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Journal of Neurolinguistics 19 (2006) 341–345

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Guest editorial

Introduction to the theme issue on foreign accentsyndrome

Foreign accent syndrome (FAS) is a neurologically based speech disorder, in which arelatively sudden and subtle change in the patient’s speech occurs. They remain perfectlyintelligible and are mostly fluent, but friends and relatives who are familiar with theirformer accent remark on the ‘‘overnight change’’. The patient’s speech now resembles thatof a non-native (hence the name FAS), or possibly a native speaker from another region ofthe country (sometimes giving rise to the alternative terms, ‘‘changed’’ or ‘‘altered accentsyndrome’’). The aetiology is varied, and the syndrome can arise from various kinds ofneurological accidents, including mild strokes or closed head injuries. The condition isrelatively rare, compared, for example, to cases of aphasia, dysarthria, or apraxia ofspeech. Consultant neurologists or speech therapists may encounter one or at most a fewcases during their entire career. A recent survey we conducted of 100 UK adult-speech andlanguage therapists (SLTs) revealed that 20/100 (20%) had seen a total of 30 FAS casesduring their careers, and no individual SLT had seen more than three. These SLTs hadpracticed for an average of 14 years (SD 6.95, range 1.5–28). On average, then, each hadseen one and a half cases, or one case every ten years. Yet the literature on single-casestudies is now quite extensive, and some researchers (such as those whose work is includedhere) have studied a number of cases. As case studies accumulate, and as tools for digitalrecording and analysis of speech have become much more widely available, it is timely tobegin to seek to understand the syndrome more comprehensively. We may look forcommonalities in the underlying injuries, or in the features of speech that are affected. Wemay ask how the symptoms relate to other kinds of neurolinguistic disorders, and we mayquestion whether there is a single syndrome, or a variety of disorders sharing somesymptoms.

Our survey indicated that the personal cases reported were initially seen between 1983and 2002, with 64% (16/25) referred from 1994 onwards. The highest number of cases peryear increased to a peak of 6 in 2002.

To check whether this increase was linked to increased publication levels, we conducteda PubMed bibliographic citation search using the descriptor ‘FAS’. A total of 19publications were listed, dating from 1985 to 2004 (Fig. 1). It could be argued that SheilaBlumstein’s group were largely responsible for the renewed interest (Blumstein, Alexander,Ryalls, Katz, & Dworetzky, 1987; Ryalls & Reinvang, 1985). Thirty-two percent of thesepublications have appeared in the last 2 years alone. Of these cases, the female:male patient

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ARTICLE IN PRESSGuest editorial / Journal of Neurolinguistics 19 (2006) 341–345342

ratio was nearly equivalent at 1:1.17, and the median age of onset was lower for males(40s), than females (50s), with ranges from the 20s to 60+ for both. From Fig. 2 it can beseen that the male–female age of onset distributions also differ, in that male onset peaks intheir 40s, whereas females’ peaks a decade later.According to our questionnaire, the FAS patients were seen by SLTs in a variety of

treatment settings: 27% acute care (N ¼ 7), 65% rehabilitation (rehabilitation center,hospital out-patient, or community hospital) (N ¼ 17), and 8% domiciliary (N ¼ 2), withsome seen in acute care or rehabilitation settings. In three quarters (77%; N ¼ 20) of FAScases, the aetiology was vascular (i.e. stroke), but a further twenty percent (19.23%, N ¼ 5)resulted from head injury, and there was also one case in the context of Guillain–Barresyndrome. Three quarters of these changed accents were described as sounding European(19/25) (e.g. German, Italian, Swedish), with the rest having acquired different accents ofEnglish (N ¼ 2) (Irish, American), other accents (N ¼ 2) (e.g. East European, SouthAfrican, ‘deaf-sounding’), or unclassified (N ¼ 2) (i.e. unspecified ‘foreign-sounding’).With respect to additional speech and language impairments, over half (19/30; 63%) alsopresented with some form of aphasia. By contrast, only a quarter (8/30; 26%) weredescribed as dyspraxic, and an eighth (4/30; 13%) as dysarthric. Follow-up reports wereonly available for 50% of the cases: of these, half (7/14) persisted at 3-year post-onset, withapproximately equal numbers resolving after 1 year (N ¼ 4) or two (N ¼ 3). There appearsto be a clear association between an increase in the number of additional symptoms(especially dyspraxia), and the persistence of FAS at 3 year post-stroke; five cases forwhom there was follow-up fell into this category. A similar number of cases had resolvedby 3-year post-onset: 3 cases resolved at 2 years, and 1 at 1 year. Each of these had onlyone additional symptom: three were aphasic, and one dysarthric, but none were alsodyspraxic. There was no distinction between type of accent for these cases, most of whichwere classified as European (usually unspecified).The papers in this theme issue bring together recent work by some of the leading FAS

researchers. The papers offer a stocktaking of prior work, and (collectively as much as

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Fig. 1. Number of FAS cases reported per 5-year period (PubMed search).

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Fig. 2. Gender differences in age of onset: Number of UK FAS cases reported by SLTs.

Guest editorial / Journal of Neurolinguistics 19 (2006) 341–345 343

individually) give rise to new questions that should shape future case studies. We draw outsome of these questions in our Conclusion, at the end of the volume.

In The FAS: A Perspective, Sheila Blumstein and Kathleen Kurowski address threefundamental questions: (1) whether FAS is indeed a syndrome in its own right, distinctfrom e.g. aphasia, dysarthria or apraxia of speech; (2) whether the features of the disordercan be explained in terms of a single underlying mechanism; and (3) whether there is acommon neural substrate lesion which gives rise to the disorder. On the first question, theauthors argue that FAS is indeed distinct, though the question is made problematic byother disagreements in the field as to whether or to what extent aphasia and apraxia ofspeech contribute to the FAS. They draw attention to the fact that aphasic or apraxicspeech is typically perceived as pathological, whereas FAS speech is not: it is merely judgedto be ‘‘foreign-sounding’’, i.e. it is taken to be within the limits of normal speech variation.Blumstein and Kurowski, like many other authors, regard the various FAS cases withwhich they are familiar as being primarily a disorder of linguistic prosody (as distinct fromemotional or affective prosody). Although segmental changes are also found in FAS, theyconsider these to be secondary to the basic prosodic disorder. Indeed, it is now generallyrecognised by phonologists that the distinction between ‘‘segmental’’ vs. ‘‘prosodic’’features of speech is not always clear-cut, as various aspects of prosody, such as stress,rhythm, syllable structure, and intonational phrasing, may have short-term (‘‘segmental’’)as well as longer-domain (‘‘suprasegmental’’) phonetic correlates (Beckman & Edwards,1994; Firth, 1948; Jun, 1995; Trubetzkoy, 1969, pp. 170–207, 275–277). On the question ofa common neural substrate, Blumstein and Kurowski argue that ‘‘nearly all cases of FAShave resulted from a left hemisphere lesion which is anterior’’.

Speech Encoding Models and FAS, by Rosemary Varley, Sandra Whiteside, ClaireHammill and Katherine Cooper, also addresses the similarities and differences betweenFAS and other neurological speech disorders. As well as examining the observed phoneticcharacteristics of the changed speech of a single subject, they used a battery of tests to tryand disentangle the roles of conceptual-semantic, lexical and phrasal factors inthe disorder. They report that low imageability, low frequency, high phonetic complexityand greater word length all contributed to increased pronunciation changes. They thusidentify FAS as a disruption of automatized speech control processes—they argue that

ARTICLE IN PRESSGuest editorial / Journal of Neurolinguistics 19 (2006) 341–345344

it is essentially a mild form of apraxia of speech—but with compensatory mechanismsin place so that the speaker can maintain some degree of phonological accuracy inspeech.

FAS, speech rhythm and the functional neuroanatomy of speech production, by SophieScott, Frances Clegg, Peter Rudge and Paul Burgess, likewise examines the changed speechof a single case. Unlike many prior studies, they focus on stress, timing and rhythmdifficulties and they give as much weight to these prosodic problems as to the obviousmispronunciations of some vowels and consonants. The patient in this case had a smallwhite matter lesion, ventral to primary motor cortex, a region that might be involved in theintegration of phonological forms with separately represented suprasegmental features,such as stress. The locus of the lesion in this case is therefore quite similar to that in severalother previously reported cases, as reviewed by Carbary, Patterson, and Snyder (2000) andBlumstein and Kurowski (this volume).In their paper, Nick Miller, Anja Lowit, and Helen O’Sullivan ask What makes acquired

FAS foreign? As well as employing a battery of neuropsychological tests and an analysis oferrors in their subject’s speech, they measure an impressive selection of phonetic variables,which they compare to speech of a healthy control speaker of the same North-Easterndialect of British English. An interesting and valuable component of their methodology is aperceptual test in which listeners rated the ‘‘degree of foreignness’’ of a set of speakers,including the FAS case, four age-matched female speakers of the same local accent, four‘‘true’’ foreign accent speakers, and one speaker with a mild apraxia of speech, in anattempt to understand better the perceptual question posed in the title of the paper. Aregression analysis revealed that stress errors, schwa insertions and vowel errors togetheraccount for around 45% of the variance in foreignness rating. As in the other papers in thisspecial issue, a combination of segmental and prosodic factors appears to be involved.Inger Moen’s Analysis of a case of the FAS in terms of the framework of gestural

phonology employs a specific, articulatory-based framework (Kent, 1997) to interpret thechanged pronunciation of a Norwegian case. Whereas prior descriptions of pronunciationerrors are given in terms of the omission, insertion or substitution of one sound byanother, the framework adopted by Moen enables her to interpret the changed speech ofher subject in terms of two other factors: abnormal scaling of articulatory gestures andincorrect phasing of gestures. The former of these is exemplified by the under-scaling of lipprotrusion in rounded vowels, incorrect scaling of tongue tip and tongue body movementsin liquid consonants, and incorrect pitch movements due to mis-scaling of vocal cordtension. Incorrect phasing of articulatory gestures leads to incorrect synchronisation, suchas voicing commencing too soon in [k] or not early enough in [r], giving rise to over- andunder-voicing, respectively. Misalignment of the Norwegian tonal contours with thevowels and consonants is also interpreted as an instance of incorrect phasing. Although, asin Blumstein and Kurowski’s and Scott et al.’s cases Moen’s subject has a prosodicdisturbance, the framework she adopts enables her to describe or even account for theprosodic and segmental errors in a unified manner, in terms of two general types ofarticulatory problems.In our conclusion, FAS: Best practise, theoretical issues and outstanding questions, we

shall examine the main questions raised by this leading-edge research. Our discussion ofthem falls under three main headings: (1) best practice in the examination and study ofFAS cases, (2) the central scientific issues raised by research into FAS, and (3) the mostpressing unanswered questions for subsequent studies to address.

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References

Beckman, M. E., & Edwards, J. (1994). Articulatory evidence for differentiating stress categories. In P. A. Keating

(Ed.), Phonological structure and phonetic form: Papers in Laboratory Phonology III (pp. 7–33). Cambridge:

Cambridge University Press.

Blumstein, S. E., Alexander, M. P., Ryalls, J. H., Katz, W., & Dworetzky, B. (1987). On the nature of the foreign

accent syndrome: A case study. Brain and Language, 31, 215–244.

Carbary, T. J., Patterson, J. P., & Snyder, P. J. (2000). Foreign accent syndrome following a catastrophic second

injury: MRI correlates, linguistic and voice pattern analyses. Brain and Cognition, 43, 78–85.

Firth, J. R. (1948). Sounds and prosodies. Transactions of the Philological Society. Oxford: Oxford University

Press (Reprinted in Firth J. R. (1957). Papers in Linguistics 1934– 1951 (pp. 121–138)).

Jun, S.-A. (1995). Asymmetrical prosodic effects on the laryngeal gesture in Korean. In B. Connell, & A. Arvaniti

(Eds.), Phonology and phonetic evidence: Papers in Laboratory Phonology IV (pp. 235–253). Cambridge:

Cambridge University Press.

Kent, R. D. (1997). Gestural phonology: Basic concepts and applications in speech-language pathology. In M. J.

Ball, & R. D. Kent (Eds.), The new phonologies (pp. 247–268). London: Singular Publishing.

Ryalls, J., & Reinvang, I. (1985). Some further notes on Monrad–Krohn’s case study of foreign accent syndrome.

Folia Phoniatrica, 37, 160–162.

Trubetzkoy, N. S. (1969). Principles of phonology. Berkeley: University of California Press.

John ColemanPhonetics Laboratory,

University of Oxford,

UK

Jennifer GurdNeuropsychology Unit,

Department of Clinical Neurology,

University of Oxford, UK