Applied Neuropsychology: Adult

ISSN: 2327-9095 (Print) 2327-9109 (Online) Journal homepage: http://www.tandfonline.com/loi/hapn21

Poststroke delusions: What about the
neuroanatomical and neurofunctional basis?
Michele Torrisi, Rosaria De Luca, Patrizia Pollicino, Simona Leonardi, Silvia
Marino, Giuseppa Maresca, Maria Grazia Maggio, Adriana Piccolo, Placido
Bramanti & Rocco Salvatore Calabrò
To cite this article: Michele Torrisi, Rosaria De Luca, Patrizia Pollicino, Simona Leonardi,
Silvia Marino, Giuseppa Maresca, Maria Grazia Maggio, Adriana Piccolo, Placido Bramanti &
Rocco Salvatore Calabrò (2018): Poststroke delusions: What about the neuroanatomical and
neurofunctional basis?, Applied Neuropsychology: Adult, DOI: 10.1080/23279095.2017.1421536
To link to this article: https://doi.org/10.1080/23279095.2017.1421536

Published online: 19 Jan 2018.

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APPLIED NEUROPSYCHOLOGY: ADULT
https://doi.org/10.1080/23279095.2017.1421536

none defined

Poststroke delusions: What about the neuroanatomical
and neurofunctional basis?
Michele Torrisi, Rosaria De Luca, Patrizia Pollicino, Simona Leonardi, Silvia Marino, Giuseppa Maresca,
Maria Grazia Maggio, Adriana Piccolo, Placido Bramanti and Rocco Salvatore Calabrò
IRCCS Centro Neurolesi “Bonino Pulejo”, Messina, Italy
ABSTRACT

KEYWORDS

Delusion is a belief about yourself, people, or events that has no accordance with reality. Although
it is known that stroke could cause various psychiatric and psychological effects, including
depression, anxiety, and aggressiveness, psychotic symptoms, especially delusions, are rather
uncommon. The most investigated poststroke delusions are paranoid type, nihilistic, and Fregoli
syndrome. We will describe two patients showing delusion symptoms (Cotard-like and erotomanic
ones) that occurred after a stroke involving the right temporal lobe, the basal ganglia and insular
region, persisting for a long period after the stroke onset. We have, therefore, supposed that the
simultaneous involvement of these brain areas could be involved in the neuroanatomical basis of
delusions, as also demonstrated by the neurofunctional evaluation.

Basal ganglia; Cotard
syndrome; erotomanic
delusions; functional
magnetic imaging; insula

Introduction
Delusion is a belief about yourself, people, or events that
has no accordance with reality. Patients can believe
different delusions: that someone wants to hurt them
(paranoid delusion), to be a famous or historic person
(grandiose delusion), to have a connection with God
(religious delusion), to feel dead (nihilistic delusion),
to mistake relatives and strangers (Capgras and Fregoli
delusion), to believe that their partners betray them
(jealousy delusion), to be seduced by someone
(erotomanic delusion), and/or to suffer from a mortal
disease or that their body has a deformity (somatic
delusion). Generally, delusions occur in psychotic
diseases, including schizophrenia. Actually, some other
diseases could cause them, such as dementia (Cipriani,
Danti, Vedovello, Nuti, & Lucetti, 2014; Torrisi et al.,
2016), traumatic brain injury (Guerreiro, Navarro, Silva,
Carvalho, & Gois, 2009), and stroke; moreover,
delusions may be due to drug effects. Although it is
known that stroke could cause various psychiatric and
psychological effects, including depression, anxiety,
and aggressiveness, psychotic symptoms, especially
delusions, are rather uncommon. In a large case series
including 360 patients affected by stroke, Kumral and
Oztürk (2004) found delusions in only 15 patients.
The most investigated poststroke delusions are the
paranoid (Devine et al., 2014) and nihilistic types,

(Sottile et al., 2015), as well as those that characterize
the Fregoli syndrome (de Pauw, Szulecka, &
Poltock, 1987).
Herein, we will describe two patients showing
delusions that occurred after a stroke involving the right
temporal lobe, the basal ganglia, and the insular region.
The patients and 5 age-sex matched normal controls
(NC) underwent high field magnetic resonance imaging
(MRI) examination, to evaluate whole brain atrophy,
normalized cerebral measurements, and functional MRI
resting state, by using tools that are a part of the FMRIB
software library (FSL - http://www.fmrib.ox-.ac.uk/fsl).

Case-report 1
A 49-year-old female, housewife, divorced with a son,
smoker and affected by hypertension and thyroid
dysfunction, without a clinical history of psychiatric
diseases, was admitted in a neurology ward owing
to an ischemic stroke. Around 12 hours after the
thrombolysis treatment, she developed a hemorrhagic
stroke in the right temporal lobe spreading to insula,
caudate nucleus and internal capsule,(Figure 1A). At a
neurological evaluation, she presented a left hemiplegia
and moderate hemianesthesia, without loss of consciousness. The day after the hemorrhagic complication,
the patient showed paranoid delusions mainly related to

CONTACT Rocco Salvatore Calabrò
salbro77@tiscali.it
IRCCS Centro Neurolesi “Bonino-Pulejo”, S.S.113 Via Palermo C/da Casazza, Messina 98123, Italy.
Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/hapn.
© 2018 Taylor & Francis Group, LLC

2

M. TORRISI ET AL.

Figure 1. (A) Axial T2- weighted, Axial FLAIR and Sagittal T1–weighted, showed intraparenchymal hematoma at the level of right
basal ganglia. Ischemic lesions in right cortical sub-cortical parietal lobe. (B) Functional magnetic resting state showed brain decreased
activation in: Right Angular Gyrus, Right Middle Frontal Gyrus, Left Paracingulate Gyrus - Right Supramarginal Gyrus (posterior and
anterior division), - Left Insular Cortex, Left Tempolar Lobe, Left middle temporal gyrus, - Precentral gyrus, postcentral gyrus, right
cingulate gyrus.

the healthcare professionals, asserting that “nurses
want to hurt or kill me” or “this hospital is false, it is
all a sham, the patients are real but the staff is fake.”
Each treatment carried out by nurses was considered
an act of aggression or carelessness. Progressively,
the frequency of delusions decreased. However, a
nihilistic/Cotard-like delusion began to appear, referred
to beliefs of death or loss of body’s parts; indeed, she
often said: “I have died and reborn eight times,” “My
feet were removed and replaced with others.” These
delusions were associated with an intense distress. There
were no hallucinations. The cognitive level, tested by
verbal neuropsychological instruments because of the
inability of using her hands (left hand plegia, and
arterial thrombosis at the right thumb, second and
third fingers) showed normal orientation, memory
(Rey 15-item Memory Test Equivalent Scores ¼ 4),
attention (Digit Span Forward E.S. ¼ 4), and language,
whereas abstracted reasoning skills were abnormal
(Raven’s Progressive Matrices E.S. ¼ 0). After one
month from stroke, she was administered risperidone
(3 mg/die) and escitalopram (20 mg/die), with a rapid
disappearance of delusions. The patient underwent
MRI examination to evaluate normal brain volume NBV (1466454 mm3) and normal cortical volume NCV (748341 mm3). Resting state evaluation showed a
decreased connectivity in the right angular gyrus, right
middle frontal gyrus, left paracingulate gyrus, right
supramarginal gyrus (posterior and anterior division),
left insular cortex, left tempolar lobe, left middle
temporal gyrus, precentral gyrus, postcentral gyrus,
and right cingulate gyrus (Figure 1B).

Case report 2
A 55-year-old female, teacher, unmarried, smoker, and
affected by diabetes and hypertension, without previous
psychiatric symptoms, was admitted to the hospital
following subarachnoid hemorrhage due to aneurysm
rupture. She, therefore, underwent embolization of
the left internal carotid and stent implant of the right
internal carotid. Immediately after the procedure, she
developed an ischemic damage to the caudate, the
lenticolar nuclei and right insular region (Figure 2A),

Figure 2. (A) Axial T2- weighted and Sagittal T1-weighted,
showed right middle carotid artery intraparenchymal ischaemic
lesion at the level of right basal ganglia. Ischemic lesions in right
cortical sub-cortical fronto-temporal lobe. (B) Functional
magnetic resting state showed brain decreased activation
in: Supracalcarine cortex, Precuneus cortex, - Planum
temporale, - Postcentral gyrus.

APPLIED NEUROPSYCHOLOGY: ADULT

with psychiatric symptoms including erotomanic
delusions. Specifically, the patient believed that some
nurses had fallen in love with her and later had betrayed
her with other patients. Moreover, her behavior
presented disinhibited and histrionic behaviors. There
were no hallucinations. At her neuropsychological
evaluation, she presented a moderate to severe
deterioration. Temporal orientation, memory, attention,
and executive functions were impaired (Moca test:
20/30; Trial Making Test A equivalent score ¼ 0, Trial
Making Test B equivalent score ¼ 0, Trial Making Test
B-A equivalent score ¼ 0, Rey 15 item Memory Test
equivalent score ¼ 1, Frontal Assessment Battery
equivalent score ¼ 0). The patient showed delusions
during the whole duration of the hospitalization, but
in consideration of the fact that she had no distress
concerning the delusions, we decided to treat only the
inappropriate behavior by administering oxcarbazepine
(900 mg/die), with a complete remission of the
symptomatology at three-month follow-up. The patient
underwent MRI examination to evaluate NBV
(1327365 mm3) and NCV (675664 mm3). Resting
state evaluation showed a decreased connectivity in
supracalcarine cortex, precuneus cortex, planum
temporale, and postcentral gyrus.

Discussion
We have described the cases of two patients who,
following a brain lesion, have developed delusions.
The absence of pre-existing psychiatric symptoms,
besides their onset after the event, let us argue that
the cause of delusions was the cerebrovascular accident.
Anyway, it is reasonable to suppose that specific
personality traits had influenced delusion features, at
least with regard to their contents. Both the patients
were suffering from a subcortical lesion in the basal
ganglia and right insular region, and these lesions have
been investigated by a high field MRI, to better define
localization and extent. Delusions are beliefs that
remain fixed despite evidence that they are incorrect.
Although the exact neural mechanism of delusional
belief remains to be clarified, a predominance of
right-hemisphere lesions has been reported in patients
with organic delusional syndromes. Several mechanisms
have been postulated to explain the development of
psychotic symptoms following acquired brain lesions,
including direct injury to the frontal lobe or disruption
of the connections between the prefrontal cortices,
associative areas, and subcortical structures causing
impairment of reality monitoring functions (Gurin &
Blum, 2017). Although there is no agreement on which

3

regions are correlated with these manifestations, as
they occur after temporal, parietal (Sottile et al., 2015),
frontal (Devine et al., 2014), and subcortical lesions,
we supposed that the simultaneous involvement of the
basal ganglia and insula could play a pivotal role in
causing delusions. Several studies have suggested the
role of insula in the genesis of psychiatric diseases
(Crespo-Facorro et al., 2000) and in regulation of
emotions (Gu, Hof, Friston, & Fan, 2013), but data on
stroke as a possible etiology are scant. With this report,
we have confirmed that delusions could be a
consequence of stroke involving insular region, and it
is likely that such symptoms may be misdiagnosed
and underreported. Indeed, insula is believed to be
involved in consciousness and play a role in diverse
functions usually linked to emotion or the regulation
of the body’s homeostasis. These functions include
compassion and empathy, perception, motor control,
self-awareness, cognitive functioning, and interpersonal
experience. In relation to these, it is involved in psychopathology and it is possible that lesions of different
insular regions and/or its connections with the frontal
lobe may cause delusions (Underwood, Kumari, &
Peters, 2016).
Otherwise, there are some studies showing a likely
influence of the lesions to the basal ganglia in the onset
of psychotic symptoms, especially those involving the
caudate nucleus (McMurtray, Sultzer, Monserratt, Yeo,
& Mendez, 2008; Narumoto et al., 2005), corona radiata
and lentiform nucleus (Abdullah, Saini, Sharip, &
Rahman, 2015), and putamen (Kitabayashi et al.,
2006). Interestingly, Huber, Karner, Kirchler, Lepping,
and Freudenmann (2008) described cases of parasitosis
delusion due to right striatal infarctions, confirming the
importance of this region in inducing psychosis. The
simultaneous presence of different hallucinations have
also been reported, (McMurtray et al., 2014), and this
could be due to a dysfunction of the connections
between prefrontal and subcortical areas following a
stroke.
In both our cases, the brain lesions involved the right
hemisphere, and this is consistent with the majority of
poststroke delusions, given that they are rarely caused
by lesions of the left hemisphere (McMurtray et al.,
2014). Moreover, the delusion time of manifestation
in the two cases confirms the findings by other studies
that delusions generally occur few days after the
vascular event. A delayed onset of poststroke
delusion is an uncommon event (Barboza, De Freitas,
Tovar-Moll, & Fontenelle, 2013). Otherwise, although
they generally last for a short period, in our case report
2 we observed the presence of delusions for a long

4

M. TORRISI ET AL.

period, and we cannot affirm whether or not their
disappearance could be attributable to the risperidone
effect in case report one. However, we believe that to
describe the eventual onset of poststroke delusions is
of utmost importance, given that they have been
associated with poorer prognosis and, as found by
Almeida and Xiao (2007), and they increase death’s
probability after 10-years from the vascular event.
Moreover, our patients showed a decreased NCV, as
compared to NC (P < 0.1). These results are consistent
with pervious voxel-based morphometry studies,
which showed grey matter reduction in the medial
frontal/anterior cingulate cortex and bilateral insula
(Wolf et al., 2013). Finally, resting state functional
MRI showed a decreased connectivity in bilateral
insular regions, as reported by other studies (Vicens
et al., 2016).
Although we are not completely able to exclude that
the influence of insula and basal ganglia damage on the
onset of delusions is a mere coincidence, the presence
of the same damaged brain regions in the two cases,
without a previous psychiatric symptomatology, is a
good reason to hypothesize this association. The
presence of the same damaged brain regions in the two
cases also supports the idea that the neuroanatomical
basis of delusions may encompass these complex and
interconnected areas, beyond a neurobiological model
of disrupted prefrontal control over somato-sensory
representation.
Clinicians, including neuropsychologists, should
be aware about/know the neuroanatomical basis of
psychosis to timely diagnose and promptly manage
stroke patient presenting with psychiatric symptoms.

Acknowledgment
The authors wish to thank Prof. Agata Grosso for English
editing.

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