comparison between verbal and
nonverbal auditory processing in the same patients.
Those that did compare performance between
domains had used different tasks or tests in the two
domains and did not control for factors such as stim-
ulus frequency and identifiability, or the relationship
between the auditory and visual stimuli. In addition,
previous studies had used 4 or 5 picture displays in
sound to picture matching tasks, entailing a lengthy
visual processing component to the task and thus were
limited to analyzing accuracy data only, losing
potentially important information about the time
course of processing. In a large neuropsychological
and lesion mapping study, our group addressed these
gaps in knowledge and assessed the relationship
between verbal and nonverbal comprehension of
complex, meaningful information in the auditory
modality by examining aphasic patients’ abilities to
match environmental sounds and corresponding
linguistic phrases to associated pictures (Saygin
et al., 2003, 2005). Task demands, stimulus character-
istics, and semantic features were all carefully
controlled to reduce confounds, and to focus on
the relationship between verbal and nonverbal
domains (Fig. 1).
452 A.P. SAYGIN AND L.E. MILLER

A Verbal stimuli and related distracter

“cow mooing”

[Speech Sound]

B Nonverbal stimuli and related distracter

Moooo o
o o. . .
[Environmental Sound]

C Verbal stimuli and unrelated distracter

“cow mooing”

[Speech Sound]

D Nonverbal stimuli and unrelated distracter

Moooo o
o o. . .
[Environmental Sound]

Fig. 1. Summary of experimental design (Saygin et al., 2003, 2005). Domain (verbal/nonverbal) and distracter type (related to target/unrelated
to target) were within-subject factors. As an example, the target “cow” appeared four times, twice with verbal sound stimuli (the phrase “cow
mooing”), twice with nonverbal stimuli (the sound of a cow mooing), twice with “sheep” as the distracter (related condition), and twice with
“violin” as the distracter (unrelated condition). 45 pictures and sounds were used as targets and related and unrelated distracters, giving rise to
45 triplets such as “cow–sheep–violin”.

Results from 30 LHD and 5 RHD patients (along
with 21 neurologically intact age-matched control
subjects) showed that RHD patients were only mildly
impaired in the task, performing similarly to mild
(anomic) aphasic LHD patients, but significantly
worse than controls. Aphasic patients’ deficits were
not restricted to the verbal domain; rather, patients
were impaired to the same extent in comprehending
speech and environmental sounds, as measured by
both accuracy and reaction time measures. Impair-
ments in both domains were significantly correlated
with language impairments as measured by the West-
ern Aphasia Battery. Performance within the task
between the two domains went hand in hand, with a
strong correlation between accuracy and reaction time
for speech and environmental sounds suggesting that
the two domains utilize some shared perceptual and
neural mechanisms (Fig. 2).
We then used both lesion overlays (Saygin et al.,
2003) and a novel lesion-symptom mapping method
called Voxel-Based Lesion-Symptom Mapping or
VLSM (Bates et al., 2003b) and found that damage
to posterior regions in the left middle and superior
temporal gyri and to the inferior parietal lobe was a
predictor of deficits for both speech and environmen-
tal sounds (Fig. 3). The posterior portion of
Brodmann’s area 22 (as roughly identified in stereo-
taxic space) corresponds to the original Wernicke’s
area. In our data, this area and the surrounding middle
temporal and inferior parietal regions were found
implicated also in environmental sound processing
(Fig. 3). In fact, Wernicke’s area itself, in the posterior
CENTRAL DISORDERS OF AUDITORY PROCESSING 453

A B
Accuracy Reaction Time
Patient M
100 * 3000

Verbal

Verbal
*
Patient M

80 1000
80 100 500 3500
Nonverbal Nonverbal
Fig. 2. Correlation of performance in the verbal and nonverbal domains within the aphasic group for (A) accuracy and (B) reaction time
(Saygin et al., 2003). Linear fits and density ellipses using a confidence interval of 95% are shown. Correlations are significant
( p < 0.0001 for both, r ¼ 0.75 and 0.95, respectively) indicating that the aphasic patients were impaired to the same extent in comprehending
language and environmental sounds. Marked with a * is patient M’s accuracy and reaction time (Saygin et al., 2010a), the only quantifiable
dissociation in the sample (Bates et al., 2003a, 2005).

VERBAL
3.3

-3.5
Middle Temporal Superior Temporal Inferior Parietal

NONVERBAL

Middle Temporal Superior Temporal Inferior Parietal

Fig. 3. Axial slices through middle temporal, superior temporal and inferior parietal areas of VLSM maps, showing the extent to which
damage to each voxel was associated with task deficits in speech (verbal) and environmental (nonverbal) sound comprehension (Saygin
et al., 2003). The values displayed at each voxel are t statistics comparing the accuracy of patients lesioned at that voxel to the patients intact
at that voxel (Bates et al., 2003b; Dronkers et al., 2004; Saygin, 2007). High t scores top the scale in red, indicating areas where damage led to
significant deficits in task performance. Voxels denoted in blue reflect negative t scores, which arise when patients with lesions to those voxels
performed better than those who did not (but had lesions elsewhere).Voxels which are not color coded were not well represented in the lesions
in our sample.

superior temporal gyrus, was more strongly associated
with performance in the nonverbal domain than the
verbal domain (p < 0.01; Saygin et al., 2003).
We followed up on our neuropsychological studies
with neuroimaging studies in healthy controls. In a
functional magnetic resonance imaging (fMRI) study
with healthy controls, we found that the more consis-
tent lesion-deficit mapping in a given region, the more
that same region tended to be activated in the fMRI
experiments in the healthy brain (Dick et al., 2007).
Recent studies with primary progressive aphasia have
also revealed concomitant deficits in verbal and
454
nonverbal sound processing in this patient population
(Goll et al., 2010a). Our stimuli and/or tasks have also
been used in a variety of developmental and clinical
populations (Cummings et al., 2006, 2008, 2009;
Cummings and Ceponiene, 2010). Overall, although
there are no doubt differences in the processing of ver-
bal and nonverbal sounds, there appear to be shared
perceptual, neural and cognitive resources utilized
for both types of sounds.
Although an association is the norm between speech
and nonverbal sounds, dissociations in neuropsychol-
ogy can also be informative, even when rare (Bates
et al., 2003a, 2005). Varney (1980) had reported deficits
in nonverbal comprehension only in patients who also
exhibited deficits in verbal comprehension, but did not
find dissociations in the opposite direction. Clarke et al.
(1996) reported a patient who was deficient in the non-
verbal auditory domain but had no diagnosed verbal
comprehension deficits (although formal testing was
not reported). When both the tasks and stimuli were
closely matched across domains as we have done, def-
icits in the two domains largely went hand in hand. Pre-
vious studies reporting dissociations between verbal
and nonverbal auditory processing (Varney, 1980;
Clarke et al., 1996) had classified impaired perfor-
mance as performing below the level of the worst con-
trol subject. According to these criteria, we had 9
patients who performed worse than the poorest per-
forming control subject in the verbal domain, and
8 patients in the nonverbal domain: 3 patients were
more impaired in verbal processing compared to non-
verbal, and 2 patients were more deficient in the non-
verbal domain than the verbal.
Instead of using such cutoffs, we advocate
assessing dissociations quantitatively and statistically
A Patient M: LH
Peak MNI = –48, –9, –18
Fig. 4. Sagittal sections through patient M’s brain showing fMRI data as the patient listened in the scanner to speech and environmental sounds
(Saygin et al., 2010a). There were two clusters in which activation for speech sounds was significantly greater than activation for environ-
mental sounds: a perilesional cluster in the left anterior temporal cortex (A, LH), and a large contralateral cluster in the right temporal cortex
extending along the superior temporal sulcus (B, RH).
A.P. SAYGIN AND L.E. MILLER
(Bates et al., 2003a, 2005). Doing so, we found three
outliers, of which only one, patient M, showed a dis-
sociation between the two domains (Fig. 2). M, a right-
handed individual who suffered a left hemisphere
stroke, had a persistent difficulty with environmental
sound comprehension, but had recovered language
function to within normal levels. We carried out exten-
sive audiological and behavioral testing in order to
characterize the patient’s unusual neuropsychological
profile (Saygin et al., 2010a). We also examined the
patient’s and controls’ neural responses to verbal
and nonverbal auditory stimuli using fMRI.
We verified that the patient exhibited persistent and
severe auditory agnosia for nonverbal sounds in the
absence of verbal comprehension deficits or periph-
eral hearing problems. Acoustical analyses suggested
that his residual processing of a minority of environ-
mental sounds might rely on his speech processing
abilities. In the patient’s brain, contralateral (right)
temporal cortex as well as perilesional (left) anterior
temporal cortex were strongly responsive to verbal,
but not to nonverbal sounds (Fig. 4), a pattern that
stood in marked contrast to the controls’ data
(Fig. 5). This substantial reorganization of auditory
processing may have supported the recovery of M’s
speech processing.
In summary, performance in verbal and nonverbal
domains is highly correlated following brain injury.
It is possible to identify not only patients who perform
worse in the verbal domain (i.e., the expected result
based on an aphasic sample and Varney (1980)), but
we can also reliably identify patients who perform
worse in the nonverbal domain, an unexpected and
rarely reported outcome (Saygin et al., 2010a). It is
possible that these dissociations are due to variation
B Patient M: RH
Peak MNI = 48, –27, –6
CENTRAL DISORDERS OF AUDITORY PROCESSING 455

A B
Patient M: LH Patient M: RH

Parameter Estimate
2 2
p<0.0001 p<0.0001

1 1

0 0

Env Sounds Speech Env Sounds Speech

Peak MNI = –48, –9, –18 Peak MNI = 48, –27, –6

C Controls: LH D Age Matched Controls: LH

[N=8] [N=2]
2
n.s. n.s. n.s.

E F
Controls: RH Age Matched Controls: RH
[N=8] [N=2]
2
n.s. n.s. n.s.

Fig. 5. Evidence for post-stroke functional reorganization in patient M’s brain (Saygin et al., 2010a). Effect sizes from the areas shown in
Fig. 4 are shown for patient M (A, B), a group of younger adult controls (N ¼ 9; C, E), and for two age-matched, older adult controls (D,
F) listening to the same sounds. Error bars are S.E.M. As clearly follows from the way these peaks were defined, there was significantly more
activation for speech sounds compared with environmental sounds in M’s data (A, B, p < 0.0001). However, no such difference was found in
the controls’ data (C–F, for all comparisons p > 0.5, not significant (n.s.)). Thus, regions that are preferentially active for speech sounds in M’s
brain (shown in Fig. 4) show no evidence of being speech-sensitive areas in the healthy brain, suggesting M may have recovered his speech
functions via post-stroke functional reorganization in both hemispheres.

between individuals’ premorbid brain organization for
these functions, as well as nonuniform post-stroke
recovery patterns across patients and across domains.
23.2.2. Word deafness
23.2.2.1. Clinical features and lesion sites
Word deafness (WD), sometimes also called pure
word deafness (PWD), was first described in the
19th century and is a rare neurological condition char-
acterized by a dramatic deficit in speech comprehen-
sion (Buchman et al., 1986; Polster and Rose, 1998;
Poeppel, 2001; Stefanatos et al., 2005). Whereas early
auditory processing is normal in patients with PWD,
they present with profound deficits in the compre-
hension and repetition of spoken language. Patients
also have preserved performance in other language
functions such as reading, writing, and speaking.
Thus, WD is arguably not a result of deficits in
“central” language processing (although it often
progresses to or from Wernicke’s aphasia). Patients
with WD should also be able to comprehend other
complex sounds such as music and environmental
sounds (though this is not always assessed, see
below). Patients with WD may describe speech as
sounding like “noise” or “jabbering” (Buchman
et al., 1986). Some patients report speech sounds
“like a foreign language” or that “words come too
quickly”, indicating an ability to recognize but not
perceive speech (Albert and Bear, 1974). Patients
may be able to compensate for their deficits
through lip-reading (Auerbach et al., 1982; Miceli,
1982; Shindo et al., 1991) and the use of contextual
cues (Saffran et al., 1976).
456
The exact neuroanatomical locus of lesions leading
to WD is not clear. Most cases have had bilateral tem-
poral lobe (Miceli, 1982; Tanaka et al., 1987; Yaqub
et al., 1988; Buchtel and Stewart, 1989; Praamstra
et al., 1991; Shindo et al., 1991; Wirkowski et al.,
2006), unilateral left temporal lobe (Saffran et al.,
1976; Caramazza et al., 1983; Metz-Lutz and Dahl,
1984; Wang et al., 2000; Stefanatos et al., 2005; Slevc
et al., 2011) or subcortical lesions (Hayashi and
Hayashi, 2007). A review of the literature reported
the majority of WD cases had bilateral lesions of the
superior temporal cortex (42 out of 59 reviewed
cases); unilateral lesions of the left temporal cortex
(16 out of the 59 reviewed cases) tended to extend
deep into subcortical transcallosal projections
(Poeppel, 2001; Takahashi et al., 1992). Cases of
WD due to unilateral damage could therefore be due
to a “disconnection syndrome”.
23.2.2.2. Specificity, associations, and dissociations
WD has often been considered evidence for domain
specificity for processing speech sounds. According
to these models, specific types of auditory information
are segregated into different functional streams
(Polster and Rose, 1998). While the characterization
of PWD as a disorder of speech comprehension is rel-
atively straightforward, the existence of truly pure cases
of the disorder is a matter of debate. Although by def-
inition, patients with PWD should not have deficits in
auditory processing of other kinds of sounds or other
aspects of language, a closer look reveals that patients
often do present with other conditions including non-
verbal auditory agnosia (Miceli, 1982; Tanaka et al.,
1987) and amusia (Auerbach et al., 1982; Tanaka
et al., 1987). Due to high comorbidity with these other
disorders, dropping “pure” from the diagnosis and
renaming the syndrome “word deafness” was consid-
ered more appropriate (Buchman et al., 1986).
Although cases that can be classified as “pure” do
exist in the literature (Metz-Lutz and Dahl, 1984;
Yaqub et al., 1988; Stefanatos et al., 2005; Hayashi
and Hayashi, 2007; Slevc et al., 2011), as in the case
of nonverbal auditory agnosia discussed above, many
studies did not assess performance in other domains
as rigorously. For instance, Yaqub et al. (1988) reported
that their WD patient could “recognize and appreciate
music”, but no formal testing was carried out. It is pos-
sible that the patient had subtler deficits in music
perception that escaped the experimenters. In that vein,
using more controlled laboratory tests, Pinard et al.
(2002) found that a patient who was previously
A.P. SAYGIN AND L.E. MILLER
classified as a “pure” case of WD (Mesulam, 1982) also
had deficits in environmental sound and music
processing.
The exact nature of the deficit in WD is also a mat-
ter of debate. Several studies have used psycholinguis-
tic measures to characterize the deficit in WD (Saffran
et al., 1976; Auerbach et al., 1982; Miceli, 1982;
Caramazza et al., 1983; Praamstra et al., 1991; Jacobs
and Schneider, 2003). Patients often exhibit impaired
processing of consonants with relatively spared while
the processing of vowels (Saffran et al., 1976; Auerbach
et al., 1982; Yaqub et al., 1988; Pinard et al., 2002;
Stefanatos et al., 2005) – though there are exceptions
(Tanaka et al., 1987; Praamstra et al., 1991). Whereas
vowels are characterized acoustically by slow formant
frequency transitions (100–150 ms), the formant
frequency transitions of consonants are very rapid
(20–50 ms), leading to the view that WD may be
linked to deficits in temporal processing (for review,
see Phillips and Farmer, 1990; Stefanatos et al.,
2005). In support of this view, it has been reported
that patients’ accuracy in speech processing will
often improve when speech is slowed down (Albert
and Bear, 1974). Deficits in processing dynamic non-
verbal stimuli have also been reported in WD. For
example, using a discrimination task between pairs
of dynamically changing sine wave stimuli, Wang
et al. (2000) found that their WD patient scored at
chance, demonstrating a profound inability to fully
process rapidly changing auditory stimuli. Other stud-
ies have found problems of temporal resolution at the
prephonemic level of processing in WD. Whereas
controls required around 1–3 ms between two clicks
to perceive them as distinct, patients with WD
required between 15 and 300 ms (Albert and Bear,
1974; Auerbach et al., 1982; Tanaka et al., 1987;
Buchtel and Stewart, 1989; Hayashi and Hayashi,
2007). Patients with WD were also unable to count
clicks presented above 2 Hz, well below the level of
controls (9–11 Hz) (Albert and Bear, 1974; Auerbach
et al., 1982; Yaqub et al., 1988). While most studies
have restricted their stimuli to the auditory domain,
temporal processing deficits of the patients may
also extend to the somatosensory and visual domains,
raising the possibility of a supramodal deficit in WD
(Tanaka et al., 1987).
The relationship between nonverbal deficits in tem-
poral processing and the speech processing deficits in
WD remains unclear. Whereas in one patient, the res-
olution of WD led to the normalization of click fusion
time (Godefroy et al., 1995), others have failed to find
CENTRAL DISORDERS OF AUDITORY PROCESSING
deficits in click fusion time despite evidence for a def-
icit in temporal processing (Stefanatos et al., 2005).
Training on rapid auditory events improved a patient’s
ability to perceive rapid temporal differences for non-
speech, but not for speech sounds (Slevc et al., 2011).
Whereas prephonemic temporal processing deficits
may contribute to WD, the theory would need to be
extended to account for these findings.
Auerbach et al. (1982) proposed dividing WD into
two sub-types: a prephonemic temporal processing dis-
order that results from bilateral temporal lobe lesions,
and a phonemic processing disorder that results from
unilateral damage to the left temporal lobe (leading
to disconnection). Temporal processing should there-
fore be spared following unilateral left temporal dam-
age. This model was further refined by Poeppel
(2001) to include different temporal integration win-
dows for acoustic processing in the left (20–50 ms)
and right (150–250 ms) hemispheres (see also Hickok
and Poeppel, 2007). According to this model, damage
to the right hemisphere should be required for the dis-
ruption of prephonemic processing. This claim has
recently been tested in a patient with WD due to a uni-
lateral left hemisphere lesion (Slevc et al., 2011). Dif-
fusion tensor imaging (DTI) revealed that transcallosal
white matter projects from the right auditory areas to
the left temporal lobe. While this provides some evi-
dence against the claim that all cases of unilateral
PWD are the result of disconnection, the evidence is
not conclusive since DTI is unable to determine
whether the tracts are in fact functionally intact.
23.3. Summary and conclusion
In this review, we briefly presented the literature on
auditory agnosias. We discussed both nonverbal and
verbal types of auditory agnosia, the latter also known
as (pure) word deafness. While neuropsychological
cases exhibiting dissociations between domains or
modalities are important in shaping theories of human
perception and cognition, these are the exception rather
than the norm in the domain of auditory agnosias. For
example, patients with speech comprehension deficits
also have nonverbal sound comprehension deficits that
go hand in hand. Despite the label “pure” word deaf-
ness, cases of verbal auditory agnosia with unequivo-
cally spared nonverbal sound comprehension are rare.
Patients with auditory agnosias tend to present with
concomitant deficits in other domains, and sometimes
also other modalities. We also noted other open ques-
tions concerning the nature of the deficits in auditory
457
agnosia and their neural bases. Further research is
needed to improve our understanding of both auditory
agnosias and functional specialization in human audi-
tory perception and cognition more broadly.
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