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Journal of Neurolinguistics 19 (2006) 346–355

www.elsevier.com/locate/jneuroling

The foreign accent syndrome: A perspective

Sheila E. Blumstein, Kathleen Kurowski
Department of Cognitive and Linguistic Sciences, Brown University, Box 1978, Providence, RI 02912, USA
Received 8 November 2005; accepted 14 March 2006

Abstract

Although there are now a fair number of reported case studies of the foreign accent syndrome,
there is little consensus about it. We provide a perspective on the foreign accent syndrome focusing
on three areas for which there is as yet disagreement in the literature. These include whether the
foreign accent syndrome is indeed a syndrome in its own right, whether the features of the disorder
can be explicated in terms of a single underlying mechanism, and whether there is a common neural
substrate that gives rise to this disorder. Based on a review of the literature and our own work, we
propose that the foreign accent syndrome is properly considered a syndrome and that it is distinct in
both its characteristics and underlying mechanism from an apraxia of speech, a dysarthria, and an
aphasic speech output disorder. We hypothesize that a deficit in linguistic prosody underlies the
foreign accent syndrome. And finally, we argue that the foreign accent syndrome emerges as a
consequence of damage to the dominant language (usually left hemisphere) speech output motor
system affecting the primary motor cortex and either its cortico-cortical connections or its cortico-
subcortical projections.
r 2006 Elsevier Ltd. All rights reserved.

Keywords: Foreign accent syndrome

1. Introduction

The foreign accent syndrome has been of great interest in the neurolinguistic and
neuropsychological literature as well as in the popular press in part because of the very
unique features it displays and in part because of the challenge it provides for our
understanding of the neural systems underlying speech production. While there are now a

Corresponding author. Tel.: +1 401 863 2849; fax: +1 401 863 2255.
E-mail address: Sheila_Blumstein@brown.edu (S.E. Blumstein).

0911-6044/$ - see front matter r 2006 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jneuroling.2006.03.003
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fair number of reported cases, there is still little consensus about this syndrome. There is
disagreement about whether the foreign accent syndrome is indeed a syndrome in its own
right or a subtype of an apraxia, aphasia, or dysarthria. There is disagreement about
whether the features of the disorder can be explicated in terms of a single underlying
mechanism. And there is disagreement about whether there is a common neural substrate
that gives rise to this disorder. In the following, we consider each of these issues in an
attempt to provide a perspective on the foreign accent syndrome.
The proposals that we will outline concerning the basis of the foreign accent syndrome,
its underlying mechanism, and its neuropathology are just that, hypotheses which will need
further study. One of the factors which has contributed to the difficulty of determining the
nature of the foreign accent syndrome has been the very different approaches that have
been taken in the analyses of the individual case studies. Some studies have focused on
descriptive assessments of listeners, others have focused on analysis of broad and/or
narrow phonetic transcriptions, and still others have used instrumental analyses to
quantitatively assess the speech patterns of the patients. The stimulus materials have varied
widely across studies, making direct comparisons across subjects difficult. The focus of
these studies has also been different. Some have tried to determine whether the features of
their patient’s output matched a particular foreign accent or dialect, and others compared
the productions to the patient’s native language. And finally, the range of different native
languages of the patients studied has varied considerably, making it difficult to assess
whether different patterns across studies reflect the impairment of different mechanisms
across patients or the different phonetic-phonological structures of the languages studied.
Nonetheless, the studies of the foreign accent syndrome to date have provided a rich set of
data which are beginning to show some important commonalities that we believe allow for
some general hypotheses about the nature of the syndrome, its basis, and its neural
underpinnings.

2. Towards a differential diagnosis of the foreign accent syndrome

The task of delineating what constitutes the foreign accent syndrome has proven difficult
because, although the behavioral data suggests that foreign accent syndrome patients have
broadly similar phonetic characteristics, the particular patterning, direction, and extent of
anomalous features differ across patients. Moreover, in 68% of the cases, the foreign
accent syndrome emerges in a setting complicated by the co-occurrence of aphasic,
apraxic, and/or dysarthric deficits (Aronson, 1990), leading some researchers to define the
foreign accent syndrome as only a subtype of another speech disorder such as apraxia
(Coelho & Robb, 2001; Moen, 2000) or as an aphasic epiphenomenon (Ardila, Rosselli, &
Ardila, 1988).
One approach to the problem of specifying the constellation of speech deficits uniquely
subsumed under the foreign accent syndrome is to distinguish the speech pattern of these
patients from that of other speech output disorders. Perhaps the most critical difference is
also the most obvious: foreign accent syndrome patients sound like normal speakers who
have acquired a foreign accent rather than like impaired speakers whose productions
violate the phonetic features of natural language. This is because the characteristic features
of the speech of these patients are still potential attributes of natural language, while
the speech of patients with apraxia of speech, Broca’s aphasia or dysarthria is
characterized by distortions of natural language properties (Blumstein, Alexander, Ryalls,
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Katz, & Dworetzky, 1987). Acoustic and perceptual analyses to date investigating these
phonetic deficits have generally corroborated this hypothesis. We will briefly review some
of the evidence suggesting that the foreign accent syndrome is neither a sub-type nor a mild
form of dysarthria, apraxia, or Broca’s aphasia (cf. also Gurd, Bessell, Bladon, &
Bamford, 1988 for discussion).
With respect to dysarthria, Goodglass (1993, p. 63) described this speech disorder
in terms of ‘‘defects of articulation that are caused by impaired motor strength,
impaired coordination, or by structural defects of the articulatory apparatus’’. Crucially,
these deficits remain constant under all speech conditions. Since the particular
speech characteristics of the foreign accent syndrome, like aphasic errors, occur
intermittently in a patient’s speech, this factor alone would support the distinction
between the foreign accent syndrome and dysarthria, and as well, would suggest that
the foreign accent syndrome is not a mild form of dysarthria. Moreover,
dysarthric productions may violate some phonetic features of natural language. For
example, Blumstein, Cooper, Goodglass, Statlender, and Gottlieb (1980) found that their
dysarthric patient produced aspirated stops with unusually long VOTs (greater than
150 ms), due to extreme degrees of aspiration. Since no language permits such extreme
aspiration, such productions would be perceived by the listener as pathological, not
‘‘foreign’’.
With respect to apraxia of speech or verbal apraxia, research efforts are still focused on
the basic problem of defining and differentiating apraxia of speech from dysarthria and
aphasia (Croot, 2002; Rosenbek and McNeil, 1991). Kent and Rosenbek (1983, p. 231)
refer to apraxia of speech as ‘‘a controversial disorder’’, acknowledging that what they
called apraxia of speech might be called Broca’s aphasia or motor aphasia by other
researchers (1983, p. 233; see also Lesser, 1978; Buckingham, 1981). In fact, Kent and
Rosenbek’s results are in keeping with the articulatory deficits of Broca’s aphasia: (1)
frequent mis-timing and discoordination of voicing with other articulations; (2) occasional
errors of segment selection; (3) initiation difficulties; (4) slowed speaking rate; (5) slow and
inaccurate movements of the articulators to spatial targets; (6) restricted variation in
relative peak intensity across syllables but preservation of terminal F0 fall. Likewise,
Blumstein and Baum (1987), in their review of consonant production deficits in aphasia,
found that the articulatory disorder of Broca’s aphasia and apraxia of speech are for the
most part indistinguishable.
Given the possibility of collapsing across aphasic and apraxic deficits, we turn to the
question of why the foreign accent syndrome is neither an aphasic nor an apraxic disorder.
More specifically, we will consider the differences between the foreign accent syndrome
and the nonfluent aphasias that typically result from left anterior lesions. It is important to
state at the outset that, since each of these disorders is defined as a syndrome, the full array
or constellation of deficits associated with each disorder may not be found in any one
patient. However, it is possible to select some defining or essential aspects of each
syndrome for this analysis. For example, both the foreign accent syndrome and anterior
aphasia are characterized by prosodic deficits involving intonation. However, many
foreign accent syndrome patients show a range of ‘‘foreign-sounding’’ intonation contours
on the sentential level: sharply rising pitch at the end of sentences (Monrad-Krohn, 1947;
Blumstein et al., 1987; Moonis et al., 1996); excessively steep terminal falls (Ingram,
McCormack, & Kennedy, 1992); and inverted pitch contours (Takayama, Sugishita, Kido,
Ogawa, & Akiguchi, 1993). In contrast, Broca’s aphasics show a flat (monotonic)
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intonation with a restricted fundamental frequency range. On the segmental level, foreign
accent syndrome patients demonstrate a range of anomalous features of vowel production
in sharp contrast to aphasic patients who show a predominance of impairments in the
production of consonants. In fact, analyses of the patterns of vowel productions in Broca’s
aphasics have shown some, but not many vowel substitution errors, and normal formant
frequency and duration distributions of vowels. The pathological aspects of aphasic vowel
production involved increased variability (standard deviations) in vowel formant
frequencies and in vowel duration (Ryalls, 1987).
Again, we may consider why the speech of patients with the foreign accent syndrome is
perceived as ‘‘foreign’’ whereas aphasic speech is perceived as pathological. In English, the
occurrence of the following foreign accent syndrome characteristics are all within the
category of potential attributes of natural language: syllable-timed speech rhythm instead
of stress-timed speech rhythm; the insertion of epenthetic vowels which change syllable
structure; tense vowel systems in place of tense/lax systems; sentential intonation patterns
with rising contours. These alterations would produce the effect of making the English
speaker sound as if s/he had a foreign accent but not a speech disorder. In contrast, no
language has an intonation system which is atonal and monotonic or a consonantal system
which allows for a voiceless phonetic category with exaggerated voice-onset time and/or
aspiration values. In such cases, the speech of that speaker would be perceived as
pathological precisely because there is no language that has such attributes as part of its
inventory.
Having considered the distinction between the foreign accent syndrome and dysarthria,
aphasia, and apraxia, we briefly turn to three recent cases of the foreign accent syndrome
which afford us the opportunity to refine our criteria for defining the syndrome. The first
two cases involve patients who were exposed to more than one language and re-acquired
an accent. Seliger, Abrams and Horton (1992) described a 65-year-old left-handed woman
with a New York or Bronx accent premorbidly who began speaking with an Irish brogue
after a neurological event that caused dysarthria and right hemiplegia; the CT scan was
negative. Although the patient’s mother spoke with an Irish brogue, the patient did not
explicitly recall having the accent as a child. Seliger et al. speculated that the Irish brogue
represented the return of a suppressed prosody pattern. Likewise, Roth, Fink, Cherney,
and Hall (1997) reported a 45-year-old man re-acquiring his native Dutch accent which he
had lost as a young man. Both cases fail to meet what may be considered essential
attributes of the foreign accent syndrome: namely, the sudden appearance of an unlearned
generic accent. As Seliger et al. note, cases of previously acquired accents that suddenly re-
appear after neurological insult do open interesting questions of cortical reorganization
and/or potential different anatomic localizations of languages learned at different ages.
However, in such cases, the particular foreign accent was a part of the speaking/listening
environment of the patient premorbidly.
Reeves and Norton (2001) reported on a case of ‘‘Foreign Accent-Like Syndrome’’ in
which a schizophrenic patient began speaking with a British accent only during severe
psychotic episodes. The patient’s history revealed that he had a British caregiver as a child.
While Reeves and Norton described this case as foreign accent-like, it again points to the
need to exclude any patient with previous long-term exposure to a second language or
dialect if the purported foreign accent is that of the earlier language or dialect. Lastly, it
must be stressed that the etiology of the foreign accent syndrome is neurogenic not
psychiatric.
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3. The basis of the foreign accent syndrome

Having considered what the foreign accent syndrome is not, it is worth focusing on those
attributes which may serve as definitional properties of the disorder. In one sense, the label
used to characterize the syndrome, the foreign accent syndrome, is unfortunate, since it
suggests in its name an ‘explanation’ that is untrue. As has been clearly attested in many
studies, the foreign accent syndrome is not an acquired dialect or foreign accent. That is,
the patient does not assume a speech output pattern that corresponds to an altered
phonetic-phonological output consistent with a particular foreign language or dialect. In
point of fact, perceptual judgments of listeners including trained phoneticians are
remarkably inconsistent within the same patient. It is not uncommon for descriptions of
the same patients to ‘sound like’ they are native speakers of several different languages
(Aronson, 1990; Blumstein et al., 1987; Coelho & Robb, 2001; Gurd et al., 1988). For
example, Ingram et al. (1992) report that their English-speaking Australian subject
sounded Asian, Swedish, or German. Moen (2000) describes an English-speaking patient
who was reported as sounding Italian, Polish, or Czech. And Monrad-Krohn’s (1947)
Norwegian patient sounded either German or French. It is worth noting that judgments of
the speech patterns that listeners perceive often cut across different language families
(Germanic, Romance, Balto-Slavic, Sino-Tibetan), which typically have different
phonological and phonetic systems. Thus, it is clear that from a descriptive point of
view listeners are essentially being ‘fooled’ into attributing the sound pattern of their
subjects to a foreign language or dialect. Of interest, such judgments may occur
irrespective of the experience or familiarity of the listener with a broad range of languages
and language families. Even phoneticians show disagreements in their assessment of the
‘origins’ of the purported foreign accent.
Consistent with the descriptive findings are the results from those studies which have
investigated the acoustic characteristics of the speech output of these patients. The
quantitative data indicate that the acoustic patterns of speech do not reflect the acoustic-
phonetic patterns or even vestiges of a particular language or dialect. One way to explore
this question is to select an attribute of the foreign accent and investigate whether the
speech pattern of the patient is consistent with that attribute. For example, voice-onset
time, a measure of voicing in stop consonants, displays different patterns in English
compared to the Romance languages. Thus, it is possible to examine directly whether an
English speaking patient with a ‘French’ sounding foreign accent produces voicing that is
consistent with a French speaker or an English speaker. Blumstein et al. (1987) showed
that their English speaking patient, who sounded ‘French,’ produced voicing patterns in
stop consonants that were consistent with English, not French. Moreover, even if there is
some consensus that the patient sounds like s/he speaks a particular dialect, acoustic
analyses have shown little evidence for the presence of features typical of the particular
accent (Dankovičová et al., 2001).
Having said all of this, the question remains as to what is the foreign accent syndrome
and why has there been no consensus on a characterization of the features that give rise to
this syndrome. In our view, the foreign accent syndrome is a speech output disorder that is
primarily a disorder of linguistic prosody (as distinct from emotional or affective prosody).
Broadly construed, prosody encompasses those properties of speech relating to pitch,
stress, and quantity (Lehiste, 1970). Deficits in prosody would affect many aspects of
speech output but would have the greatest effect on the production of vowels (their
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duration and tenseness), on stress patterns of words affecting the overall rhythm of speech
as well as syllable structure and the phonetic characteristics of both vowels and consonants
in the immediate environment, and on local pitch manifestations as well as more global
intonation patterns. As a consequence, segmental errors may occur, but they are secondary
to the prosodic disturbance. For example, as discussed by Blumstein et al. (1987), changes
in speech rhythm from stress-timed to syllable-timed could have been the basis for a
number of the segmental errors that their foreign accent syndrome patient made including
the addition of epenthetic vowels, the production of full stops instead of flaps
intervocalically, and changes in vowel length and tenseness.
Nearly, all papers in the literature claim that deficits in linguistic prosody emerge as a
characteristic feature of the speech pattern in foreign accent syndrome patients (Berthier,
Ruiz, Massone, Starkstein, & Leiguarda, 1991; Coelho & Robb, 2001). In a review of the
literature, Coelho and Robb (2001) report that 93% of the cases of foreign accent
syndrome have a prosodic disturbance. Prosody is used as a cover term to characterize
local pitch reductions, increased pitch excursions, and the more global characteristic of
prosody including rhythm and timing as well as pitch or intonation. That this disorder is
linguistic and not a more generalized prosodic disturbance is supported by the fact that
these patients typically are reported to be within normal limits or have minimal
impairments in their production of affective prosody (Berthier et al., 1991; Carbary,
Patterson, & Snyder, 2000; Takayama et al., 1993).
Nonetheless, it is the case that not all features of a prosodic disturbance emerge in all
patients. As a consequence, some have questioned whether indeed the foreign accent
syndrome is truly a syndrome and whether it is a unitary disorder (Ardila et al., 1988;
Moen, 2000; for discussion see Kurowski, Blumstein, & Alexander, 1996). That the
patterns of speech output vary across patients could be suggestive of different underlying
mechanisms encompassing the foreign accent patients. However, an alternative possibility
is that, similar to all neuropsychological disorders, there are differences in the severity of
impairment across patients. That is, there is a common syndrome for all patients who are
diagnosed with the foreign accent syndrome but the severity of their impairment varies. If
this were the case, some characteristics of the speech pattern would be present in virtually
all cases although the extent of that characteristic might vary. Other characteristics would
emerge only in some cases and not in others.
Prosodic characteristics that seem to be present in all cases of foreign accent
syndrome are changes in timing and rhythm affecting stress and quantity. Such changes
result in the production of segments with manifestations particularly in the production of
vowels and some aspects of consonant production. In contrast, while there appear to be
local changes in intonation resulting in a reduced pitch range, the more extensive
modulations of intonation in which there are larger than expected pitch changes
particularly at the end of phrases or sentences do not emerge in all patients
(cf. Dankovičová et al., 2001; Kurowski et al., 1996). Thus, we hypothesize that intonation
changes emerge as a more severe manifestation of the foreign accent syndrome. In fact,
there have been few cases reported of patients whose intonation patterns include
occurrence of the large pitch excursions at the ends of sentences or phrases (cf. Blumstein
et al., 1987; Moen, 2000; Monrad-Krohn, (1947); Moonis et al, 1996). These large pitch
excursions occur only sporadically, but they are so unusual and noticeable that their
presence appears as a dominant descriptive characteristic for these patients (cf. also
Ingram et al., 1992).
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Evidence against the hypothesis that the presence of intonation impairments reflects a
more severe manifestation of the foreign accent syndrome would be the presence of a
patient who displayed impairments only in the production of intonation as described
above and the absence of deficits in rhythm and timing. As far as we know, no such case
has been reported in the literature. Berthier et al. (1991) report two cases of patients who
had recovered from the foreign accent syndrome and indicate that the only residual deficit
is one of intonation. However, these two patients show a local deficit in the production of
intonation characterized by a restricted range of intonation, and not the larger intonation
excursions which we have proposed emerge only in the more severe patients.

4. Neural underpinnings

One of the challenges with all single case research is determining the underlying neural
basis of the disorder. With relatively few cases identified in the literature and, of these, only
a subset with any details on lesion localization, it has been difficult to identify a clear-cut
pattern of neuropathology. Nonetheless, if one assumes that focal lesions impair networks
rather than discrete isolated areas with a particular function, then a pattern of
neuropathology is beginning to emerge which suggests certain commonalities across
patients.
Nearly all cases of foreign accent syndrome have resulted from a left hemisphere lesion
which is anterior. Most foreign accent patients have smaller lesions (relative to those found
in the aphasias) which appear to involve Broca’s area, the adjacent inferior motor strip,
and/or the middle frontal gyrus (Berthier et al., 1991; Berthier, 1994; cf. also summaries of
Blumstein et al., 1987; Carbary et al., 2000). There are reported cases of lesions restricted
to subcortical areas, but these appear to involve basal ganglia structures. Taken together,
these findings suggest that the foreign accent syndrome emerges as a consequence of
damage to the speech output motor system affecting the primary motor cortex and either
cortico-cortical connections with it or its cortico-subcortical projections.
There are four cases which appear to be exceptions to this pattern. In particular, there
are three reported cases of patients with the foreign accent syndrome who were reported to
have lesions in the right hemisphere (Berthier et al., 1991; Critchley, 1970; Dankovičová et
al., 2001) and a reported case of a patient with a left parietal lobe lesion (Roth et al., 1997).
These cases would appear to challenge the claim that the neuropathology of the foreign
accent syndrome is restricted to left hemisphere pathology of the frontal speech motor
system. However, further consideration of the individual cases suggests that they may
indeed not serve as ‘exceptions’.
With respect to the cases with right hemisphere pathology, the emergence of the foreign
accent syndrome could well be due to the fact that these patients have an anomalous
dominance. In such a case, it would be expected that similar lesion loci to those found in
left hemisphere patients would result in the foreign accent syndrome. The evidence from
the three reported cases of a foreign accent syndrome subsequent to a right hemisphere
lesion is consistent with this view. The one case where there are detailed neuropathological
findings (Berthier et al., 1991) reported a right hemisphere lesion which was subcortical
‘involving most of the white matter underlying the middle portion of the right precentral
and postcentral gyri’ (Berthier et al., 1991, p. 136). Critchley (1970) reported that his
patient had a crossed Broca’s aphasia which evolved into the speech output pattern of the
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foreign accent syndrome. The presence of an aphasia with right hemisphere damage
supports the view that this patient did indeed have anomalous dominance.
The third case of the foreign accent syndrome following right hemisphere damage was
reported by Dankovičová et al. (2001) and presents a more complicated picture. This
patient had a subarachnoid hemorrhage presumably from a large terminal carotid
aneurysm, and subsequently a large infarct in the right middle cerebral artery. Further
details of the lesion were not available. This patient is particularly interesting in
considering whether the foreign accent emerges with either right or left hemisphere damage
irrespective of language dominance. She appeared to have problems with pragmatic
aspects of language consistent with a pattern of right hemisphere lesions in a left
hemisphere language dominant individual. Moreover, she showed no evidence of a mild
Broca’s aphasia, often shown in the early course of the syndrome. However, early post-
onset, she did have some features characteristic of an aphasia. She had a mild dysarthria
and used sentences which were lengthy, convoluted, and often unintelligible. She also
spoke rapidly and without self-monitoring. Importantly, she was reported to have no
difficulties with affective prosody, a pattern consistent with left hemisphere damaged
patients with the foreign accent syndrome, but inconsistent with patients with right
hemisphere language dominance. That is, left language dominant patients with right
hemisphere damage typically display deficits with affective prosody (Ross, 1981). The lack
of an impairment in affective prosody coupled with some signs of aphasia is suggestive of
either a crossed or mixed dominance for language in this right hemisphere damaged
foreign accent syndrome patient.
Finally, only one patient has been reported who had a foreign accent syndrome as a
consequence of a left hemisphere parietal lobe lesion (Roth et al., 1997). Nonetheless, it is
not clear that this patient can be considered as an example of the foreign accent syndrome.
This patient displayed the emergence of a previously learned foreign accent. One of the
primary characteristics of the foreign accent syndrome is the emergence of a new speech
pattern, one which in point of fact sounds like a foreign accent but cannot be attributed
either to the individual’s premorbid accent or to an actual existing dialect or language.
Thus, this patient cannot be considered as an exception to the neuropathology shown for
patients with the foreign accent syndrome.
There is no doubt that further detailed descriptions of the lesion localization in patients
with the foreign accent syndrome are necessary. However, the syndrome appears to emerge
with damage to the language dominant frontal neural systems underlying speech and
motor control.

5. Summary

On the basis of consideration of the various case study reports in the literature and our
own work, we have proposed that the foreign accent syndrome is properly considered a
syndrome and that it is distinct in both its characteristics and underlying mechanism from
an apraxia of speech, a dysarthria or an aphasic speech output disorder. We also proposed
that the foreign accent syndrome is primarily a disorder of linguistic prosody. And finally,
we proposed that the foreign accent syndrome emerges as a consequence of damage to the
dominant language (usually left hemisphere) speech output motor system affecting the
primary motor cortex and either its cortico-cortical connections or its cortico-subcortical
projections. Clearly, more research will be required to test these hypotheses. However, it is
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our hope and expectation that as we apply more sophisticated techniques in the analysis of
the speech output of these foreign accent syndrome patients and as we begin to have more
consistent analyses of the neuroradiological findings, we will come to a deeper
understanding of this interesting and challenging speech output disorder.

Acknowledgements

This research was supported in part by NIH Grant DC00314 to Brown University.

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