Rare disease

Transient foreign accent syndrome
Hanul Srinivas Bhandari
Neurology Department, UT Southwestern Medical Centre, Austin, Texas, United States
Correspondence to Dr Hanul Srinivas Bhandari, hbhand@mednet.swmed.edu

Summary
Foreign accent syndrome (FAS) is a poorly understood and studied syndrome as it is indeed a rare entity. Since its first description in 1907 by
French neurologist Pierre Marie involving a patient who presented with an Alsatian accent, there are approximately only 60 cases reported
in the literature. The majority of such cases of FAS have been secondary to cerebrovascular accidents. Of the cases in the literature, none
report such a transitory nature of FAS. In this particular case, a 55-year-old male presented with a foreign accent. This FAS was triggered by
ischemia and was reversed after a seizure, the first reported in the literature.

BACKGROUND

INVESTIGATIONS

Foreign accent syndrome (FAS) is a rare syndrome in itself,
with only 60 cases reported in the literature. Moreover,
this is the first case where the FAS was reversed after a
seizure. This rare presentation should be included in published literature so it can aid in understanding FAS, which
is truly an enigmatic entity.

There were no abnormalities on laboratories. An initial
emergency department CT of his head showed encephalomalacia in the left parietal lobe, precentral gyrus and middle frontal gyrus, without evidence of acute findings.
Following the seizure, further testing performed included
a transthoracic echocardiogram and an electroencephalogram that did not reveal new findings. MRI of his brain
revealed restricted diffusion in the left parieto-occipital
region and in the left middle frontal gyrus (figure 1A,B). No
mass lesions and no evidence of pathologic enhancement
were seen. Magnetic resonance angiography of his head
was normal appearing.

CASE PRESENTATION
A 55-year-old Texan male, presented with a day history of
another accent. His son noted his pronunciation of words
as ‘foreign’. He denied issues with writing, reading, or
grammar and denied any other systemic symptoms including neurological deficits. His medical history included
hypertension, obstructive sleep apnoea syndrome, hypertriglyceridemia and cerebrovascular accidents (CVAs): left
frontal infarction (2003) and left parieto-occipital infarction
(2007). No medications or allergies were significant to this
case. He smoked half pack per day for 20 years and denied
illicit drug use. Family history is non-contributory.
Physical examination revealed vital signs within normal limits. His mental status via the Montreal Cognitive
Assessment was scored as 29/30. There was no right-left
disorientation. He followed complex commands and his
speech was clear and fluent. Of note, multiple medical
personnel noted that the patient sounded as if he had a
Cockney accent. The patient did not recognise his accent as
foreign. Language showed minor disruptions as alterations
of syllable structure. There was no change in tone, rate, or
pitch, no sound substitutions, perseveration, or echolalia,
no difficulty with speech initiation and there was preservation of syntax. No alexia or agraphia of mono-syllable and
multi-syllable words, phrases, or sentences were noted.
Additionally, he could copy a paragraph, and there was no
evidence of acalculia. No deficits in executive functioning
were noted. No other cortical signs were noted. The rest of
his neurological examination did not reveal any deficits.
Within minutes of the examination, the patient exhibited right head version followed by a Jacksonian march up
his right arm, which was witnessed. This evolved into a
tonic-clonic generalised seizure lasting 30 s. Postictal confusion lasted 30 min.
BMJ Case Reports 2011; doi:10.1136/bcr.07.2011.4466

OUTCOME AND FOLLOW-UP
Subsequently, his neurological examination remained similar to the initial examination except that he reverted to his
Texan accent. The patient has not been to Britain and does
not have relatives/friends there. This was no re-occurrence
of his FAS at discharge. He was lost to follow-up.

DISCUSSION
Only 60 cases report FAS since it was first described in 1907
by French neurologist Pierre Marie. It results from damage
to the processes involving articulation. FAS is characterised
as a pseudoaccent, where listeners categorise speech alterations as resembling a foreign accent,1 but actually is an
impairment of the finer linguistic abilities such as pauses
and vocal stress.2 FAS is postulated to be due to changes
in accentuation of syllables. It is not the result from previous experience from another language and patients with
FAS have usually never visited the country their accent
resembles.3
It has been associated with various aetiologies as surveyed in the literature. The most common aetiology
involves a vascular lesion affecting the motor speech areas
in the language dominant hemisphere.4 But it has been
linked to other aetiologies such as metastatic breast carcinoma,5 traumatic brain injury,1 and even as an initial
symptom of multiple sclerosis.6 Additionally, migraines
have been implicated as well.
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Figure 1 (A,B) MRI brain, selected axial images (Flair, top and diffusion-weighted imaging (DWI), bottom) showing correlated areas of
ischemia of the left frontal, involving the middle frontal gyrus, and parieto-occipital regions after the seizure event.
Furthermore, the areas affected in FAS are scattered. The
majority of cases involve the motor speech areas, but the
dominant precentral gyrus, inferior central gyrus, corpus
callosum and insula also have been implicated in FAS.7 8
Other case reports have shown involvement in the nondominant rolandic and temporal areas.6 In a review of 16
cases of FAS, both cortical and subcortical processes were
found to be involved.9 Therefore, there is no clear lesion
which can explain FAS consistently. Due to the intricate
nature of speech production, possibly a subtle disruption
of the motor speech network may lead to FAS, while major

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disruptions can lead to aphasias. Furthermore, it has been
theorised that FAS may be due to a mild deficit in motor
planning,10 where this intricate network is disrupted. In
most case reports of FAS, lesion size has been minimal
where it is usually less than three centimeters in diameter
and typically involves only a single gyrus,11 this is consistent with the patient’s case. Another theory involves the
possibility of increased activity of certain areas rather than
deficiencies. One report describes an ischemic event of the
left putamen in which functional MRI was performed. The
authors noted statistically increased activity of the ventral

BMJ Case Reports 2011; doi:10.1136/bcr.07.2011.4466

angular gyrus and the central sulcus.12 They concluded
these areas are implicated in FAS.
In the differential diagnosis of FAS, apraxia of speech
(AOS) is necessary to be ruled out; it is surmised that FAS is
not an AOS variant. Unlike AOS, FAS patients do not have
difficulties with speech initiation.13 In diagnosing AOS,
the Academy of Neurologic Communication Disorders
and Sciences urged that certain clinical characteristics be
employed: slow rate of speech, sound distortions resulting
in slurred speech, distorted sound substitutions and prosodic abnormalities.14 These abnormalities were not seen
in the patient In diagnosing FAS, certain clinical characteristics have been theorised. These characteristics include
the speculation that vowels are more affected than consonants, vowel pronunciation is longer or laxer and lexical
stress patterns are affected.15 Another report states that the
main characteristic of FAS was a change in emphasis of
syllables.3
FAS is a rare phenomenon, but its reversal is rarer. One
particular case followed the resolution of FAS. It involved
a patient with a left frontoparietal infarct resulting in
FAS; subsequently the FAS reversed after a right cerebellar haemorrhage.8 These CVAs were separated by 3 years.
The authors concluded that the mechanisms in accented
speech production depend on a delicate bihemispheric
balance between cerebral and cerebellar connections.8
Furthermore, no literature shows the mercurial reversal of
FAS after a seizure. The acute ischemia of the left middle
frontal gyrus resulted in the patient’s FAS. The semiology
of the seizure suggests a focus in the vicinity of the new
ischemia. This provides the possibility that the increased
metabolic demand from the seizure resulted in anoxic damage to the penumbra or even non-adjacent areas containing
efferent pathways that fine tuned functions of the initial
lesion. This resulted in additional lesions in the described
cortical motor speech network,11 thereby correcting the
FAS. This concept has been described,8 where the first
insult lead to FAS and another deficit in the network corrected the aberrations in fine speech control due to another
pathway in the network activated or disinhibited. Due to
the rapid reversal of the FAS, dedicated speech testing was
not performed. The patient declined further language batteries after the reversal and he was lost to follow-up.
Our case describes FAS and its sudden reversal after a
seizure, the first reported of its kind. As theorised in the
patient, FAS can involve multiple pathways of the complex
motor speech network.11 FAS is a rare phenomenon, one
that needs to be better understood.

BMJ Case Reports 2011; doi:10.1136/bcr.07.2011.4466

Learning points
FAS is a poorly understood phenomenon; it is most
likely not a true accent change, rather the perception
to the listener as a foreign accent.
▶ FAS is not a variant of AOS.
▶ A single cortical area is not responsible for total
speech pronunciation, rather it is a complex motor
speech network, involving multiple areas.
▶ This is the first reported case of FAS that was reversed
after a seizure.
▶

Acknowledgements I would like to thank my mentor, Horatio R Aldredge,
MD, for his support and time.
Competing interests None.
Patient consent Obtained.

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