Snyder et al. BMC Neurology
(2020) 20:370
https://doi.org/10.1186/s12883-020-01949-0

CASE REPORT

Open Access

Artery of Percheron infarction with
persistent amnesia: a case report of
bilateral paramedian thalamic syndrome
Hannah E. Snyder1, Sheliza Ali2,3, Joanna Sue2,4, Ayse Unsal2,4, Crystal Fong5 and Zhihui Deng2,6*

Abstract
Background: The artery of Percheron is an uncommon anatomic variant which supplies the bilateral paramedian
thalami and rostral midbrain. While infarction of its vascular territory can result in a wide range of symptoms,
paramedian thalamic syndrome is classically described as a triad of symptoms including vertical gaze disturbances,
fluctuating level of consciousness, and amnesia. There is minimal evidence to date to characterize the long-term
cognitive consequences of infarction of the artery of Percheron utilizing neuropsychological assessment.
Case presentation: We describe a 40-year-old female patient initially presenting with dizziness, confusion and falls
with unremarkable head CT scans. Subsequent MRI, more than 24 h after symptom onset, identified evidence of
bilateral thalamic and rostral midbrain infarction. Neuropsychological testing was administered at 4 months poststroke, with follow up testing at 1 year. The patient was found to have profound anterograde and retrograde
amnesia, which did not change significantly over the first year of rehabilitation, and which was not easily
identifiable in everyday encounters due to her relatively intact working memory and social skills.
Conclusions: As early diagnosis of infarction of the artery of Percheron is challenging, patients have frequently
missed the time window for acute management of ischemic stroke. Moreover, this case study highlights the need
for further research in deciphering the role of the paramedian thalamus in memory and cognition, as well as the
importance of standardized neuropsychological testing for the artery of Percheron stroke patients to identify safety
and rehabilitation concerns that may be overlooked.
Keywords: Artery of Percheron, Paramedian thalamus, Neuropsychological assessment, Anterograde and retrograde
amnesia

Background
The artery of Percheron (AOP) is an uncommon anatomic variant first described by Gérard Percheron in
1973. It refers to a single arterial trunk originating from
one of the proximal posterior cerebral arteries to supply
bilateral paramedian thalami and rostral midbrain [1].
The AOP is thought to occur in up to 33% of the
* Correspondence: dengz22@mcmaster.ca
2
Regional Rehabilitation Centre, Hamilton Health Sciences, Hamilton, Canada
6
Division of Physical Medicine and Rehabilitation, Department of Medicine,
McMaster University, Hamilton, Canada
Full list of author information is available at the end of the article

population, with a majority of individuals having independent hemispheric vascularization of these structures
[2]. Infarction of this artery is often characterized by a
triad of symptoms including altered level of consciousness, memory deficits, and supranuclear and vertical
gaze palsies [3]. Rarer clinical presentations have been
described, including patients presenting with severe
bradycardia, parkinsonism and convulsive seizures [4–6].
Infarction within the vascular territory of the AOP is an
important differential diagnosis to consider in an individual presenting to the Emergency Department (ED)
with fluctuating level of consciousness (LOC), especially

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Snyder et al. BMC Neurology

(2020) 20:370

when considering that initial head computed tomography (CT) is typically normal [7]. Magnetic resonance
imaging (MRI) is currently the gold standard for diagnosis of bilateral paramedian thalamic infarction.
On a macroscopic scale, the thalamus has been welldefined as a set of diencephalic nuclei which distributes
motor and sensory information to and from the cortex.
Meanwhile, the specific roles of individual nuclei within
the paramedian thalamus, such as the dorsomedial and
intralaminar nuclei, are still an area of controversy [1, 8].
The paramedian region is postulated to contribute to
arousal, memory, personality and behavior based on various case reports describing sequelae such as reduced level
of alertness, amnesia, apathy, and disinhibited behavior
following bilateral infarction of this territory [3, 8]. Thus,
neuropsychological assessment is an important component of initial testing of individuals with AOP infarction
to determine degree of deficit in various cognitive domains. To our knowledge, only one case study of AOP infarction with neuropsychological assessment at two
timepoints exists, and it describes a dramatic improvement of behaviour and cognition from 3 months to 1 year
post-stroke [9]. Here, we present a case of a patient who
similarly suffered bilateral paramedian thalamic infarction,
but with a profoundly different outcome of severe amnestic syndrome and other cognitive deficits as identified by
neuropsychological testing at 4 months and 1 year.

Case presentation
Our patient was a 40-year-old right-handed woman with
a previous history of recurrent deep vein thrombosis
(DVT), reportedly related to oral contraceptive use and
not managed medically. Otherwise, her past medical history was unremarkable for stroke risk factors. She awoke
one morning complaining of dizziness and shortly thereafter began to act strangely, including missing a step
while walking and getting into a low-impact collision
while driving her son to work. She was alert and speaking clearly following this event, and her son suggested
that she walk the short distance home. A couple of
hours later, the patient was dysarthric and confused. She
was subsequently found with evidence of trauma likely
due to falls, including contusions on her feet, shin, and
face for which she was not able to provide a history. Her
initial Glasgow Coma Scale (GCS) was documented to
be between 8 and 10 by Emergency Medical Services.
Upon arrival at the ED, our patient’s GCS deteriorated
to 6 (motor 4, eyes 1, verbal 1) and she was temporarily
intubated. Neurological exam was significant for subtle
anisocoria with right pupil dilation, but both pupils were
equally reactive to light and there was no gaze deviation.
Initial medical workup including lumbar puncture and
electroencephalography was unremarkable. CT head without contrast showed no acute intracranial abnormalities.

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A repeat CT head with angiogram performed the same
day were also unremarkable. Finally, a brain MRI with
angiogram the following day demonstrated evidence of
acute infarcts in the bilateral thalami and midbrain (Fig. 1)
with angiographic findings suggestive of occlusion of the
right artery of Percheron (Fig. 2). Unfortunately, our patient was past the time window for thrombolysis. She was
managed conservatively and then admitted to a local rehabilitation centre for post-stroke rehabilitation once
medically stable. Investigations for stroke etiology, including coagulopathy screen, ultrasound for DVT, and transthoracic echocardiogram with contrast bubble study for
intracardiac shunting, were unremarkable. A thorough
vasculitis workup was not performed given the lack of evidence of brain angiitis on imaging or clinical signs of a
systemic rheumatologic disease.
She was ultimately transferred to an Acquired Brain Injury (ABI) Rehabilitation Program 59 days following her
initial presentation. Her admitting neurological examination revealed slightly reduced left-sided strength in both
her upper and lower extremity without other focal neurological deficits. Meanwhile, significant cognitive impairment was identified, specifically involving her memory
and executive functioning. Regarding functional status,
she was using a wheelchair regularly for safety and cognitive reasons but was physically able to perform transfers
and climb stairs with supervision, she was alert but not
oriented, she was occasionally incontinent of urine, and
she displayed lack of judgement and some impulsiveness.
A trial of neurostimulants (amantadine up to 100 mg BID
and methylphenidate up to 15 mg BID) aimed at improving her cognition did not lead to any functional benefit.
As an inpatient on the ABI unit, our patient underwent several days of standardized neuropsychological assessment at four months following her initial event. A
battery of tests was administered over several sessions,
which assessed her intellectual functioning, processing
speed, attention, working memory, visuospatial function,
memory, and executive functioning. She was noted to
have a profound memory deficit, with performance in
the lowest percentile on nearly all tests of immediate recall, delayed recall, and recognition (i.e. she was unable
to recall or recognize either verbal or visual information
after delays of approximately 20 to 30 min). While she
tended to perform in the low average to average range
on tests of working memory, she could not encode these
memories into long-term storage. Moreover, consistent
with a severe anterograde and retrograde amnesic syndrome, she self-reported an inability to form any new
episodic memories or recall any events which occurred
before her stroke, including the inability to recall memories of her childhood. While she also performed poorly
on tests of executive function, it was difficult to determine the true extent of these deficits as her ability to

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Fig. 1 MRI findings of acute infarction in bilateral thalami and midbrain. Axial magnetic resonance images 1 day post-stroke demonstrating acute
infarcts of the thalami and midbrain bilaterally (yellow arrow) as confirmed with increased signal on diffusion weighted imaging (a-d),
corresponding signal drop out on apparent diffusion coefficient map (e-h), and hyperintensity on fluid attenuation inversion recovery sequences
(i-l). For each row of images, axial slices are arranged caudally to rostrally

perform these tasks and learn from feedback may have
been confounded with her memory deficits. Importantly,
her relatively intact basic attention, working memory,
and social skills made it extremely difficult for those
around her to determine the extent of her memory impairments. At 1 year follow-up, the patient’s neuropsychological assessment showed mild improvement in
her visual memory functioning, but her other memory
scores remained weak and consistent with her previous
assessment (Table 1). Prior recommendations including
24-h supervision, repetition of information, provision of
one-step instructions, and gradually increasing physical
and mental activity were still being employed by her
family with good tolerance of these strategies.

Discussion and conclusions
AOP infarction is an often-delayed diagnosis due to various factors. First, the AOP is an uncommon anatomic
variant and its stroke syndrome is not commonly encountered. Next, ischemia of this region can present in a
variety of ways and is not limited to the classically described paramedian thalamic syndrome [3]. Finally, MRI
is the gold standard for diagnosis of AOP infarction,
while CT is routinely used as first-line imaging for
standard stroke diagnosis [7]. In our case, MRI was performed more than 24 h after the patient’s initial

symptom onset that identified restricted diffusion within
the thalami and midbrain bilaterally. The early recognition of thalamic stroke syndromes as a cause of decreased LOC and coma is essential since hyperacute
AOP infarction can be treated effectively with intravenous heparin and thrombolysis [10, 11].
This case emphasizes the need for neuropsychological assessments at various time points following AOP infarction to
identify the true extent of cognitive impairment. While there
have been cases where AOP infarction led to an amnestic
presentation similar to Korsakoff syndrome with its pathognomonic symptom of confabulation, our patient’s profound
anterograde and retrograde amnesia was not immediately
obvious to caregivers due to her strong social skills and relatively intact working memory [12]. The extent of her deficit
was only identified when she completed neuropsychological
testing, which also allowed for appropriate care recommendations and prognosis to be delivered.
Although our patient did not show significant recovery, Krolak-Salmon et al. described a case of AOP infarction with memory impairment 1 month post-stroke, but
complete recovery after 1 year [9]. While recovery trajectory has not been specifically analyzed in this population,
a major study of anterior circulation ischemic strokes
showed that functional outcome was best predicted by
neurologic improvement at only 2 days post-infarction

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Fig. 2 Angiographic findings suggestive of occlusion of right artery of Percheron. Contrast-enhanced magnetic resonance imaging (a) and CT
angiogram (c) demonstrated normal opacification and diameter of the vertebrobasilar arterial trunk, excluding top of the basilar artery syndrome.
There was slight asymmetry of the posterior cerebral arteries (PCAs) with relative narrowing of the right P1 segment compared to the left (yellow
arrows in a and c), raising the possibility of incomplete P1 occlusion or stenosis and occlusion at the level of the perforating branches of the
right PCA, namely artery of Percheron. However, the filling of the more distal part of the right PCA appeared normal, likely due to the
contribution from a robust posterior communicating artery (yellow arrows in b). Magnetic resonance venogram (d) demonstrated normal
opacification and filling of the internal cerebral veins (yellow arrows) and intracranial venous sinuses, excluding deep cerebral venous infarct

[13]. Accordingly, our patient’s outcome may be more
representative of the typical stroke patients.
Regarding memory impairment, researchers have noted
that patients with damage to the dorsomedial and intralaminar thalamic nuclei, which are impacted by AOP infarction, may present with similar memory difficulties as
those with bilateral hippocampal damage [14]. On the
other hand, prefrontal cortex (PFC) dysfunction is associated with executive function impairments [15] and some
researchers have proposed that the memory deficits seen
in AOP stroke are secondary to impairments in executive
function, supported by the correlation between thalamic
substructures and PFC [16]. Increasing evidence indicates
interconnections between the PFC and the dorsomedial
thalamus, although the mechanism of PFC-thalamic functional connectivity underlying higher cognitive function is
not completely understood [17]. While there may be a relationship between our patient’s executive function and
memory, given the severity of her memory deficits (i.e.,
anterograde and retrograde amnesic syndrome), it is unlikely that her executive abilities would fully account for
all aspects of her memory impairment, such as her inability to form basic episodic memories.

Limitations of the current study include differences between administration of neuropsychological assessment at
4 months and 1 year after stroke. Particularly, the initial
assessment was completed over several days, whereas
follow-up was obtained in 1 day and included self-report
measures of behaviour and personality as opposed to extensive clinical interviewing. Although testing was completed in different settings (inpatient versus outpatient)
and there was some variation in the measures utilized,
both were conducted by licensed neuropsychologists and
similarly trained psychometrists. Future studies may take
a more experimental approach by having a standard assessment protocol at each timepoint.
In closing, AOP infarction is an important differential
diagnosis to consider when a patient presents with fluctuating consciousness characteristic of stroke but initial
head CT is normal, since early diagnosis and management
may significantly improve clinical outcome. We described
a case of a 40-year-old female presenting with profound
anterograde and retrograde amnesia who missed the time
window for thrombolysis following AOP occlusion.
Neuropsychological assessment at 4 months and 1 year
post-stroke showed limited improvement over time.

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Table 1 Neuropsychological profile post-injury at 4 months and 1 year post-injury

Neuropsychological testing at 4 months (black) and 1 year (grey) post-stroke. Performances that span across ranges represent variability within that domain.
Simple visuospatial functioning and inhibition were tested at the 4 month timepoint only.

Importantly, her relatively intact social skills and working
memory prevented appreciation of the true extent of her
memory deficit in the absence of neuropsychological testing. Thus, this case study emphasizes the need for thorough neuropsychological testing to document areas of
impairment and to identify strategies for rehabilitation
and safety in AOP stroke patients. It also supports the role
of the paramedian thalamic territory in executive function
and memory as has been described by previous works, but
additional research is needed to decipher the functions of
specific thalamic nuclei, such as the dorsomedial nucleus,
in moderating these cognitive domains.
Abbreviations
AOP: Artery of Percheron; ABI: Acquired brain injury; CT: Computed
tomography; DVT: Deep vein thrombosis; ED: Emergency department;

GCS: Glasgow Coma Scale; LOC: Level of consciousness; MRI: Magnetic
resonance imaging; PFC: Prefrontal cortex
Acknowledgements
We thank the patient described in the study as well as all team members
who cared for her on the Acquired Brain Injury Rehabilitation Unit.
Authors’ contributions
Conception and design of the work – AU, HES, JS, ZD. Drafting the work or
substantively revising it – AU, HES, JS, SA, ZD. Acquisition and interpretation
of neuroimaging – CF, ZD. All authors read and approved the final
manuscript.
Funding
No funding was received for this study.
Availability of data and materials
The authors declare that all the data are contained within the manuscript.

Snyder et al. BMC Neurology

(2020) 20:370

Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent for publication was obtained and is available upon
request.
Competing interests
The authors declare no conflicts of interest.
Author details
1
Michael G. DeGroote School of Medicine, McMaster University, Hamilton,
Canada. 2Regional Rehabilitation Centre, Hamilton Health Sciences, Hamilton,
Canada. 3Department of Psychology, University of Victoria, Victoria, Canada.
4
Department of Psychiatry and Behavioural Neurosciences, McMaster
University, Hamilton, Canada. 5Department of Radiology, McMaster
University, Hamilton, Canada. 6Division of Physical Medicine and
Rehabilitation, Department of Medicine, McMaster University, Hamilton,
Canada.
Received: 8 June 2020 Accepted: 30 September 2020

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