Neurocase
The Neural Basis of Cognition

ISSN: 1355-4794 (Print) 1465-3656 (Online) Journal homepage: http://www.tandfonline.com/loi/nncs20

Persistent anterograde amnesia due to the artery
of Percheron occlusion: a case report
Birsen Ince & Furkan Asan
To cite this article: Birsen Ince & Furkan Asan (2018): Persistent anterograde amnesia due to the
artery of Percheron occlusion: a case report, Neurocase, DOI: 10.1080/13554794.2018.1458884
To link to this article: https://doi.org/10.1080/13554794.2018.1458884

Published online: 02 Apr 2018.

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NEUROCASE, 2018
https://doi.org/10.1080/13554794.2018.1458884

Persistent anterograde amnesia due to the artery of Percheron occlusion: a case
report
Birsen Ince and Furkan Asan
Department of Neurology, Division of Cerebrovascular Disease, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
ABSTRACT

ARTICLE HISTORY

Bilateral thalamic infarction involving the artery of Percheron (AOP) can cause diagnostic difficulties due
to the varying clinical presentations. AOP infarcts presented with isolated memory impairment are not
common and the factors affecting the persistence of memory disorders are still unknown. A 41-year-old
male patient was hospitalized with acute unconsciousness. MRI disclosed bilateral paramedian thalamic
infarction The patient had isolated memory deficit and his anterograde amnesia continued without any
change in the past decade. More cases might answer the questions concerning the intra- and extrathalamic structures responsible for the amnesic syndrome and the factors affecting the persistence of
the symptoms.

Received 27 April 2017
Accepted 16 March 2018

Introduction
Blood supply to the thalamus has many anatomic variations.
The artery of Percheron (AOP) is a rare vascular variant
supplying both paramedian thalami. Occlusion of this
uncommon vessel results in symmetrical bilateral thalamic
infarcts with or without mesencephalic infarctions. The complex anatomy, vascular supply and functions of thalamus are
responsible for the variable clinical presentations leading
the physician to think of an etiology other than stroke.
AOP infarcts are mainly characterized by a triad of altered
mental status, gaze palsy, and memory impairment (Arauz
et al., 2014). The prognosis of AOP infarction is usually good
with low mortality and often rapid reversal of the coma, but
the outcome of memory deficits after the acute phase of
the disease is unknown. All cases with AOP infarction might
not pursue a similar long-term course, raising the burning
question why some cases have only temporary memory
disorder after the incident while others are obliged to live
with lifelong memory deficit. We report a case with longterm anterograde amnesia due to AOP occlusion by questioning the factors that contribute to the persistence of the
symptoms.

Case report
A 41-year-old male patient with no history of illness,
tobacco, or alcohol consumption was hospitalized with
acute unconsciousness. There was no focal neurological
deficit on admission. His Glasgow Coma Scale was 7/15
(eye 2, verbal 1, motor 4). He was treated at the intensive
care unit (ICU) without requiring mechanical ventilation.
Although he demonstrated fluctuations in his level of consciousness ranging from coma to somnolence, his pupils
were equal and reactive to light bilaterally. MRI disclosed

CONTACT Birsen Ince

bince@istanbul.edu.tr

© 2018 Informa UK Limited, trading as Taylor & Francis Group

KEYWORDS

Percheron; anterograde
amnesia; thalamic infarction;
amnesia; persistent amnesia

bilateral paramedian thalamic infarction; MR angiography,
blood biochemistry, serological tests, and markers of vasculitis were completely normal. Transthoracic echocardiography revealed ejection fraction to be 35% and diffuse
hypokinesia. Etiology was evaluated as cardioembolic and
anticoagulant therapy was started. The patient was examined after regaining consciousness, where orientation to
person, place and time, reading, writing, copying, and
verbal expression were all found insufficient. Within a
month, all language functions completely returned to normal, but anterograde amnesia continued without any
change. Mini Mental State Examination (MMSE) score was
9/30. He is 50 years old now and has been living for the
past decade without being able to turn his life into memories. He has no retrograde amnesia, no memory deficit
regarding his past life but he has not been able to record
any new memories since the cerebrovascular accident
10 years ago. He is a retired worker, he could chat with
his family and old friends, but never remembering what he
talked about more than a few minutes. He cannot recognize his now grown-up children, but he knows their names
in order. The patient does not show any behavioral disorders but is usually in a depressive mood, probably since
he is aware of his incompetencies. We administered MMSE
to see if the score stayed the same and it was 10/30 after
10 years. Montreal Cognitive Assessment (MOCA) score was
11/30. The worst part of assessment was the delayed
record. The recall of word list after 5 min was impossible.
Naming and attention were normal, although visuospatial
skills, orientation and abstraction were insufficient in the
test. Although he has no stroke recurrence under the
adjusted-dose warfarin treatment and no other neurological disabilities, daily life is very distressing for the patient
as well as his family.

2

B. INCE AND F. ASAN

Discussion
A number of studies have been carried out on thalamic amnesia, with the aim of clarifying the role of thalamic nuclei and
bundles in memory processes (Danet et al., 2017). Thalamic
abnormalities occur in some of the earliest stages of
Alzheimer’s disease. Appreciating the importance of the thalamic nuclei for memory may provide the understanding of
Alzheimer’s disease (Aggleton, Pralus, Nelson, & Hornberger,
2016). To date, cognitive outcome has been assessed in single
cases and small case series, some of which have reported
residual memory deficits, and others apparent recovery following limbic encephalitis (Butler et al., 2014), but there is no
sufficient data on long-term prognosis of memory deficit following thalamic stroke. The prognosis of AOP infarctions is
usually good. Life threatening complications have been
reported very rarely (Zappella et al., 2014). Recent reviews
and case reports on this topic cover the early phase of the
disease thoroughly (Lamot, Ribaric, & Popovic, 2015; Zappella
et al., 2014) and just temporary memory deficit has been
reported in three-month follow-up (Bailey & Khadjooi, 2016).

(a)

Only Arauz et al. reported a long-term follow-up (a mean of
55 months) for the case series of 15 patients including 2
patients with anterograde amnesia, but if there was any
change in the level of amnesia, it was not mentioned. It was
pointed out that the presence of midbrain extension was
meaningful in the persistence of clinical findings. Their observations suggested that the non-extension to the midbrain
explains the favorable outcome in 67% of the cases mostly
presenting with the behavioral amnesic impairment and mental status disturbance (Arauz et al., 2014). Cerebral MRI of our
patient on the 10th year demonstrates bilateral thalamic paramedian infarction (Figure 1(a,b)) due to the AOP occlusion
without the extension to the brainstem (Figure 1(c, d)) and
there are no lesions at the other regions of the brain.
Similar clinical features and outcomes were recorded in
patients with AOP infarction identified in the literature, of
whom 13 required ICU management. In stroke patients who
required mechanical ventilation, 1-year mortality rates range
from 40–70% and cognitive impairments persist in 63–75% of
survivors (Zappella et al., 2014). Our patient was treated at the

(b)

(c)
Figure 1. MRI shows bilateral paramedian thalamic infarction (a, b) without midbrain involvement (c, d).

(d)

NEUROCASE

ICU but the need of mechanical ventilation did not arise.
Embolic heart disease is one of the most common types of
etiology which occludes the AOP leads to bilateral paramedian
thalamic infarction (Jumean et al., 2016). Our patient has a
cardioembolic etiology with diffuse hypokinesia, but it is
reported that unfavorable outcome is not related to the etiology of stroke (Arauz et al., 2014).
Intra- and extra-thalamic structures primarily responsible for
the amnesic syndrome are still unknown. Vascular thalamic
amnesics often present dysexecutive and behavioral deficits
similar to those observed in patients with frontal damage, but
our case showed no behavioral dysfunctions. Data reported in a
few single cases provide support for the hypothesis that thalamic regions connected to distinct areas of the mesiotemporal
lobe play differential roles in recollection and familiarity processes (Carlesimo, Lombardi, & Caltagirone, 2011). The connections link hippocampal and parahippocampal regions with the
mammillary bodies, the anterior thalamic nuclei, and the cingulate gyrus, all structures now strongly implicated in memory
functions (Bubb, Kinnavane, & Aggleton, 2017). Unfortunately,
findings from the literature review did not allow identifying
consistent localization and criteria for the persistence of the
memory disorder. The fact that our case did not have any
recurrent infarcts, its “single attack-single location” characteristic and the unchanging severity of amnesia for a decade suggests a clarifying effect regarding the location of amnesia.
In conclusion, our patient is the first case with a 10-year
history of anterograde amnesia due to AOP occlusion; more
cases with long-term follow-up may provide 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 infarction presenting with isolated memory disorder.

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

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