Neurocase
The Neural Basis of Cognition

ISSN: (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/nncs20

A brain origin for factitious disorder
(Munchausen’s) with malingering? A single case
with an old frontal lobe lesion
Jan Adriaan Coebergh , Aliza Amlani , Mark Edwards , Yee-Haur Mah & Niruj
Agrawal
To cite this article: Jan Adriaan Coebergh , Aliza Amlani , Mark Edwards , Yee-Haur Mah & Niruj
Agrawal (2020): A brain origin for factitious disorder (Munchausen’s) with malingering? A single
case with an old frontal lobe lesion, Neurocase, DOI: 10.1080/13554794.2020.1858110
To link to this article: https://doi.org/10.1080/13554794.2020.1858110

Published online: 11 Dec 2020.

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NEUROCASE
https://doi.org/10.1080/13554794.2020.1858110

A brain origin for factitious disorder (Munchausen’s) with malingering? A single case
with an old frontal lobe lesion
Jan Adriaan Coebergha,b, Aliza Amlanib, Mark Edwardsc, Yee-Haur Mahd,e and Niruj Agrawalf
a

Department of Neurology, Ashford St. Peter’s Hospital NHS Foundation Trust, Chertsey, UK; bDepartment of Neurology, St. George’s Hospital,
London, UK; cNeuroscience Research Group, Institute of Molecular and Clinical Sciences, St George’s University of London, London, UK; dKing’s
College Hospital NHS Foundation Trust, London, UK; eSchool of Biomedical Engineering & Imaging Sciences, KCL, London, UK; fDepartment of
Neuropsychiatry, St George’s Hospital NHS Foundation Trust, London, UK
ABSTRACT

ARTICLE HISTORY

We describe a patient who presented with gender identity dysphoria and stroke-like symptoms who we
diagnosed with Munchausen’s syndrome (factitious disorder). We discuss whether a brain lesion in the
left frontal cortex is a possible risk factor, and support this hypothesis through neuropsychological
investigation, EEG abnormalities, and a personality assessment. This case report supports previous
suggestions that underlying brain disease/lesions might be risk factors for Munchausen’s syndrome
(factitious disorder).

Received 7 October 2020
Accepted 26 November 2020

Case description
A 50 year old man presented with a headache followed by leftsided paralysis of arm and leg and was initially treated as
a possible stroke. He reported that he recently arrived in the
United Kingdom from another country intending to study for
a PhD (doctorate degree). He said he had been prescribed hormo­
nal medication as part of gender reassignment by a General
Practitioner at the airport. He requested to wear a pink hospital
gown and to be called by a female forename. Due to single-sex
hospital bays in the hospital, he was given a private side room. His
MRI head showed an old left frontal lesion with increased signal on
gradient echo, consistent with his reported history of a previous
head injury. His limb weakness was variable and Hoover’s sign was
positive. He reported he previously ran a head injury charity and
had been active in politics. On day four a neurologist discussed the
clinical suspicion of functional neurological symptoms and the
need for more evidence before starting hormonal medication.
There was no next of kin available for collateral history nor location
Yushkevich of discharge. After looking up his (later deleted) profile
on Wikipedia we asked him about previous convictions for fraud
mentioned on the profile, and for more details about his PhD.
There were numerous inconsistencies in the details provided by
him, leading us to the conclusion that they were untrue. When
made aware of the possibility of having to pay for health-care
costs as a non-UK resident he self-discharged after 10 days having
regained full neurological function. We became aware that in the
next two months he visited at least four hospitals in the area with
similar symptoms, and received thrombolysis for suspected stroke
on multiple occasions and admissions often lasted about a week
to 10 days. During one of the later admissions Electroenc
ephalography (EEG) was carried out which showed frontal slow
waves and a neuropsychological assessment was done. When he
was seen by one of the authors (who had also met him in another
CONTACT Jan Adriaan Coebergh

jan.coebergh@nhs.net

© 2020 Informa UK Limited, trading as Taylor & Francis Group

KEYWORDS

Brain lesion; factitious
disorder (Munchausen’s);
EEG; malingering

hospital) he refused to discuss his recent contacts with health
services and turned down an in-depth explanation of the MRI,
EEG, and neuropsychological findings and self-discharged. He has
not re-attended since. In the seven years since he has remained
active as a male on publicly available internet sites.

Investigation results
He completed a gender identity/dysphoria (GID) questionnaire
for adolescents and adults (GIDYQ-AA). He scored an average of
2.41 on the 27 questions (Always-Often-Sometimes-RarelyNever; 1–5); the lower the score the more gender identity
dysphoria (For the GIDYQ–AA mean score a cut-point of 3.00
showed sensitivity of 90% for the GID adults, and specificity was
100% for the control adults) (Singh et al., 2010).
During detailed neuropsychological testing he was highly
sociable and appeared very engaged and motivated to do well.
He passed a test of effort. His verbal comprehension was on the
75th percentile, perceptual reasoning and organization 92nd
percentile, working memory and concentration 42nd percentile,
and speed of information processing 34th percentile. There was
no memory or executive impairment. He self-reported moder­
ate levels of anxiety and no symptoms of depression.
On a 320 item of personality structure (Morey & McCredie,
2019) which includes indices of response consistency, impres­
sion management, and a range of validity indicators, alongside
numerous clinical scales he showed significant elevation on the
paranoia index denoting increased vigilance for monitoring the
environment for potential harm; a tendency to be resentful and
hold grudges and a readiness to spot inequities in the way he
has been treated. He also had markedly elevated scores on the
dominance index on the interpersonal scale. The interpretative
manual suggests the person may be driven to appear compe­
tent and authoritative but others might view them as

Department of Neurology, Ashford St. Peter’s Hospital NHS Foundation Trust, Chertsey KT17 0PZ, UK

2

J. A. COEBERGH ET AL.

Figure 1. EEG at rest.

Figure 2. Lesion in blue.

overbearing and self-important. There was some elevation on
a mania scale suggesting restlessness and impulsivity; other­
wise, all indices were within normal ranges.
EEG at rest showed fairly frequent intermittent burst of high
amplitude irregular slow waves sometimes intermixed with sharp
components over the right fronto-temporal and fronto-parietal
regions. It was occasionally bilateral but more prominent on the right.
The lesion was segmented using the original CT brain image
and the program ITK (Insight Segmentation and Registration
Toolkit)-snap (Yushkevich et al., 2006). The original CT scan was
signal adjusted prior to spatial normalization using a reversible
transformation (Rorden et al., 2012). The signal processed CT
brain image was spatially normalized using the combined seg­
mentation-normalization routine in Statistical Parametric
Mapping (SPM)12, with the derived normalization parameters
used to transform the original CT brain image and segmented
lesion mask into MNI (Montreal Neurological Institute) space.
The images provided were created using mricroGL.

The Talairach (Lancaster et al., 2000) location is z 55–69. The
location of the lesion lies within the region of x-14; y-8; z61
which would place it in the left superior frontal gyrus/paracen­
tral lobule. The lesion involves 1.03% of the total superior
frontal gyrus and 2.26% of the total supplementary motor
cortex in the left hemisphere. The volume of the lesion is
0.832 cm3 (Du et al., 2006)

Discussion
Munchausen’s syndrome (factitious disorder) was first defined
by Richard Asher as a syndrome where a person repeatedly
presents to hospital with a dramatic illness history made up of
falsehoods, after which he or she discharges themselves
against advice (Asher, 1951). According to DSM V; the latest
diagnostic criteria, patients with Munchausen’s (factitious dis­
order) intentionally produce physical or psychological symp­
toms with the sole motivation of assuming the sick role

NEUROCASE

3

Figure 3. Lesion in red.

((C. C. Bass & Halligan, 2016; Christopher Christopher Bass &
Halligan, 2014; Kanaan & Wessely, 2010)). It is difficult to be sure
the diagnosis in this case was not malingering since a degree of
gain in the form of free accommodation and food was present.
It is therefore possible there is an overlap between the two
diagnoses. To our knowledge feigning a desire to have gender
reassignment has not previously been described as
a presentation, but the obvious benefit of it was a private room.
Although there is little understanding of the pathogenesis of
Munchausen’s syndrome (factitious disorder) (Yates & Feldman,
2016) advances in imaging mean that identifying brain pathol­
ogy is possible. Relevant to this, the neurological basis of lying
has been studied using fMRI. The prefrontal cortex is strongly
activated during lying (Yang et al., 2005). It has been shown
that the right anterior prefrontal cortex (aPFC) is more involved
in lies that are well rehearsed, whereas the anterior cingulate
cortex (aCC) is more active during spontaneous generation of
non-memorized lies (Lee et al., 2002). Langleben and others
(Langleben et al., 2002) observed increased activity in the
superior frontal gyrus and anterior cingulate cortex in
deception.
Pathological liars without antisocial traits were found to
have a 22% increase in prefrontal white matter and a 14%
reduction in prefrontal gray matter compared to healthy con­
trols (Yang et al., 2005). Further studies have shown an increase
in white matter in the orbitofrontal, inferior frontal, middle
frontal, and superior frontal cortices in pathological liars
(Yang et al., 2007). The question of whether preexisting differ­
ences in the prefrontal structure cause increasingly deceptive
behavior or whether the act of lying increases the white matter
volume in this region of the brain remains unanswered
(Bengtsson et al., 2005).
Literature relating to factitious disorder has alluded to the
possibility of “organic” causes including by Asher in 1953

(Asher, 1951). In one case, bilateral fronto-temporal atrophy
preceded the behavior (Babe et al., 1992). King and Ford
described that 40% of patients with pseudologia fantastica
had a history of brain abnormality; 15% had primary epilepsy
and 7% had an abnormal EEG, previous brain infection, or head
trauma (King & Ford, 1988).
Our patient presented with seemingly intentionally induced
neurological and psychological symptoms which quickly
improved when challenged, and subsequent similar presenta­
tion to other hospitals. His presentation is consistent with
Munchausen’s syndrome (factitious disorder). In our patient,
we can suggest that the personality traits of high dominance
and paranoia are possible contributors to this behavior (Baek
et al., 2017). However, he also had evidence of mainly right
fronto-parietal and fronto-temporal slowing on EEG and
a lesion of the left superior frontal gyrus. These are areas high­
lighted in lying and (self-) deception studies. It must be noted
that superior frontal gyrus/supplementary motor area function
is altered in functional neurological disorder (FND) where there
is impaired awareness of motor intention (Baek et al., 2017;
Voon et al., 2011) and our patient had positive signs for this
(Hoover’s sign (McWhirter et al., 2011)). Two cases of supple­
mentary motor area (SMA) strokes presenting with signs of
contralateral functional neurological disorder have been pub­
lished (inconsistent weakness and positive clinical signs)
(Mathew et al., 2018; Mohebi et al., 2019). It must be noted
that in our patient the weakness was ipsilateral. The SMA has
also been associated with a loss of self-awareness during com­
peting sensorimotor activity (Goldberg et al., 2006) One can
wonder about self-awareness of the deception in our patient.
This literature demonstrates that self-awareness of movement
is a continuum and a simple involuntary versus voluntary
dichotomy might not be sustainable. For example, FND/disso­
ciative seizures as a rule are perceived as involuntary but we

4

J. A. COEBERGH ET AL.

have met patients that acknowledge inducing symptoms
when, as so often, they are not taken seriously (willful
exaggeration).
It is possible that the brain lesion described in this patient
has the potential to disturb widespread cortical and sub cor­
tical networks. We note that although incidental EEG abnorm­
alities in healthy people are relatively common, intermittent
significant frontal slowing is an unusual incidental finding. It
superficially supports the theory that the frontal lobe brain
lesion may have led to an alteration in brain function in this
person. Future exploration through functional studies and
structural and functional connectivity analysis might help us
understand the pathophysiology of Munchausen’s syndrome
(factitious disorder).
We have to be modest however in linking an area of brain
damage to altered behavior decades later but the notion that
brain pathology could be a risk factor for Munchausen’s syn­
drome (factitious disorder) and malingering is potentially impor­
tant with regards to the often complex management and
societal/health care professional attitudes toward such patients.

Disclosure statement
No potential conflict of interest was reported by the authors.

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