Chapter 20

AUDITORY AGNOSIA
AND AMUSIA
Russell M. Bauer
Tricia Zawacki

The term auditory agnosia refers to an impaired ous characteristics of heard music. Table 20-1 lists
capacity to recognize sounds in the presence of the major clinical features of each syndrome.
otherwise adequate hearing as measured by stan-
dard audiometry. Historically, the term has been
used broadly to refer to impaired capacity to rec- CORTICAL DEAFNESS AND CORTICAL
ognize sounds in general and in a narrow sense to AUDITORY DISORDER
refer to a selective deficit in recognizing nonverbal
sounds only. Terminological confusion abounds, Patients with cortical deafness show profound im-
with such terms as cortical auditory disorder,•1 2 pairments in processing auditory stimuli of any
auditory agnosia,3.4 and auditory agnosia and word kind and often have electrophysiologic signs of
dea fness5 all being used to describe similar phe- primary impairment in auditory-perceptual acuity.
nomena. In most cases, impairment in the recogni- The behavior of patients with cortical auditory
tion of both speech and nonspeech sounds is pres- disorders is similar, though auditory evoked re-
ent to some degree. The relative severity of these sponses are more often normal in this population.
impairments depends on lesion localization, on Both groups show a range of impairments in audi-
premorbid lateralization of linguistic and nonlin- tory perception, discrimination, and recognition
guistic skills in the individual patient, and on which that affect verbal and nonverbal materia l.9•10 If
hemisphere is first or more seriously damaged6 present, aphasic signs are mild and do not prevent
(but see Ref. 7). Complicating the picture even the patient from identifying visual or somesthetic
further is the fact that many patients evolve from stimuli. Difficulties in elementary auditory func-
one disorder to another as recovery takes place.8 tion, including temporal auditory analysis and lo-
In regard to generalized auditory agnosia, we pre- calization of sounds in space, are common.
fer the theoretically neutral term cortical auditory In our view, cortical auditory disorders and
disorder, and we first discuss this entity together cortical deafness are related in much the same way
with cortical deafness. We then discuss more "se- as visual agnosia is related to cortical blindness.
lective" deficits, including pure word deafness (a If so, then cortical auditory disorders can take
selective impairment in speech-sound recogni- apperceptive or associative11 forms, though some
tion), auditory sound agnosia (selective impair- degree of perceptual deficit is apparent in nearly
ment in recognizing nonspeech sounds), and para- all cases where the evaluation of auditory abilities
linguistic agnosias (in which recognition of has been sufficiently comprehensive. This state-
prosodic features of spoken language is impaired). ment is true even in cases where pure tone audiom-
Finally, we describe patients with receptive (sen- etry is relatively normal. Jerger and coworkers12•13
sory) amusia, loss of the ability to appreciate vari- reported impairments in auditory perception (ear
fol 267
---------------------- --------------------------...
Pc:,N t rl1f-tIl-\ LY\11)
268 PART 3/DISORDERS OF PERCEPTION, ATTENTION, AND AWARENESS

Table 20-1
Clinical features of various forms of auditory agnosia

Cortical Auditory Sensory/

Cortical auditory Pure word sound receptive
deafness disorder deafness agnosia amusia

Audiometric sensitivity +I- + + +

Speech comprehension + +
Speech repetition + +
Spontaneous speech + +a +a + +
Reading comprehension + + + + +
Written language + + + + +
Recognition of familiar sounds + ?
Musical perception
_b
+!-
Recognition of vocal prosody + ?
Key: + = spared ability; - = impaired ability; ? = insufficient information in literature to generalize.
"May be some paraphasia.
bWhen tested (rarely). musical perception has been shown to be impaired in these patients.
Sources: Adapted from Buchman et al. 7 and Oppenheimer and Newcombe,3 with permission.

suppression in dichotic listening, abnormal click
fusion thresholds, and impaired discrimination of
basic sound attributes) in patients with cortical
auditory disorders. These sometimes evolve from
a state of cortical deafness, making it difficult to
distinguish between the two entities. Michel and
colleagues14 argued that the cortically deaf patient
looks and feels deaf, whereas the patient with cor-
tical auditory disorders insists that he or she is not
deaf. This turns out to be a poor criterion, because
the subjective experience of deafness in the former
condition is typically so transient and patients in
both groups are "deaf" when subjected to appro-
priate tests. Although it was once believed that
bilateral cortical lesions involving primary audi-
tory cortex resulted in total hearing loss, evidence
from animal experiments1,5 •16 cortical mapping of
the auditory area,17 and clinicopathologic studies
in humans18.19 indicate that complete destruction
of primary auditory cortex does not lead to perma-
nent loss of a diometric sensitivity. Thus, clinical,
pathologic, and electrophysiologic data question
the distinctive nature of cortical deafness1•·9 10 and
suggest that it is one of a spectrum of auditory
impairments that runs from generalized distur-
bances in detecting and discriminating basic sound
attributes to more complex and selective impair-
ments in auditory recognition.
Cortical deafness is most often seen in bilat-
eral cerebrovascular disease. The course is usually
biphasic, with an initial deficit (often aphasia and
hemiparesis) related to unilateral damage, fol-
lowed by a second (contralateral) deficit associ-
ated with sudden transient total deafness.1, 2 1,3 2,0 21
A biphasic course is also typical of cortical audi-
tory disorders. In cortical deafness, bilateral de-
struction of the auditory radiations or the primary
auditory cortex (Heschl's gyms) has been a con-
stant finding. 20 The anatomic basis of cortical audi-
tory disorders is more variable. Lesions can be
quite extensive,3 though the superior temporal gy-
ms and efferent connections of Heschl's gyms are
often involved. Two recent Japanese cases22•23 sug-
gest that cortical auditory disorders can result from
bilateral lesions sparing the cortex entirely. Thus,
the lesions in cortical auditory disorders seem to
CHAPTER 20/ AUDITORY AGNOSIA AND AMUSIA ["E\1-l 4 fl\lLtrt\ 269
. l\ \l J
involve either intrinsic or disconnecting lesions of writing and reading disturbances disappear, the
auditory association cortex, with relative sparing patient still does not comprehend spoken language
of Heschl's gyrus. but can communicate by writing. Deafness can be
ruled out by normal audiometric pure-tc;me thresh-
olds. At this point, the patient may experience
PURE WORD DEAFNESS (AUDITORY auditory hallucinations or may exhibit transient
AGNOSIA FOR SPEECH, AUDITORY euphoric34 or paranoid35ideation. The inability to
VERBAL AGNOSIA) repeat poorly comprehended speech stimuli distin-
guishes pure word deafness from transcortical sen-
The patient with pure word deafness is unable to sory aphasia; the absence of florid paraphasia and
comprehend spoken language although he or she of reading and writing disturbance distinguishes it
can read, write, and speak in, a relatively normal from Wernicke's aphasia. This having been said,
manner.7 Writing to dictation is typically impaired, it should be recognized that "aphasic" and "ag-
though copying of written material is not. By defi- nosic" symptoms may both be present, though dif-
nition, comprehension of nonverbal sounds is rela- ferent in degree, in the individual case.7
tively spared, but nonverbal auditory recognition Many patients are responsive to speech input
is impaired in the majority of cases in which it has but complain of dramatic, sometimes aversive
been evaluated.7 Thus, the syndrome is "pure" in changes in their subjective experience of speech
that (1) the patient is relatively .free of signs of sounds.8The pure word deafness patient may com-
posterior aphasia (see Chap. 9) and (2) the im- plain that speech is muffled or sounds like a foreign
pairment in speech sound recognition is dispropor- language. Hemphill and Stengel's36 patient stated
tionately severe. The disorder was first described that "voices come but no words." Klein and Har-
by Kussmau l.24 Li chteim25 later defined it as an. per's31 patient described speech as "an undifferen-
isolated deficit and postulated a bilateral subcorti- tiated continuous humming noise without any
cal interruption of fibers from ascending auditory rhythm" and "like foreigners speaking in the dis-
projections to the left "auditory word center." tance." Albert and Bear's30 patient said "words
With few exceptions, pure word deafness has been come too quickly" and, "they sound like a foreign
associated with bilateral, symmetric corticosub- language." The speech of these patients is often
cortical lesions of the anterior part of the superior slightly louder than normal. Performance on
temporal gyri with some sparing of Heschl's gyrus, speech perception tests is inconsistent and highly
particularly on the left. Some patients have subcor- dependent upon context37 and linguistic com-
tical lesions of the dominant temporal lobe only, plexity.38
presumably destroying the ipsilateral auditory ra- Many studies of pure word deafness have
diation as well as callosal fibers from the contralat- emphasized the role of auditory-perceptual pro-
eral auditory region.26- 28 It is generally agreed that cessing in the genesis of the disorder.1·8,.12, 3038 Prob-
the lesion profile results in a bilateral discon- lems with temporal resolution30 and phonemic dis-
nection of Wemicke's area from auditory input. 29 crimination39-41 have also received attention.
The fact that it involves an unusually placed, cir- Auerbach and coworkers 38 suggest that the disor-
cumscribed lesion explains the low incidence of der may take two forms: (1) a prephonemic tempo-
pure word deafness. In the review performed by ral auditory acuity disturbance associated with bi-
Buchman and colleagues,7 the lesions in 30 of 37 lateral temporal lesions or (2) a disorder of
reviewed cases were of cerebrovascular origin. phonemic discrimination attributable to left tem-
When first seen, the patient is often recov- poral lesions and closely linked to Wernicke's
ering from a Wemicke's aphasia, though occasion-· aphasia,. Albert and Bear30 suggest that the prob-
ally pure word deafness may actually give way to lem in pure word deafness is one of temporal reso-
30
a Wernicke's aphasia. - 33 As the paraphasias and lution of auditory stimuli rather than specific pho-
270 PART 3/DISORDERS OF PERCEPTION, ATTENTION, AND AWARENESS
netic impairment. Their patient demonstrated
abnormally long click-fusion thresholds, and im-
proved in auditory comprehension when speech
was presented at slower rates. Saffran and col-
leagues,41 on the other hand, showed that in-
forming their patient of the nature of the topic
under discussion significantly facilitated compre-
hension. Thus, the disorder appeared to arise at
different levels in these two patients. This variabil-
ity supports the contention of Buchman and co-
workers7 that pure word deafness describes a spec-
trum rather than an individual disorder.
On tests of phonemic discrimination, pa-
tients with bilateral lesions tend to show distinctive
deficits for the feature of place of articula-
tion.38·39.42 Those with unilateral left hemispheric
disease (LHD) show either impaired discrimina-
tion of voicing41 or no distinctive pattern.40 In di-
chotic listening, some patients show extreme sup-
pression of right-ear perception,30.41 suggesting the
inaccessibility of the left hemispheric phonetic de-
coding areas (Wemicke's area) to auditory mate-
rial that has already been acoustically processed
by the right hemisphere. Several studies have re-
ported brainstem and cortical auditory evoked re-
sponses in pure word deafness patients.14 Brain-
stem auditory evoked potentials (BAEPs) are
almost always normal, suggesting intact processing
up to the level of the auditory radiations-.30-3843
Results from studies of cortical auditory evoked
potentials (AEPs) more variable, consistent with
variable pathology.38 For example, the patient of
Jerger and colleagues12 had no appreciable AEP,
yet heard sounds. The patient of Auerbach and
associates38 showed normal Pl, Nl, and P2 re-
sponses to right-ear stimulation but had minimal
response over either hemisphere to left-ear stimu-
lation.
Although patients with pure word deafness
are supposed to perform relatively well with envi-
ronmental sounds, many show subnormal perfor-
mances when such abilities are formally tested.7
Similarly, the appreciation of music is often dis-
turbed. Some patients may recognize foreign lan-
guages by their distinctive prosodic characteristics,
and others can recognize who is speaking, sug-
gesting preserved ability to comprehend paralin-
l \C\ l)
guistic aspects of speech. Coslett and associates44
described a word-deaf patient who showed a re-
markable dissociation between the comprehen-
sion of neutral and affectively intoned sentences.
He was asked to point to pictures of males and
females depicting various emotional expressions.
When instructions were given in a neutral voice,
he performed poorly, but when instructions were
given with affective intonations appropriate to the
target face, he performed normally (at a level com-
mensurate to his performance with written instruc-
tions). This patient had bilateral destruction of
primary auditory cortex with some sparing of audi-
tory association cortex, suggesting at least some
direct contribution of the auditory radiations di-
rectly to association cortex without initial decod-
ing in Heschl's gyrus.44 These authors speculate
that one reason why pure word deafness patients
improve their auditory comprehension with lip
reading is that face-to-face contact allows them to _
take advantage of visual cues (gesture and facial
expression) that are processed by different brain
systems. Another explanation is that lip reading
provides visual information about place of articu-
lation. a linguistic feature that is markedly im-
paired at least in the bilateral cases.38 In either
case, the preserved comprehension of paralinguis-
tic aspects of speech in pure word deafness patients
further reinforces the widely held belief that com-
prehension of speech and nonspeech sounds are
dissociable abilities.
AUDITORY SOUND AGNOSIA
(AUDITORY AGNOSIA FOR
NONSPEECH SOUNDS)
Patients with auditory sound agnosia have selec-
tive difficulty recognizing and identifying nonver-
bal sounds. The disorder is rare, less common by
far than pure word deafness, but its existence has
raised interest because it suggests the same type
of "domain-specificity" in the auditory system that
has received much recent attention in the study
of visual recognition disorders_45- 47The lower inci-
dence of auditory sound agnosia may be due in
part to the fact that such patients are less likely
CHAPTER 20 / AUDITORY AGNOSIA AND AMUSIA
to seek medical advice than are those with a disor-
der of speech comprehension and also because
nonspecific auditory complaints may be dis-
counted when pure tone audiometric and speech
discrimination thresholds are normal. This is un-
fortunate, since normal audiometry does not rule
out the possibility of primary auditory percep-
tual defects. 48.49
Vignolo9 argued that there may be two forms
of auditory sound agnosia: (1) a perceptual-dis-
criminative type associated mainly with right
hemisphere damage and (2) an associative-seman-
tic type associated with left hemisphere damage
and linked with posterior aphasia. The former
group makes predominantly acoustic (e.g., "man
whistling" for birdsong) errors on picture-sound
matching tasks, while the latter makes predomi-
nantly semantic (e.g., '·train" for automobile en-
gine) errors. This division follows the original clas-
sification of Kliest,50 who distinguished between
the ability to detect/perceive isolated sounds or
noises and the inability to understand the meaning
of sounds. In the verbal sphere, the analogous
distinction (at least on the input side) is between
pure word deafness (perceptual-discriminative)
and transcortical sensory aphasia (semantic-asso-
ciative). Relatively few cases of "pure" auditory
sound agnosia have been reported.-51 55
The patient of Spreen and colleagues 54 is a
paradigm case. He was a 65-year-old right-handed
male who complained of "nerves" and headache
when seen 3 years after a left hemiparetic episode.
Audiometric testing revealed moderate bilateral
high-frequency loss and speech reception thresh-
olds of 12 dB for both ears. The outstanding abnor-
mality was the inability to recognize common
sounds. There was neither aphasia nor any other
agnosic deficit. Sound localization was normal, but
scores on the pitch subtest of the Seashore Tests
of Musical Talent were at chance level. The patient
performed well on a matching-to-sample test, sug-
gesting that his sound recognition disturbance
could not be attributed to serious acoustic distur-
bance. He claimed no musical experience or talent
and refused to cooperate with further testing of
musical ability. Postmortem examination revealed
a sharply demarcated old infarct of the right hemi-
271
sphere centering around the parietal lobe and in-
volving the superior temporal and angular gyri as
well as a large portion of the inferior parietal,
inferior. and middle frontal gyri and the insula.
Other cases with unilateral pathology were re-
ported by Fujii and coworkers52 (small posterior
right temporal hemmorhagic lesion of the middle
and superior temporal gyri), Neilsen and Sult 53
(right thalamus and parietal lobe), and Wortis and
Pfe ffe r55 (large lesion of the right temporoparie-
tooccipital junction).
These data suggest that an inability to recog-
nize environmental sounds can occur after unilat-
eral right hemisphere damage. Such a defect is less
commonly seen in the context of bilateral dis-
ease,51 but these cases are less ''pure.. at least in
the acute stage. The association of auditory sound
agnosia with right hemisphere damage implies that
acoustic processors within the right hemisphere
are preferentially involved in dealing with nonlin-
guistic sounds. The left hemisphere is likely in-
volved in providing linguistic labels for identified
sounds. and in performing semantic-associative
functions supporting sound recognition and identi-
fication.
"PARALINGUISTIC AGNOSIAS":
AUDITORY AFFECTIVE AGNOSIA
AND PHONAGNOSIA
The auditory speech signal conveys not only lin-
guistic meaning but also-through variations in
volume. timbre, pitch, and rhythm-information
about the emotional state of the speaker (see
Chap. 56). Recent clinical evidence suggests that
comprehension of affective tone can be selectively
impaired. Heilman and coworkers 56 showed that
patients with hemispatial neglect from right tem-
poroparietal lesions were impaired in the compre-
hension of affectively intoned speech (a deficit
they called "auditory affective agnosia") but
showed normal comprehension of linguistic
speech content. Patients with left temporoparietal
lesions and fluent aphasia showed normal compre-
hension of both linguistic and affective (paralin-
guistic) aspects of speech. Whether this defect is
 f(1 E "\- mftr\ l\ \ 7 )
272 PART 3/DISORDERS OF PERCEPTION, ATTENTION, AND AWARENESS
"agnosic" in nature remains to be seen, since audi-
tory sensory/perceptual skills were not assessed.
It is possible that auditory affective agnosia is a
subtype of auditory sound agnosia (i.e., that it rep- hemispheres contribute in complex ways. Dichotic
resents a category-specific auditory agnosia), but
further studies are necessary before this can be
asserted with any certainty.
Recent studies by Van Lancker and associ-
ates57-59 have revealed another type of paralinguis- to be important in the processing of sequential
tic deficit after right hemisphere damage. In these
studies, patients with unilateral right hemisphere
damage showed deficits in discriminating and rec-
ognizing familiar voices, while patients with left
hemisphere damage were impaired only on a task
that required a discrimination between two fa-
mous voices. Although the exact nature of this
distinction is elusive, it seems to parallel that be- rhythm factors become more important for distin-
tween episodic (personally experienced) versus se-
mantic (generally known) memory in amnesia re-
search. Evidence. from computed tomography
(CT) suggested that right parietal damage resulted
in voice-recognition impairment, while temporal
lobe damage in either hemisphere led to deficits
in voice discrimination. The authors refer to this
deficit as "phonagnosia," but, like auditory af-
fective agnosia, it remains to be seen whether it
is truly agnosic in nature.
SENSORY (RECEPTIVE) AMUSIA
The subject of amusia has been reviewed in detail
by Wertheim, °Critchley and Henson, and Gates
6 61
62
and Bradshaw. Sensory amusia refers to an in-
ability to appreciate various characteristics of
heard music. Impairment of music perception oc-
curs to some extent in all cases of auditory sound
agnosia and in the majority of cases of aphasia 62
and pure word deafness, though its exact preva-
lence in such populations is unknown. Loss of mu-
sical perceptual ability is probably underreported
because a specific musical disorder rarely inter-
feres with everyday life.
Wertheim 60 believed that receptive amusia
occurs more frequently with left hemisphere dam-
age, while expressive musical disabilities are more
apt to be associated with right hemisphere dam-
age. More recent evidence suggests that music per-
ception is a multicomponent process to which both
listening studies show that the right hemisphere
plays a more important role than the left in the
processing of musical and nonlinguistic sound pat-
terns.63·64 However, the left hemisphere appears
(temporally organized) material of any kind, in-
cluding musical series. The dominant hemisphere
may process heard music more analytically or with
more attention to specific features of the music,
such as temporal order or rhythm.62·65 According
to Gordon,64 melody recognition becomes more
dependent on sequential processing as time and
guishing tone patterns (see Ref. 66). The multi-
componential nature of music perception makes
it difficult to define receptive amusia and to local-
ize the deficit to a particular brain region. Further
complicating the picture is the fact that pitch, har-
mony, timbre, intensity, and rhythm may be af-
fected to different degrees and in various combina-
tions in the individual patient.
Many clinical studies distinguish between
"instant" perceptual processes governing - judg-
ments of pitch, harmony, timbre, and intensity
(loudness) and more "sequential," time-depen-
dent processes governing melody recognition and
judgments of rhythm and duration. Tentative
clinical support for this kind of distinction exists
in a double dissociation between the perceptual
processing of pitch and the processing of tempo-
ral sequences,67 dissociations that also hold true
for reading music and for singing. There is further
evidence that aspects of musical denotation (the
"real-world" events referred to by lyrics) and
musical connotation (the formal expressive pat-
terns indicated by pitch, timbre, and intensity) are
selectively vulnerable to focal brain lesions.68·69
Gordon and Bogen70 reported that during the
right hemispheric anesthesia by the WADA pro-
cedurn. singing was impaired with disrupted pitch
production but ·preserved rhythmic expression.
Hallucinations of voices and musical sounds have
 ( \ 7)
CHAPTER 20/ AUDITORY AGNOSIA AND AMUSIA 273

been reported with electrical stimulation of the gested to be dependent upon on the degree of
lateral and superior surfaces of the first tem- these preillness characteristics.72
poral convolutions in either hemisphere with
more frequent occurrence on the nondominant
side.71 SUMMARY
Peretz and colleagues 68 applied comprehen-
sive nonverbal auditory testing to two patients In this chapter, we have briefly reviewed major
with bilateral lesions of auditory cortex. In their types of auditory recognition disorders. Although
patients, the perception of speech and environ- certain identifiable syndromes exist, our review
mental sounds was spared, but the perception of suggests a bewildering array of clinical symptoms
tunes, prosody, and voice was impaired. Based and assessment methods. A fundamental problem
on these behavioral dissociations. they argue that concerns the lack of a comprehensive theory of
music processing is distinct from the processing of auditory cognition. Compared to vision, for exam-
speech or environmental sounds. Their data led ple, we know relatively littie about the cognitive
them to argue for a task- and process-specific ap- architecture underlying auditory identification of
proach to the analysis of cases of auditory agnosia. voices or environmental sounds. This theoretical
They suggest that nominally "auditory" tasks anarchy has led to terminologic confusion and has
should be broken down into their functional sub- slowed development of a cognitive taxonomy of
components and that more extensive component- auditory disorders because it has been unsafe to
based analysis of auditory processing deficits is assume that different authors are using such terms
warranted. For example, they distinguish between in the same way. Another problem is that rela-
processes involved in the recognition of specific tively little agreement exists regarding necessary
voices or musical instruments (which is timbre- and sufficient methods of testing in patients with
dependent), and processes involved in recognition auditory recognition disturbances. Thus, for exam-
of tunes (which is pitch-dependent). The notion ple, it is not uncommon for claims of a specific
that nominally distinct classes of auditory material defect in one area of auditory processing to be
(e.g., melodies, prosody, and voice) share common made when, in fact, such specificity is a spurious
processes may be critically important in devel- result of incomplete testing. This problem has
oping a functional taxonomy of auditory recogni- been noted by others,9 and it is obvious that further
tion disorders in general and of amusia in par- theoretical development in the area of auditory
ticular. recognition disturbances will depend on the ability
This suggestion points out certain significant of researchers to devise more comprehensive and
deficiencies in the evaluation of amusic patients. theoretically driven assessments of auditory
Although theories linking brain function to music function.68
perception have long been available,60 •72• 73 such Despite these problems, some progress has
theories do not often contain sufficient process been made in identifying potentially important dis-
specificity to guide the clinical evaluation of sociations within auditory recognition distur-
amusic patients. Thus, for example, relatively little bances that may eventually reveal the underlying
is known regarding which musical features will be structure of higher auditory processes. Dissocia-
most informative in constructing a neuropsycho- tions between verbal (pure word deafness) and
logical model of music perception. Another obsta- nonverbal (auditory sound agnosia) deficits and
cle to systematic study of acquired amusia is the between perceptual-discriminative and semantic-
variability of preillness musical abilities, interests, associative forms of recognition disturbance have
and experience (see Wertheim 60 for a system of been described. Recent findings of impairments in
:f classifying musical ability level). The cerebral or- recognizing affective prosody, tunes, and voice are
ganization of musical perception has been sug- exciting because they raise the further possibility

1s

274 PART 3/DISORDERS OF PERCEPTION, ATTENTION, AND AWARENESS
of " category-specificity" 47·74·75 (or process-speci-
ficity) in auditory recognition, as has been de-
scribed for vision (see Chaps. 17 and 18).
It seems clear at this point that further divi-
sions within the concept of auditory agnosia are
necessary and that a more comprehensive, pro-
cess-based approach to evaluating auditory func-
tion is required. If this approach is developed fur-
ther, the important building blocks in the structure
of auditory cognition will eventually become ap-
parent through behavioral dissociations.46 In our
view, the clinical approach to a patient suspected
of auditory agnosia should consist, at a minimum,
of the following steps. First, extensive testing of
nonauditory language functions and of general
neuropsychological status should be conducted in
order to rule out the contribution of aphasia or
dementia to the auditory recognition deficit. Sec-
ond, detailed testing of auditory-perceptual abili-
ties should be conducted, including but not neces-
sarily limited to pure tone audiometry, speech-
detection thresholds, temporal auditory acuity
(e.g., click fusion thresholds), auditory discrimina-
tion,76 and sound-localization tasks. When possi-
ble, brainstem and cortical auditory evoked re-
sponses should be evaluated in order to ascertain
the "level" at which the patient's deficit occurs.
Third, a broad evaluation of auditory capacities
should be conducted, including evaluation of the
patient's ability to recognize speech, environmen-
tal sounds, and music. Performance in other areas
not typically assessed in these patients (e.g., voice
recognition, singing and related expressive behav-
ior, and evaluation of the patient's ability to recog-
nize linguistic and nonlinguistic prosody) should
be assessed. In order to sharpen the hazy distinc-
tions between auditory agnosia (identification and
recognition disturbances) and auditory compre-
hension deficits associated with aphasia, it might
also be fruitful to routinely subject aphasic groups
to the same kind of comprehensive auditory test-
ing instead of assuming that their impairment in
speech comprehension is a straightforward conse-
quence of linguistic impairment. The interested
reader should consult Peretz and associates68 for
a useful and reasonably comprehensive instantia-
y
f
tion of this kind of approach to the study of audi-
tory agnosias.
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