BRAIN AND LANGUAGE 1, 195-204 (1974)

Auditory Agnosia for Speech

(“Pure Word-Deafness”)

A Historical Review with Current Implications

MARVIN N. GOLDSTEIN
Department of Neurology, Monroe Commanity Hospital and
University of Rochester School of Medicine & Dentistry, Rochester, New York 14603

Received August 2 1, 1973

A historical review of thought about the existence. clinical presentation. and

mechanism of auditory agnosia for speech is presented. Implications of recent
contributions which shed more light on this syndrome are discussed.

Auditory agnosia for speech has been recognized clinically since at

least 1877 (Kussmaul). “Word-deafness” is diagnosed when the ability
to understand and repeat speech and write from dictation is lost. In pure
or isolated word-deafness, reading, copying written material, spontane-
ous writing and speech remain largely unaffected (Lichtheim, 1885).
Other auditory agnosias have been described as occurring in “pure”
form, in association with each other, or with aphasia. Sensory amusia
and agnosia for non-verbal sounds also are described in “pure” forms
(Nielsen, 1939; Spreen et al., 1965; Feuchtwanger, 1930; Wertheim,
1963).
The literature is confusing in that word deafness has often been con-
sidered as part of Wernicke’s aphasia, as a separate entity or as a limited
“cortical deafness,” or even as due to a peripheral sensory deficit. More
modern studies demonstrate anew the difficulty in discreetly separating
these conditions. In fact, many of the classical case reports describe the
simultaneous presence of auditory defect, word deafness and some
degree of aphasia.
In 1874, Wernicke described in detail a syndrome resulting from
lesions of the posterior third of the left superior temporal gyrus. Patients
with this so-called sensory aphasia were described as being unable to un-
derstand speech and unable to repeat words as well as having disturbed
reading and writing ability. The speech reception disturbance was postu-
lated by Wernicke as being due in part to a limited deafness involving
those sound frequencies used in human speech. This was alternatively
described as loss of mental speech sound images or memory. Some of
his patients, however, also showed disturbances of expressive speech.
195
196 MARVIN N. GOLDSTEIN

Naming disorders, paraphasias and agraphia were noted in some of Wer-

nicke’s patients. Wernicke thought that the paraphasia resulted directly
from lack of intact sound images which were necessary for a feedback
control of motor speech. Agraphia and alexia were explained as also
related to loss of speech-sound memories. The credit given to Wernicke
for describing word-deafness as part of his sensory aphasia complex was
disputed by Bastian. In 1869, Bastian published a paper on speech
disorders, in which he wrote:
Most aphasic patients can understand perfectly what is said to them and can follow
and feel interested when they hear others read aloud. . . . In certain of the severe
cases of aphasia . . it is distinctly stated that the patient either did not gather all or
with difficulty and imperfectly, the import of words when he was spoken to, though he
could be made to understand with the utmost readiness by means of signs and ges-
tures. Must we not suppose in such a condition either the communication of the af-
ferent fibres with the auditory perceptive centres is cut off, or that this centre itself, in
which the sounds of words are habitually discriminated and associated with the things
to which they refer is more or less injured?
While Bastian’s description alludes to the concept of word-deafness,
this argument about academic precedence pales when one considers the
description by Lordat (1843) of his own symptoms after an attack in
1828: “I know the words but cannot perceive them.” Syntax was dis-
ordered; he showed paraphasia. However, Lordat also noted that he in-
verted syllables in words and used totally incorrect words. An even ear-
lier account of auditory agnosia is ascribed to Ambrose Pare by Hen-
schen, but when one reads this report, it is lacking even simple details
(Hamby, 1960).
Kussmaul (1877) separated a condition in which there was lack of un-
derstanding of spoken words (he coined the term word-deafness) with no
disturbances of hearing or expressive speech from isolated reading dis-
ability. These two syndromes, when they appeared together, were con-
sidered to represent Wernicke’s sensory aphasia. Word-deafness was
thought by Kussmaul to be the major result of destruction of the first left
temporal gyrus. He ascribed word-blindness to lesions of the left angular
and supramarginal gyri.
Lichtheim (1885) conceived of a language as developing through
acquisition of auditory word-impressions and motor or kinesthetic word-
impressions, each controlled by a specific brain center. Disturbances of
these centers resulted in motor or in sensory aphasias, respectively.
Lichtheim’s scheme of language disorders included a condition in which
the understanding of language and the subsequent repetition of spoken
words and the ability to write to dictation are lost. Motor speech, volun-
tary writing, reading and copying are intact in this syndrome and para-
phasia and paragraphia are said to be absent. This, Lichtheim called
isolated speech deafness and considered it to be the result of a disrup-
 WORD-DEAFNESS 197

tion in the pathway from the auditory reception center to the center for
auditory word impression. He distinguished isolated speech deafness,
which he also called subcortical word-deafness, from Wernicke’s
aphasia. In the latter condition, he considered that the ability to repeat
words and write to dictation are intact. A case first reported by Burk-
hardt (1882) was used to illustrate this type of disability. This patient
was further studied by Lichtheim over a two year period.
The patient was a teacher and journalist who suffered an “apopleptic
fit” in 1877, at the age of 55. Handedness was not described. Some left
facial weakness was accompanied by paraphasia, paragraphia when writ-
ing to dictation and disturbed spontaneous writing. Auditory language
perception was considered intact. These symptoms cleared, but five
years later there was a sudden increase in facial weakness and difficulty
in speaking. He was completely word-deaf. One year later reading and
spontaneous writing as well as speaking were found to be unimpaired by
Lichtheim, but the word-deafness remained. The patient was apparently
able to recognize at least the sound of a bell, but lost the ability to recog-
nize familiar melodies. He was unable to write to dictation or repeat
spoken words. Copying and reading aloud were unimpaired. Lichtheim
analyzed this case as representing at first a Wernicke’s sensory aphasia
which cleared partly, leaving the patient with isolated word-deafness.
Wernicke thought such a syndrome was very rare and due to subcortical
lesions in the left posterior temporal lobe.
Bastian (1897) apparently considered that pure word-deafness and
aphasia were related in a reverse fashion. In his work, he considered
partial damage to the “left auditory word centre” or loss of function of
that area to result in verbal amnesia, especially amnesia for names of ob-
jects with unimpaired ability to repeat speech. Destruction of the same
left auditory word center was concluded by Bastian to result in complete
word-deafness. He located this auditory word center in the posterior
part of the middle temporal gyrus. Later in his book, Bastian theorized
as to why in patients with lesions in this same area, some maintained
normal voluntary speech and others were severely aphasic or showed
paraphasia. He raised these possibilities:
(a) complete word-deafness with fairly intact voluntary speech
might result from isolation of the auditory word center rather than
its destruction.
(b) partial dysfunction of this auditory word center may leave
enough functioning for the production of paraphasic speech.
(c) paraphasia could be produced by the incomplete substitution
by the visual word center for lost functions of the auditory. This
latter possibility could produce word blindness in addition to audi-
tory word perception difficulties.
198 MARVIN N. GOLDSTEIN

A fourth theory listed was that the temporal lobe of the right hemisphere
substitutes partially for the destroyed area of the opposite side.
Liepmann ( 1898) and Liepmann and Starch ( 1902) described a patient
with word-deafness and inability to identify songs. This patient (Gor-
stelle) was found to have normal spontaneous speech. He was ap-
parently illiterate prior to the onset of his word-deafness so testing for
reading and writing disabilities was impossible. The brain showed a
subcortical lesion in the left temporal lobe, isolating the auditory associ-
ation area from auditory input from both right and left hemispheres. This
was thought to confirm Bastian’s and Wernicke’s thoughts about the
mechanism of production of pure word-deafness. Liepmann (1912) also
reported the autopsy findings of a patient of Wernicke’s (Hendschel)
with similar lesion localization. Van Gehuchten and Goris’ (19 10) patient
had a subcortical abscess in the left middle temporal gyrus. Their patient
had normal reading ability and spontaneous writing. He was paraphasic.
Potzl (1919) Henneberg (1926), Henschen (1920), Schuster and Ta-
terka (1926) and Kleist (1934) further documented similar cases with the
same unilateral localization of brain destruction.
Among other early cases, those of Giraudeau (1882), Pick (1892),
Dejerine and Serieux (1898). Ballet (1903), Bonvicini (1905) Barrett
(1910), and Henschen (1919, 1920) showed bilateral involvement of
temporal lobes at postmortem examination. One of Henschen’s (1919)
cases (Clara Nilsson) is described because it is frequently quoted as an
important study. The patient was a 54 year old woman who developed
right hemiparesis in 1901 which apparently cleared. The next year left
hemiparesis appeared. The patient was unable to name objects although
she recognized them, could not read, and refused to write. She did not
understand what was said to her, and showed some difficulty in pronun-
ciation. Re-examination in 1904 demonstrated normal reading, writing,
and calculation, as well as clear speech. Audiometric examination with
multiple tuning forks was normal. She could recognize familiar melodies
and sing them. She had . . . “great difficulty in understanding what is
said to her, and it is necessary to repeat it many times in order to be un-
derstood.”
The patient died in 1904. At autopsy, bilateral lesions were found.
The posterior portions of the left first and second temporal gyri and
lower part of the transverse gyrus were softened. This extended also
into nearby areas of occipital and lower temporal cortex. On the right
side similar destruction was noted but was more widespread. Henschen
proposed the term “perceptive word deafness” for this syndrome.
Almost all of the patients reported, with few exceptions, showed
paraphasia. Because the patients described in the above reports fulfilled
all of the other criteria for word-deafness, (Lichtheim, 1885; Dejerine,
 WORD-DEAFNESS 199

1898) and were similar as to site of brain destruction, perhaps para-

phasia should not be raised as a serious objection to their inclusion as
representative of this syndrome.
Many of these patients acted as if deaf when spoken to, but most of
the reports include some mention of response to low intensity non-
verbal sounds by the patients. Pick’s (1898) patient seemed to have a
major hearing loss. Freud (1891) stated that the lesion responsible for
word-deafness was “not a simple disruption of tracts but incomplete
bilateral lesions of auditory cortex.” He believed that there was a strong
possibility that peripheral hearing loss was necessary for development of
isolated word-deafness. Freund (1895) described two patients (one of
these had previously been reported in Wernicke’s monograph) with sub-
cortical sensory aphasia and disturbances of labyrinthine function. He
concluded that auditory word recognition disturbance was not related to
the aphasias but was primarily due to hearing loss. Wernicke (1894) had
already raised the possibility of limited deafness as a possible major
factor. Bay’s more recent work (1950) on the mechanism of production
of agnosias again raises the question of peripheral sense organ disabil-
ities.
Theorizing that previously reported cases called pure word-deafness
were most frequently patients with unrecognized “deficits of auricular
transmission,” Marie (1906) called this syndrome “a simple myth”:
1 must declare, first of all. that to my knowledge pure word deafness does not exist
from either the clinical or the anatomico-pathological point of view. From the
clinical point of view I have never observed a case of pure word deafness, nor any-
thing which approached it, and the observations which I have read have hardly sat-
isfied me. . I do not hesitate to declare that it is impossible to find an authentic
case of this pretended clinical form.

Perhaps the tone of these passages should be interpreted in the light

that they are included in an article responding to Dejerine’s statement
that Marie was busy “crossing out with the stroke of a pen all the works
accumulated on aphasia since 1825.”
Freund (1903) himself later reported the autopsy finding of a patient
clinically thought to have pure word-deafness on the basis of bilateral
labyrinthine dysfunction whose brain was shown to have contained a
tumor. This was situated in the first temporal gyrus on the left side. Bon-
vicini (1905) had, in fact, studied his patient’s auditory acuity with a
graded series of tuning forks and concluded that hearing was sufficiently
acute to detect speech. Barrett’s (19 10) patient had been totally deaf in
the right ear following explosion of a firearm nearby but graded tuning
forks and Galton whistle notes were heard normally on the left. Hen-
schen’s (1910) patient with normal responses to auditory testing was
described above. Hemphill and Stengel (1940) reported the carefully
200 MARVIN N. GOLDSTEIN

studied case of a 34 year old man with post-traumatic pure word-

deafness, no paraphasias and relatively minor hearing disturbance for
high tones in the left ear. The audiogram was normal on the right. Their
patient survived and thus no autopsy was performed. Reinhold’s (1950)
patient was noted to be talking strangely and acting as if she were unable
to understand the speech of others. After many months, spontaneous
speech was unimpaired, but the patient was unable to understand spoken
words. She could read and write correctly and repeat non-verbal sounds.
Perception of rhythm and musical notes was disturbed also as was iden-
tification of non-verbal sounds. Audiological evaluation suggested no im-
pairment in hearing test sounds.
Another patient was studied by Wohlfart, Lindgren and Jernelius
(1952). This man demonstrated almost total acoustic agnosia for speech,
music and non-verbal sounds after two episodes of right hemiparesis
followed by left hemiparesis. He was left with global aphasia which
cleared to leave the auditory agnosia and minimal paraphasia. Audiom-
etry showed only slight reduction in acuity in higher frequencies, bilat-
erally. Autopsy demonstrated multiple, bilateral areas of softening in
cerebral and cerebellar hemispheres, including both posterior portions of
superior temporal gyri. Ziegler’s (1952) first patient was similar.
Klein and Harper (1956) reported the case of a similar patient who
stated he could even hear a leaf falling but could not understand speech.
Audiometric testing revealed only moderately decreased acuity in the
left ear. Mildly disturbed spelling and musical sense was also noted.
Some degree of improvement occurred over eighteen months.
Lemoyne and Mahoudeau’s (1957, 1959) patient demonstrated loss of
musical sense and verbal auditory agnosia again with normal writing and
with paraphasia. Again only mild high tone hearing loss was demon-
strated. Autopsy demonstrated bilateral temporal lesions of vascular ori-
gin. Brain (1965) concluded that hearing impairment plays no part in the
production of word deafness.
More recently, patients with bilateral temporal lesions have been sub-
jected to discriminating tests of auditory function. Jerger, Weikers,
Sharbrough and Jerger (1970) reported careful studies on a patient who
suffered two episodes of cerebral infarction affecting both posterior
temporal regions. At first he appeared to be deaf. Some paraphasia
was present. Pure tone audiometry demonstrated bilateral high grade hear-
ing loss affecting all frequencies at first. Bone and air conduction re-
sults were similar. Later, improvement occurred, especially in speech
frequencies. High frequency loss was present in the right ear but recov-
ered to a large extent in the left. Speech audiometry showed no signifi-
cant speech frequency loss. Bekesy audiometry demonstrated even more
marked right ear hearing loss. Performance studies with phonetically
 WORD-DEAFNESS 201

balanced words demonstrated that speech understanding was markedly

and bilaterally deficient. Loudness discrimination was impaired on the
right but not left. Perception of temporal order was poor bilaterally.
Averaged cortical evoked responses to pure-tone and click signals were
reported as being easily elicited in a control subject but not in the pa-
tient. Although this patient failed to demonstrate word-deafness in usual
bedside tests, he did show word hearing deficits under controlled test sit-
uations. This case report may be a useful guide for future studies of pa-
tients with clinically apparent word-deafness.
An even more recent study by Kanshepolsky, Kelly and Waggener
(1973) of a patient also with bilateral temporal lobe infarction, proven by
autopsy, demonstrated mild loss of acuity for pure tones, unilaterally im-
paired loudness discrimination and bilaterally deficient threshold-dura-
tion function. Tests of temporal ordering gave normal results. Speech
audiometry demonstrated severely impaired perception. This patient
spontaneously complained that he could hear but could not understand
the words.
Schuknecht and Woellner (1955) demonstrated that pure tone thresh-
olds may be normal with poor speech discrimination even in peripheral
involvement of the acoustic nerve (their patient had an acoustic
neurinoma). These studies appear to offer conclusive evidence that
normal or only slightly impaired pure-tone audiometric examinations do
not offer evidence against the contribution made by disordered primary
perception of auditory stimuli.
In discussing visual agnosias, Lissauer (1890) attempted to distinguish
between apperception, the conscious perception of sensation; and asso-
ciation, the analysis of perceptions in relation to meaning and other per-
ceptions. Bay’s studies (1950, 195 1) have demonstrated that under con-
ditions of reduced visual efficiency, subjects acted as if they suffered
visual agnosia. With the advent of sophisticated techniques for the
testing of auditory apperception, patients similar to those deseribed ear-
lier have been noted to show significant defects of audition. Even pa-
tients with the more common and widely accepted condition of sensory
aphasia have been found to have impaired auditory perception (Vignolo,
1960).
While it is not necessary to imply the presence of peripheral acoustic
apparatus deficits for the production of word-deafness, it is apparent that
recently reported cases have all shown definite apperceptive limitation
when carefully studied (Brown, Goldstein, and Hollander, 1972: Jerger,
Weikers, Sharbrough, and Jerger, 1970; Kanshepolsky, Kelly, and
Waggener, 1973). Perhaps further studies of the effects of central
nervous system lesions on the functioning of primary sensory perception
would be a profitable endeavor. The effects of disease limited to the
202 MARVIN N. GOLDSTEIN

cerebrum and more “peripheral ” sensory impairment need not be mutu-

ally exclusive.
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