938946
case-report2020

JMHXXX10.1177/1557988320938946American Journal of Men's HealthSaida et al.

Case Report

Artery of Percheron Stroke as an Unusual
Cause of Hypersomnia: A Case Series and
a Short Literature Review

American Journal of Men’s Health
July-August 2020: 1­–10
© The Author(s) 2020
Article reuse guidelines:
sagepub.com/journals-permissions
https://doi.org/10.1177/1557988320938946
DOI: 10.1177/1557988320938946
journals.sagepub.com/home/jmh

Imen Ben Saida1,2 , Helmi Ben Saad2,3 , Maroua Zghidi1,
Emna Ennouri1, Radhouane Ettoumi1,2, and Mohamed Boussarsar1,2

Abstract
The thalamus and the mesencephalon have a complex blood supply. The artery of Percheron (AOP) is a rare anatomical
variant. Occlusion of this artery may lead to bithalamic stroke with or without midbrain involvement. Given its broad
spectrum of clinical features, AOP stroke is often misdiagnosed. Usually, it manifests with the triad of vertical gaze
palsy, memory impairment, and coma. In this article, we report three cases of bilateral thalamic strokes whose clinical
presentations were dominated by a sudden onset of hypersomnia. We also reviewed last 5 years’ publications related
to the AOP strokes in males presenting sleepiness or equivalent terms as a delayed complication. The AOP stroke may
present a diagnostic challenge for clinicians which should be considered in the differential diagnosis of hypersomnia.
Keywords
hypersomnolence, Percheron infarction, bithalamic
Received April 17, 2020; revised June 1, 2020; accepted June 5, 2020
The thalamus is an egg-shaped structure of gray matter on
the human diencephalon (Khanni et al., 2018). Its vascular supply is complex and presents multiple anatomical
variants. The artery of Percheron (AOP), which is a rare
anatomical variant, is characterized by a solitary common
arterial trunk arising from the posterior cerebral artery
(Lamboley et al., 2011). Occlusion of this artery is rare
and may lead to a bilateral paramedian thalamic infarction with or without midbrain involvement (Lamot et al.,
2015). This uncommon ischemic stroke syndrome, with
its broad spectrum of clinical presentations, is often misdiagnosed and therefore represents a diagnostic challenge
for physicians. Acute hypersomnia is an unusual complication of this stroke (Bollu et al., 2017). Here, we report
three cases of bithalamic stroke whose clinical presentations were dominated by altered mental status, mainly
consistent with hypersomnia. We also briefly report the
results of the published cases/case series (2015–2020
period) of male patients presenting an AOP stroke.

of the case series’ retrospectively obtained and anonymized data. However, written informed consents were
obtained from the three patients for the publication of
their cases.

Cases

Corresponding Author:
Helmi Ben Saad, Laboratory of Physiology, Faculty of Medicine of Sousse,
University of Sousse, Rue Mohamed Karoui, Sousse 4000, Tunisia.
Email: helmi.bensaad@rns.tn

The Ethics Committee of Farhat Hached Teaching hospital waived the need for ethics approval for the publication

Case 1
A previously healthy 73-year-old man presented to the
emergency department with altered consciousness. On
admission, his signs were within normal range. On the
neurological examination, the patient had a fluctuant consciousness state fully reversible under pain stimuli,
excessive daytime sleepiness, and nocturnal agitation. He

1

Medical Intensive Care Unit, Farhat Hached University Hospital,
Sousse, Tunisia
2
Research Laboratory N° LR12SP09, Heart Failure, Faculty of
Medicine of Sousse, University of Sousse, Sousse, Tunisia
3
Laboratory of Physiology, Faculty of Medicine of Sousse, University
of Sousse, Sousse, Tunisia

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons
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2

American Journal of Men’s Health 

Figure 1. Head computed tomography scan illustrates bilateral thalamic hypodensities (arrows) compatible with an ischemic
stroke.

had neither sensitive nor motor focal signs. All blood
tests (e.g., electrolytes test, complete blood count [CBC],
and liver function tests) were normal. A head computed
tomography (CT) performed 2 hr after the symptoms
onset was normal. This situation misled to an initial diagnosis of a coma secondary to viral encephalitis. Fortyeight hours after admission to the intensive care unit, a
new brain CT scan showed bilateral thalamic hypodensities in the paramedian territory (Figure 1). Further evaluation aiming at identifying the stroke etiology revealed a
rapid atrial fibrillation at electrocardiogram without
abnormalities on Doppler ultrasound and transthoracic
echocardiography, findings consistent with an embolic
mechanism or a heart-brain syndrome. Treatment with
anticoagulation (enoxaparin) and amiodarone was started.
Two weeks later, there was a marked improvement in the
clinical condition (somnolence and behavioral impairment). The patient was transferred to the cardiology
department.

Case 2
A 43-year-old man with a past medical history of hypertension was brought to the emergency department after
20-hr of unarousable sleepiness. There was no recent history of drug abuse, head injury, trauma, or seizure. On the
physical examination, the patient was afebrile and his
blood pressures were high at 230/120 mmHg. On the neurological examination, the patient had a Glasgow coma
scale of 7 points (2, 2, and 3 points for ocular, verbal, and

motor components) requiring invasive mechanical ventilation. No other abnormalities were noted (neither meningeal syndrome nor focal neurological deficit). On
admission, the infectious, toxic, and metabolic encephalopathy tests (e.g., CBC, blood urea nitrogen, creatinine,
plasma glucose, liver function tests, and urine drug
screen) were normal. Initial CT scan was normal. Twentyfour hours later, a new brain CT scan revealed bilateral
paramedian thalamic hypodensities, which were not present on the first CT examination (Figure 2). A 9-lead electrocardiogram showed a right bundle-branch block. A
transthoracic and transesophageal echocardiogram,
carotid, and vertebral Doppler ultrasound revealed no
abnormalities. There was a gradual improvement in the
patient’s clinical state. A detailed neurological examination after extubation revealed fluctuating arousal, complete vertical gaze palsy, thalamic aphasia, and behavior
changes with agitation and increased impulsivity. The
aforementioned psychiatric disorders were managed with
haloperidol. Two weeks after hospitalization, the patient
was discharged and referred to a neurologist.

Case 3
An 82-year-old man with a past medical history of hypertension, diabetes mellitus, and myocardial infarction presented
to the emergency department with a brief loss of consciousness, followed by drowsiness episodes which were initially
neglected and then worsened in a crescendo pattern. On the
physical examination, the patient was sleepy, apathetic, and

Saida et al.

3

Figure 2. Head computed tomography on an axial view illustrates an ischemic stroke (arrows) in the paramedian artery
territory of both thalami.

Figure 3. Axial T2-weighted magnetic resonance imaging of the brain illustrates hyperintense bilateral lesions of the paramedian
thalami (arrows) compatible with an acute ischemic stroke.

presented no other abnormalities. Results of the routine
blood tests (e.g., electrolytes test, blood urea nitrogen, creatinine, plasma glucose, and CBC) were within the normal
range. During the hospital course, the patient presented
many periods of irrepressible need for sleep, and he was
unable to stay awake and alerted during the major daytime

waking episodes. Brain magnetic resonance imaging (MRI)
showed bilateral paramedian thalamic infarcts (Figure 3).
Doppler ultrasound and transthoracic echocardiography
were unremarkable. A significant improvement in hypersomnolence during the hospital stay was noted and the
patient was discharged on day six following the stroke.

4

Figure 4. Artery of Percheron (AOP) illustration.
BA = basilar artery; PCA = posterior cerebral artery;
T = thalamus.

Discussion
The AOP was first described by Gerard Percheron in
1973 (Agarwal et al., 2014; Caruso et al., 2017). This
artery arises from the proximal posterior cerebral arteries
and supplies both the paramedian thalami and the mesencephalon (Figure 4). AOP is a rare anatomical variant that
is present in 4%–12% of the population (Arauz et al.,
2014; Kaya et al., 2010; Kocaeli et al., 2013; Uz, 2007).
The prevalence of bilateral thalamic infarction caused by
AOP occlusion is unknown since it is often misdiagnosed
(Arauz et al., 2014). It “seems” that AOP stroke represents 0.1% to 2.0% of ischemic strokes and 4% to 18% of
thalamic infarcts (Agarwal et al., 2014; Caruso et al.,
2017; Garcia-Grimshaw et al., 2018; Lamot et al., 2015).
There is no predilection as regards sex, race-ethnicity,
and age in the reported cases of AOP stroke in literature.
According to Garcia-Grimshaw et al. (2018), the aforementioned data depend on the etiology of the AOP stroke.
Firstly, the latter can occur at any age, but it is particularly
common in patients after their 30s mostly between 60 and
70 years (Lin et al., 2018). Secondly, there is a slight male
predominance with a male to female ratio of 3:2 (Hermann
et al., 2008; Stamm et al., 2018; Suzuki et al., 2016).
On May 27, 2020, a personal literature review based
on a 2015–2020 PubMed search [key items: “artery of
Percheron” AND (“case report” OR “case-series”)]
found 73 papers published in English language (30, 37,
and 6 papers included females, males, and both sexes,
respectively). Among the 37 studies including only

American Journal of Men’s Health 
males, 13 reported sleepiness or equivalent terms (i.e.,
hypersomnolence, drowsiness, or excessive daytime
sleepiness) as a delayed complication of an AOP stroke
(Table 1; Afana et al., 2019; Aryan et al., 2016; Bailey &
Khadjooi, 2016; Goico & Mikesell, 2018; Harisuthan
et al., 2018; Ince & Asan, 2018; Kamasak et al., 2015;
Khanni et al., 2018; Oliveira et al., 2018; Shah & Ali,
2018; Vasconcellos et al., 2016; Zelante et al., 2015;
Zhou et al., 2015).
The shape of the infarct can deduce the presence of
AOP stroke because this anatomical variant typically
causes bilateral paramedian thalamic-mesencephalic
infarction (Agarwal et al., 2014; Lopez-Serna et al.,
2009). The risk factors of AOP stroke are similar to those
of ischemic ones. The two most frequent risk factors are
microangiopathy and cardiac embolism (Arauz et al.,
2014; Garcia-Grimshaw et al., 2018). The clinical presentations of AOP stroke are extremely variable. The most
common clinical features are bilateral vertical gaze palsy
(65%), memory impairment (anterograde and retrograde
amnesia) (58%), and coma (42%; Garcia-Grimshaw
et al., 2018; Lamboley et al., 2011; Lamot et al., 2015).
The remaining clinical features reported in the literature
include hypersomnolence (29%), akinetic mutism, and
behavioral disorders (apathy, agitation, and aggressiveness; Agarwal et al., 2014; Caruso et al., 2017; GarciaGrimshaw et al., 2018; Lamboley et al., 2011; Lamot
et al., 2015; Lazzaro et al., 2010).
In the three reported cases, we found some of the clinical features reported in the previous series, including
hypersomnia, coma, vertical gaze palsy, and neuropsychiatric disorders (Table 1). Altered mental status is a
classic manifestation of AOP stroke and can range from
hypersomnia to coma (Table 1). However, hypersomnia
is rarely reported as a first complaint (Cases 1 and 3)
since it is usually misdiagnosed as coma or it is lately
diagnosed after recovery from coma (Case 2; Bassetti
et al., 1996; Hammersley et al., 2017; Hermann et al.,
2008; Oliveira et al., 2018). Hypersomnolence (i.e.,
excessive daytime sleepiness and/or prolonged sleep) in
bithalamic stroke is explained by the crucial role of the
thalamus in sleep regulation and in maintaining arousal.
Hypersomnolence has been attributed to the interruption
of noradrenergic and dopaminergic impulses from the
ascending reticular activating system to the thalamus
(Bassetti et al., 1996; Bollu et al., 2017; Goyal et al.,
2012). Sleep-wake disturbances are more pronounced in
bilateral than in left-sided or right-sided thalamic infarcts
(Hermann et al., 2008). Sleep needs have been reported
to remain increased after this stroke (Goyal et al., 2012;
Hermann et al., 2008). Unfortunately, we have no follow-up information about the three patients after their
discharge.

5

Goico and Mikesell (2018)

Oliveira et al. (2018)

Khanni et al. (2018)

Afana et al. (2019)

Authors

n = 1 (56 Yrs, Brazil)
Excessive daytime sleepiness
Memory impairment
Left-sided weakness
n = 1 (72 Yrs, United States)
Somnolence
Vertical gaze palsy

n = 1 (39 Yrs, State of Palestine)
Coma
Slurred speech
Hypersomnia
Loss of interest
Right-sided ptosis
Vertical gaze palsy
Diminished light reflex
Amnesia
Right upper limb paralysis
n = 1 (59 Yrs, Haiti)
Hypersomnolence

Number of cases (age/country)/
main complaints

Brain MRI with DWI

Brain MRI

Brain CT scan
Brain MRI

Brain CT scan
Brain CTA
Brain MRI

Medical imagery

(continued)

•• Suspect AOP stroke in a patient with a decreased conscious level,
ophthalmologic signs, and cardio-embolic risk factors
•• Early diagnosis is best obtained with a brain MRI with DWI
•• Treatment of AOP stroke depends on the pathophysiologic mechanism
•• Prognosis is subject to the extent of infarction but considered relatively good
with regard to mortality and permanent deficits

•• Acute AOP strokes continue to present a diagnostic challenge for clinicians
in the acute setting owing to the diversity and inconsistency in presentation,
frequent lack of localizing signs, and poor resolution on initial imaging
•• This has implications for treatment and prognosis, especially in settings
offering tissue plasminogen activator (tPA), where early detection and
intervention significantly impact functional outcomes for patients
•• It may not be cost-effective to perform a complete stroke workup on all
patients presenting with vague, atypical symptoms, but clinicians should keep
thalamic pathology on the differential diagnosis given its involvement in many
diverse neurological roles
•• Maintaining a high suspicion for thalamic infarct, with AOP stroke as one
etiology, and a low threshold for MRI in patients presenting acutely with
otherwise
•• Awareness of the clinical and neuroimaging features of the AOP stroke
syndrome is essential for timely diagnosis and appropriate management

•• This experience demonstrates the need for surgeons performing anterior
cervical discectomy with fusion (ADCF) procedures to be aware of this
potential complication
•• There are many other prophylactic treatments of this complication such as
maintaining appropriate cervical positioning during surgery or prevention of
postoperative dehydration
•• Care should be taken to avoid intimal disruption of the vertebral artery by
overly dilating the intervertebral space

Conclusion

Table 1. Results of the 13 Cases/Case-Series, Published During the 2015–2020 Period, Including Males Suffering From an Artery of Percheron (AOP) Stroke and Reporting
Sleepiness or Equivalent Terms (Such as Hypersomnolence, Drowsiness, or Excessive Daytime Sleepiness) as a Delayed Complication.

6
Brain CT scan
Brain MRI

Brain CT scan
Brain MRI

Brain MRI
Brain MRA

n = 1 (45 Yrs, India)
Dizziness
Diplopia
Ocular movement abnormalities
Hypersomnolence

n = 1 (41 Yrs, Turkey)
Fluctuations in the level of
consciousness (coma to somnolence)
Retrograde amnesia
Depressive mood

Harisuthan et al. (2018)

Ince and Asan (2018)

Medical imagery

n = 1 (39 Yrs, United Kingdom)
Hypersomnolence

Number of cases (age/country)/
main complaints

Shah and Ali (2018)

Authors

Table 1. (continued)

(continued)

•• In a patient presenting with drowsiness/somnolence, a posterior circulation stroke
should be considered if no evidence of other more common causes is found
•• A CT head must be followed by an MRI to confirm the diagnosis and
subsequent focus should be on eliciting risk factors and careful evaluation for
etiologies
•• The present case is the only one reported to have just dysfunction of arousal/
conscious and no other focal neurological findings
•• In an emergency setting, sudden dip in sensorium with localizing neurology
findings to midbrain and thalamus (e.g., coma and vertical gaze palsy) could be
due to multiple causes
•• Embolic stroke of the proximal AOP should be one of the differentials
•• Anytime the initial imaging is normal, perform a follow-up head CT or MRI as
early, to make the correct diagnosis
•• If the diagnosis was made within the stroke window period, thrombolytic
therapy could still be done, and the outcome can be fairly good
•• This patient is the first case with a 10-year history of anterograde amnesia
due to AOP stroke
•• More cases with long-term follow-up may provide a better understanding of
the clinical persistence of the symptoms and the thalamic structures primarily
responsible for the amnesic syndrome
•• This case highlights the difficulty in the prediction of the prognosis in the
AOP stroke presenting with an isolated memory disorder

Conclusion

7

Vasconcellos et al. (2016)

n = 1 (40 Yrs, India)
Brain MRI
Complication following re-exploratory
trans-sphenoidal surgery for a pituitary
adenoma
n = 1 (59 Yrs, Brazil)
Brain MRI
Abrupt drowsiness
Decreased level of consciousness
Coma
Cervical dystonia (spasmodic torticollisanterocollis)
Ataxic gait
Vertical gaze palsy (upward and
downward)
Convergence insufficiency
Mydriatic nonreactive pupils and light
intolerance

Aryan et al. (2016)

Brain CT scan
Brain MRI

Medical imagery

n = 1 (47 Yrs, United States)
Low level of alertness (deep coma to
mild somnolence)
Memory problems

Number of cases (age/country)/
main complaints

Bailey and Khadjooi (2016)

Authors

Table 1. (continued)

(continued)

•• AOP stroke is an uncommon cause of coma presenting in elderly and middleaged individuals
•• The patient may have a source of cardioembolism or classical cardiovascular
risk factors
•• Reduced consciousness can range from a deep coma to hypersomnolence
•• Ophthalmological signs and neuropsychological deficits may also be evident
•• Despite an investigation, the cause remains undetermined in the majority of
cases
•• Overall the prognosis is good with low mortality and often rapid reversal of
the coma, necessitating early diagnosis and optimal supportive care
•• Reaching the correct diagnosis in patients presenting with nontraumatic coma
can be challenging, but incorrect diagnosis can result in delays in appropriate
management and potential for harm due to employment of unnecessary
treatments and ongoing symptoms
•• This case highlights the difficulty in recognizing a stroke syndrome presenting
as isolated reduced consciousness and the importance of revisiting a diagnosis
when a patient fails to respond to initial treatment
•• A case of an AOP stroke occurring in a patient following endoscopic transsphenoidal surgery
•• This rare complication should be thought about in the setting of reexploratory pituitary surgery
•• Great degree of awareness of stroke syndromes can improve patient
outcome with early recognition and suitable treatment option like
thrombolysis or vascular interventions

Conclusion

8
Brain MRI
Brain MRA

•• Some evidence suggests that posterior communicating artery (PCoA)
hypoplasia per se predisposes to thalamic lacunar stroke because of the
critical role of PCoA in the collateral supply of proximal posterior cerebral
artery territory
•• We suggest that the occurrence of the two anatomic variants might have led
to a hemodynamic infarction due to a poor regional collateral flow

•• A case of a patient with acute AOP stroke resulting in bilateral mirror-like
median thalamic infarctions involving the dorsomedial and intralaminar nuclei
bilaterally
•• There was an initial difficulty in diagnosis due to the presence of altered
mental state only
•• A unique feature of this presentation included the evolution of symptoms into
the Korsakoff syndrome, characterized by memory deficits and confabulation
•• Involvement of the mammillothalamic pathways bilaterally has been implicated
in its causation
•• The proximity of the lesions caused by infarction in the territory of the AOP
to the mammillothalamic pathways is probably the cause of the syndrome in
this patient
•• A literature review did report a few cases with Korsakoff syndrome in
bilateral thalamic infarctions
•• The better outcome in relation to management in an intensive care setting
•• The importance of neuroimaging in the presence of unexplained altered
mental state and cognitive difficulty to diagnose the underlying problem is
important, particularly because of available therapeutic intervention in acute
stroke syndromes
•• Bilateral strokes of the paramedian thalamus may result in severe illness and
impairment
•• Common clinical manifestations include disorientation, confusion,
hypersomnolence, deep coma and “coma vigil,” or akinetic mutism (awake
unresponsiveness), as well as severe memory impairment

Conclusion

Note. CT = computed tomography; CTA = CT angiography; DWI = diffusion-weighted imaging; MRA = magnetic resonance angiography; MRI = magnetic resonance imaging; n = number; Yrs = years.

Zelante et al. (2015)

Brain MRI

n = 2 (5 Yrs, Turkey)
Case 1: Mutism and ataxia after
chickenpox infection
Case 2: Headache, somnolence,
agitation, speech dysfunction following
an upper respiratory tract infection
n = 1 (65 Yrs, Italy)
Drowsiness
Gait instability
Dysarthria
Right ptosis, vertical gaze palsy
Hypoesthesia and hemiparesis

Kamasak et al. (2015)

Medical imagery

n = 1 (68 Yrs, United States )
Brain CT scan
Coma
Brain MRI
Behavior changes (agitation and
Brain MRA
aggression)
Cognitive and communication
impairment
Fluctuating arousal and orientation
Impaired learning and memory (impaired
anterograde and retrograde memory)
Paraphasia
Monotonous speech with hypophonia
Auditory and visual hallucinations
Vertical gaze paralysis

Number of cases (age/country)/
main complaints

Zhou et al. (2015)

Authors

Table 1. (continued)

Saida et al.

9

The complexity and polymorphism of AOP stroke
semiology explain why bithalamic infarction is often
misdiagnosed, lately detected, or even not detected. It
is a real diagnostic challenge for clinicians to detect
this condition in a timely fashion. Its diagnosis and
treatment may be delayed because of the wide spectrum of its clinical features. Moreover, the initial CT
scan can be normal (Khanni et al., 2018; Xu et al.,
2017). Diagnosis of AOP stroke is often made retrospectively beyond the thrombolysis or endovascular
treatment window. MRI is the neuroimaging of choice
to be conducted when AOP stroke is highly suspected
(Lamboley et al., 2011). MRI typically shows a hyperintense signal in the region supplied by AOP (Song
et al., 2017).
In the three case series, the patients recovered completely. This is in line with previous studies which reported
good prognosis of patients with AOP stroke (Arauz et al.,
2014; Kichloo et al., 2019; Song et al., 2017).
In conclusion, these case series highlighted the difficulties of recognizing the AOP stroke in a timely fashion.
These observations also illustrated the importance of considering this stroke syndrome as one of the differential
diagnoses of hypersomnolence.
Acknowledgments
Authors wish to thank Professor Samir Boukattaya for his
invaluable contribution to the improvement of the quality of the
writing in the present article.

Authors’ Contributions
I.B.S., H.B.S., M.Z., and M.B. substantially contributed to the
conception and design, acquisition of data, or analysis and interpretation of data. I.B.S., H.B.S., M.Z., E.E., R.T., and M.B.
drafted the article or revised it critically for intellectual content.
I.B.S., H.B.S., M.Z., E.E., R.T., and M.B. gave final approval of
the version to be published.

Declaration of Conflicting Interests
The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication
of this article: H.B.S. reports personal fees from AstraZeneca,
Saiph, Teriak, Hikma, and Chiesi. The remaining authors
declare that they have no conflicts of interest concerning this
article.

Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.

ORCID iDs
Imen Ben Saida
Helmi Ben Saad

https://orcid.org/0000-0001-8698-9339
https://orcid.org/0000-0002-7477-2965

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