BRAIN
AND
LANGUAGE
14, 235-271 (1981)
An Investigation of Repetition and Language Processing in a
Case of Conduction Aphasia
ALFONSOCARAMAZZA
The Johns Hopkins University
ANNAMARIA G. BASILI AND JERRY J. KOLLER
Fort Howard Veterans Administration
Medical Center
AND
RITA SLOAN BERNDT
The Johns Hopkins University
A study is reported of a single case of conduction aphasia. A battery of tasks
designed to investigate the parameters of the patient’s severe repetition deficit
is supplemented by tests of several language functions. The results provide
extensive information on a wide range of the patient’s language abilities and are
used to evaluate the adequacy of four models that have been offered to account
for conduction aphasia. An argument is made in support of the suggestion that
the syndrome of conduction aphasia should be divided into two subgroups based
on patients’ ability to select and realize phonemes in speech output. It is concluded that the best explanation for the disorder of patients with repetition deficit
but without significant speech output problems is the hypothesis that repetition
ability is compromised by a pathological limitation of auditory-verbal short-term
memory. This hypothesis is extended to account for the pattern of results obtained in the language tasks.
In 1874 Carl Wernicke predicted the syndrome of conduction aphasia
on the basis of his neuroanatomical
model of the distribution and interaction of language functions in the dominant hemisphere. Lichtheim’s
The research reported here was supported by NIH Research Grant 14099 to the Johns
Hopkins University. We would like to thank John Hart for designing the oral reading
tasks, and for his help in testing the patients on several of the tasks. We would also like
to thank Edgar Zurif for his helpful comments on an earlier draft of this paper. Address
reprint requests to Dr. Alfonso Caramazza, Department of Psychology, The Johns Hopkins
University, Baltimore, MD 21218.
235
0093-934X/81/060235-37$02.00/0
Copyright
0 1981 by Academic Press, Inc.
All rights of reproduction
in any form reserved
236
CARAMAZZA
ET AL.
(1884) clinical description of the first case of conduction aphasia provided
a verification of Wernicke’s prediction, as well as an elaboration of the
syndrome to include a deficit of repetition ability as a major symptom.
Numerous cases of conduction aphasia have been reported in the neurological and neuropsychological
literature since Lichtheim’s
original
report (see Benson, Sheremata, Bouchard, Segarra, Price, & Geschwind,
1973; Green & Howes, 1977). There now appears to be some agreement
that the lesion site in the left hemisphere associated with conduction
aphasia is the posterior third of the first temporal gyrus and the supramarginal gyrus, with possible involvement
of the arcuate fasciculus
(Benson et al., 1973). There is less agreement on the underlying functional
features: a marked and disproportionate
difficulty repeating spoken
words; relatively good comprehension
(on clinical testing) and fluent
speech; occasional word-finding difficulties; the occurrence of occasional
literal or verbal paraphasias; difficulties in spelling and writing; and some
problems with oral reading.
The explanation offered by Wernicke and Lichtheim for the clinical
features of conduction aphasia rests on the assumption that specific
components of language representation
(e.g., sound images) are organized in cortical centers that are connected to one another; language
functions such as speaking and comprehension
require the normal participation of these various cortical centers. Conduction aphasia was assumed to be a “disconnection”
syndrome in which Broca’s area (center
for articulatory
gestures) is severed from Wernicke’s area (center for
sound images), resulting in a dissociation of two components of a word.
Since Broca’s and Wernicke’s areas are presumably spared, the patient
should have normal comprehension and articulatory ability. His language
deficit should be restricted to occasional word choice difficulties in spontaneous speech and a disproportionate
problem with repetition (see also
Geschwind, 1965).
This view of conduction aphasia did not go unchallenged. Freud (1891)
and later Goldstein (1948) criticized Wernicke’s disconnection
model.
While accepting the existence of the clinical picture offered for conduction aphasia, Goldstein strongly disagreed on the interpretation
of the
mechanisms responsible for the deficit. He assumed that conduction
aphasia (which he renamed “central aphasia”) involved a disruption of
all speech perforthe mechanisms of “inner speech”; consequently,
mance should be affected to some extent, with repetition especially impaired. Hecaen and his collaborators have further refined and elaborated
Goldstein’s interpretation
of conduction aphasia to focus on the encoding
of inner speech forms into the motor output program (Dubois, Hecaen,
Angelergues, de Chatelier, & Marcie, 1964; Hecaen & Albert, 1978;
Hecaen, Dell, & Roger, 1955). Other interpretations
of conduction
aphasia have been offered that differ in important ways from the dis-
CONDUCTION
APHASIA
237
connection model (e.g., Alajouanine
& Lhermitte,
1964; Kinsbourne,
1972; Kleist, 1916). A feature shared by all of these hypotheses is that
the disproportionate
repetition deficit that is the cardinal feature of conduction aphasia is regarded as a symptom secondary to a more general
language deficit.
Over the last decade Warrington and Shallice have suggested that, at
least in some cases, the symptoms of conduction aphasia result from an
impairment
of auditory-verbal
short-term memory @TM) (Shallice &
Butterworth, 1977; Shallice & Warrington, 1970, 1974, 1977; Warrington,
Logue, & Pratt, 1971; Warrington & Shallice, 1969, 1972). In a series
of detailed analyses of several case studies, Warrington and Shallice
have provided compelling evidence and arguments to support this thesis.
A number of critical replies have been published (Kinsbourne,
1972;
Strub & Gardner, 1974, Tzortzis & Albert, 1974), and debate continues
over whether or not conduction aphasia should be considered primarily
a disorder of memory. This debate comprises the primary theoretical
focus of the studies reported here. The details of the STM-deficit
hypothesis, and the points raised by its detractors, will be discussed in
detail as the data are presented.
In this paper we report a case study of a relatively pure case of
conduction aphasia. After a brief presentation of the patient’s history
and his performance on various standardized tests, we will present some
data on his repetition ability. Discussion of repetition is followed by an
analysis of his ability to read, to comprehend, and to produce language.
An assessment of the patient’s performance on these latter language
functions is reported in order to evaluate the hypothesis that the repetition deficit in this patient is secondary to a language processing disorder.
Stated differently, a detailed picture of the patient’s language and repetition performance is necessary in order to impose reasonable constraints on a model of conduction aphasia.
CASE HISTORY
MC is a black male who was 58 years old at the time this study was
initiated. He is a high school graduate who was employed for 30 years
as a machinist. In June of 1976 MC suffered a left-cerebrovascular
accident, which resulted initially in a mild right-sided hemiparesis and
“moderately
severe mixed aphasia.”
The patient was followed as an outpatient in the Department of Audiology and Speech pathology at the Fort Howard Veterans Administration Medical Center, and by the summer of 1978 he had progressed
to a condition in which his overall language functions were judged to be
only mildly impaired on clinical testing. He was classified at that time
as a conduction aphasic on the basis of the Boston Diagnostic Aphasia
Examination
(Goodglass & Kaplan, 1972).
238
CARAMAZZA
ET AL.
Audiological examination revealed a mild conductive hearing loss, with
residual capacities judged to be adequate for speech. MC’s visual acuity
is corrected, with no visual field impairments.
On first impression, MC’s language disability appears to be minor. He
is attentive in social situations and seems to communicate
without difficulty in casual conversation.
However, close scrutiny of his verbal
output in structured conversation reveals moderate word-finding difficulties and occasional paragrammatism.
MC’s comprehension
of sentences is quite impaired when assessed rigorously, and, of course, he
exhibits a striking inability to repeat words presented aurally. Results
of some standard clinical tests are presented in Table 1. It is evident
that MC’s comprehension
of single words (Peabody; BDAE Word Discrimination
and Body Part Identification
subtests) is spared relative to
his comprehension of sentences (Token Test; BDAE Commands subtest).
Other subtests of the Boston Diagnostic rule out his classification as a
Wernicke’s or an anemic aphasic.
CT scan reveals a focal lesion in the left posterior and superior temporal
PERFORMANCE
Boston Diagnostic Aphasia
Examination,
5178
OF PATIENT
TABLE 1
MC ON STANDARD
Peabody Picture
Vocabulary Test,
7/76 (Form B)
TESTS
Auditory comprehension
64179
15120
6/S
8/12
z = +.5
o<z< + .5
- l.O<z< - .5
o<z< + .5
Naming
Responsive naming
Confrontation naming
Animal naming
Body part naming
16/30
88195
9
23130
.5<z<I.O
z = +.5
z = +.5
Oral reading
Word reading
Sentence reading
30130
lO/lO
z = +1.0
z > +1.0
9/10
118
018
z= +.5
z = -1.0
z = -1.0
Word discrimination
Body part identification
Commands
Complex material
Repetition
Words
High-probability
Low-probability
Token Test,
2178
CLINICAL
Subtests
1
7
sentence
sentences
II
3
Raw score = 106
III
2
IV
2
v
1
Percentile = 41
z=o
CONDUCTION
APHASIA
239
and inferior parietal regions, with extensive involvement
of the white
matter in this region. This lesion is consistent with the classical and
widely accepted neuroanatomical
correlate of conduction aphasia (see
Benson et al., 1973).
The patient lives alone, independently,
and has worked occasionally
as a janitor since his illness. His primary activities are reading, visiting
libraries and museums, and watching television.
REPETITION
TASKS
The extent and nature of MC’s repetition deficit was assessed by a
set of tasks that was designed to address two broad sets of issues. First,
it was necessary to establish that MC’s repetition performance was comparable to the recent case reports that have provided the data base for
the interpretation
of conduction aphasia as an auditory-verbal
STM disorder. Second, the tasks were designed to address a number of specific
issues that have assumed considerable prominence in recent discussions
of conduction aphasia: (1) whether the repetition difficulties in conduction
aphasia are better characterized as a “reproduction”
or a true repetition
deficit; (2) the effect of modality of input (auditory/visual)
on the repetition deficit; and (3) whether the repetition defect is related only to
memory load (list length) or is importantly affected by the type of verbal
material that comprises the list or memory set.
Repetition
of Digits
under Different
Recall Delays
The first task employed the serial recall Brown-Peterson
test procedure, using digits as the items to be recalled. List lengths of one, two,
and three digits were presented at an item rate of approximately
one per
second under several conditions of delay (0, 3, 6, 9, and 12 set). The
digits from 1 to 9 comprised the test items. The only constraint on the
composition of the lists was that no item was repeated within a list. In
the conditions with delay, rehearsal was prevented by having the patient
name a random series of colors as the examiner pointed to a number of
colored blocks. Twenty trials of each of the delay conditions were
blocked by list length, and each condition was presented once in a visual
and once in an auditory mode. The results, expressed as number of
correctly-repeated
digit strings, are presented in Table 2.
There are three aspects of these data that should be emphasized. First,
there is a major effect of mode of presentation:
MC’s performance,
summed over list lengths and delay conditions, shows that he could
correctly repeat 200 items (67%) in the visual mode of presentation but
only 117 (39%) in the auditory mode. Indeed, it appears that MC’s
memory span for auditory material is reduced to one item, while it may
be two items long for visual input. Second, there is a clear effect of list
length, or memory load, on repetition performance: MC’s memory span
240
CARAMAZZA
NUMBER
OF
ET AL.
TABLE 2
Dlclr LISTS REPEATED
IN CORRECT
ORDER
Delay (set)
List
length
0
3
6
9
12
Auditory
presentation
1
2
3
19
8
3
15
7
2
13
8
2
16
5
0
13
6
0
Visual
presentation
1
2
3
20
19
11
18
18
7
16
14
3
18
17
5
19
12
3
Note. Maximum
score for each condition
= 20.
is at best two items long. Third, though it is not dramatic, there is some
decline in correct performance with increasing delay of recall.
To examine further the locus of the repetition defect, the total number
of correct items repeated was calculated independently
of whether an
entire string was repeated correctly. The data for the three-digit lists are
presented in Table 3.
The most striking feature is the clear serial position effect (a primacy
effect) in correct item recall as a function of delay. Recall of the first
position item is quite good, but there is a major drop in performance for
the last item; there is absolutely no indication of a recency effect.
The repetition performance of our patient parallels that of conduction
aphasics described in recent reports by other investigators (e.g. Kinsbourne, 1972; Shallice & Warrington, 1977; Strub & Gardner, 1974). This
type of repetition performance, when present with other symptoms, has
been interpreted as consistent with a number of different theories of
TABLE
NUMBER
OF DIGITS
REPEATED
WITHOUT
3
RESPECT
TO ORDER
Auditory
presentation
(THREE-DIGIT
Visual
presentation
Position
correct
Delay (set)
0
3
6
9
12
Total
1 2 3
(37)
(33)
(37)
(25)
15-11-11
15-ll7
16-11-10
11- 7- 7
12- 9- 4
(25)
Note. Maximum total score for each condition
LISTS)
Position
correct
Total
1 2 3
(53)
18-16-19
19-19-14
17-14-l 1
16-15-12
16-15- 9
(52)
(42)
(43)
(401
= 60.
CONDUCTION
APHASIA
241
conduction aphasia. In order to motivate more clearly the other tasks
employed, we will briefly discuss the major theories of the repetition
deficit in conduction aphasia by analyzing how each of these would
explain the data reported thus far.
Three major classes of explanation have been offered for the repetition
deficit in conduction aphasia. One type of explanation is a variant of the
classical disconnection theory (Wernicke, 1874; Lichtheim, 1884; Geschwind, 1965; Kinsbourne, 1972). Within this argument, the repetition disorder results from a failure to transmit verbal information
adequately
from a short-term store to the output mechanisms. Auditory input is
processed normally, and STM representations are unimpaired. Transfer
of information
from short-term to long-term memory (LTM), and language comprehension,
are also said to be unaffected.
In Kinsbourne’s
explanation of the repetition defect, the disorder
“ . . . has to be attributed to a communication
channel with pathologically
limited capacity” (1972, p. 1131). Kinsbourne accounts for the other
features of conduction aphasia by invoking a neuroanatomical
explanation originally offered by Kleist (1916), in which the observed symptoms reflect the underdeveloped
linguistic functioning of the right hemisphere which has been released from inhibition as a result of damage
to the dominant left hemisphere.
The disconnection model has little difficulty explaining the well-known
digit repetition results that we have replicated here. In the auditory input
condition, the conduction aphasic can adequately process the input and
store it in STM. He has difficulty when required to recall the digits,
however, because information is not flowing normally from the storage
buffer to the output mechanisms. The model can easily explain the decline
in performance with increasing delay of recall by assuming a natural
decay function in memory. One aspect of the repetition data that the
disconnection model has some difficulty explaining is the superior performance obtained in the visual input condition. To account for this
result, the model must assume that information from a visual store can
directly communicate with the speech output mechanism. This assumption is explicitly made by Kinsbourne, but it is not clear how lexical-visual
information specifies the phonemic structure of lexical items so that the
speech output mechanism can be activated for repetition. In other words,
at some point in the process of repetition the visual-lexical
input must
be translated into an auditory-verbal
representation to serve as a model
for the required speech response. This is an important issue that needs
considerable elaboration if the model is to be taken seriously.
A second class of explanations of conduction aphasia was inspired by
Goldstein’s critique of the disconnection model and his suggestion that
the syndrome represents a disturbance of “inner speech”-the
representation of word concepts. Goldstein’s own account of conduction
242
CARAMAZZA
ET AL.
aphasia is not sufficiently specific to motivate an explanation of recent
data, but Hecaen’s elaboration of Goldstein’s model has been applied
to that purpose (Dubois et al., 1964; Hecaen et al., 1955; Tzortzis &
Albert, 1974; Yamadori & Ikumura,
1975). The central assumption in
this work is that the repetition deficit and other symptoms of conduction
aphasia result from a disturbance of “the first articulation”-the
mechanisms that transform an abstract acoustic mode1 or, more generally,
abstract lexical representations, into the phonological forms that in turn
guide the phonetic, articulatory,
and graphemic mechanisms of speech
output.
There are two variants of Goldstein’s general formulation that can be
distinguished on the basis of where in the chain of processing the exact
locus of impairment is to be situated. Dubois et al. (1964), Yamadori and
Ikumura (1975), and Tzortzis and Albert (1974) locate the deficit directly
at the level of encoding the phonological targets for output (henceforth,
the “encoding deficit” model). Strub and Gardner (1974) argue that the
deficit is at the level at which the abstract representation that guides the
selection of phonological
forms is constructed from a decoding of the
auditory input (henceforth, the “decoding deficit” model).
As in the case of the classical model, these newer theories can account
for the repetition deficit traditionally
found in conduction aphasia. The
encoding deficit model assumes that the patient can adequately process
both visual and auditory input but that the internal representation constructed from these inputs cannot be readily encoded for output purposes
because of a disruption of the output programming
mechanism. It assumes further that as the input becomes more complex, the strain on
the encoding device produces not only errors of omission and paraphasias, but also ordering problems in which the elements of a string
are encoded in the wrong order. This model explicitly addresses an
aphasic symptom that is assumed to be an important component of
conduction aphasia: phonemic paraphasias. It completely fails, however,
to provide an explanation of the superior repetition of words presented
visually.
The decoding deficit mode1 argues that the repetition deficit in conduction aphasia is the result of reduced efficiency in decoding speech,
which places various levels in the decoding process in competition
for
limited processing space. This model has the advantage of being able to
explain subtle comprehension
deficits that can be found in conduction
patients. As in the case of the encoding deficit model, however, it fails
to offer a motivated account for the disparity in repetition performance
for the visual and auditory input conditions.
The most thoroughly developed mode1 of the repetition disorder found
in conduction aphasia is the auditory-verbal
STM deficit mode1 proposed
by Warrington and Shallice (1969). This mode1 assumes that the repetition
CONDUCTION
243
APHASIA
deficit is not secondary to a disturbance of specifically linguistic mechanisms. Rather, the impairment
is a reduction of auditory-verbal
STM
capacity to a memory span that is much reduced from the normal storage
capacity of approximately
seven units of information (Miller, 1956).
This model can account for repetition performance in the auditory
condition; more importantly,
the superior performance for the visual
input condition can be explained by assuming that a visual STM store
is functioning normally. This model can also handle quite naturally a
number of interesting aspects of the repetition data and other types of
memory performance. For example, it correctly predicts that conduction
aphasics should be able to make effective use of long-term memory in
repetition tasks because semantic information can be entered directly
into LTM without the necessity of short-term storage. Finally, this model
assumes that aphasic symptoms associated with conduction aphasia are
secondary to the STM deficit. For example, the comprehension
difficulties found in these patients reflect the inadequate support of a working
memory system during sentence parsing and interpretation.
These issues
will be discussed further below.
Now that we have presented the three classes of models that have
been proposed to account for the repetition disorder in conduction
aphasia, we can evaluate each of them by considering our patient’s
performance on several repetition and recognition tasks.
Single-Item Probe (Recognition
Task)
This task was designed to assess MC’s STM without requiring him to
retain serial list information or to repeat the items in the list. A memory
probe technique was used that was similar to that employed by Shallice
and Warrington (1970). A four-item list was read, followed by a singleprobe item, and the patient was to say whether the probe item had been
part of the list. One hundred sixty lists of concrete nouns were prepared
and the probe item was part of the list on half the trials. The patient’s
task was to decide whether the probe item was contained in the list he
had just heard. The number of correct responses for each serial position
probed (out of a possible 20 correct) is shown in Table 4.
The overall rate of performance (74% correct) was comparable to the
TABLE
NUMBER
OF CORRECT
Number
correct
Note. Maximum
RESPONSES
TO SINGLE
4
ITEM
PROBE
FOR EACH
SERIAL
POSITION
1
Serial position
2
3
4
17
11
14
17
score for each position = 20.
244
CARAMAZZA
ET AL.
performance of Warrington
and Shallice’s patient KF (76% correct).
Importantly,
there appears to be a serial position effect for both primacy
and recency items. What should be emphasized about these results is
that, although MC’s performance here is superior to his performance in
recall tasks (see next experiment), it is nonetheless markedly impaired.
This suggests that, for MC as well as for KF, the STM representation
for a four-item list is not normal.
The results of this experiment are consistent neither with the disconnection model nor with the encoding deficit explanation of the repetition
deficit. Both of these assume that the input is processed adequately and
that a normal internal representation of the input string is constructed.
The decoding deficit model and the auditory-verbal
STM model can
easily accommodate the results of this experiment because both predict
that the internal representation of the input string should not be normal.
The first two experiments have established that MC has a profound
repetition deficit that cannot be explained as a disconnection or as an
encoding disorder. MC’s performance on the repetition task is qualitatively identical to the cases reported by Warrington and Shallice (1969),
Saffran and Marin (1973, Tzortzis and Albert (1974), Strub and Gardner
(1974), and Kinsbourne (1972). Interestingly however, Kinsbourne’s two
cases had a remarkable list recognition ability that contrasted sharply
with their repetition performance. The recognition ability of these patients presents a striking contrast to the performance of Warrington and
Shallice’s patient and to that of MC. This discrepancy will be considered
further in the Discussion.
Repetition of High-Frequency
Function Words
Nouns, Low-Frequency
Nouns and
One of the characteristics of repetition performance that Warrington
and Shallice have interpreted as support for the STM disorder hypothesis
is that their patient’s ability to repeat items appears to be related to the
length of the list rather than to the types of items in the list. This argument
is at variance with the widely reported clinical observation that conduction aphasics have considerably more difficulty repeating the grammatical function words-articles,
auxiliaries,
conjunctions,
etc.-than
repeating nouns (e.g. Goodglass 8z Kaplan, 1972). If this clinical observation is correct, it could be a source of difficulty for the STM hypothesis,
as well as for the decoding deficit hypothesis. In this experiment,
we
tried to quantify the reported clinical impression of a differential repetition impairment
as a function of list material.
Three types of words were used: high-frequency concrete nouns, lowfrequency concrete nouns, and function words. The two noun sets contained an equal number of one-, two-, and three-syllable words. The
experimental
paradigm used was the Brown-Peterson
serial recall pro-
CONDUCTION
APHASIA
245
cedure with 0- and 9-set delays. List lengths were one, two, three, and
four words presented at a rate of approximately
one item per second in
25-list blocks. There were separate auditory and visual presentation conditions. Results for this task (number of correct lists recalled) are shown
in Table 5.
Three aspects of these data should be emphasized. First, as in Experiment 1, there is a marked effect of mode of presentation, with the
visual condition superior to the auditory condition. Second, there is a
slight effect of frequency, with high-frequency nouns recalled better than
low-frequency nouns in the visual presentation condition. Third, and
most important. is the difference in the patient’s ability to recall function
words relative to nouns in the two modes of presentation. MC had serious
difficulty recalling even a single function word when these words were
presented aurally; when they were presented visually he could recall
them as well as nouns in both the immediate and the delay conditions.
To obtain a more precise assessment of MC’s repetition performance,
we analyzed item recall independently of serial recall performance. These
data (in the form of percentage of total items correct without regard to
whether they were recalled in the correct order) are presented in Tables
6 (three-word lists) and 7 (four-word lists). The data are averaged over
delay conditions, where relevant, as no appreciable differences were
obtained as a function of delay. These data replicate in part the results
obtained in Experiment
1. More importantly,
they show an effect of
word frequency that is considerably stronger in the visual than in the
auditory presentation condition. A further aspect of these data to be
emphasized is the very small number of function words recalled in the
auditory condition: 15 and 7% for the three- and four-item lists, respectively.
The data from this experiment were reanalyzed to address the issue
of whether item repetition performance was a function of the number
of syllables in the words to be repeated. A number of investigators have
reported that some conduction aphasics have more difficulty repeating
long than short words (Dubois, et al., 1964; Yamadori & Ikumura, 1975).
This form of deficit (termed a “reproduction”
disorder) is necessarily
predicted by both the disconnection and the encoding deficit models,
although it is not inconsistent with any of the hypotheses that have been
offered. Shallice and Warrington (1977) have suggested that a reproduction problem may reflect a different type of disorder than the classic
repetition deficit and that we should treat patients with these two types
of symptoms separately. To determine whether MC’s repetition difficulties were primarily a reproduction disturbance, we analyzed repetition
of high-frequency nouns in the auditory presentation condition as a function of syllable length. Table 8 presents these data for words of one,
two, and three syllables in the form of proportion of correct items recalled. It is immediately
clear that there were no appreciable differences
1
Visual
presentation
25
25
13
I
111
1
22
Hi-freq.
nouns
25
25
5
0
141
0
21
Low-freq.
nouns
AND
24
20
I
0
01
0
13
Functors
NOUNS
FUNCTION
1
2
3
4
23
4
1
List
length
(words)
WORDS)
TABLE 5
LISTS REPEATED IN CORRECTORDER
24
18
7
0
1
0
NT 0
NT
12
Functors
23
16
NT
1
25
21
4
2
130
24
Low-freq.
nouns
142
24
Hi-freq.
nouns
Delay (9 set)
No&. Maximum score for each condition = 25.
” Patient was nor rested on a condition if he failed to produce at least one correct repetition of the preceding list.
2
3
4
23
4
I
presentation
Auditory
List
length
(words)
No delay
NUMBER
OF
(CONCRETE
F
2
F
P
$
$
CONDUCTION
TABLE
PERCENTAGE
OF WORDS
REPEATED
CORRECTLY
(THREE-WORD
247
APHASIA
6
WITHOUT
RESPECT
TO CORRECT
ORDER
LISTS)
Percentage serial
position correct
Total percentage
correct
3
Nouns
Auditory presentation
Frequency
High
Low
Mean
percentage
correct
Visual presentation
Frequency
High
Low
Mean
percentage
correct
Auditory presentation
Visual presentation
49
49
78
78
38
38
30
32
49
78
38
31
71
53
72
78
64
52
78
30
62
75
58
54
32
72
8
58
4
50
Function words
I5
60
in repetition as a function of syllable length. This result strongly suggests
that MC’s difficulties in repetition should not be characterized as a disorder of reproduction.
Several aspects of the results of this experiment are inconsistent with
the disconnection,
the encoding and the decoding deficit hypotheses.
None of these models can explain the superior performance for visually
presented lists or the fact that function words were very poorly repeated
in the auditory, but not in the visual, condition.
The STM deficit hypothesis successfully predicts the advantage of
visual input, but appears to have some difficulty explaining other aspects
of these results. First is the observation that a frequency effect was
obtained in the visual rather than in the auditory condition. Warrington
and Shallice have argued that recall in the auditory input task consists
primarily of information
from LTM, whereas recall in the visual input
task is from an undamaged visual STM in addition to LTM. By this
reasoning, it is expected that the frequency effect (which reflects information coming from LTM) should be most strongly manifested in the
auditory mode condition.
However, our results showed the opposite
effect: a greater effect of frequency in the visual condition.
248
CARAMAZZA
TABLE
PERCENTAGE
OF WORDS
REPEATED
CORRECTLY
ET AL.
7
WITHOUT
RESPECT
TO CORRECT
ORDER
(FOUR-WORD LISTS)
Percentage serial
position correct
Total percentage
correct
1
2
3
4
42
32
76
76
48
32
20
4
24
16
39
76
43
I5
21
63
39
70
68
66
28
44
24
72
34
50
69
47
34
53
Function words
7
12
37
68
8
46
4
24
4
8
Nouns
Auditory presentation
Frequency
High
Low
Mean
percentage
correct
Visual presentation
Frequency
High
Low
Mean
percentage
correct
Auditory presentation
Visual presentation
Perhaps a more disturbing result is the effect of presentation mode
(visual vs. auditory) on the patient’s repetition of function words relative
to nouns. MC’s ability to repeat function words when presented aurally
is severely limited. This limitation
cannot be attributed to an ordering
output problem (Tzortzis & Albert, 1974), since MC had difficulty repeating even single-word lists of function words (see Table 5). It appears
TABLE
PROPORTION
8
OF THREE-,
Two-,
AND ONE-SYLLABLE
HIGH-FREQUENCY
CORRECTLY
(AUDITORY
PRESENTATION,
~-SEC DELAY)
NOUNS
REPEATED
Number of syllables
List length
(words)
1
2
3
4
Mean proportion
correct
3
2
1
1.0
1.0
.50
.85
I.0
.88
.56
.48
1.0
.88
.72
.38
.78
.63
.65
CONDUCTION
249
APHASIA
that the form of the representation that MC can construct for aurally
presented words is particularly impoverished for function words.
Warrington and Shallice have argued that “a reduction in all auditory
verbal span tasks, performance being related to the ‘string’ length rather
than the characteristics of individual speech sounds, is prima facie evidence of an impairment
of the short term memory store” (Warrington
et al., 1971, p. 385). Since our patient’s repetition performance was
significantly affected by the type of stimulus material presented, we must
consider whether the STM hypothesis can be interpreted to accommodate
this result. For example, it might be argued that, unlike nouns, function
words lack clear (nonsyntactic) meaning when presented without a sentence context and that they are, therefore, not processed as fully as
nouns. Under such circumstances, the LTM representation for function
words is not developed or is developed poorly. The lack of a welldeveloped LTM representation would force the patient to recall function
words strictly from STM, which is impaired, thus leading to the severely
impoverished
repetition performance. This is not an implausible line of
reasoning, and it leads to a testable prediction: when function words are
used in the normal syntactic role they should receive adequate “semantic” analysis to produce a strong LTM representation. That is, recall
of function words should improve when they are embedded in phrasal
contexts.
Repetition of Phrases
To test this prediction, we asked MC to repeat ten function word/noun
phrases. Each phrase was read slowly but with normal intonation. As
shown in Table 9, MC repeated correctly all ten nouns, but only one
function word. He was fully aware that two words were presented on
each trial, and he even seemed aware of the fact that the first word was
TABLE
REPETITION
Stimulus
item
The gun
in bed
a dog
among friends
between cars
at home
few people
under blankets
up ladders
some flowers
OF FUNCTION
9
WORD/NOUN
PHRASES
Patients’
responses
-gun
in bed
--dog
(“dog . . . dog
on friends
beneath cars
on home
-people
“und” blankets
on ladders
on flowers
something dog”)
250
CARAMAZZA
ET AL.
a function word. The incorrect function words he produced were articulated normally. It should be emphasized here that MC’s problem with
function words is a repetition-induced
pathological behavior; in conversational speech and writing he uses function words in a relatively normal
way.
The assumption motivating this experiment was that function words
used in a syntactic context would receive semantic processing that would
result in an adequate LTM trace that could be used to aid repetition.
It is possible that the manipulation
employed here (isolated two-word
phrases) did not in fact lead to a more effective semantic analysis of
function words. Alternatively,
it may be that function words do not in
general receive a semantic analysis and that there is no condition in
which repetition of function words could rely on an LTM component.
If either of these alternatives is true, this experiment was not a fair test
of the STM-deficit
hypothesis.
Finally, it should be noted again that the results obtained in this and
in the previous experiment are not consistent with any of the hypotheses
that have been offered to explain conduction aphasia. That is, predictions
about differential
repetition performance as a function of form class
distinctions do not follow naturally from any of these hypotheses as they
were originally formulated.
Repetition
of Nouns with h4anipulations
of Delay
The last experiment in this section was designed to assess the effects
of two other presentation parameters on repetition performance to allow
further distinctions among the four hypotheses concerning the nature of
conduction aphasia. One question was whether allowing the patient to
rehearse the input (unfilled delay condition) would improve his performance relative to performance in a condition in which rehearsal was
blocked by an extraneous task (filled delay). The other issue explored
was the effect of rate of presentation on the patient’s repetition. If impaired repetition is based on the patient’s inability to encode the items
for output (encoding deficit hypothesis), these input manipulations
should
have little effect on performance.
Three conditions were employed, all using 25 three-word lists composed of high-frequency nouns. In one condition the patient was presented aurally with the three-word lists at a rate of one item per second
and a filled, 9-set delay preceded recall of the list. The distractor task
was, as in previous cases, the rapid naming of colored blocks. The second
condition was identical to the first except that no distractor task was
interspersed between the presentation of the list and the point of recall.
That is, the patient was allowed to rehearse the list for 9 set prior to
recall. In the third condition, items were presented at the rate of one
CONDUCTION
251
APHASIA
every 3 set, and an unfilled delay of 3 set was introduced between the
third item and the point of recall. Thus, the time between the presentation
of the first item and recall was about equal for the three experimental
conditions, but the potential for rehearsal was varied.
Table 10 presents the number of serially correct lists recalled, the total
number of items recalled, and the number of items recalled for each
serial position for the three conditions. The total number of words recalled is about equal for each condition. However, there are clear interactions of delay condition by number of serially correct lists recalled,
and of delay condition by serial position of items recalled. From these
results it appears that the major effect of preventing rehearsal is on serial
recall performance, whereas rate of presentation most clearly affects the
serial position of items recalled.
The results of this experiment present insurmountable
difficulties for
the encoding deficit hypothesis. This model assumes that the locus of
the disorder is in the encoding of a relatively well-constructed and wellpreserved internal representation into a phonological string for output.
However, as a comparison of the filled and unfilled delay conditions
indicates, serial recall performance is a function of differential forgetting
of order information from STM due to the prevention of rehearsal. Furthermore, the encoding deficit hypothesis fails to provide a motivated
account for the recall of items from different serial positions in the
unfilled delay condition and the slow rate of presentation condition.
Consideration of these two tasks suggests that item recall as a function
of serial position is determined by some input variable that affects the
form of the internal representation and is apparently unrelated to any
hypothesized disruption of the encoding mechanism. It should be emphasized that these differences in serial position performance occur in
TABLE
NUMBER
OF HIGH-FREQUENCY
10
NOUNS
RECALLED
CONDITIONS
(THREE-WORD
AS A FUNCTION
LISTS)
OF THREE
DELAY
Serial position
correct
Delay condition
9 set,
with distractor
9 set,
no distractor
3 set,
between items
Seriallv correct
lists
Total words
correct
1
2
3
2
46
22
14
IO
8
48
21
17
10
8
51
16
17
18
Note. total number of lists for each delay condition
= 25
252
CARAMAZZA
ET AL.
the context of equal performance in serial recall and total item recall.
This pattern of performance cannot be explained by assuming a disruption
at the level of the encoding of output.
The disconnection hypothesis has comparable difficulty accounting for
the pattern of results we have reported. That is, this hypothesis also fails
to predict the interactions for the two comparisons we have made above.
Both the STM and the decoding deficit hypotheses are successful in
accounting for one of the interactions between conditions, but both fail
to account for the other comparison. In order to discuss the predictions
made by the STM hypothesis we need consider in more detail Shallice
and Warrington’s
model (1970). This model assumes that there are parallel inputs into STM and LTM, as well as a “rehearsal loop” that
provides a means for keeping information “active” in STM. Shallice and
Warrington argue that the repetition deficit results from a pathological
limitation
of the short-term store, but this limitation
should not prevent
the “normal”
functioning of the rehearsal circuit. The fact that rehearsal
is possible, though perhaps with reduced efficiency, allows the generation
of fairly normal LTM representations
of lists that do not exceed the
capacity of the impaired short-term store in conditions that allow for
rehearsal. One prediction that follows from this is that there should be
a different pattern of serial position recall as a function of rate of presentation. In the condition with delay between items, the patient can
presumably rehearse each word sufficiently to achieve an adequate LTM
representation.
When items are presented more rapidly, the patient cannot make efficient use of the rehearsal system and the later items on the
list are processed inadequately for LTM storage.
A similar prediction,
based on different principles, is made by the
decoding deficit hypothesis. This model assumes that in the slow presentation condition each item can be processed adequately; in contrast,
in the rapid presentation condition the inefficient decoding system cannot
process to a sufficient extent the later items in the list. Thus, both
hypotheses successfully predict a different pattern of serial position results for the rate of presentation contrast.
Although these two hypotheses correctly predict a difference in serially
correct performance for filled and unfilled delay conditions, they encounter difficulties with the serial position data. Specifically, both of
these hypotheses predict a recency effect for the unfilled delay condition.
In the case of the STM hypothesis, a recency effect is predicted by the
assumption that the rehearsal system is normal and thus the last item
should receive normal rehearsal. The decoding deficit hypothesis similarly assumes that the last item before the unfilled delay should receive
“deeper” processing than the last item in the filled delay condition since
there is no interfering process to block the “deeper” processing needed
for good recall.
CONDUCTION
Both hypotheses can account for the major portion
but neither explains the entire pattern.
DISCUSSION
253
APHASIA
OF REPETITION
of these results,
TASK RESULTS
There are four major features that characterize MC’s repetition abilities
in the tasks we have presented to him. Two of these features have also
characterized the recent cases of conduction aphasia reported in the
literature-severely
restricted memory span and superior repetition of
visually relative to aurally presented material. A third aspect of MC’s
repetition performance distinguishes our case from some of the other
cases reported. Specifically, MC has no deficit in the fluency of his
speech; he could repeat three-syllable words about as well as he could
repeat monosyllables (see Table 8). In this respect he is similar to cases
KF and JB reported by Warrington and Shallice, and case IL reported
by Saffran and Marin. All of these cases clearly differ, however, from
the cases reported by Kinsbourne, by Dubois et al., and by Yamadori
and Ikumura, all of whom were described as having considerable difficulties in the “reproduction”
of presented targets. Finally, MC presented
an exaggerated deficit in repetition of aurally presented function words
in comparison to nouns, but no differential effect of form class when the
items were presented visually. Although this particular pattern of deficits
involving form class distinctions has not previously been reported in
case studies of conduction aphasia, it is not unexpected when we consider
the clinical descriptions of that disorder (e.g. Goodglass & Kaplan, 1972).
Shallice and Warrington (1970) have made an attempt to distinguish
between subgroups of patients having difficulty with repetition: one group
can be said to have a disorder of “reproduction,”
and they have particular difficulty with multisyllabic
words; the other subgroup is characterized by a “pure” repetition deficit that is less affected by the number
of syllables in the words that are to be repeated (See also Luria, 1976).
This distinction is heuristically valuable in that it provides the opportunity
for formulating theories of cognitive disorders for relatively homogeneous
populations of patients. Shallice and Warrington argue that the classification “conduction
aphasia” should be restricted to those patients
whose spontaneous and imitative speech output is clearly paraphasic,
and whose repetition difficulties are based on a deficit of speech reproduction. Patients who have comparable difficulty repeating long and short
words, and whose spontaneous and imitative speech is not paraphasic,
should be classified as patients with an STM deficit, rather than as
conduction aphasics.
We agree with Shallice and Warrington that the patients who have
been described as conduction aphasics do not constitute a homogeneous
group. It is clear that the two cases reported by Kinsbourne, for example,
are different from our case and from the cases reported by Warrington
254
CARAMAZZA
ET AL.
and Shallice. From the clinical description that Kinsbourne presents, his
patients appear to have lesions in the anterior language regions, whereas
our case presents the classically established parietal-temporal
involvement. In addition, Kinsbourne’s
two cases had the remarkable ability
to discriminate identical pairs of eight item lists from nonidentical pairsan ability that appears to rule out an STM impairment. MC’s performance
is significantly inferior, as he achieved only a 75% level of accuracy in
a single item probe of a four-word string (see also Shallice & Warrington,
1970). The patients described by Tzortzis and Albert and by Yamadori
and Ikumura also appeared to have difficulties with the reproduction of
speech. Indeed, a major factor underlying the formulation of the encoding
deficit hypothesis was the presence of literal paraphasias in their patients’
speech.
It must be noted that the distinction drawn here is not an easy one
to make-MC,
as well as Strub and Gardner’s patient LS, produced
occasional paraphasias in spontaneous speech. Nonetheless,
the neuroanatomical
and behavior discrepancies apparent in the recent case
reports strongly support Shallice and Warrington’s
efforts to narrow
discussion to more homogeneous cases.
Considering the distinctions drawn above, it would appear that MC’s
performance should be classified as a relatively pure repetition disorder.
The experimental results presented here indicate that the source of MC’s
impairment cannot be attributed to the classically defined disconnection
of the language areas, nor is it possible to attribute it to a disorder of
the “first articulation”
as defined by Dubois et al. (1964) and further
developed by Tzortzis and Albert (1974) and Yamadori and Ikumura
(1975). Rather, it appears that MC’s repetition defect is based on a
disruption of the memory trace that serves as a model for repetition. The
evidence for this assessment consists of the following features of MC’s
performance. First, the results of the memory probe task clearly indicate
that his memory representation for a four-item list is seriously impaired.
Second, the experimental
parameters that affected MC’s repetition performance (e.g., rate of presentation, the prevention of rehearsal during
delay, etc.) were primarily factors that determine the form of the internal
representation
that is constructed upon the presentation of the to-berepeated material. Third, differences in repetition performance as a function of mode of input suggest a specifically auditory storage deficit.
Fourth, the differential effect of form class on repetition indicates that
an inadequate representation
is constructed for function words when
they are presented aurally.
Although the results suggest that our patient’s disorder should be
considered as occurring at the level of memory representation, the precise
nature of this disorder is far from clear. Specifically, such a disorder
could result from several sources, including the pathological limitation
CONDUCTION
APHASIA
255
of capacity in the short-term store suggested by Warrington and Shallice,
or the decoding deficit offered by Strub and Gardner.
The first two of the results summarized above can be accommodated
equally well by the decoding deficit hypothesis and by the STM-deficit
hypothesis. The third finding-superior
repetition of visually presented
material-is
naturally predicted by the STM deficit hypothesis but not
by the decoding deficit view. Strub and Gardner have argued that there
may be an alternative route for processing visual information,
but this
“explanation”
is not motivated by any independent considerations.
If
this account is accepted, however, it implies that visual processing in
all tasks should be superior to auditory processing. This is an important
point to which we shall return.
The fourth result-disproportionately
impaired repetition of aurally
presented function words-is
not easily accommodated
by either the
STM deficit or the decoding deficit hypothesis. We have suggested that
the representation of function words is particularly affected in the case
of disordered memory representation because these words have little
semantic information
to supplement the short-term representation that
is presumably coded phonologically.
Although these arguments can reasonably be made, they considerably expand both hypotheses as they
were originally formulated.
At this point we may want to reassess whether a unitary deficit hypothesis can account for the observed pattern of deficits in even a single
conduction patient. This need for a reassessment becomes even more
pressing if we broaden the scope of our explanatory theories to include
aphasic symptoms in addition to the repetition defect. Thus, for example,
how do the decoding and the STM deficit hypotheses account for the
very poor performance of our patient, the patient of Strub and Gardner,
and those of Warrington and Shallice on the Token Test? How is the
STM deficit in Shallice and Warrington’s case KF related to that patient’s
reported reading disorder (Shallice & Warrington, 1975)? Does the fact
that our subject does not share KF’s reading deficit have any bearing
on the issue of whether a similar disorder characterizes these two cases?
In order to characterize fully a patient’s disorder, it is of paramount
importance to analyze his performance not only on the major symptom
of interest but also on related behaviors. Broadening the focus beyond
the most readily apparent deficit serves two important functions: first,
it helps distinguish among the cases that are taken to be clear instances
of a syndrome; and second, a careful analysis of the patterns of cooccurrences of symptoms should importantly
constrain the development
of theories of aphasia. By assessing patients’ abilities on a wide range
of tasks, we may avoid the real danger of selecting the symptoms to fit,
rather than to inform, our theories.
256
CARAMAZZA
ET AL.
LANGUAGE TASKS
In an effort to provide a comprehensive picture of our patients’ aphasic
symptoms, we tested MC’s language performance in four areas: oral
reading, speech production, sentence comprehension (auditory and visual), and sentence construction
(anagram). These particular language
functions were tested in order to obtain information comparable to that
available on some of the other reported cases of “conduction
aphasia”
(e.g., KF on oral reading); to explore more fully MC’s difficulties with
function words; and to obtain a relatively precise assessment of MC’s
language processing capacities.
Oral Reading
In their comprehensive review of studies on conduction aphasia, Green
and Howes (1977) report that the majority of conduction patients present
moderate reading impairments.
The overall ratings that they report do
not reveal the nature of the reading difficulties exhibited by the patients,
and few of the case studies reported describe the reading disorders of
conduction aphasics. Thus, we have no knowledge of whether these
patients were “deep dyslexics,” as was case KF reported by Shallice
and Warrington (1975), or whether the patients’ reading difficulties were
primarily at the level of visual confusions or “literal”
paralexias that
might be related to an output encoding disorder.
MC was presented with 205 single words and 39 sentences which he
was asked to read aloud. The single words consisted of high- and lowfrequency concrete nouns, abstract nouns, verbs, adjectives, function
words, nonword pseudo-homophones
(e.g. “bate”), and pronounceable
letter strings (e.g., “bewlet”).
The sentences contained both abstract
and concrete nouns and included indirect object constructions, prepositional phrases, WH questions, imperatives, passives, and subordinate
clause constructions.
Single words and sentences were typed on cards and the patient was
given as much time as he needed to read the words aloud. MC’s oral
reading of the single words is presented in Table 11 in the form of
percentage correct. This table also shows data obtained from a patient
classified as a Broca’s aphasic, who was tested for comparison purposes.
A Broca patient was chosen because of MC’s special difficulties in repeating function words. It is well known that Broca’s aphasics have
particular problems processing function words (Caramazza & Berndt,
1978), and it is important to compare those problems with the difficulties
that conduction aphasics experience with that class of words.’
’ A mildly impaired Wemicke’s aphasic was also tested on all tasks reported here. This
patient was included to assure that the syntactic disturbances that are of interest cannot
be said to occur as a general feature of aphasia. The Wemicke patient showed no evidence
of syntactic processing difficulties, nor selective disruption of function words relative to
other classes of words.
CONDUCTION
APHASIA
257
TABLE 11
PERCENTAGEOF WORDSREAD CORRECTLYIN EACH FORM CLASS
Nouns
High-frequency,
concrete (N= 23)
Low-frequency,
concrete (N = 23)
Abstract
Patient MC
Broca Patient
100
96
96
70
86
43
Verbs (N= 20)
95
75
Adjectives (N = 20)
95
65
Function words (n = 20)
95
20
50
10
60
5
Nonwords
Pseudo-homophones
(N= 10)
Pronounceable
strings (N = 20)
An inspection of this table reveals that MC had no serious reading
problems, at least for real words. His overall performance with real
words is 95% correct. The few errors that occurred were literal paralexias. He had more trouble reading nonwords, and seemed poorly disposed to attempting these “strange”
items. In contrast to MC, the
Broca’s aphasic had a lower level of performance overall for every category tested, and also displayed marked difficulty reading function words,
abstract words, and nonwords. Indeed, this patient’s pattern of performance is similar to KF, the deep dyslexic case reported by Shallice and
Warrington.
MC’s reading of sentences was also excellent. He made only 7 errors
in 39 sentences and these were local and relatively insignificant.
For
example, he read “what is your near idea” instead of “what is your new
idea.” In general, MC had no difficulty reading function words. In contrast, the Broca’s aphasic did not read a single sentence correctly and,
as expected, had considerably more difficulty reading the sentences with
abstract nouns and those with a preponderance of function words.
From these results it appears that MC can process visually presented
words sufficiently well to assign them a correct phonological representation and can then use this representation to determine the articulatory
form necessary for the proper production of the word.
Although MC has difficulty repeating aurally presented function words
he has no special trouble reading words of this type. The Broca patient,
on the other hand, was severely impaired in his ability to read function
words.
258
CARAMAZZA
ET AL.
Sentence Production (Story Completion Task)
We have emphasized that MC’s spontaneous speech production is
relatively normal. To quantify that clinical impression, we elicited speech
samples using the Story Completion
Test (Goodglass, Gleason, Bernholtz, & Hyde, 1972). This test involves the presentation of a two- or
three-sentence “story” which leads to a sentence fragment that the patient is required to complete. For example, when presented with the
sequence: “the grass needs to be cut. I give my son the lawn mower
and I tell him . . .,” the patient is expected to complete the sentence
with an imperative construction.
There are 28 items designed to elicit
14 different types of syntactic frames. The test was administered to MC
twice, once aurally and once visually. The Broca patient was given only
the auditory version of the task.
Results of this task are presented in Table 12. In the auditory version
of the test, MC produced four inappropriate
responses and one “no
response,” while more than half of the Broca patient’s responses were
inappropriate.
If responses are assessed strictly in terms of whether they
are agrammatic,
MC produced only two deviant responses, while considerably more of the Broca patient’s responses were agrammatic. Finally, although MC’s responses were for the most part appropriate in
terms of context, they were often not given in the form elicited by the
story fragment.
MC’s performance on the visual version of the test was somewhat
worse than his performance on the auditory version in that he produced
a larger number of inappropriate
responses (indicating poorer comprehension of the visually presented material). The actual form of his reTABLE
NUMBER
AND
ANALYSIS
OF COMPLETIONS
12
SUPPLIED
IN STORY
Patient MC
Classification of
patient’s response
Correct completions
Appropriate response,
but not target
constructions
Completion
inappropriate, but
not agrammatic
Completion
agrammatic
No response
Note: Total items = 28.
Standard
administration
COMPLETION
TASK
Broca Patient
Visual
administration
Standard
administration
11
9
1
10
5
5
4
12
11
2
1
-
11
-
2
CONDUCTION
APHASIA
259
sponses, when assessed for the proper use of function words and grammatical well-formedness,
did not differ appreciably from the level of
performance in the auditory version of the test.
The results obtained in this task reveal that MC has considerable
mastery of the use of function words, although his comprehension of the
“story” fragment is somewhat disturbed. In particular, it appears that
MC gets the general gist of the story fragment without fully processing
the syntactic form of the sentences that he is expected to complete. The
Broca patient’s comprehension
performance represents an essentially
more severe form of MC’s deficit.
Comprehension
of Sentences
As we have indicated, MC’s language comprehension,
although near
normal on clinical testing, is quite impaired when assessed more rigorously. His performance on the story completion task suggests poor syntactic comprehension
in both visual and auditory modalities. Similarly,
MC’s comprehension on the Token Test (DeRenzi & Vignolo, 1962) was
significantly impaired in both modalities. The presence of poor comprehension in conduction aphasia is more prevalent than would be assumed
from the clinical description. Warrington and Shallice and Strub and
Gardner report that their patients have severe comprehension difficulties
when assessed by the Token Test. Furthermore, Green and Howes (1977)
report that most of the conduction cases reviewed in the literature have
impaired comprehension.
Of the 37 cases reported in which comprehension performance was tested in both modalities, 25 are described as
having mild to moderate auditory comprehension impairments, with visual comprehension significantly poorer. A comparison of comprehension
in individual cases reveals that 22 of 37 patients were more impaired in
the visual than in the auditory modality, 11 showed an equal impairment
and 4 showed a reversal.
Two recently published studies report that conduction aphasics produced a pattern of comprehension
deficit that was identical to that of
Broca’s aphasics (Caramazza & Zurif, 1976; Heilman & Scholes, 1976).
For example, Caramazza and Zurif showed that conduction and Broca’s
aphasics (as a group) had good comprehension of sentences in which the
meaning could be uniquely determined by comprehension of the major
lexical items without regard to syntactic relations (e.g., “the apple that
the boy is eating is juicy”). Both patient groups performed at chance
level with semantically reversible sentences, that is, sentences in which
an appreciation of the syntactic relations among major lexical items is
necessary for the assignment of a semantic interpretation (e.g., “the boy
that the girl is chasing is tall”).
One other indication of the nature of the comprehension deficit can
be inferred from a case report by Saffran and Marin (1975), who asked
260
CARAMAZZA
ET AL.
their patient to repeat semantically constrained or semantically reversible
sentences. When attempting to repeat, their patient often produced accurate paraphrases of semantically constrained sentences, but tended to
reverse the meaning when repeating semantically reversible (passive)
sentences. This result suggests that the patient did not recover the proper
syntactic structure for the semantically reversible sentences and assigned
them incorrect meanings.
The studies by Caramazza and Zuriff, Heilman and &holes, and Saffran and Marin suggest that the comprehension
deficit in conduction
aphasia can be characterized as resulting from an inability to process or
to represent syntactic information adequately. This hypothesis was tested
with respect to MC’s comprehension
impairment.
A sentence-picture
matching task was used. Of 72 items, 36 sentences
were semantically reversible (e.g. “the cat is being chased by the dog”)
and 36 were semantically constrained (e.g. “the bone is being eaten by
the dog”). Several syntactic forms were included: actives, passives, and
subject-relative and object-relative subordinate clause constructions. The
sentences were presented to the patient twice, once visually and once
aurally. In the visual presentation condition, the patient was given as
much time as he needed to study the sentence before choosing one of
four pictures. Similarly, in the auditory presentation condition the patient
was given as many repetitions of the sentence as he wanted before he
decided to respond. The pictures were not in front of the patient while
he was reading or hearing the sentences; thus, he could not systematically
eliminate inappropriate
pictures using partial information.
The four pictures presented with each sentence consisted of a correct depiction of
the sentence; one picture that differed from the correct one in that
different objects from those described in the sentence participated in the
action described by the verb (lexical distractor); one picture (for the
reversible sentences only) that reversed the relation between the two
objects named in the sentence (the syntactic distractor); and one picture
(or two in the semantically constrained sentences) that differed in both
objects and actions from the target picture (lexical distracters).
The number of correct responses and the distribution of error types
are shown in Table 13. Overall, MC’s performance was slightly better
than that of the Broca patient. Of particular interest is the comparison
of performance on the semantically
constrained and the semantically
reversible sentences for the two patients. Both performed worse on the
reversible sentences than on the semantically
constrained sentences.
More importantly,
an analysis of error types shows that both MC and
the Broca patient made substantially more “syntactic”
than lexical errors
in the visual presentation condition.
Two aspects of these results should be emphasized. First, the pattern
of comprehension
for the conduction aphasic is remarkably similar to
CONDUCTION
TABLE
ANALYSIS
Sentence type
13
OF RESPONSES-SENTENCE
Presentation
mode
261
APHASIA
COMPREHENSION
TASK
Error
Total correct
Patient MC
Lexical
type
Syntactic
Nonreversible
Visual
Auditory
32
29
4
7
-
Reversible
Visual
Auditory
21
16
2
9
13
11
Nonreversible
Visual
Auditory
22
27
14
9
-
Reversible
Visual
Auditory
17
16
2
10
17
10
Broca patient
Note: Maximum number correct in each condition
= 36.
that of the Broca patient in that both made more syntactic than lexical
errors in the reversible sentences. This result supports Caramazza and
Zurif’s (1976) suggestion that conduction aphasics may have asyntactic
comprehension.
Second, there is a marked interaction of error type by
input modality for both patients. This result shows that neither patient
could adequately recover the syntactic structure of sentences even when
given unlimited time to process the sentences.
Sentence Construction (Anagram) Task
Thus far we have found that MC has asyntactic comprehension like
a Broca patient, but that, unlike the Broca’s aphasic, he is not agrammatic
in the production of sentences or in oral reading. To investigate further
this intriguing dissociation of syntactic processes we tested MC and the
Broca control on an anagram task. All the lexical information, including
syntactically relevant cues such as function words and bound grammatical morphemes, is given to the patient. His task is to rearrange the
words to produce a meaningful sentence. It is assumed that in this situation the performance of the patient reflects fairly directly his grammatical knowledge of the language (von Stockert & Bader, 1976; Kremin
& Goldblum,
1975). There are no output constraints such as articulatory
and encoding difficulties, or word finding problems to mask the patient’s
knowledge of the syntactic and semantic organization of a sentence.
The 15 sentences used in this task were varied in syntactic form from
simple active, affirmative sentences to questions, passives, and indirect
object constructions. Each word of a sentence was printed on a separate
card and the cards were presented to the patient in a scrambled order.
262
CARAMAZZA
ET AL.
The patient was given as much time as he needed to rearrange the cards
into a meaningful sentence. The results of this experiment provide a
striking contrast in performance between the two patients. MC rearranged all 15 scrambled sentences to produce correct responses. He was
provided with cues (next word in the string) in only two sentences. In
all other instances he had no major difficulty successfully completing the
task, but he performed quite slowly and carried out the task with what
appeared to be a trial-and-error
strategy. In contrast, the Broca patient
failed to rearrange 6 of 15 sentences, despite considerable cueing. The
patient was able to rearrange only two of the sentences without assistance. It was clear that the Broca’s aphasic did not appreciate the syntactic
function of grammatical
morphemes. Examples of the two patients’ attempts to rearrange a scrambled sentence are presented in Table 14. One
striking aspect of the Broca patient’s,behavior
was that he appeared to
be totally insensitive to the grammatical
violations in the strings. he
produced. Unlike the Broca’s aphasic, MC was quite aware of the syntactic role of function words, although he appeared to use a trial-anderror strategy in solving the task.
The results of this experiment offer another example of the differences
in language processing abilities between the conduction and the Broca’s
aphasics. While the Broca patient does not seem to have access to
syntactic information
in any of the language functions tested, the conduction aphasic can, under appropriate circumstances, gain access to
syntactic knowledge to guide his language performance.
DISCUSSION
OF LANGUAGE TASKS
MC’s performance on these four language tasks reveals an interesting
pattern: “normal”
performance in oral reading, speech production, and
TABLE
SAMPLE
RESPONSES-SENTENCE
14
CONSTRUCTION
(ANAGRAM)
TASK
Target sentence: “The boy gave it to the dog.”
Patient MC
the boy gave
the dog gave it
the boy gave it to the dog
Broca patient
boy gave dog
the to the it
the boy gave dog
to the it
the it boy gave dog
to the
the it boy gave the to dog
the boy gave the dog to it
Comments
moves slowly
rejects; says “no”
correct
substantives/functors
on separate lines
placed
focus on attempts to move words
from bottom to top line
cue: “the boy gave”
indicates satisfaction
CONDUCTION
APHASIA
263
sentence construction, but moderately impaired comprehension of aural
and written language. This dissociation is the more interesting in that
the form of the comprehension defect is similar to that found in Broca’s
aphasia; i.e., it is asyntactic. However, the basis of MC’s comprehension
deficit is certainly not the same as the basis of the Broca patient’s
problem.
The pattern of performance for the Broca patient revealed a uniform
impairment
in all language functions at the level of the processing of
syntactic information.
That is, the patient was especially impaired in
reading function words (words that serve primarily a syntactic function);
his production in the story completion task was almost entirely agrammatic; his comprehension
was asyntactic and his performance on the
sentence anagram task revealed a profound impairment in syntactic organization. This pattern of performance supports the hypothesis that
Broca’s aphasia results from a disruption of the syntactic parser of the
language processing apparatus (Berndt & Caramazza, 1980; Caramazza
& Berndt, 1978; Zurif & Caramazza, 1976). The basis for this claim is
that the language component is shown to be affected in all language
functions tested (Caramazza & Zurif, 1976; Whitaker, 1971). By this
argument, the syntactic parser is not assumed to be impaired in conduction aphasia, even though these patients appear to have asyntactic
comprehension,
because their performance in other language functions
reveals a normally functioning syntactic component.
If we accept that conduction aphasia spares the syntactic parsing device we must look for an explanatory model that places the locus of the
disorder at a point between the perceptual processing mechanism (both
phonological
and graphemic), which appear on the basis of the oral
reading task to be functioning relatively normally, and the syntactic and
semantic processing systems, which seem to be unimpaired based on
performance in the sentence anagram task. Each of the remaining two
hypotheses can be elaborated to account for the pattern of MC’s performance in the language tasks reported here.
The decoding deficit hypothesis assumes that the patient can process
the input stimulus sufficiently well to recover the phonological and/or
the graphemic representations of a word. Beyond this, however, the
patient has difficulty carrying out further lexical analysis bearing on the
syntactic and semantic properties of the word. The idea here is simply
that a less-than-normal lexical representation is formed from a presented
word stimulus so that any further processing of the lexical information
will be based on an impoverished
representation. This hypothesis can
explain many of the features that characterize MC’s language performance.
The hypothesis must be developed further, however, if we are to
account for the dissociation between his impaired comprehension on the
one hand, and his relatively normal speech production and sentence
264
CARAMAZZA
ET AL.
anagram performance on the other. To explain MC’s asyntactic comprehension, we need to make the assumption that the processing of
grammatical morphemes is relatively more impaired than the processing
of other lexical forms. This assumption can be motivated on the basis
of a linguistic analysis that assigns to grammatical morphemes primarily
or exclusively a syntactic description (e.g., Bolinger, 1975; Kimball,
1973, 1975). Thus the representation
of function words in the lexicon
would be strictly in terms of syntactic description.
By this account, when a patient is presented with a sentence he processes the input at a “normal”
level up to the assignment of a phonological description of the input string. Beyond this point, further lexical
processing is disturbed in such a way that the internal representation
constructed contains less than the normal amount of lexical information
ordinarily used in language comprehension.
Major lexical items will be
more richly specified in the sentence representation because of the dual
nature of the information
represented in the lexicon (syntactic and semantic). Function words, however, are represented in the lexicon only
in terms of their syntactic value and consequently will have a correspondingly impoverished
status in the representation formed by the patient during the comprehension
process. The argument developed here
suggests that the conduction patient will construct an internal representation of a sentence that has a relatively more richly specified semantic
content than syntactic structure, leading to an exaggerated reliance on
lexical-semantic
information.
Since by this hypothesis the disorder is specified in terms of lexical
processing, it is predicted that the patient should have some difficulty
with the story completion task in discerning the type of response he
should provide. However, there should not be any impairment
in the
grammaticality
of the selected response. The results we have reported
are consistent with this prediction: MC did produce a number of inappropriate responses that reflect his poor comprehension
of the story
fragment, but the responses produced were grammatically
and semantically well formed.
The decoding deficit hypothesis can also explain MC’s performance
on the sentence anagram task. The type of processing required in this
task combines features of the sentence comprehension and the sentence
production tasks. As in the comprehension
task, the patient must understand the individual lexical items presented; as in the production task,
he must “spontaneously”
generate a syntactic frame in which to embed
the lexical items presented. Although it is assumed that the lexical processing capacities of the patient are limited, the format of the task allows
an adequate level of performance to be achieved, but in a laborious and
groping fashion. That is, the lexical information is continuously available
in the anagram task, which allows the patient to make use of the im-
CONDUCTION
APHASIA
265
poverished representation
he can construct by slowly and laboriously
arranging and rearranging the words until he has produced a sentence.
To the extent that we accept these arguments to account for performance on the sentence anagram task, we may be undermining our explanation of MC’s asyntactic comprehension
in the sentence-picture
matching task. In that experiment, the sentence and picture were not
presented together but the patient had ample opportunity to study the
sentence. It might be expected that under such circumstances the patient
could again use a trial-and-error method to construct an adequate internal
representation of the sentence. Unfortunately,
we have no way of assessing the force of this argument with regard to asyntactic comprehension since semantically reversible sentences cannot meaningfully be used
in the sentence anagram task; i.e., both versions would be correct. However, if we consider only comprehension
of nonreversible sentences,
MC’s performance was very good and at a level comparable to his
performance in the anagram task.
The STM deficit hypothesis can also be used as a basis for explaining
the language deficits exhibited by MC. This hypothesis predicts that oral
reading of single words should be unimpaired since the phonological and
semantic components of the system are functioning normally. The finding
of asyntactic comprehension
is also compatible with this model. It is a
basic assumption of all language processing models that normal sentence
comprehension requires the functioning of a “working memory” to store
the sentence input and/or the results of analyses carried out on the input
in the process of assigning a semantic interpretation to the sentence (e.g.
Clark & Clark, 1977). A disruption of STM would naturally result in
impaired comprehension.
To explain the asyntactic form of this comprehension deficit, Saffran and Marin (1975) have argued that the patient
with impaired working memory may adopt a strategy of “serial semantic
processing” together with a strategy of “assigning syntactic relations in
the SVO order” (Bever, 1970). This assumption was developed to account for errors in repetition of reversible passive sentences in the conduction case they studied, and it can also be used to explain poor syntactic comprehension.
There is an implicit assumption in Saffran and Marin’s hypothesis that
should be made explicit as it will play a role in our discussion of comprehension failure of visually presented material. The argument that conduction aphasia involves a limitation of the short-term store means that
only a limited segment of the sentence input is available in STM at any
one time. It is as if we were looking through a narrow window moving
along the sentence; what is visible through the window can be seen quite
well, but most of the sentence is not available. This is a basic premise
of the STM hypothesis; further assumptions concerning serial semantic
processing must be motivated on independent grounds since they are not
266
CARAMAZZA
ET AL.
a logical consequence of the STM deficit hypothesis. Actually, the serial
processing assumption is not needed to explain Saffran and Marin’s and
Shallice and Butterworth’s
(1977) repetition data, nor is it needed to
explain our patient’s comprehension.
Saffran and Marin’s implicit assumption is that syntactic processing
in real time is not possible with a pathologically
limited working memory.
Syntactic processing normally requires storing and updating syntactic
analysis to the level of a clause (Fodor, Bever, & Garrett, 1974), which
exceeds the limitations of the impaired working memory. A consequence,
by default, is that the only useful information a patient may have available
upon hearing a sentence is the semantic information represented by the
major lexical items. Comprehension of a sentence could be based on this
lexical-semantic
information,
together with the SVO strategy suggested
by Bever (1970).
MC’s comprehension
of visually presented sentences was moderately
impaired, even though he had unlimited time to study the stimulus sentences. His asyntactic performance can be explained if we assume that,
although MC can perform local syntactic and semantic analyses, he
cannot perform a full syntactic analysis on a sentence since this requires
the storage in working memory of the output of the local syntactic analyses performed at each point along the sentences. Thus, here again the
patient can rely only on the semantic information
from major lexical
items activated in LTM. Indeed, it is predicted that if the patient has
unlimited time to process the sentence he should obtain a very accurate
representation of the major lexical items such that the only errors in the
sentence-picture
matching task should be restricted to syntactic ones.
The results obtained here (see Table 13) are largely in agreement with
this prediction.
MC’s performance on the sentence anagram task can be explained by
assuming that the patient can carry out “local” syntactic analysis within
the confines of the “narrow window.” MC performed very well on this
task, albeit slowly and in a trial-and-error fashion. Since MC can perform
“local” syntactic analyses he can make pair combinations (e.g., Determiner + Noun) either serially (e.g., (Determiner
+ noun) + Aux
+ Noun), (Aux +
. . . ) or by first generating pairs (e.g., (Determiner
Verb)) and then linking the pairs by further local analyses at the boundary
between pairs (e.g., (Determiner
+ Noun) + (Aux + Verb)). If the
patient were to proceed in this fashion to solve the anagram task, we
would expect his performance to be not unlike MC’s, which we have
described as effortful and groping.
We have offered two explanations of the language performance of MC
that appear to do about equally well in accounting for the obtained
results. These explanations should also be evaluated in terms of how
CONDUCTION
APHASIA
well they can account for the repetition
other data available in the literature.
GENERAL
267
results and, where relevant,
DISCUSSION
A number of different hypotheses have been proposed to explain the
repetition deficit in conduction aphasia. As we have noted in separate
discussions of the repetition and language tasks reported here, the performance of MC cannot be accommodated within the classical disconnection hypothesis, nor can it be explained by the encoding deficit hypothesis. These hypotheses cannot provide motivated accounts for
performance on the probe task, the differential repetition as a function
of mode of presentation, or for the differential effects of form class and
delay manipulations
on repetition. They are even less successful in explaining MC’s performance on the language tasks, in particular asyntactic
comprehension cooccurring with normal syntactic production. However,
in light of our remarks about different subgroups within conduction
aphasia, it could be maintained that these two hypotheses were developed
to explain the behavior of a type of conduction aphasic who is different
from our patient. In this case the analyses we have carried out of MC’s
performance have little bearing on the validity of the two hypotheses
with regard to the range of facts that these models were originally developed to explain. By this argument, however, these two hypotheses
lose their status as explanations of “conduction aphasia” in general and
must be considered as hypotheses about the nature of the disorder that
underlies one subclass of conduction aphasics.
The two other hypotheses we have considered, the decoding deficit
and the auditory-verbal
STM deficit hypotheses, are moderately successful in accounting for the pattern of results obtained separately in the
repetition and language processing tasks. However, if we consider both
sets of results we find that the auditory-verbal
STM hypothesis continues
to provide a reasonable account of MC’s performance, while the decoding
deficit hypothesis is confronted with unresolvable conflicts.
There are two major problems that confront the decoding deficit hypothesis. One concerns the patient’s better repetition of visually presented than of aurally presented items. One attempt by Strub and Gardner
to deal with this problem is a simple restatement of the results: “visual-semantic
connections may be better preserved” (p. 253); in another
case they offer a vague appeal to an alternative route for processing
visual information.
However, even if we were to accept the account they
offer for the better performance of repetition of visually presented over
aurally presented items, they would still be unable to explain the total
pattern of performance of visual and auditory tasks. That is, if it is
indeed the case that visual processing is relatively normal, then the
268
CARAMAZZA
ET AL.
decoding deficit hypothesis would fail to explain our patient’s asyntactic
comprehension of visually presented sentences. That is, to explain MC’s
performance on the language tasks, particularly his performance on the
story completion and reading comprehension
tasks, we had to assume
that the decoding deficit was a general lexical processing deficit, independent of mode of stimulus input. The decoding deficit hypotheses, to
remain internally consistent, necessarily fails to explain one of two major
resuts-either
the better repetition of visual over auditory inputs, or poor
comprehension
of visually presented sentences.
The other problem that confronts the decoding deficit hypothesis concerns the very nature of the lexical decoding impairment.
Shallice and
Warrington (1977) have already objected to the vague claims about lexical
decoding disturbances that are assumed to underlie the repetition defect.
Indeed, the position that conduction aphasics manifest a lexical processing deficit should be motivated on independent grounds. We have
not been able to support this hypothesis in our assessment of MC’s
performance on various tasks that require lexical processing. For example, we have reported in this paper that MC’s oral reading performance
was excellent. Reading is a complex process that involves both orthographic and phonological
processing of lexical forms, and no serious
impairments were detected in either of these two processing components.
Thus, there is no evidence that MC has a specific lexical decoding deficit
that underlies the repetition defect or the asyntactic comprehension
we
have reported. These objections to the decoding deficit hypothesis are
serious enough to rule it out as a possible explanation of the disorder
that characterizes our patient’s aphasic performance.
The hypothesis that can best account for MC’s complex performance
on repetition and language processing tasks is the auditory-verbal
STM
deficit hypothesis. The only major result in the repetition tasks that
presents some difficulties for the hypothesis is repetition of function
words. It appears that MC’s especially marked inability to repeat aurally
presented function words is incompatible
with the STM hypothesis, unless we assume that function words are processed differently from other
lexical forms. There is some independent evidence that function words
and content words are processed differently, at least in sentence production (Garrett, 1973, and it is intuitively
obvious that they receive
minimal semantic analysis. With regard to MC’s inability to repeat function words when these were presented in phrasal contexts, we need to
assume that even in such cases function words are represented only
phonologically
in short-term store, although they play a crucial role in
the syntactic analysis of sentences. By this assumption, aurally presented
function words should be especially affected by a disorder of auditory-verbal STM, since the only code of representation available to such
lexical forms is the modality in which the impairment is realized.
CONDUCTION
APHASIA
269
The STM hypothesis does very well in explaining MC’s performance
on the language tasks. This is especially interesting when the complexity
of the obtained results is considered. Most important is the fact that the
hypothesis can explain the results obtained in the language tasks without
recourse to the ad hoc introduction
of new mechanisms: the account
given is based entirely on consequences of a disruption of short-term
memory and the assumptions concerning the processing and representation of function words that were developed to explain the repetition
results.
One elaboration of the STM deficit hypothesis that was needed to
explain the language comprehension performance of our patient was the
claim that MC could apply his unimpaired syntactic knowledge only to
a small segment of the presented material at a time. In particular, it was
assumed that MC could apply local analyses-analyses
between pairs
of words-but
could not make use of working memory to store the output
of syntactic analysis. This assumption, which follows naturally from the
hypothesis of pathologically
reduced capacity in the STM store, predicts
MC’s asyntactic comprehension of sentences.
To conclude, we have reported an extensive analysis of the repetition
and language processing performance of a conduction aphasic. Of the
four hypotheses considered, the only one that could provide a motivated
account of all the major features of performance was the auditory-verbal
STM deficit hypothesis. If our analysis is correct, we have provided a
strong demonstration
of the relationship between a nonlinguistic
processing component and particular aphasic symptoms in a patient. The
study of patients of this type should be especially fruitful for an analysis
of the contribution of auditory-verbal
STM to various language functions.
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