Unusual presentation of more common disease/injury

Case report

Behavioural changes as the first manifestation of a
silent frontal lobe stroke
Rafael García Carretero,1 Blanca-Nieves Beamonte-Vela,1
Jose-David Silvano-Cocinero,1 Ana Alvarez-Mendez2
1

Internal Medicine, Hospital
Universitario de Mostoles,
Mostoles, Spain
2
Intensive Care Medicine,
Hospital Universitario de
Mostoles, Mostoles, Spain
Correspondence to
Dr Rafael García Carretero,
​rgcarretero@​salud.​madrid.​org

Summary
A 67-year-old man was admitted to our hospital after
his relatives found him to have severe personality and
behavioural changes. His behaviour was inappropriate
and uninhibited. The patient reported no symptoms
and he showed poor insight into his own behaviour.
Neuroimaging showed an orbitofrontal lesion, due to an
infarction of the anterior cerebral artery. The patient was
diagnosed with frontal lobe syndrome.

Accepted 18 December 2018

Background

Frontal behavioural syndromes caused by strokes
are rarely reported, it therefore remains unclear
whether a frontal lobe infarction is actually silent
or asymptomatic.1 The frontal lobe, due to its size,
is commonly involved in strokes. Most strokes are
caused by ischaemic or haemorrhagic involvement
of the middle cerebral artery, and clinical manifestations are therefore mainly due to injury to the
precentral gyrus (pre-Rolandic area), which is a
motor cortex.
However, strokes due to involvement of the
anterior cerebral artery confined to the prefrontal
cortex have been designated as silent or asymptomatic, but whether they are truly asymptomatic is not
clear, since psychiatric symptoms, personality and
behavioural changes must be considered as neurological manifestations.1
Clinical manifestation of frontal lobe involvement depends on the size of the lesion, side (left or
right), depth and type of injury. These personality
changes in the frontal lobe can be hard to recognise
because of their subacute onset. The clinical spectrum can be wide: from impulsiveness and disinhibition, to apathy, abulia or amotivational state.2

Case presentation

© BMJ Publishing Group
Limited 2019. No commercial
re-use. See rights and
permissions. Published by BMJ.
To cite: García Carretero R,
Beamonte-Vela B-N,
Silvano-Cocinero J-D,
et al. BMJ Case Rep
2019;12:e227617.
doi:10.1136/bcr-2018227617

A 67-year-old man was admitted to our hospital
after his relatives found him to have changes in his
personality for the last 10–15 days. He had been a
responsible, mild-mannered man, who worked as a
bank manager. For the past 2 weeks, he had been
showing behavioural changes: he was rude when
eating food; he did not wait until his relatives were
at the table; he did not always use a knife and fork;
he used foul language while eating; he sometimes
used inappropriate sexual words when addressing
his relatives; his wife said he showed inappropriate
sexual behaviour, such as masturbation without
shame while she was present. However, he showed

no concern regarding these changes. Aggression
or verbal abuse were not present as behavioural
symptoms.
He had hypertension and type 2 diabetes mellitus,
and was on ramipril 2.5 mg daily and metformin 1 g
twice a day.
On physical examination, his temperature was
36.2°C, he had a heart rate of 78 bpm, blood pressure of 143/84 mm Hg and oxygen saturation of
97% on room air. On auscultation, heart sounds
and lungs were normal. On neurological examination, the patient did not show any focal or lateralising neurological signs.

Investigations

Laboratory tests were normal, with a white cell
count of 6.7×109/L, haemoglobin 14.1 g/L and
platelets 179×109/L. Kidney and liver panels were
also normal. The chest X-ray showed no acute
process. However, the brain CT scan showed a
right frontal cortical–subcortical hypodensity area
(5.5×2×6 cm), with no mass effect and no abnormal
enhancement after intravenous contrast administration (figure 1A). As the lesion could have resembled
a non-aggressive brain tumour, a brain MRI was
performed. The MRI (figure 1, slides B–D) showed
a right frontal cortical–subcortical hyperintensity
in T2 and hypointensity in T1. These radiological
findings led us to establish the diagnosis of subacute
anterior cerebral artery stroke.

Outcome and follow-up

Echocardiography, carotid ultrasound, 24 hours
Holter monitoring and electroencephalogram were
also performed, but they did not find any abnormalities. We started aspirin 100 mg daily and atorvastatin 20 mg daily.
Our patient remained in the admissions ward
for 1 week to complete the work-up. During his
stay, the patient got better and his neurological
symptoms improved. As a plausible hypothesis,
we think the patient started recovering some days
before he was admitted. It sounds reasonable, since
the onset was subacute. His relatives said he once
again became nice, judicious, prudent, thoughtful
and well-mannered. He was discharged and was
scheduled for a follow-up 3 months later. Generally speaking, he continued to be the person he
was before the stroke, but he was never aware of
his changes, and his family said he had problems in
interpreting others’ moods.

García Carretero R, et al. BMJ Case Rep 2019;12:e227617. doi:10.1136/bcr-2018-227617

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Unusual presentation of more common disease/injury

Figure 1 Neuroimaging (brain CT scan and MRI) of the frontal
lobe. Slide A shows a right frontal cortical–subcortical hypodense
area (arrow); this lesion causes no mass effect and no abnormal
enhancement after intravenous contrast administration. Slide B (T1weighted MRI) shows a hypodense lesion in a sagittal plane of the wide
frontal lobe lesion (arrow). Slides C (fluid-attenuated inversion recovery)
and D (T2-weighted turbo spin-echo) show a right frontal cortical–
subcortical hyperintensity (axial plane, arrows pointing the lesion).

Discussion

Mental changes after frontal lobe injury have been reported
since the 1940s. It is well known that higher mental functions
are affected after frontal lobe damage.3 Human behaviour is
involved, and emotions, attention, interest and will are therefore affected. Patients with so-called frontal lobe syndrome can
have a complete change in personality as an expression of the
above-mentioned damage. Size, extension and side of the lesion
are essential in developing certain symptoms.1 4
Diffuse neurodegenerative diseases, as well as focal lesions such
as stroke, head trauma, neoplasm and bacterial abscess formation,
can cause personality changes when the frontal lobe is involved, by
compromising the frontal cortical and subcortical structures.4
The most common denomination of frontal lobe syndromes
is ‘frontal lobe personality’. Clinical manifestations of these
syndromes, in which mood, behaviour and cognition are
involved, include not only disinhibition and impulsiveness, but
also apathy and abulia.4
There are several ways to classify frontal lobe syndrome, in
an attempt to develop a clinical-topographic correspondence.
Patients with orbitofrontal syndrome show impulsiveness, fearlessness, abnormal sexual behaviour, hyperactivity and disregard
for others’ emotions. Patients with anterior cingulate syndrome
are apathetic and aboulic, and they become quiet. Patients with
dorsolateral prefrontal cortex syndrome tend to be less organised
and lack the ability to plan (the so-called executive dysfunction).
However, if the lesion involves the subcortical circuitry, patients
can have combined syndromes. Therefore, clinical manifestations can sometimes be heterogeneous, since the frontal lobe
disorder may be caused by a wide cortical lesion or interruption of the frontal-subcortical circuitry.4 However, predicting
symptoms based on neuroanatomic injuries can be challenging,
and patients with a lesion in the frontal lobe might not develop
personality or behavioural changes.4 5 It is worth noting that
lateralisation is important due to the functional differences
between both cerebral hemispheres, as some clinicopathological
2

correlations can be set. Therefore, behavioural changes correlate
with the involved arterial domain. If left anterior cerebral artery
is involved, amotivational and apathetic features may arise. On
the contrary, delayed response deficits with impulsivity, social
improprieties, deficient social pragmatics, social anarchy and
emotional regulation deficits may arise on stroke of the right
anterior cerebral artery.6–9
Probably due to the above-mentioned reasons (low incidence
of stroke in the frontal lobe, heterogeneous clinical presentation, difficulties in predicting symptoms and outcome), frontal
behavioural syndromes due to stroke are uncommon in the
medical literature and have been rarely reported, when compared
with other diseases (such as abscesses and brain tumours).5
Some instruments have been developed in order to measure
personality, in an attempt to compare premorbid traits of personality versus current changes, but these tools have proven not to
be useful for assessing real-life predictions.4
Therapy is not easy to initiate, as identification and assessment of
these frontal syndromes can be difficult. Furthermore, patients often
have no insight into the disorder, and cannot identify situations in
which their behaviour is inappropriate. This leads to a failure to
respond to reinforcers trying to modify emotional responses.10

Learning points
►► Stroke is characterised by an acute onset of neurological

symptoms, which are usually motor-related. However,
personality changes such as impulsiveness and disinhibition
can be explained by fronto-cortical damage.
►► Frontal lobe personality includes emotional disorders or
executive dysfunction, but the symptoms are uncommon
and sometimes difficult to identify: abnormal emotional
responses, jealousy, abnormal sense of humour, lack of
empathy, apathy.
►► Frontal lobe syndromes can be misdiagnosed and therefore
left untreated. Clinicians should be aware when relatives
are concerned about personality or behavioural changes in
the patient, particularly when patients are unable to control
emotions or experience emotional changes.
►► Frontal strokes will remain silent only if clinicians are unable
to identify characteristic symptoms.
Contributors RGC wrote the first draft. BNBV fixed spelling and grammar
mistakes. JDSC edited the MRI images. AAM revised the final manuscript.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

References

1 Nagaratnam N, Bou-Haidar P, Leung H. Confused and disturbed behavior in the
elderly following silent frontal lobe infarction. Am J Alzheimers Dis Other Demen
2003;18:333–9.
2	Scheffer M, Monteiro JK, de Almeida RMM. Frontal stroke: Problem solving, decision
making, impulsiveness, and depressive symptoms in men and women. Psychol
Neurosci 2011;4:267–78.
3 Goldstein K. The mental changes due to frontal lobe damage. J Psychol
1944;17:187–208.
4 Chow TW. Personality in frontal lobe disorders. Curr Psychiatry Rep
2000;2:446–51.
5 Bogousslavsky J. Frontal stroke syndromes. Eur Neurol 1994;34:306–15.
6	Poletti M, Lucetti C, Logi C, et al. Cognitive correlates of negative symptoms in
behavioral variant frontotemporal dementia: implications for the frontal lobe
syndrome. Neurol Sci 2013;34:1893–6.

García Carretero R, et al. BMJ Case Rep 2019;12:e227617. doi:10.1136/bcr-2018-227617

Unusual presentation of more common disease/injury
7 Berlin HA, Rolls ET, Kischka U. Impulsivity, time perception, emotion and
reinforcement sensitivity in patients with orbitofrontal cortex lesions. Brain
2004;127:1108–26.
8	Rosen HJ, Wilson MR, Schauer GF, et al. Neuroanatomical correlates of impaired
recognition of emotion in dementia. Neuropsychologia 2006;44:365–73.

9	Rankin KP, Gorno-Tempini ML, Allison SC, et al. Structural anatomy of empathy in
neurodegenerative disease. Brain 2006;129:2945–56.
10	Rolls ET, Hornak J, Wade D, et al. Emotion-related learning in patients with social
and emotional changes associated with frontal lobe damage. J Neurol Neurosurg
Psychiatry 1994;57:1518–24.

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