Brain & Language 119 (2011) 119–128

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Brain & Language

journal homepage: www.elsevier.com/locate/b&l

Conduction aphasia, sensory-motor integration, and phonological short-term

memory – An aggregate analysis of lesion and fMRI data
Bradley R. Buchsbaum a,⇑, Juliana Baldo b, Kayoko Okada d, Karen F. Berman e, Nina Dronkers b,
Mark D’Esposito c, Gregory Hickok d,⇑
a
Rotman Research Institute, Toronto, Ontario, Canada
b
VA Northern California Health Care System, Center for Aphasia and Related Disorders, Martinez, CA, USA
c
Department of Psychology, University of California, Berkeley, CA, USA
d
Department of Cognitive Sciences, University of California, Irvine, CA, USA
e
Section on Integrative Neuroimaging, National Institute of Mental Health, Bethesda, MD, USA

a r t i c l e i n f o a b s t r a c t

Article history: Conduction aphasia is a language disorder characterized by frequent speech errors, impaired verbatim
Accepted 11 December 2010 repetition, a deficit in phonological short-term memory, and naming difficulties in the presence of other-
Available online 21 January 2011 wise fluent and grammatical speech output. While traditional models of conduction aphasia have typi-
cally implicated white matter pathways, recent advances in lesions reconstruction methodology
Keywords: applied to groups of patients have implicated left temporoparietal zones. Parallel work using functional
Conduction aphasia magnetic resonance imaging (fMRI) has pinpointed a region in the posterior most portion of the left pla-
Working memory
num temporale, area Spt, which is critical for phonological working memory. Here we show that the
Speech production
Planum temporale
region of maximal lesion overlap in a sample of 14 patients with conduction aphasia perfectly circum-
Brain lesion scribes area Spt, as defined in an aggregate fMRI analysis of 105 subjects performing a phonological work-
Sensorimotor integration ing memory task. We provide a review of the evidence supporting the idea that Spt is an interface site for
Phonological short-term memory the integration of sensory and vocal tract-related motor representations of complex sound sequences,
such as speech and music and show how the symptoms of conduction aphasia can be explained by dam-
age to this system.
Ó 2011 Elsevier Inc. All rights reserved.

1. Introduction monitoring – and attempting to correct – their own errors in

speech output. This self-correcting behavior often results in re-
Conduction aphasia, first described in 1874 by Carl Wernicke, is peated unsuccessful efforts to correct a phonological speech error
a syndrome that is characterized by frequent phonemic parapha- (e.g., ‘‘baselaw, lacelaw, basecall, casecall . . .’’ for baseball), a
sias (sound-based speech errors) with attempts at self-correction, behavior that is sometimes referred to as conduite d’approche
impaired verbatim repetition, and naming difficulties in the pres- (Goodglass, 1992).
ence of otherwise fluent and grammatical speech output. In con- The main symptoms of conduction aphasia point to a deficit at a
trast to these deficits in speech production, patients with phonological level of processing. The paraphasic errors made by
conduction aphasia have relatively spared auditory comprehension patients with conduction aphasia are overwhelmingly of a phone-
(Baldo, Klostermann, & Dronkers, 2008; Benson et al., 1973; Dama- mic variety (Bartha & Benke, 2003; Goodglass, 1992), the repetition
sio & Damasio, 1980; Goodglass, 1992). deficit appears to reflect a deficit in phonological short-term mem-
The phonological production deficits in conduction aphasia are ory (Baldo & Dronkers, 2006; Baldo et al., 2008), and the naming
linked to articulatory planning load, so that picture naming or rep- deficit is frequently associated with tip-of-the-tongue states and
etition of multi-syllabic words, sentences, and phrases is especially is benefitted by phonemic cueing (Goodglass, Kaplan, Weintraub,
impaired (Goodglass, 1992). Due to their relatively preserved audi- & Ackerman, 1976). Of course, there is considerable syndromic var-
tory comprehension, conduction aphasics are capable of accurately iation among patients with conduction aphasia; however, in the
current study, we use the diagnostic label ‘‘conduction aphasia’’
⇑ Corresponding authors. Address: Rotman Research Institute, Baycrest Hospital, to refer to aphasic patients that share a similar pattern of language
3560 Bathurst St., Toronto, ON, Canada M4Y1 M2. Fax: +1 416 785 2862 (B.R. deficits that include relatively preserved auditory comprehension
Buchsbaum). Center for Cognitive Neuroscience, Department of Cognitive Sciences, in the presence of fluent but paraphasic speech output and dramat-
University of California, Irvine, Irvine, CA 926978, USA (G. Hickok). ically impaired repetition.
E-mail address: [email protected] (G. Hickok).

0093-934X/$ - see front matter Ó 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.bandl.2010.12.001
120 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128

Neurological tradition has attributed conduction aphasia to action of sensory and motor systems during speech production and
damage to a white matter tract, the arcuate fasciculus that con- phonological short-term memory. Thus, the phonemic paraphasias
nects the two major language centers, Wernicke’s and Broca’s area and repetition difficulties that characterize conduction aphasia are
(Geschwind, 1965). Thus, conduction aphasia has often been re- the result of a damaged sensory-motor integration circuit that
ferred to as a ‘‘disconnection syndrome’’ because the lesion to leads to an impairment in the capacity for auditory representations
the arcuate fasciculus is assumed to interrupt communication be- of speech to constrain and guide the corresponding articulatory
tween the sensory and motor modules of the classically defined representations thought to be stored in the inferior frontal gyrus
speech language system. More recent evidence, however, indicates and ventral premotor cortex (Hickok & Poeppel, 2000, 2004; Wise
that damage to the arcuate fasciculus is not a prerequisite of con- et al., 2001). To date, the correspondence between the functionally
duction aphasia (Dronkers, 2000; Shuren et al., 1995). Moreover, defined area Spt and the lesion sites associated with conduction
electrical stimulation of the left superior temporal gyrus (STG) in aphasia has been indirect, approximate, and anatomically impre-
an epileptic patient has been shown to induce phonemic parapha- cise. With the emergence of methods such as voxel-based lesion
sias and auditory-verbal repetition deficits, a finding suggesting mapping, however, and the ability to place functional neuroimag-
that cortical dysfunction alone is sufficient to produce the symp- ing results in the same normalized anatomical space as lesion data,
toms of conduction aphasia (Anderson et al., 1999). Finally, most we now have the ability to directly test whether indeed conduction
of the available anatomical evidence suggests that conduction aphasia involves damage to area Spt.
aphasia is most often caused by damage to the left superior tempo- Simple tests of phonological working memory that involve an
ral gyrus and/or the left supramarginal gyrus, that is, a region cen- unfilled delay period interposed between speech stimulus presen-
tered around the posterior portion of the Sylvian fissure (Axer, von tation and a memory test require that a subject can both accurately
Keyserlingk, Berks, & von Keyserlingk, 2001; Baldo & Dronkers, register and encode an input stimulus sequence and can maintain
2006; Damasio & Damasio, 1980; Green & Howes, 1977; Turken an internal representation of that code during the delay. We have
et al., 2008). hypothesized that area Spt is critical for the transformation from
Functional neuroimaging research in the last 15 years has indi- an auditory ‘‘input’’ code to an articulatory, or ‘‘output’’, code that
cated an important role for this temporoparietal zone in tasks of must occur during tests of simple repetition as well as phonologi-
phonological short-term memory and speech production. Studies cal working memory. In the context of functional neuroimaging,
of object naming (Hickok et al., 2000; Okada, Smith, Humphries, however, the temporal separation between encoding, mainte-
& Hickok, 2003), single-word repetition (Price et al., 1996), silent nance, and response components of the task allows for a separate
reading (Buchsbaum, Olsen, Koch, Kohn, et al., 2005), and covert assessment of brain activation for each phase. Thus, as a practical
articulation of syllables (Paus, Perry, Zatorre, Worsley, & Evans, matter, phonological working memory tasks offer a useful way of
1996; Wildgruber, Kischka, Ackermann, Klose, & Grodd, 1999) have isolating regions that are active during stimulus perception,
shown elevated activation in the posterior superior temporal area, short-term maintenance – or both.
even in the absence of auditory input or feedback (e.g. during cov- In the present study, we have gathered 105 single subject fMRI
ert production). Moreover, several studies have shown that during scans on a phonological working memory paradigm, collected
speech production tasks, posterior superior temporal activity is across five studies and three laboratories, and performed an aggre-
modulated by phonological variables such as word length and fre- gate analysis on the entire set of statistical activation maps (see
quency (Graves, Grabowski, Mehta, & Gordon, 2007; Graves, Yarkoni, Barch, Gray, Conturo, & Braver, 2009). To compare the spa-
Grabowski, Mehta, & Gupta, 2008; Levelt, Praamstra, Meyer, tial pattern of activation in the fMRI phonological working memory
Helenius, & Salmelin, 1998; Okada et al., 2003). Studies examining analysis with the lesion distribution of conduction aphasia, we per-
phonological short-term memory that have used auditory-verbal formed a conjunction analysis of the aggregate fMRI map with the
stimuli and a relatively extended covert maintenance period have lesion distribution in stereotaxically normalized space of 14
consistently shown that a region in the posterior portion of the pla- patients with chronic conduction aphasia (Turken et al., 2008).
num temporale, area Spt (Sylvian-parietal–temporal), activates We predicted and confirmed that the area of maximum lesion
during both perception (stimulus encoding) and convert rehearsal probability among patients with conduction aphasia would
in tests of phonological memory (for a review, see Buchsbaum and contain within its bounds area Spt, as defined in fMRI studies of
D’Esposito (2008), Chein, Ravizza, and Fiez (2003) and Jacquemot phonological working memory. In the Discussion, we review evi-
and Scott (2006)). Examination of single subject activations in dence supporting the idea that conduction aphasia is a disorder
these studies (Buchsbaum, Hickok, & Humphries, 2001; Hickok, of sensory-motor integration that is caused by damage to area Spt.
Buchsbaum, Humphries, & Muftuler, 2003) reveals that the area
of maximal activity during phonological rehearsal tasks is most
often located in planum temporale at the posterior end of the left 2. Methods
Sylvian fissure, inferior to the supramarginal gyrus. Finally, the
peak Talairach coordinate reported for delay period activity in 2.1. Aggregate fMRI analysis
studies of phonological working memory is nearly identical to
the coordinates reported in basic speech production tasks The data entered in the aggregate fMRI analysis were taken
(Buchsbaum, Olsen, Koch, Kohn, et al., 2005; Graves et al., 2007, from five verbal working memory studies carried out by the
2008). In short, Spt activates during the performance of behaviors authors in the last 5 years. The studies were selected because each
that are impaired in conduction aphasia (repetition, naming, verbal involved auditory presentation of verbal material followed by a de-
short-term memory), and is located in an area of cortex often dam- lay period involving verbal rehearsal, and because relevant con-
aged in patients with the disorder. trasts for these ‘‘encoding’’ and ‘‘delay’’ phases of the task were
One hypothesis that has recently been advanced (Hickok & available (in non-normalized ‘‘native’’ image space) for each of
Poeppel, 2004, 2007) is that Spt functions as an interface site for the 105 individual subjects (age range: 8–42) that took part in
the integration of sensory and vocal tract-related motor represen- the studies. We did not include two studies (Buchsbaum et al.,
tations of complex sound sequences, including speech and music 2001; Hickok et al., 2003) from our laboratories because the data
(Hickok, Okada, & Serences, 2009; Pa & Hickok, 2008). According sets were relatively small (13 subjects combined) and because
to this hypothesis, conduction aphasia is a deficit that is caused the data had been archived and were not readily available. Aside
by damage to Spt and surrounding tissue, which disrupts the inter- from these two omissions, we included all studies that were
 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128 121

carried out in our collective laboratories and met our inclusion cri-
teria (further detailed below).
Two of these studies have been previously published
(Buchsbaum, Olsen, Koch, & Berman, 2005; Hickok et al., 2009),
and three others (Finn et al., in preparation; Buchsbaum et al.,
submitted for publication; Buchsbaum et al., in preparation) are
currently unpublished (see Table 1). Each of the studies used a sim-
ilar task paradigm and shared the following features: (1) auditory
presentation of phonological stimuli during a short stimulus
encoding period, (2) at least an 8 s delay period in which subjects
were instructed to covertly rehearse to the to-be-remembered
items, and (3) a response phase in which memory for the presented
items were tested via serial recall or a recognition memory probe
requiring a yes/no response. In each study, then, an estimate of
both stimulus-related and maintenance-related activation during
phonological working memory could be assessed by separately
modeling the encoding and delay phases of the trial (see Fig. 1).
For more detail on the task and scanner parameters for the studies,
see Supplementary appendix 1. Fig. 1. General task structure and fMRI modeling of Phonological Short-term
The analysis of delay-period activation was performed on the memory paradigms. Each of the five fMRI tasks included in the aggregate analysis
contrast maps representing the difference in activation during followed the same basic structure: there was an encoding phase during which
the retention interval and a baseline estimate of BOLD activity. In auditry-verbal stimuli were presented; this was followed by a delay period in which
subjects were instrcuted to covertly rehearse the just-presented items; this was
each of the five studies, the full trial was modeled with a set of
followed by a test phase, in which subjects were instructed to either overtly recall
temporally shifted hemodynamic regressors (see Fig 1.), one for the items in order, or to make a recognition judgment.
each phase (encoding, delay, recall/probe). The activation magni-
tude for any of the three phases corresponds to the beta estimate
for the appropriate term in the multiple regression model. These statistical significance of the contrast at the group level. Instead,
raw magnitude estimates of the activity in each phase of the trial for each voxel in normalized space, we counted the number of sub-
were then assessed for statistical significance using one-tailed jects with a z-statistic for the contrast of interest that exceeded
t-tests. In each study entering the analysis, the first level (i.e. 2.05 (p < 0.01, one-tailed). The threshold was chosen to be rela-
within-study) statistical analyses were computed in native (non- tively lenient so as to increase sensitivity to smaller effects. Note
spatially normalized) image space and then were transformed to that this threshold was not used to determine statistical signifi-
stereotaxically normalized space (using the MNI template). cance at the group level (see resampling procedure described be-
To ensure consistency in the method of normalization across low) but only for the purposes of counting the number of
studies, where available (93 out 105 subjects), high resolution subjects with an above-threshold activation at each voxel. This
structural MRIs were normalized to the same stereotaxic reference raw count was then converted to a percentage, and a corrected sig-
space using the MNI atlas. A nonlinear volumetric image registra- nificance threshold was determined through a permutation-based
tion program (FNIRT; http://www.fmrib.ox.ac.uk/fsl/fnirt) was resampling procedure (Nichols and Holmes, 2002). To derive a null
used to warp each subject’s MRI to normalized MNI space. The distribution for the expected proportion of activated voxels given
nonlinear registration parameters were then used to transform the empirical distribution of the z-statistics in the set of 105 con-
all of the native space statistical contrast maps to normalized tem- trasts, the spatial indices (excluding non-brain voxels) of each of
plate space. This normalization procedure was applied even for the the 105 normalized contrast maps were randomly permuted. The
set contrasts that had come from previously published data sets proportion of z-statistics exceeding 2.05 was computed for each
(Buchsbaum, Olsen, Koch, et al., 2005; Hickok et al., 2009) – which voxel in the set of spatially permuted contrast maps, and the max-
had applied slightly different normalization routines – so as to imum value across the entire reshuffled volume was recorded. This
maximize the degree of cross-study consistency. For the 12 sub- was repeated for 100 iterations and the threshold for statistical sig-
jects for which the original high-resolution MRIs were not avail- nificance was determined to be the 5th largest (for a corrected
able, a low resolution EPI image was instead used for linear (12 p < .05 alpha) value in the set. Thus, the end result was a whole-
parameter affine model) spatial normalization to the MNI template brain (or family-wise) correction for multiple comparisons that
using the program FLIRT (Jenkinson & Smith, 2001). was based on the empirical distribution of z-statistics in the set
Because the studies differed in a variety of ways including the of 105 contrast maps. Because the empirical distributions were
field strength (3T or 4T) of the MRI scanner, the number of trials slightly different for the encoding and delay contrasts, this method
in the session, the precise imaging sequence used, etc., we did yielded different thresholds for the two contrasts, namely 37% for
not compute a typical parametric one-sample t-statistic to access the encoding maps and 28% for the delay maps. Thus, a voxel

Table 1
Basic information about studies that entered fMRI meta-analysis.

Study N Stimuli Encoding (s) Delay (s) Probe

Buchsbaum, Olsen, Koch, et al. (2005) and Buchsbaum, Olsen, Koch, Kohn, et al. (2005) 12 Two words 4 10 Recall
Buchsbaum et al. (submitted for publication) 10 Six letters 6 10 Recognition
Finn et al. (in preparation) 23 Seven letters 6 8 Recall
Buchsbaum et al. (in preparation) 34 Nine letters 8 12 Recall
Hickok et al. (2009) 22 Jabberwocky sentences 3 12 Oddball detection

Study = the study contributing the fMRI contrast maps; N = number of subjects; Stimuli = the type of verbal stimuli used in working memory task; Encoding = the duration of
the stimulus encoding phase; Delay = the duration of the delay phase; Probe = the manner in which memory was tested following the delay period.
122 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128

was declared significant across the group if 37% or 28% of subjects gist, who was blind to the patients’ diagnoses and goals of the
had a z-statistic exceeding 2.05 in the encoding and delay con- study, reviewed the lesion reconstructions for accuracy. Next, the
trasts, respectively. A null hypothesis distribution for the conjunc- scans were non-linearly transformed into MNI space (MNI-152
tion of encoding and delay phases – i.e. the percentage of subjects template) using SPM5 running on Matlab software (Mathworks,
with significant values (p < 0.01) for both encoding and delay Natick, MA). Lesion masks were used for each reconstruction so
phases – was generated using the same resampling scheme and that the SPM normalization procedure was not affected by the
yielded a threshold of 22%. Analyses of the test phase (probe or re- presence of the lesion (i.e., cost function masking) (see Brett, Leff,
call) periods were not performed due to the heterogeneity in the Rorden, & Ashburner, 2001). When digital images were not avail-
tasks employed and because the main point of theoretical interest able (N = 7), the same board-certified neurologist reconstructed
was the encoding and delay phases. the lesions onto an 11-slice template based on the atlas of
DeArmond et al. (see Friedrich, Egly, Rafal, & Beck, 1998; Knight,
2.2. Lesion overlap mapping Scabini, Woods, & Clayworth, 1988). These 11-slice reconstructions
were digitized and then non-linearly transformed into MNI space
2.2.1. Participants using SPM5. To do this, the two templates were aligned using 50
The sample consisted of fourteen patients (4 women and 10 control point pairs to match anatomical features. The slices were
men) who suffered a single, left hemisphere (LH) middle cerebral then aligned using a local weighted mean transformation imple-
artery stroke resulting in a chronic conduction aphasia. Patients mented by the cpselect, cp2tform and imtransform functions in
were selected from a large pool of patients at the Center for Apha- Matlab 6.5. These algorithms were applied to warp the lesion
sia and Related Disorders, VA Northern California Health Care Sys- reconstructions from the 11-slice template into MNI space. All 14
tem (VANCHCS) based on the following criteria: Native English patients’ reconstructed lesions were then overlaid to reveal regions
speakers in the chronic phase of stroke (>12 months post-onset), of maximal lesion overlap.
with no pre-morbid history of psychiatric illness, dementia or neu-
rologic illness. The diagnosis of conduction aphasia was made
based on the pattern of performance on the Western Aphasia Bat- 3. Results
tery (WAB) (Kertesz, 1982), namely, impaired repetition (0–69%
correct), moderate to preserved fluency (50–100% correct), and rel- 3.1. Aggregate fMRI analysis
atively good comprehension (70–100% correct). Spontaneous
speech and naming errors in this group were primarily phonemic As can be seen in Fig. 2, activation during both the encoding and
in nature. Patients’ overall languages scores on the WAB ranged delay periods was most prominent in frontal, lateral temporal, and
from 40 to 88 (out of 100), which were all below the cut-off for parietal cortices, bilaterally. During encoding, almost the entire ex-
normal language performance (i.e., all patients were aphasic). tent of the auditory and multisensory cortex of the bilateral supe-
Patients’ mean age was 61.6 (SD = 9.3; range 48–77); mean educa- rior temporal lobe was active. During rehearsal, however, activity
tion was 13.0 (SD = 3.7; range = 5–18); and number of months in the superior temporal area was confined only to a few areas,
post-stroke was 56.1 (SD = 55.8; range = 13–247). See Table 2 for including the left posterior planum temporale (Area Spt), the left
performance scores for each subject on the subtests of the WAB. posterior superior temporal sulcus (pSTS), and the middle superior
All patients were pre-morbidly right-handed, except for one temporal sulcus (mSTS), bilaterally. Activation in the frontal cortex
patient who was left-handed and one patient who reported being during both encoding and delay was most robust in the left hemi-
ambidextrous. sphere along the dorso-ventral axis comprising premotor cortex,
the inferior frontal gyrus, and the anterior insula (see Fig. 2). The
2.4. Lesion overlay analysis supplementary motor area on the medial wall and superior parietal
cortex, bilaterally, were also reliably active during rehearsal. The
Patient lesions were reconstructed from CT and MRI scans ac- single most consistent region of rehearsal-related activity in the
quired around the time of testing. For cases where digital MRI brain, with 77% of subjects showing a significant effect in the peak
images were available (N = 7), lesions were traced directly onto voxel (MNI: x = 51, y = 12, z = 41), was located in the dorsal por-
T1 scans using MRIcro software (Rorden & Brett, 2000). A neurolo- tion of the precentral gyrus.

Table 2
Characterization of individuals with conduction aphasia.

Subject AQ Rep. Naming Comp. Digit span Word span single syll. Word span multi syll.
1063 75 56 72 78 2 2 –
0806 40 9 2 70 0 0 0
1138 65 16 68 80 2 1 0
1133 70 56 76 90 3 1 1
1015 67 49 80 84 2 2 2
1137 73 51 83 89 – – –
0736 74 48 64 98 2 2 2
0626 88 61 79 98 2 4 4
0694 83 64 82 96 3 2 3
0822 67 52 36 88 3 2 2
0718 74 64 79 84 2 2 2
0820 72 49 71 82 2 2 2
0639 80 58 87 82 – – –
0655 78 53 76 82 – – –

Notes. AQ = aphasia quotient (out of 100); Rep. = WAB repetition percentage; Naming = WAB naming percentage; Comp. = WAB auditory comprehension percentage; Word
Span Single Syll. = maximum number of single-syllable words repeated aloud; Word Span Multi Syll. = maximum number of multi-syllabic words repeated aloud; – = data not
available.
 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128 123

Fig. 2. Proportion of subjects showing reliable activation during encoding and delay phases. Each of the four brain surfaces shows the percentage of subjects showing
significant activity (p < 0.01 at single subject level) for the either encoding > baseline or the delay > baseline contrasts. These images are unthresholded so that entire cortical
pattern can be visualized. Whole-brain thresholds corrected for multiple comparisons were 37% (for encoding) and 28% (for delay).

3.2. Conjunction of encoding and delay contrasts Table 3

MNI coordinates of activated clusters for encoding \ delay conjunction.
To examine regions that were active both during stimulus Cluster size Max% X Y Z Label
encoding and verbal memory maintenance, we performed a con-
1701 69 51 9 42 Precentral sulcus
junction analysis between the delay and encoding meta-contrasts. 580 46 30 54 39 Intraparietal sulcus
The purpose of this contrast was to distinguish regions that are ac- 529 62 0 9 51 Supplementary motor area
tive both during auditory-perceptual encoding and during covert 503 43 27 63 21 Cerebellum
467 33 57 6 42 Precentral sulcus
rehearsal from those that are active exclusively in one of the two
255 44 45 36 45 Intraparietal sulcus
task phases (e.g. pure sensory or pure rehearsal-related areas). 178 33 36 18 6 Anterior insula
We have previously used this contrast to identify area Spt (e.g. 103 44 21 6 0 Putamen
Hickok et al., 2003), which activates robustly both to auditory 70 33 51 42 21 Posterior planum temporale
input and during covert rehearsal. Thus, if Spt has sensory-motor 33 27 60 30 3 Superior temporal sulcus
30 29 63 24 0 Superior temporal sulcus
properties it should therefore show robust activity both during
28 28 30 3 51 Middle frontal gyrus
auditory-verbal perception and during covert speech or covert 9 23 12 6 0 Caudate nucleus
rehearsal.
As can be seen in Fig. 3, a number of regions were active during
both task phases, including dorsal and ventral portions of the pre- right nor left auditory cortex was reliably activated during
frontal cortex the intraparietal sulcus, STS bilaterally, and area Spt rehearsal, a finding that is consistent with previous reports (e.g.
in the left planum temporale (see Table 3 for MNI coordinates of Buchsbaum, Olsen, Koch, et al., 2005; Hickok et al., 2003). In
activated clusters; maximum coordinate: 51, 43, 20). Neither addition, while area Spt and a region in the posterior STS were

Fig. 3. Proportion of subjects showing reliable activation for the conjunction of encoding and delay phases. Left and right brain inflated surfaces showing areas active both
during encoding and during the delay period. The surfaces are thresholded at 22%, corresponding to a whole-brain corrected p-value of 0.05.
124 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128

active only in the left hemisphere in the conjunction analysis, the activated regions in fMRI studies of phonological short-term mem-
middle portion of the STS was reliably active in both hemispheres ory was in the left posterior planum temporale region, area Spt, a
(see Fig. 3). site which has been argued to support sensory-motor integration
The peak percentage of overlap in Spt was what might appear to for vocal tract actions (Hickok et al., 2009). In what follows, we will
be a relatively modest value of 33% (35 out of 105 subjects). This summarize the arguments for Spt as a sensory-motor integration
number, however, reflects to some extent the neuroanatomical var- area and discuss how this claim can illuminate the symptom com-
iability of the posterior portion of the planum temporale, which is plex of conduction aphasia.
difficult to align across subjects due to individual differences in
the trajectory of the Sylvian fissure (Westbury, Zatorre, & Evans, 4.1. Sensory-motor integration in area Spt
1999). Visual inspection of single subjects activation reveals a clus-
ter of activity in the posterior planum temporale. To illustrate this, a By sensory-motor integration, we mean the mechanism by
single slice (in MNI space; z = 24) showing single-subject encoding which sensory information can be used to guide action. Visually
\ delay activation for all 14 subjects from study #2 (as numbered guided reaching/grasping is a canonical example. Visual informa-
in Table 1) is displayed in Supplementary Fig. 1. Each subject’s acti- tion about the location and shape of a coffee cup can be used to
vation is overlaid on the subject’s own MRI after nonlinear registra- guide a reach toward and grasp of that cup. To achieve this task,
tion to MNI space. Although all of the 14 subjects have a cluster of location and shape information from the visual system must be
activation in the posterior planum temporale, the peak value in transformed from visual representations into some representation
the group overlap map is only 50%. Thus, even with 100% of subjects that can inform action. During the action itself, sensory feedback is
in a group showing activation in the immediate vicinity of planum also critical to ensure accuracy of the movement. Thus sensory-
temporale, anatomical variation (as well as variation in the mapping motor integration is critical for motor control (Kawato, 1999;
between function and structure) is sufficiently large that it cannot Shadmehr & Krakauer, 2008). In the speech domain, there is
be fully corrected by nonlinear registration. unequivocal evidence for sensory involvement of speech produc-
tion. For example, delayed auditory feedback of one’s own voice
disrupts speech fluency (Stuart, Kalinowski, Rastatter, & Lynch,
3.3. Comparison with conduction aphasia
2002; Yates, 1963). Other forms of altered speech feedback have
similar effects: shifting the pitch or first formant (frequency band
To directly compare the area of activation associated with pho-
of speech) in the auditory feedback of a speaker results in rapid
nological working memory in the temporal lobe with the distribu-
compensatory modulation of speech output (Burnett, Senner, &
tion of lesions in conduction aphasia (Baldo et al., 2008), the fMRI
Larson, 1997; Houde & Jordan, 1998). Altered auditory feedback
conjunction (encoding + delay) analysis was compared with a
has been found to activate the posterior planum temporal region
lesion overlay map based on 14 patients with chronic conduction
relative to unaltered speech (Tourville, Reilly, & Guenther, 2008),
aphasia. In the left two panels of Fig. 4, the two overlap maps are
suggesting that Spt is involved in this form of sensory-motor inte-
shown on a left hemisphere cortical surface. The region most often
gration. Levelt (1983) has also documented the importance of feed-
compromised in this group of patients with conduction aphasia
back monitoring in speech production.
was centered in left temporoparietal cortex, in an area encompass-
The functional properties of sensory-motor systems have been
ing parts of the supramarginal and angular gyri as well as the pos-
studied extensively in the context of the visual system. For exam-
terior superior temporal cortex. The area of maximum overlap (85%
ple, it has been found that in the parietal lobe of the macaque, the
lesion overlap and significant encoding/delay fMRI conjunction)
intraparietal sulcus (IPS) contains a constellation of functional
between the lesion overlap map and the fMRI conjunction map is
regions that support sensory-motor integration (Andersen, Snyder,
displayed in the rightmost panel of Fig. 4, where it can be seen that
Bradley, & Xing, 1997; Colby & Goldberg, 1999; Grefkes & Fink,
the peak area of cross-study overlap is located squarely in the pos-
2005). These regions are organized around motor effector systems
terior portion of the planum temporale (area Spt).
(for a recent review see (Grefkes & Fink, 2005).
Spt has been shown to exhibit functional properties character-
4. Discussion istic of sensory-motor areas in the macaque IPS. Spt shows sen-
sory-motor response properties responding both during the
The main result of our analysis was that the maximum overlap perception and production of speech (Buchsbaum, Olsen, Koch,
between the distribution of lesions in conduction aphasia and the Kohn, et al., 2005; Buchsbaum, Olsen, Koch, et al., 2005;

Fig. 4. A comparison of conduction aphasia, phonological working memory in fMRI, and their overlap. The uninflated surface in the left panel shows the regional distribution
lesion overlap in patients with conduction aphasia (max is 12/14 or 85% overlap). Middle panel shows the unthresholded conjunction of encoding and delay maps in the
aggregate fMRI analysis (see Fig. 3 for thresholded and inflated view of the same data). The right panel shows the area of maximal overlap between the lesion and fMRI
surfaces (lesion >85% overlap and significant fMRI activity for conjunction of encoding and delay).
 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128 125

Buchsbaum et al., 2001; Hickok et al., 2003) as well as for non- noted as is typical in conduction aphasia) (Howard & Nickels,
speech vocal tract actions such as humming melodic stimuli (Hickok 2005; Jacquemot, Dupoux, & Bachoud-Levi, 2007). This pattern of
et al., 2003; Pa & Hickok, 2008). A recent study has demonstrated sparing and loss was interpreted in one report as evidence for a
that the pattern of activity across voxels in Spt is different during disconnection between phonological input and output codes
the sensory and motor phase of such tasks indicating partially (Jacquemot et al., 2007), which is in line with our proposed expla-
distinct populations of cells, some sensory-weighted and some nation of conduction aphasia. Interestingly, there is also evidence
motor-weighted (Hickok et al., 2009). A similar distribution of cell that conduction aphasics are less affected by delayed auditory
types has been found in monkey IPS sensory-motor areas (Grefkes feedback than controls as would be expected if the repetition def-
& Fink, 2005). Spt activity is tightly correlated with activity in fron- icit results from disruption of sensory-motor integration systems
tal speech-production related areas, such as the pars opercularis (BA (Boller, Vrtunski, Kim, & Mack, 1978).
44) (Buchsbaum et al., 2001) suggesting that the two regions are This explains the repetition deficit, but what about paraphasias
functionally connected. Spt activity is motor-effector selective, in spontaneous speech output where there is not a sensory trace to
responding with greater magnitude when the output task involves maintain? There is reason to believe that speakers rely to some ex-
the vocal tract compared to the manual effectors (Pa & Hickok, tent on an auditory-phonological memory of words they are
2008). Finally, Spt includes cortex on the posterior planum tempo- attempting to produce, as Wernicke proposed, or in modern motor
rale. The planum temporale is often considered an auditory region. control terminology that the targets of a motor speech act are audi-
However, human cytoarchitectonic studies (Galaburda & Sanides, tory in nature as argued explicitly by Guenther, Hampson, and
1980) and comparative studies in monkeys (Smiley et al., 2007) Johnson (1998). If motor control of speech production is driven
indicate that the posterior PT region is not part of unimodal auditory by auditory speech targets and if the link between auditory and
cortex. Consistent with this, recent functional studies have found motor systems is disrupted, one expects an increase in the error
that Spt responds also to visual input that is relevant to vocal tract rate in speech production, i.e., paraphasias in spontaneous speech.
actions such as visual speech (lip reading) (Okada & Hickok, Further, one expects that the error rate would increase as a func-
2009). Taken together, this constitutes strong evidence for Spt as a tion of processing load as is the case with conduction aphasics.
sensory-motor integration area for the vocal tract. Consistent with this, functional imaging studies have shown word
length and word frequency effects in auditory-related areas,
4.2. Sensory-motor integration and conduction aphasia including Spt and STS, during speech production: longer or lower
frequency words yield greater activation than shorter or higher fre-
It has been proposed that deficits in repetition and speech quency words in picture naming tasks (Graves et al., 2007; Okada
production typical of conduction aphasia may be viewed as a sen- et al., 2003; Wilson, Isenberg, & Hickok, 2009). Thus the present
sory-motor integration deficit resulting from damage to area Spt model provides an explanation for phonemic paraphasias in speech
(Hickok & Poeppel, 2000, 2004; Hickok et al., 2003). This hypothe- production.
sis explains paraphasic speech output fairly straightforwardly on A prevalent view in the literature is that conduction aphasics
the assumption that speech production relies on auditory guidance have a phonological short-term memory deficit (Baldo et al.,
(e.g., auditory feedback control) at least under some circumstances. 2008; Caramazza, Basili, Koller, & Berndt, 1981; Shallice &
It has already been established that the auditory system guides Warrington, 1977), specifically affecting the phonological store
speech production rapidly and automatically in cases of altered component (Baddeley, 1992). This component is assumed to be a
auditory feedback at the phonetic level (an example of auditory temporary store for phonological information that is distinct from
guidance from self-monitoring). It is also clear that higher-level auditory-phonological processing systems involved in speech com-
auditory information (e.g., sequences of sounds) can guide speech prehension. The contents of the phonological store can be kept
output. For example, it is trivial for healthy individuals to listen to active via articulatory rehearsal. The phonological store, together
and then parrot back a sequence of nonsense syllables (e.g., ba- with the articulatory rehearsal mechanism, constitutes the phono-
da-ga) or even a non-speech stimulus such as a novel melody or logical loop (Fig. 5A). This model explains not only the poor repeti-
sequence of tones (an example of auditory guidance from external tion via disruption of the phonological store, but also the preserved
input). Because nonsense syllables or tones are not represented in
conceptual-semantic memory, the repetition of such sequences
requires some form of auditory-motor interface capable of trans-
lating a sequence of sounds into a sequence of motor commands.
In short, it is clear that at least under some circumstances, includ-
ing both self- and other-generated speech, acoustic information
guides speech production.
Conduction aphasics typically have difficulty with verbatim
repetition of speech, and this difficulty is exacerbated by length
and decreased familiarity and/or decreased semantic constraint
(such as ‘‘He is the one who did it’’, or nonwords) (Goodglass,
1992). These situations require the patient to rely more extensively
on the auditory-phonological trace for successful repetition (How-
ard & Nickels, 2005). If Spt is damaged, the auditory-motor trans-
lation system will be dysfunctional, leading to more errors in
situations that require increased reliance on the auditory trace of
the input. Indeed a recent study found precisely that conduction
aphasics fail in situations that require retention of the auditory-
phonological trace of a perceived utterance (Baldo et al., 2008).
Several case studies have also been presented in which patients Fig. 5. Schemetic diagram showing the role of Spt in the phonological loop. (A) A
diagram showing the architecture of the phonological loop as typically presented
with conduction aphasia-like symptoms have disproportionate dif- (e.g. Baddeley, 1992). (B) Reinterpretation of the phonological loop as emerging
ficulty in repeating nonwords relative to intact speech perception from sensorimotor interaction between perceptual and motor speech centers,
and relatively preserved speech production (some errors were which is mediated by Spt.
126 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128

comprehension via the preserved auditory-phonological process- lateral superior temporal gyrus (STG) and posterior superior tem-
ing system. The sensory-motor account is not incompatible with poral sulcus (STS). These regions have also been implicated in pho-
this view. In fact it promotes a similar architecture, although with nological processing on the basis of their activation in a range of
different functional operations associated with the various archi- tasks including speech production (Indefrey & Levelt, 2000, 2004;
tectural components. Price et al., 1996; Wilson et al., 2009), speech perception (Binder
According to the sensory-motor account, phonological short- et al., 2000; Hickok & Poeppel, 2007; Liebenthal, Binder, Spitzer,
term memory is an emergent property of the sensory-motor circuit Possing, & Medler, 2005; Okada & Hickok, 2006; Scott & Wise,
(Fig. 5B) (Buchsbaum & D’Esposito, 2008; Buchsbaum, Olsen, Koch, 2004; Vaden, Muftuler, & Hickok, 2010), and auditory-phonological
et al., 2005; Hickok & Poeppel, 2007; Hickok et al., 2000, 2003; short-term memory (present result and (Buchsbaum, Olsen, Koch,
Postle, 2006). On this view, the articulatory rehearsal mechanism et al., 2005; Hickok et al., 2003)). We suggest that these STG/STS
is the same as in the phonological loop model, but the ‘‘phonological regions correspond to the ‘‘phonological processing’’ system in
store’’ is not a distinct, specialized buffer, but the same auditory- Fig. 5B. This raises a question: if left STG/STS regions support pho-
phonological system that is involved in processing speech for nological processing for comprehension and if these same regions
comprehension. A recent large-scale lesion study (N = 210) has pro- are damaged in at least some conduction aphasics, why is speech
vided evidence for this claim by demonstrating an association comprehension preserved in these patients? The answer is that
between STM function (digit span) and lesions involving the left speech recognition is bilaterally organized such that the right
STG/STS (Leff et al., 2009). In addition, the linkage between sensory STG/STS can support speech sound perception sufficiently well to
and motor components is mediated by a sensory-motor interface allow for good comprehension (Hickok & Poeppel, 2004, 2007;
component. The functional deficit in conduction aphasia, then, in- Hickok et al., 2000). Evidence for this view comes from chronic
volves damage to this sensory-motor interface, i.e., area Spt. This stroke studies which indicate that damage to the STG/STS is not
model (i) explains the phonological short-term memory deficit associated with substantial phonemic perception deficits in speech
because the articulatory mechanism can no longer refresh the recognition tasks (Baker, Blumstein, & Goodglass, 1981; Miceli,
contents of the ‘‘phonological store’’ (the auditory-phonological Gainotti, Caltagirone, & Masullo, 1980), from acute stroke studies
processing system), (ii) explains phonemic paraphasias because which show that phonemic perception deficits are mild even in
auditory-phonological information cannot be used normally to sup- acute stages of disruption (Rogalsky, Pitz, Hillis, & Hickok, 2008),
port speech production, and (iii) explains preserved comprehension and from Wada studies which indicate that even deactivation of
because auditory-phonological processing systems are not dam- the entire left hemisphere fails to substantially impair the ability
aged. Thus, the sensory-motor account not only explains phonolog- to distinguish subtle phonemic contrasts in auditory comprehen-
ical short-term memory parsimoniously as an emergent property of sion (Hickok et al., 2008). Thus, damage to auditory-phonological
a system that is needed independently for speech processing, and systems in the left hemisphere STG/STS only partially disrupts this
links this circuit to a class of sensory-motor circuits known to exist bilateral system, leaving comprehension minimally impaired.
in the primate parietal lobe, but also explains the co-occurrence of Another question raised by the STG/STS involvement in conduc-
phonological STM deficits and phonemic paraphasias in conduction tion aphasia is whether damage to this region results in distinct
aphasia. deficits compared to damage to Spt. From a functional standpoint,
One complication for this view is the existence of a small num- one might expect conduction aphasia-like symptoms to result from
ber of cases in the literature of nominal conduction aphasics damage to either the left hemisphere auditory-phonological sys-
(‘‘short-term memory patients’’ or ‘‘repetition conduction apha- tems or to the network (Spt) that interfaces these systems with
sics’’) that have difficulty with repetition and verbal STM and yet the articulatory systems (assuming that it is primarily the left
have little or no impairment in naming and spontaneous speech hemisphere auditory-phonological networks that interface with
production. The first thing to note is that none of the present sam- the motor system). Damage to either component could produce
ple of 14 patients with conduction aphasia could be classified as paraphasic errors and deficits in repetition and phonological STM
‘‘repetition conduction aphasics’’ as all had significant naming either because intact auditory-phonological systems cannot inter-
impairments and were well below the normal cut-off for perfor- face with the motor system (Spt damage) or because the auditory-
mance on a language battery. This is consistent with the fact that phonological system itself – that is, the portion of the system that
only a very small number of patients with ‘‘pure’’ verbal STM def- interfaces with the motor system – is disrupted (STG/STS damage).
icits in the presence of unimpaired spontaneous speech1 have been There is one symptom of conduction aphasia that may distinguish
reported in the literature (reviewed in Shallice & Vallar, 1990). The the contributions of these two components: word-finding. Word-
rarity of these STM cases suggests that they reflect an atypical func- finding deficits are common in conduction aphasia and these defi-
tional organization (or reorganization Nadeau, 2001). One possibility cits typically manifest as tip-of-the-tongue-like states (Goodglass
is that repetition conduction aphasia is associated with lesions that et al., 1976), which imply a deficit in accessing phonological forms
involve the lateral superior temporal cortex but spare the more for production (Vigliocco, Antonini, & Garrett, 1998). There is no
dorsally situated Spt, leading to deficits in memory for acoustic– obvious reason why a pure sensory-motor integration deficit
phonetic material but sparing speech production processes that should cause failures to access phonological forms. That is, one
depend on auditory-motor integration (Buchsbaum, Olsen, Koch, would expect that phonological forms should be activated
et al., 2005; Leff et al., 2009). To address the functional–anatomical accurately but that attempts to produce such forms may result in
puzzle presented by repetition conduction aphasia, however, it will paraphasic errors. Thus, we propose that damage to auditory-
be necessary to conduct large sample studies that involve a mixture phonological networks in the STG/STS is primarily responsible for
of symptom severity on relevant indices of speech production and word-finding deficits in conduction aphasia. There is some sugges-
STM, combined with high-resolution MRI and fMRI activation tive evidence for this view. A study comparing conduction aphasics
paradigms. with supra- versus infra-Sylvian lesions found that infra-Sylvian
Consistent with other recent studies, we found that lesions cases had more difficulty naming than supra-Sylvian cases (Axer
resulting in conduction aphasia sometimes involve the posterior et al., 2001). That same study found that infra-Sylvian cases also
performed worse on comprehension measures, as one might ex-
pect if auditory-phonological systems are partially damaged.
1
One indication of the latter group’s rarity is that its representatives are widely Somewhat surprisingly, infra-Sylvian cases were also more
known by their initials (e.g. Shallice & Butterworth, 1977; Vallar & Baddeley; 1984). impaired on the repetition test; damage to the sensory-motor
 B.R. Buchsbaum et al. / Brain & Language 119 (2011) 119–128 127

interface should disrupt repetition at least as much as damage to of research on the cortical organization of sensory and motor sys-
phonological processing systems. However, the repetition test in- tems. The division of sensory processing streams into two broad
volved semantically meaningful items that may have caused the streams, one with a tight connection to the motor system and
effect as follows. Repetition can be achieved via a semantic route the other with only indirect, perhaps semantically-mediated con-
as long as subtle semantic distinctions are not required (Baldo nections to action systems, appears to be an organizational prop-
et al., 2008). It may be that the supra-Sylvian group was able to rely erty of cortical sensory systems generally (Hickok & Poeppel,
on the semantic route more effectively than the infra-Sylvian 2007). This result is not only a satisfying example of convergence
group who had (partial) damage to auditory-phonological net- between traditionally distinct domains of research, but also opens
works and slightly depressed comprehension scores. We would the door to cross-fertilization between fields.
predict comparable deficits on a nonword repetition task. Overall,
these findings are suggestive of functional differences between Acknowledgments
STG/STS and Spt in terms of their involvement in the various symp-
toms of conduction aphasia, but more research is needed with lar- Supported in part by NIH Grant R01 DC03681 (GH).
ger sample sizes and more precise localizations to draw any firm
conclusions.
Appendix A. Supplementary material
It was noted above that Spt is not speech specific, activating
equally well when tonal stimuli are involved (Hickok et al.,
Supplementary data associated with this article can be found, in
2003). This is consistent with the claim that Spt supports sen-
sory-motor integration for the vocal tract as the sensory-motor the online version, at doi:10.1016/j.bandl.2010.12.001.
task for the tonal stimuli involved a vocal tract behavior: hum-
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