Brain and Language 88 (2004) 83–95

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Linguistic and neuropsychological deficits in crossed

conduction aphasia. Report of three cases
Lisa Bartha,a,* Peter Mari€en,b,c Werner Poewe,a and Thomas Benkea
a
Universitaetsklinik fuer Neurologie, Anichstrasse 35, Innsbruck A-6020, Austria
b
Department of Neurology, AZ Middelheim, University of Antwerp, Belgium
c
Department of Linguistics, Free University of Brussels, Belgium

Accepted 17 June 2003

Abstract

This study describes the linguistic and neuropsychological findings in three right-handed patients with crossed conduction
aphasia. Despite the location of the lesion in the right hemisphere, all patients displayed a combination of linguistic deficits typically
found in conduction aphasia following analogous damage to the left hemisphere. Associated cognitive deficits varied across the three
patients. In addition, all cases showed deficits classically attributed to non-dominant hemisphere damage (visuoperceptual deficits
and reduced figural memory). As a result, lesion–behaviour relationships in our study sample indicate both dominant and non-
dominant qualities of the right hemisphere.
Ó 2003 Elsevier Inc. All rights reserved.

Keywords: Conduction aphasia; Crossed aphasia; Short-term memory

1. Introduction reduced auditory–verbal short-term memory (Shallice &

In 1874, Carl Wernicke introduced the concept of
conduction aphasia as a distinct type of aphasia. The
cardinal features of this syndrome consist of dispro-
portionately affected repetition and relatively intact
comprehension, word-finding difficulties, and parapha-
sic errors in spontaneous speech (Benson et al., 1973;
Caramazza, Basili, Koler, & Berndt, 1981; Goodglass,
1992; Rothi, McFarling, & Heilman, 1982). Speech
disruptions in conduction aphasia are predominantly of
the phonological type (omissions, substitutions, trans-
positions, or insertions of sounds or syllables), but may
be semantic as well for certain lexical categories (e.g.,
numbers and functors). Patients with conduction apha-
sia are generally aware of their speech problems, which
often leads to repetitive self-corrections (conduites
d’approches). Regarding the cognitive dysfunctions that
may accompany conduction aphasia, the literature is
only sparsely documented. Single case studies report
*
Corresponding author.
E-mail address: lisa.bartha@uibk.ac.at (L. Bartha).
Warrington, 1977), sentence construction deficits
(Caramazza et al., 1981), ideomotor apraxia (Benson
et al., 1973), and impaired numerical processing (Del-
azer & Bartha, 2001; Girelli, Bartha, & Delazer, 2002).
Studies on the neuroanatomical basis of conduction
aphasia have identified lesions in the supramarginal
gyrus (Brodmann area 40), the primary auditory corti-
ces, the insular cortex and the adjacent white matter
(Axer & Berks, 2001; Benson et al., 1973; Damasio &
Damasio, 1980), as well as lesions in the temporo-oc-
cipital region (Bartha & Benke, 2003) of the language
dominant hemisphere; in some but not all cases a lesion
of the arcuate fasciculus is found (Damasio & Damasio,
1980; Palumbo, 1992; Tanabe et al., 1978; Wernicke,
1874).
In genuine dextrals, aphasia caused by a right-hemi-
sphere lesion is uncommon. This condition, first termed
‘‘crossed aphasia’’ by Bramwell (1899), is currently de-
fined as a clear-cut language disorder due to a lesion in
the right hemisphere in a natural right-hander with a
structurally intact left-hemisphere and with no familial
antecedents of left-handedness or a history of early

0093-934X/$ - see front matter Ó 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0093-934X(03)00281-5
84 L. Bartha et al. / Brain and Language 88 (2004) 83–95
brain damage or epilepsy (Mari€en, Engelborghs, Vig-
nolo, & De Deyn, 2001). The estimated incidence of
crossed aphasia in dextrals varies between 0.4 and 2.0%
of the aphasic population (Bakar, Kirshner, & Wertz,
1996; Brown & Hecaen, 1976). The exact neurological
mechanisms underlying this uncommon condition are
still unknown. A wide variety of explanations have been
proposed such as absence of decussation of cortico-
spinal tracts (Souques, 1910), a familial strain of sinis-
trality (Ardin-Delteil, Levi-Valensi, & Derrieu, 1923),
involvement of phylogenetically older subcortical
structures (Habib, Joanette, Ali-Cherif, & Poncet, 1983),
a simultaneously acquired invisible small left-hemi-
sphere lesion (Castro-Caldas, Confraria, Paiva, &
Trindada, 1986), inhibitory metabolic repercussions of
the right-hemisphere lesion on left-hemisphere func-
tioning (Schweiger, Weschler, & Mazziota, 1987), and
natural variation in functional brain organization due to
the presence or absence of one single gene (Annett &
Alexander, 1996). To these, Brown and colleagues
(Brown & Wilson, 1973; Brown & Hecaen, 1976) added
the hypothesis that crossed aphasia is the product of
incomplete lateralization of language functions in the
left hemisphere during maturation.
The initial view of the semiology of crossed aphasia
has changed dramatically over the past years. Whereas
early reports (e.g., Joanette, Puel, Nespoulous, Rascol,
& Roch Lecours, 1982; Puel et al., 1982) tended to view
crossed aphasia as an atypical, non-fluent type of
aphasia with relatively intact language comprehension
and a favourable recovery, the more recent literature
presents not only atypical, non-fluent patterns (Gomez-
Tortosa, Martin, Syxhra, & Dujovny, 1994), but also
classic non-fluent aphasic syndromes like BrocaÕs
aphasia (Rey, Levin, Rodas, Bowen, & Nedd, 1994),
transcortical motor (Raymer et al., 1999), and global
aphasia (Ozeren, Mavi, Sarica, & Karatas, 1998), as well
as classic fluent types like WernickeÕs (Giovagnoli, 1993;
Trojano, Balbi, Russo, & Elefante, 1994), transcortical
sensory (Nedelec-Ciceri et al., 1996), and anomic
aphasia (Basso, Capitani, Laiacona, & Zanobio, 1985)
with a variable outcome. Thus, crossed aphasia came to
be viewed as more consistent with the classical taxon-
omy of aphasia in the last years.
We found 21 cases of crossed conduction aphasia
described in the literature (Annett & Alexander, 1996,
C8; Assal, 1982; Basso et al., 1985, C5; Berndt, Mit-
chum, & Price, 1991; Endo, Kurashima, Yanagi, Tsuk-
ada, & Makishita, 1982, C5; Foroglou, Assal, & Zander,
1975; Gomez-Tortosa et al., 1994; Haaland & Miranda,
1982; Henderson, 1983, C1; Lano€e et al., 1992; Lozano
& Clark, 1976; Mari€en et al., 2001, C5 & 9; Mendez &
Benson, 1985; Osmon, Panos, Kautz, & Gandhavadi,
1988; Perani, Papagno, Cappa, Gerundini, & Fazio,
1988, C1; Puel et al., 1982; Stefanis, Desmond, &
Tatemichi, 1997; Sugimoto, Hashimoto, & Yamaguchi,
1985; Yamadori, Yoshida, & Sugiura, 1992; Yarnell,
1981, C2). However, detailed neuropsychological ex-
amination is rarely reported, and follow-up testings are
not available. Thus, less is known about associated
cognitive deficits and the outcome of crossed conduction
aphasia.
During the past two decades, two issues have been
the primary focus of interest in crossed aphasia. First,
aphasia symptoms and lesion location have been studied
to address the question whether or not crossed aphasia
reflects classic lesion–aphasia relationships holding for
standard, uncrossed aphasia. In this respect, review
studies (Alexander, Fischette, & Fischer, 1989; Coppens
& Hungerford, 1998) have shown that 65% of the
cases display lesion–aphasia relationships comparable
to those following an analogous lesion in the left
hemisphere (mirror-image cases), while 35% of the
cases (anomalous cases) violate classically expected
lesion-aphasia relationships. The second issue concerns
dissociations among neuropsychological symptoms that
accompany language deficits in dextrals with right-
hemisphere lesions, such as a dissociation of language
and praxis, i.e., the presence of intact limb praxis in
crossed aphasia (Henderson, 1983; Mendez & Benson,
1985), and, conversely, crossed limb apraxia in patients
with intact linguistic functions (Marchetti & Della Salla,
1997). Functional dissociations like these suggest that
crossed aphasia may be the source of more detailed in-
formation about the functional organization of the
cognitive system (Berndt et al., 1991). The present study
addresses both issues. We describe three new cases of
crossed conduction aphasia, documented by formal
neurolinguistic and neuropsychological assessments and
neuroimaging. The aim of this study is to analyse lin-
guistic and neuropsychological functions, as well as le-
sion location in patients with crossed conduction
aphasia and to compare these findings with ÔclassicÕ
conduction aphasia following left-hemisphere lesions.
Since longitudinally documented cases of crossed
aphasia are rare (Roebroek, Promes, Korten, Lormans,
& van der Laan, 1999), and since the outcome of crossed
conduction aphasia is unknown, we reinvestigated all
patients in the chronic phase.
2. Methods
Language was examined by means of the Aachener
Aphasie Test (AAT) (Huber, Poeck, Weniger, & Will-
mes, 1983), the Innsbrucker Benenntest (IBT) (Bartha,
Delazer, & Benke, 2001), a 1-min semantic verbal flu-
ency task, and a German adaptation of Gallaher and
CanterÕs test (1982) tapping syntactic comprehension.
Memory was evaluated by means of the Wechsler
Memory Scale (Wechsler, 1945), the CorsiÕs Block-
Tapping task (Milner, 1971), and the Rey Osterrieth
 L. Bartha et al. / Brain and Language 88 (2004) 83–95
Complex Figure Test (Osterrieth, 1944; Rey, 1941; Vis-
ser, 1973). Visuoperceptual and visuospatial functions
were assessed by means of a selection of the Visual
Object and Space Perception Battery (VOSP) (War-
rington & James, 1991), the Visual Searchboard (Kim-
ura, 1986), a Letter and Symbol Cancellation Task
(Caplan, 1985), and a Line Bisection Test (Diller et al.,
1974). The Raven Progressive Matrices Test (Raven,
1960) was administered to measure conceptualization of
spatial design and non-verbal problem solving (numer-
ical relationship). Buccofacial praxis was investigated
for single, two-, and three-sequential oral and tongue
movements (Mateer & Kimura, 1977). Imitation of fin-
ger and hand position was tested on the basis of De
RenziÕs apraxia test (De Renzi, Mozzi, & Nichelli, 1980).
To evaluate comprehension and production of mean-
ingful, non-linguistic pantomimed actions, the New
England Pantomime Test (Duffy & Duffy, 1984) was
administered. Object use was assessed in three consec-
utive steps by means of an experimental test battery
consisting of 10 every-day objects. This required the
patients to: (1) pantomime the use of a verbally named
object, (2) to pantomime the use of a visually presented
object, and (3) to handle the real object. Objects used in
these tests were a toothbrush, comb, shaving brush,
glass, saltpot, hammer, electric bulb, lemon squeezer,
scissors, and bottle opener. One point was given for each
correct response. Arithmetical functions were assessed
using the reduced form of the EC301R battery (Deloche
et al., 1994).
3. Case reports
3.1. Case 1
3.1.1. History
In August 2000, G.S., a 40-year-old monolingual
electrician with 9 years of formal education acutely de-
veloped aphasia and paresis of the left arm. He was fully
right-handed as formally assessed by the Edinburgh
Handedness Inventory (EHI) (Oldfield, 1971) which re-
vealed a laterality quotient (LQ) of +100. He had no
history of left-handedness in his family and had not
sustained brain damage prior to this insult. Three days
after the stroke, magnetic resonance imaging (MRI) of
the brain disclosed a right temporo-parieto-occipital
infarction (Fig. 1). In-depth neurolinguistic and neuro-
psychological examinations were performed on the
fourth and fifth day post-onset (Table 1). The patient
was re-examined 12 weeks after the onset of neurologi-
cal symptoms.
3.1.2. Neurolinguistic and neuropsychological findings
In the acute phase, this patient presented fluent spon-
taneous speech with frequent phonemic paraphasias,
85
conduites dÕapproches, and word-finding difficulties.
Furthermore, some minor paragrammatic errors regard-
ing inflections and verb forms were observed, while per-
severations or neologisms did not occur. In formal testing,
(Table 1) repetition was the most impaired linguistic
function (123/150); errors included phonemic parapha-
sias (e.g., Haust€ ur [front door] ! harstur), conduites
dÕapproches (e.g., Hallenhandballweltmeisterschaft
[worldÕs championship in handball] ! hallen.. hallenpart..
hallenwelt.. hallenbadweltmeisterschaft), and phonose-
mantic blends (e.g., Hund [dog] ! Hut [hat]). Auditory
and reading comprehension of words and sentences re-
vealed only minor deficits (43/60 and 47/60, respectively);
however, the patient performed worse on the Token Test
(30 errors/50), where longer commands were significantly
more impaired than shorter ones. In addition, syntactic
comprehension was impaired (40/58). Naming revealed
word-finding difficulties, phonemic paraphasias, condu-
ites dÕapproches (e.g., Schraubenzieher [screwdriver] !
schreib.. schraubenzieher), and semantic errors (e.g.,
Schuhl€ offel [shoehorn] ! fußschemel [stool]) (106/120).
Reading was intact and writing showed some phonemic
paragraphias (18/30). Verbal fluency was reduced.
Neuropsychological testing revealed intact visual
working memory and intact figural long-term memory,
whereas verbal–auditory working memory was mark-
edly impaired (Digit Span forward 3, backward 2). G.S.
had intact visuoperceptual basic functions like spatial
location and position discrimination but presented a
mild deficit in visuo-perceptual matching tasks requiring
knowledge of objects (object recognition 15/20). He
displayed severe ideomotor apraxia as evidenced by
poor imitation of finger and hand positions (left hand
31/72, right hand 46/72), poor pantomime recognition
and expression (32/40 and 194/345, respectively), re-
duced pantomimed object use (16/20), and impaired
orofacial sequential movements (1/6). Numerical abili-
ties were intact.
Twelve weeks post-onset, G.S. substantially recov-
ered from his conduction aphasia, but still exhibited
mild word-finding difficulties and paragrammatic
errors in spontaneous speech. In formal aphasia testing,
the patient still showed mildly reduced language com-
prehension. Verbal fluency was also compromised.
However, repetition, naming, reading, and writing nor-
malized. In addition, G.S.Õ verbal–auditory working
memory improved to normal. Furthermore, he recov-
ered from apraxia and obtained normal results on oro-
facial movements, finger and hand positions, and object
use tasks.
3.2. Case 2
3.2.1. History
W.K., a 56-year-old, monolingual right-handed man
with an LQ of +100 (Oldfield, 1971) and no history of
86 L. Bartha et al. / Brain and Language 88 (2004) 83–95
Fig. 1. Patient G.S. Ischemic right temporo-occipital lesion including posterior part of the temporal lobe, lateral occipital area, supramarginal and
angular gyrus, and posterior insular cortex.
familial left-handedness or prior brain damage had 12
years of formal education and worked as a computer
scientist. In April 2000 he had a grand mal seizure. MRI
of the brain showed a tumour in the right temporal lobe
(Fig. 2A). One month after the epileptic fit the patient
developed word-finding difficulties. According to his
wife, his language deficits progressively increased. In
August 2000 the patient was referred to our laboratory. A
detailed neurolinguistic and neuropsychological exami-
nation was carried out on two consecutive days (Table 1).
W.K. presented fluent speech output with intact articu-
lation and prosody, evidenced word-finding difficulties,
phonemic paraphasias, and conduites dÕapproches. Au-
ditory and reading comprehension were good for single
words but sentence comprehension was slightly dis-
rupted. Repetition tasks revealed phonemic paraphasias
at the sentence level. Confrontation naming, reading, and
writing were normal. In addition, W.K. presented intact
mnestic functions as well as normal praxis.
Eight days after this examination the tumour was
totally resected. Histologic examination of a tumour
specimen revealed an anaplastic astrocytoma grade III.
Seven days after the operation a second neurolinguistic
examination was conducted (Table 1). The patient was
re-examined again 4 months later. W.K. did not receive
speech therapy before or after tumour resection. A re-
peat MRI was performed 5 months after the operation
(Fig. 2B).
3.2.2. Neurolinguistic and neuropsychological findings
post-operative
Seven days post-operatively this patient showed fluent
spontaneous speech with phonemic paraphasias, word-
finding difficulties, and minor paragrammatic errors. As a
result of the word-finding difficulties, W.K. frequently
produced idioms and paraphrases that preserved the
meaning. There were neither perseverations nor semantic
or phonemic neologisms. Formal aphasia testing
disclosed markedly impaired repetition with phonemic
paraphasias (e.g., Hepatitis [hepatitis] ! hipatitus),
conduites dÕapproches (e.g., Vormundschaftsgericht
[guardianship-courts] ! v€ur.. vormand.. vormandschuft..
 L. Bartha et al. / Brain and Language 88 (2004) 83–95 87

Table 1
Neuropsychological test results
Cognitive functions G.S. 1 G.S. 2 W.K. W.K. W.K. C.M. C.M. C.M. Maximum
pre post 1 post 2 pre post 1 post 2 possible
score
Time post-onset/post-operatively 4 89 7 120 11 225
(days)
Orientation
Mini mental state orientation 10 10 10 10 10 10 10 10 10
Language
Aachener Aphasie Test
Token test (errors) 30 20 5 32 21 0 22 14 50
Auditory comprehension
Words 24 28 30 22 25 30 20 21 30
Sentences 19 23 20 24 24 30 24 26 30
Written comprehension
Words 26 24 22 24 24 30 28 28 30
Sentences 21 26 23 23 29 30 20 22 30
Repetition
Sounds 30 30 30 30 30 30 28 30 30
Words 29 30 30 30 30 30 20 29 30
Foreign words 28 30 30 27 28 30 21 28 30
Compounds 21 29 27 20 20 30 13 22 30
Sentences 15 26 24 16 21 30 10 21 30
Naming
Objects 28 30 30 27 28 30 18 29 30
Colours 30 30 30 29 29 30 10 30 30
Objects (compounds) 26 28 30 24 26 30 4 20 30
Situations 22 23 30 22 23 30 16 23 30
Reading 28 30 30 27 29 30 24 30 30
Composition of letters and words 24 30 26 5 24 30 23 30 30
Writing 18 30 26 7 23 30 23 29 30
IBT naming 43 49 44 37 48 n.d. n.d. 45 50
Syntactic comprehension 40 43 52 37 40 n.d. n.d. 53 58
Verbal fluency 9 13 20 9 17 15 4 13
Memory
Rey Osterrieth Complex Figure
Copy 33 33 31 n.d. 32 36 30 35 36
Long delay free recall 21 27 26 20.5 14.5 8 11.5 36
Wechsler Memory Scale
Digit span forward—raw score 3 5 5 3 4 6 5 5
Digit span backward—raw score 2 4 4 3 3 4 4 4
Corsi Block Tapping 6 6 6 6 6 n.d. n.d. 7
Visuoperception
VOSP
Screening 20 20 n.d. n.d. 20 n.d. n.d. 20 20
Object recognition 15 20 19 20 20
Position discrimination 20 20 20 20 20
Number location 10 10 9 9 10
Searchboard
Items found in visual fields n.d. n.d. n.d. n.d.
Left 8 11 12 11
Right 12 9 8 9
Average searching time (s)
Left 7.0 6.3 4.4 6.0
Right 7.8 9.1 5.8 8.4
Cancellation (omissions) 0 0 n.d. n.d. 0 0 3 0
Line bisection n.d. n.d. 0 n.d. n.d. 0
Raven Progressive Matrices
Set A 3 6 5 6 6 5 2 6 12

Praxis
Orofacial Copying
Single movements 17 17 17 17 17 17 10 17 17
88 L. Bartha et al. / Brain and Language 88 (2004) 83–95

Table 1 (continued)
Cognitive functions G.S. 1 G.S. 2 W.K. W.K. W.K. C.M. C.M. C.M. Maximum
pre post 1 post 2 pre post 1 post 2 possible
score
Sequential movements 1 6 6 6 6 6 2 2 6
De Renzi
Imitation of finger/hand position
Left hand 31 69 69 70 72 72 66 71 72
Right hand 46 70 69 71 72 72 67 71 72
New England Pantomime Test
Recognition A 43 46 46 n.d. 44 n.d. n.d. 46 46
Recognition B 32 39 40 35 40 40
Expression 194 312 300 287 323 345
Object Use
Pantomime after verbal command 16 20 20 n.d. 20 n.d. n.d. 20 20
Pantomime with visual stimuli 16 20 20 20 20 20
Real object use 20 20 20 20 20 20
Numerical processing
EC 301 R
Number sequences 6 6 n.d. 6 6 6 6 6 6
Dot counting 2 2 2 2 2 2 2 2
Writing Arabic numbers from 12 12 6 6 12 12 12 12
dictation
Reading Arabic numbers 12 12 8 12 12 12 12 12
Mental calculation 16 16 14 10 16 16 16 16
Number positioning on a vertical 10 10 10 16 10 10 10 10
scale
Number comparison
Arabic numerals 16 16 16 16 16 16 16 16
Written verbal numbers 16 16 16 16 16 16 16 16
Spoken numbers 16 16 16 16 16 16 16 16
Written calculation
Addition 4 4 2 4 4 4 4 4
Subtraction 4 4 2 2 4 4 4 4
Multiplication 7 7 3 5 7 7 7 7
n.d., not done.

vermundschaftgerechts), phonosemantic blends (e.g.,
Umleitung [diversion] ! anleitung [guidance]), and
paraphrases (123/150). Auditory and reading compre-
hension, as measured with the AAT, showed only minor
deficits (46/60 and 47/60, respectively). However, perfor-
mance on the Token Test (32 errors/50) and syntactic
comprehension tasks (37/58) was significantly reduced.
Naming (102/120) revealed word-finding difficulties,
phonemic paraphasias (e.g., Schnecke [snail] ! sch-
neuke), conduites dÕapproches, and semantic paraphasias
(e.g., Harfe [harp] ! cello) closely related to the target
word. Reading was intact, but written language produc-
tion was significantly impaired as evidenced by compo-
sition of words and sentences (5/30), and writing to
dictation (7/30). The patient produced fluent written
language characterized by frequent phonemic paragra-
phias with omissions, transpositions, and insertions of
graphemes. Neuropsychological testing revealed reduced
verbal–auditory working memory (Digit Span forward 3,
backward 3), but intact verbal and figural long-term
memory functions, intact visuoperceptual abilities, and
normal praxic functions though some difficulties occured
in pantomime recognition (35/40). Numerical processing
was reduced: W.K. presented substitutions in number
writing and semantic paralexias in number reading, minor
difficulties in addition and subtraction facts, and more
consistent failure in multiplication facts. In the latter task,
errors consisted of operand and non-table errors.
Four months later, W.K. still displayed a conduction
aphasia. Additionally, chronic deficits were obvious
in auditory–verbal short-term memory and number
processing.
3.3. Case 3
3.3.1. History
C.M., a 29-year-old, monolingual right-handed wo-
man with an LQ of +100 (Oldfield, 1971) and no family-
history of left-handedness or prior brain damage, had 12
years of formal education and worked as a bank em-
ployee. From December 1998 to February 1999 she
developed a series of epileptic seizures. Anticonvulsive
therapy was started in February. One month later, MRI
of the brain showed a tumoural mass in the posterior
right temporal lobe (Fig. 3A). Preoperative neurolin-
guistic assessments did not disclose linguistic deficits
 L. Bartha et al. / Brain and Language 88 (2004) 83–95 89

Fig. 2. (A) Patient W.K., preoperative MR-study. Cortico-subcortical space-occupying lesion extending from the inferior angular gyrus to the
posterior infero-temporal region. (B) Patient W.K., post-operative MR-study. Area of tumor resection surrounded by edema. Post-operative lesion
includes posterior part of medial and superior temporal gyrus, angular gyrus, and underlying white matter.

(Table 1). In addition, praxis and memory testing
showed normal results. Eleven days after neurosurgical
resection of an anaplastic astrocytoma (grade III)
neurolinguistic examinations were performed. Post-op-
eratively, C.M. received one session of speech therapy
per week, for a total of 10 weeks. Five months post-
operative, repeat MRI was performed (Fig. 3B). Seven
months after the operation cognitive functions were
reinvestigated.
3.3.2. Neurolinguistic and neuropsychological findings
post-operative
Eleven days after tumour resection, this patient dis-
played fluent spontaneous speech with intact articula-
tion and prosody, contaminated with frequent phonemic
paraphasias, conduites dÕapproches, and word-finding
difficulties. Furthermore, C.M. presented semantic pa-
raphasias in spontaneous speech which were closely re-
lated to the target. There were neither perseverations
nor semantic or phonemic neologisms. In formal apha-
sia testing, C.M. displayed significantly reduced repeti-
tion (92/150) with phonemic paraphasias and conduites
dÕapproches (e.g., Strumpf [sock] ! schurp.. schlumpf..
strumpf). Language comprehension, measured with the
AAT, was only mildly reduced (auditory comprehension
44/60, written comprehension 48/60), and syntactic
comprehension was intact. However, on the Token Test
she obtained a below normal score (10 errors/50).
Naming (48/120) showed word-finding difficulties, pho-
nemic paraphasias, conduites dÕapproches (e.g., Sch-
raubenzieher [screwdriver] ! sch.. schraub.. strahl..
schraub.. schtraub.. schraufe.. strauben.. schrauben..),
and semantic errors with close semantic relationship to
the target (e.g., Zahnb€urste [tooth-brush] ! zahnpasta
[tooth-paste]). Writing was intact, whereas in reading
some phonemic paralexias occurred (24/30).
The neuropsychological examination revealed intact
verbal–auditory and visual working memory; however,
figural long-term memory was impaired (8/36). Fur-
thermore, C.M. presented mild left visuo-spatial neglect.
90 L. Bartha et al. / Brain and Language 88 (2004) 83–95
Fig. 2. (continued)
The patient made some omissions on the left side in a
cancellation task and deviations to the right side in a line
bisection task. In praxis testing, C.M. exhibited intact
imitation of finger and hand positions but showed
apraxia for single and sequential orofacial movements
(10/17 and 2/6, respectively).
Seven months post-operatively, C.M. displayed per-
sistent conduction aphasia. However, further cognitive
deficits initially present in the acute phase, including
figural memory deficits, neglect, and apraxia, receded
during follow-up.
4. Discussion
This report analyses linguistic and neuropsychologi-
cal deficits in three patients with crossed conduction
aphasia. One patient (G.S.) developed conduction
aphasia after a focal right-hemisphere stroke, and two
patients developed conduction aphasia in association
with a tumour of the right temporal lobe (W.K. and
C.S.). In C.S., conduction aphasia arose after neuro-
surgical intervention, as the patient was linguistically
unimpaired pre-operatively. In contrast, W.K. showed
already some linguistic deficits prior to operation. All
patients under consideration were right-handed, with
no family-history of left-handedness, and had no history
of brain damage or epilepsy. Thus, our patients can
be classified as representatives of crossed aphasia in
dextrals.
4.1. Language profile
In the acute phase, all three patients displayed lin-
guistic deficits similar to those found in conduction
aphasia after left-hemisphere lesions (Bartha & Benke,
2003; Goodglass, 1992). Spontaneous speech was
characterized by phonemic paraphasias, conduites
dÕapproches, and word-finding difficulties, whereas
conversational language comprehension was only mildly
reduced. On formal aphasia testing, all patients dis-
played the same quality of errors, but to a different de-
gree. Repetition was the most impaired language
function. Auditory and written language comprehension
 L. Bartha et al. / Brain and Language 88 (2004) 83–95 91

Fig. 3. (A) Patient C.M., preoperative MR-study. Cortico-subcortical, space-occupying lesion comprising the posterior temporal gyri, and lower
parts of the angular and supramarginal gyrus. (B) Patient C.M., post-operative MR-study. Area of tissue resection including posterior temporal and
inferior parietal areas roughly corresponding to preoperative lesion extension.

was only mildly reduced. Yet, in G.S. and W.K., the
Token Test revealed a more profound impairment,
probably due to the requirement of auditory–verbal
short-term memory functions for this particular test.
Reading was intact in G.S. and W.K., but mildly re-
duced in C.M. Writing was severely impaired in W.K.,
whereas only minor writing deficits were found in the
other two patients. Thus, comparing the deficits of our
patients with descriptions of uncrossed conduction
aphasia (Bartha & Benke, 2003; Benson et al., 1973;
Caramazza et al., 1981; Goodglass, 1992; Rothi et al.,
1982), the language profiles of our study sample appear
quite consistent with the classic combination of lin-
guistic deficits found in common conduction aphasia.
4.2. Cognitive deficits accompanying language impair-
ment
Various authors attributed deficits in syntactic
comprehension in conduction aphasia to reduced ver-
bal–auditory short-term memory rather than to a glo-
bal language comprehension deficit (Bartha & Benke,
2003; Caramazza et al., 1981). The present study adds
to this evidence, as both patients with auditory–verbal
short-term memory impairment (W.K. and G.S.) dis-
played significantly reduced syntactic comprehension
abilities. By contrast, the patient who exhibited normal
short-term memory functions performed flawless on the
syntactic comprehension task. Comprehension of
words and sentences, however, was only mildly reduced
in all three cases. Additional cognitive deficits were
found in ideomotor praxis and visuoperception (G.S.
and C.M.), numerical processing (W.K.), and figural
memory (C.M.). Ideomotor apraxia and deficits in
numerical processing are typically manifestations of
conduction aphasia (Benson et al., 1973; Delazer &
Bartha, 2001; Girelli et al., 2002) but visuoperceptual
deficits and figural memory impairment, as found in
the above cases, are uncommon following left temporo-
parietal lesions.
92 L. Bartha et al. / Brain and Language 88 (2004) 83–95
Fig. 3. (continued)
4.3. Outcome of crossed conduction aphasia
Conduction aphasia is generally known as a rela-
tively mild variant of language impairment, and it is
reported that many patients return home and continue
their former work (Benson et al., 1973). However, as
evidenced in this study, crossed conduction aphasia
may result in chronic linguistic deficits. Although G.S.
showed some improvement he still exhibited language
deficits, while conduction aphasia persisted in both
other patients. Additionally, W.K. still presented nu-
merical and short-term memory deficits. In this case
study, we found no transformation of conduction
aphasia into other aphasic syndromes (ÔSyndromen-
wandelÕ, Leischner, 1987). Notably, C.M.Õs and W.K.Õs
outcome, who both had undergone a tumour exstir-
pation, was worse than G.S.Õ, who developed conduc-
tion aphasia following an ischemic infarction. A
possible explanation for this finding is that surgical
interventions in the human brain cause more perma-
nent damage to the tissue involved than ischemic
lesions. Furthermore, it can be hypothesized that
language functions in G.S. were not fully lateralized in
the right hemisphere.
4.4. Brain lesions in crossed conduction aphasia
MRI studies showed that crossed conduction aphasia
in our three patients was caused by focal cortico-sub-
cortical lesions in the right hemisphere (Figs. 1–3). No
coexisting left-hemisphere lesion was found. This lesion
pattern was relatively consistent across the three subjects
including posterior temporal, inferior parietal, and lat-
eral occipital regions. With respect to lesions found in
uncrossed conduction aphasia (Axer et al., 2001; Bartha
& Benke, 2003; Damasio & Damasio, 1980; Palumbo,
1992), the lesion sites appear as being located in the
homologous, right-hemisphere brain areas.
4.5. Lesion lateralization and cognitive deficits: Mirror-
image or unique pattern?
The findings of this study suggest that language and
auditory–verbal short-term memory of the three patients
 L. Bartha et al. / Brain and Language 88 (2004) 83–95
were lateralized to the right hemisphere. The underlying
lesions were located in brain areas which are typical for
conduction aphasia, with the exception that they were
located in the right hemisphere. Thus, linguistic deficits
and lesion locations of our patients demonstrate a mir-
ror image pattern of standard conduction aphasia.
Ideomotor apraxia, when present, was also crossed. A
different pattern was found for accompanying cognitive
impairments, such as visuoperception and figural
memory. Since neuropsychological studies (e.g., Benton,
1985; Jones-Gotman, 1992) have identified these func-
tions as typical right-hemispheric abilities, the most
stringent explanation for the present findings is that the
crossed conduction aphasia patients in this study have
visuoperceptual abilities and figural memory lateralized
to the right hemisphere. We therefore conclude that vi-
sual-perceptual abilities and figural memory functions in
our patients are normally represented indicating a dis-
sociation of lateralization of language, praxis, visuo-
perception, and figural memory.
In summary, our case studies confirm recent findings
in crossed aphasia that focal right-hemispheric lesions
do not always result in non-fluent aphasia with intact
language comprehension, but can also produce classic
aphasic syndromes like conduction aphasia. In contrast
to previous reports of crossed aphasia where detailed
language examination is often not available, our study
presents comprehensive examination of various lan-
guage modalities and associated cognitive functions
including auditory–verbal short-term memory and
syntactic comprehension, thus allowing a deeper insight
in the uncommon syndrome of crossed conduction
aphasia. In addition, it shows that none of our patients
exhibited only language deficits; thus, in case of a more
in-depth investigation of cognitive functioning, crossed
aphasia turns out to be accompanied by additional
cognitive impairment—both crossed and uncrossed.
Moreover, the outcome of crossed conduction aphasia
was not known previously; therefore follow-up exam-
inations are presented which uncover crossed conduc-
tion aphasia as a potentially chronic syndrome.
The neuropsychological data also show that reduced
auditory–verbal short-term memory is an optional, not
an obligatory accompanying deficit in conduction
aphasia. Furthermore, evidence is added to the as-
sumption that impaired syntactic understanding often
found in conduction aphasia is attributed to reduced
auditory–verbal short-term memory.
Our study also demonstrates that preoperative lan-
guage assessment and language lateralization studies are
important in all patients regardless of lesion site, since
even in some strong dextrals preoperative estimation of
language outcome seems unpredictable on merely a
clinical basis. Finally, the variability of accompanying
deficits in our patients exhibits the lack of clear-cut
groups of functions lateralized to the same hemisphere
93
and underlines the need for a detailed assessment of
each cognitive domain.
Acknowledgments
The authors gratefully thank Dr. Armin Muigg for
referring the patients W.K. and C.M., as well as Dr.
Thomas Erlacher for referring the patient G.S. The
paper was prepared during a tenure of a project grant to
the first author from the O€ sterreichische Nationalbank
Jubil€aumsfonds Nr. 8741.
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