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Freak speak or lingo star? A beginner’s guide to Foreign Accent Syndrome‬

Today’s Daily Telegraph featured the story of Englishman Alun Morgan who following a stroke now speaks fluent Welsh. Doctors diagnosed the 81-year old Mr Morgan with aphasia, a form of brain damage that causes a shift in the brain’s language centre. Mr Morgan is now being taught to speak English again.

Although often treated as a joke, ‘Foreign Accent Syndrome’ (FAS) is a very rare speech disorder but now medically recognized condition. FAS is typically characterized by the (sometimes sudden) appearance of a new speaking accent, identifiably different from the person’s native language. Prior exposure and knowledge to the newly acquired accent is not needed for it to occur and it is usually perceived as foreign or dialectical by fellow natives and, usually, by the person themselves. Published case studies have reported that it is impossible to fake FAS. However, the FAS sufferers don’t suddenly acquire a foreign language (vocabulary, grammar, syntax, etc.) just the accent (although the Wikipedia entry on FAS made reference to a news report that coming out of a coma, a 13-year old Croatian girl allegedly gained the ability to speak fluent German). However, as far I am aware, there are no proven cases where someone with improved their language skills following the development of FAS.

FAS typically occurs following a traumatic brain injury (e.g., head trauma, stroke, cerebral haemorrhage) although other conditions (such as multiple sclerosis) have also led to the development of FAS. Those with FAS often suffer in other ways including poor concentration span, poor memory, and feelings related to loss of identity. Research examining the brain structures of those with FAS have highlighted there are commonalities in relation to specific parts of the brain that are (unsurprisingly areas that control various language functions). More recently, there is growing empirical evidence that the cerebellum (which controls motor function) appears to be critical in the development of some cases of FAS. For instance, Dr. D.A. Cohen and his colleagues published a case study in a 2008 issue of the journal Neurology and concluded that their case demonstrated “that abnormal right cerebellar activity can play a causal role in perpetuating the FAS rather than being merely an epiphenomenon of damage to the reciprocally connected left hemisphere”. A series of papers published by a team led by Dr. P. Mariën have all conformed the role of the cerebellum in the acquisition of FAS (Clinical Neurology and Neurosurgery, 2006; Folia Phoniatrica et Logopaedica, 2007; Cortex, 2009).

The disorder was first described over 100 years ago (in 1907) by Dr. Pierre Marie (a French neurologist). This was followed by a Czech case study published in German by Dr. A Pick in 1919. (Unfortunately, these first two cases were not written in English so I have been unable to gain any details of either of the two cases described)

The first published case study written in English is believed to be one dating back to 1947 by the neurologist Dr. Monrad-Krohn. He described the case of a 30-year old female (Astrid L) from Norway who was hit on the head by shrapnel during a German air raid on Oslo in 1941. The injury led to aphasia, hemiplegia, and seizure disorder. This caused speech problems but within a year of the injury, the woman’s speech began to improve but it was different to how she had spoken before her head injury. Monrad-Krohn described how the woman’s ‘rhythm and melody’ of her voice had dramatically altered and that she sounded like she had a foreign (German sounding) accent (even though she had never travelled outside of Norway). Consequently, she was shunned and/or ridiculed by many of her native Norwegians. Since these three early published case studies, around 60 cases of FAS have been documented worldwide including people who went from speaking British to French, American to British, Japanese to Korean, and Spanish to Hungarian. A 2006 article by Diane Garst and William Katz highlighted the common features of FAS. The ‘classic’ characteristics are:

  • Monolingual patient is frequently mistaken for being a non-native speaker.
  • Speech changes are not triggered by psychiatric or psychological problems.
  • Idiosyncratic speech errors contribute to appearance of a cohesive ‘accent’
  • Patient is aware of accent and unhappy about it.
  • Voicing changes occur in both prosody (syllable-by-syllable timing, and abnormal pitch patterns) and segmentals (consonant distortions, substitutions, deletions; frequent problems with alveolar tap/flap; omplex or unusual vowel substitutions)

Writing in a 2007 issue of the Annals of General Psychiatry, Stéphane Poulin and colleagues noted that:

Different explanations of the functional origin of FAS have been suggested, one of the more frequent being impaired access to verbal-motor patterns or a mild form of apraxia of speech. Clinical manifestations are heterogeneous among FAS patients but usually include segmental (e.g., changes in vowel length and tenseness) and prosodic (e.g., inappropriate word and sentence stress) deficits”.

A 2005 paper in the journal European Neurology by Edwards, Patel and Pople examined 35 case published case studies of FAS. Their analysis reported that the majority (n=26) of those with FAS resulted from cerebral infarct. The remainder resulted from head injury (n=6), multiple sclerosis (n=2) and psychosis (n=1). In one-third of the cases (34%), the person with FAS also had agrammatism (i.e., a form of expressive aphasia that refers to the inability to speak in a grammatically correct way). As Stéphane Poulin and colleagues note:

“In spontaneous speech, agrammatic patients speak non-fluently and produce telegraphic speech. They mainly use content words (nouns, verbs, adjectives) and tend to omit or substitute function words (prepositions, articles and auxiliaries) as well as inflections or other grammatical morphemes. Among reported FAS cases, few brain imaging studies have been done and there is no consensus regarding the precise region responsible for its occurrence. Neuroanatomically, the vast majority of the lesions described were in the dominant hemisphere and in most cases involved regions typically associated with Broca’s aphasia. Subcortical structures seem to be consistently affected”.

Thanks to the internet and broadcast media, there are many cases of FAS that have not been reported in the academic and clinical literature. I’ll leave you with a few you can check out yourself. Just click on each name to get the details.

  • Tiffany Roberts: In 1999, 57-year old American woman Tiffany Roberts (from Indiana) had a stroke and developed an English accent.
  • Linda Walker: In 2006, a 60-year old British woman with a Geordie accent (from Newcastle) had a stroke and developed a strange accent (described as Jamaican, Italian, French Canadian and Slovak).
  • Rajesh: In 2007, a 14-year old Indian boy (from Uttar Pradesh) developed a broken American accent following corporal punishment from his father.
  • Cindy Lou Romberg: In 2007, a middle aged American woman Cindy Lou Romberg (from Port Angeles, Washington) developed an English speaking Russian/German/French-sounding accent following her neck being adjusted by a chiropractor (although she had suffered a brain injury in a car crash back in 1991).
  • Julie Frazier: In 2008, a 39-year old American woman Julie Frazier (from Fort Wayne, Indiana) developed a British-Russian accent following a severe hemiplegic migraine (the first such case involving migraine as the trigger episode).
  • Sarah Colwill: In 2010, a 35-year old British woman Sarah Colwill (from Devon) developed a Chinese accent following an extreme migraine.
  • Kay Russell: In 2010, a 49-year old British woman Kay Russell (from Gloucestershire) developed a French/Russian/Eastern European accent following a migraine.
  • Karen Butler: In 2011, a middle-aged American woman Karen Butler (from Newport, Oregon) developed an Irish/Eastern European accent following oral surgery.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Ardila, A. Rosselli, M., & O. Ardila. (1988) Foreign accent: an aphasic epiphonomenon? Aphasiology, 2,5, 493-499.

Aronson, A.E. (1990). Dysprosody of pseudo-foreign dialect. In Aronson, A.E. (Ed.), (2nd ed.) Clinical Voice Disorders  (pp. 119-124) New York: Thieme-Stratton.

Berthier, M., Ruiz, A., Massone, M., Starkstein, S., & R. Leiguarda. (1991). Foreign accent syndrome: behavioural and anatomical findings in recovered and non-recovered patients. Aphasiology, 5, 129-147.

Blumstein, S.E., Alexander, M.P., Ryalls, J.H., & W. Katz. (1987). On the nature of the foreign accent syndrome: A case study. Brain and Language, 31,215-244.

Coelho, C.A., & Robb, M.P. (2001). Acoustic analysis of Foreign Accent Syndrome: An examination of three explanatory models. Journal of Medical Speech-Language Pathology, 9, 227-242.

Cohen, D.A., Kurowski, K., Steven, M.S., Blumstein, S.E. & Pascual-Leone, A. (2008). Paradoxical facilitation: the resolution of foreign accent syndrome after cerebellar stroke. Neurology, 73, 566-567.

Edwards, R.J., Patel, N.K. & Pople, I.K. (2005). Foreign accent following brain injury: syndrome or epiphenomenon? European Neurology, 53, 87-91.

Garst, D. & Katz, W. (2006). Foreign Accent Syndrome. The ASHA Leader, August 15.

Marie P. (1907). Presentation de malades atteints d’anarthrie par lesion de l’hemisphere gauche du cerveau. Bulletins et Memoires Societe Medicale des Hopitaux de Paris, 1, 158–160.

Mariën P., Verhoeven J. (2007). Cerebellar involvement in motor speech planning: some further evidence from foreign accent syndrome. Folia Phoniatrica et Logopaedica, 59, 210-217.

Mariën P., Verhoeven J., Engelborghs, S., Rooker, S., Pickut, B. A., De Deyn, P.P. (2006). A role for the cerebellum in motor speech planning: evidence from foreign accent syndrome. Clinical Neurology and Neurosurgery, 108, 518-522.

Mariën, P., Verhoeven, J., Wackenier, P., Engelborghs, S. & De Deyn, P.P. (2009). Foreign accent syndrome as a developmental motor speech disorder. Cortex, 45, 870–878.

Moen, I. (2000). Foreign accent syndrome: A review of contemporary explanations. Aphasiology, 14, 5-15.

Monrad-Krohn, G.H. (1947). Dysprosody or altered “melody of language.” Brain, 70, 405-415.

Pick, A. (1919). Über Änderungen des Sprachcharakters als Begleiterscheinung aphasicher Störungen. Zeitschrift für gesamte Neurologie und Psychiatrie, 45, 230–241.

Dead man walking: A beginner’s guide to Cotard’s Syndrome

One of the strangest and rarest mental disorders that has been studied academically is Cotard’s Syndrome (CS), and also known as the Cotard Delusion, the Nihilistic Delusion, and the Walking Corpse Syndrome, CS is where individuals hold the delusional belief that they are dead (figuratively or literally) and do not exist. Alternative versions of CS involve the individual believing they are putrefying and/or have lost their blood and/or internal organs. In even rarer instances the condition may include delusions of immortality. Unsurprisingly, CS is often found in psychotic individuals with schizophrenia but has also presented itself following adverse reactions to the anti-viral drug acyclovir (typically used in the treatment of herpes simplex virus). Some research has also indicated that individuals with impaired renal function are also at a higher risk of displaying CS symptoms.

CS is named after the 19th century French neurologist Jules Cotard who first described the condition in 1880. Cotard named the disorder the ‘negation delerium’ (le délire de négation). The severity of the disorder can differ between individuals (i.e., mild to severe). The characteristics of CS include despair and self-loathing at one end through to intense delusions and chronic depression at the other. The original case described by Cotard was a female given the pseudonym ‘Mademoiselle X’. She eventually died of starvation (because she believed she didn’t need to eat and denied that some parts of her body even existed) and believed she was eternally damned.

According to Yamada and colleagues in a 1999 issue of Acta Psychiatrica Scandinavica, CS has three distinct stages (i.e., germination, blooming and chronic). The first (germination) stage comprises psychotic depression and hypochondria. The second (blooming) stage comprises the full development of the syndrome and the delusions of negation. In the final (chronic) stage comprises severe delusions and chronic depression, and leads to a completely distorted view of the world in which they live. They also become socially withdrawn, completely neglect their hygiene, and cannot make sense of reality. As far back as 1921, Tissot described two components of the syndrome – an affective component associated with anxiety and a cognitive component associated with the presence of delusion.

Here are a couple of examples from the clinical literature.

  • Example 1: In 1996, Dr. A.W. Young and Dr. K.M. Leafhead reported a case of CS in a Scottish man who suffered brain injury following a motorcycling accident. Following his discharge from hospital, he was taken to South Africa by his mother and became convinced that he had died of septicaemia or AIDS and had gone to hell.
  • Example 2: A case study reported by Dr. D.N. Mendhekar and Dr. N. Gupta in a 2005 issue of the Indian Journal of Pediatrics described CS in a 14-year-old male epileptic. He had a history of depression, social withdrawal, talking about death, and disturbed biological function. His CS episodes occurred around twice a year (lasting 1-3 months each time). During each affected episode, the child believed that he and everyone around was dead.

Recently, Hans Debruyne and colleagues wrote an excellent review of CS in a 2011 issue of Mind and Brain, and wrote what they believed is a “classical description” of CS:

“In its early stages, Cotard’s syndrome is characterized by a vague feeling of anxiety, with a varying time span from weeks to years. This anxious state gradually augments and can result in nihilistic delusions where denial of life or denial of body parts are the prominent features. The patient loses sense of reality. Despite the delusion of being dead, these patients show an increased tendency to automutilation or suicidal behavior. Additional symptoms may include analgesia and mutism. The core symptoms always reflect a preoccupation with guilt, despair, and death”.

In the same 2011 review, the authors examined all the epidemiological studies and summarized the findings:

“The prevalence and incidence of this rare syndrome is not known. Only one study reported on prevalence in a selected psychogeriatric population in Hong Kong. In 2 out of 349 patients, Cotard’s syndrome was diagnosed suggesting a prevalence of 0.57% in this population. A prevalence of 3.2% was reached when severely depressed elderly were included. A recent study found 0.62% (n=3) of patients in a Mexican sample (screened over a 2-year period) of primary psychiatric patients having Cotard’s syndrome. Using the same methodology they found also 0.11% (n=1) having Cotard’s syndrome in a sample of neurological patients with mental disturbances”.

In 1995, Dr. G.E Berios and Dr. R. Luque (University of Cambridge, UK) carried out a statistical analysis of 100 cases of CS. They reported no differences between men and women with CS, and age appeared to increase the likelihood of someone developing CS. In relation to affective disorders and mood state, the authors reported that CS sufferers experienced depression (89%), anxiety (65%) and guilt (63%). In relation to delusions, CS sufferers experienced hypochondriacal delusions (58%) and delusions of immortality (55%). The most common nihilistic delusions concerned the body (86%) and existence (69%). The authors also carried out exploratory factor analysis and reported that the factors appeared to suggest three types of CS (i.e., Psychotic Depression Type; Cotard Type I; and Cotard Type II) and that each type may need to be treated differently and have different therapeutic implications.

  • The Psychotic Depression type includes individuals with melancholia and a few nihilistic delusions.
  • The Cotard Type I includes individuals with no depression or other disease and comprises a “pure” CS whose nosology is closer to delusional disorders (rather than the affective disorders).
  • The Cotard Type II includes individuals with anxiety, depression and auditory hallucinations and comprise a mixed group.

Neurologically, CS is thought to be related to the Capgras Syndrome (i.e., a disorder in which an individual has the delusion that someone close to them – partner, friend, or family member – has been replaced by an identical-looking imposter). Both syndromes are thought to originate from a disconnection between the areas of the brain that recognize faces and the areas that associate emotional content with such facial recognition. This can lead to feelings of derealization (i.e., an alteration in experience or perception of the external world so that it seems unreal). Brain scans show that those displaying CS often have lesions in the parietal lobe and greater brain atrophy than those in control groups. There are several reports of successful treatment in the psychiatric literature with ant-depressants, anti-psychotics, and various mood stabilizers. Therapeutic interventions such as electro-convulsive therapy have also been used to positive effect. In their 2011 review, Debruyne and colleagues concluded:

“Despite that Cotard’s syndrome was first described more than a century ago, literature on this topic remains restricted to case reports. Although the syndrome is rare, more larger scale research is needed to further clarify the pathophysiologic underpinnings of the disease and its relation to other delusions of misidentification such as Capgras syndrome”.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Berrios G.E. & Luque R. (1995) Cotard’s delusion or syndrome? Comprehensive Psychiatry, 36, 218-223.

Berrios G.E. & Luque R. (1995) Cotard Syndrome: clinical analysis of 100 cases. Acta Psychiatrica Scandinavica,  91, 185-188.

Berrios G.E. & Luque R. (1999) Cotard’s ‘On hypochondriacal delusions in a severe form of anxious melancholia’. History of Psychiatry, 10, 269-278.

Cohen, D. & Consoli, A. (2006). Production of supernatural beliefs during Cotard’s syndrome, a rare psychotic depression. Behavioral and Brain Sciences, 29, 468-470.

Debruyne H, Portzky M, Peremans, K. & Audenaert K (2011). Cotard’s syndrome. Mind and Brain, 2, 67-72.

Debruyne H, Portzky M, Van den Eynde F. & Audenaert K (2009). Cotard’s syndrome: a review. Current Psychiatry Reports, 11, 197-202.

Mendhekar, D. N., & Gupta, N. (2005). Recurrent postictal depression with Cotard delusion. Indian Journal of Pediatrics, 72, 6, 529-31.

Pearn, J. & Gardner-Thorpe, C (2002). Jules Cotard (1840-1889) His life and the unique syndrome that bears his name. Neurology, 58,1400–3.

Tissot F. (1921). De lire des negations termine par guerison. Cosiderations sur l’hypochondrie et la melancholie. Ann Med Psychol, 79, 321-328.

Yamada, K., Katsuragi, S. & Fujii, I. (1999). A case study of Cotard’s syndrome: stages and diagnosis. Acta Psychiatrica Scandinavica, 100, 396-399.

Young, A.W., Robertson, I.H., Hellawell, D.J., de, P.K.W., & Pentland, B. (1992). Cotard delusion after brain injury. Psychological Medicine, 22, 799-804.

Young, A.W. & Leafhead, K.M. (1996) Betwixt life and death: Case studies of the Cotard Delusion. In P.W. Halligan & J.C. Marshall. (Eds.), Method in Madness: Case studies in Cognitive Neuropsychiatry). Hove: Psychology Press.