Vascular Health and Risk Management

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Complex neurological symptoms in bilateral
thalamic stroke due to Percheron artery
occlusion
This article was published in the following Dove Press journal:
Vascular Health and Risk Management
22 December 2016
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Paola Caruso
Paolo Manganotti
Rita Moretti
Department of Clinical Neurology,
University of Trieste, Trieste, Italy

Abstract: The artery of Percheron is a rare anatomical variant where a single thalamic perforating artery arises from the proximal posterior cerebral artery (P1 segment) between the basilar
artery and the posterior communicating artery and supplies the rostral mesencephalon and both
paramedian territories of the thalami. Almost one-third of human brains present this variant.
Occlusion of the artery of Percheron mostly results in a bilateral medial thalamic infarction,
which usually manifests with altered consciousness (including coma), vertical gaze paresis,
and cognitive disturbance. The presentation is similar to the “top of the basilar syndrome”, and
early recognition should be prompted. We describe the case of a young female with this vessel
variant who experienced a bilateral thalamic stroke. Magnetic resonance angiography demonstrated bilateral thalamic infarcts and a truncated artery of Percheron. Occlusion of the vessel
was presumably due to embolism from a patent foramen ovale. Thrombolysis was performed,
with incomplete symptom remission, cognitive impairment, and persistence of speech disorders. Early recognition and treatment of posterior circulation strokes is mandatory, and further
investigation for underlying stroke etiologies is needed.
Keywords: thalamus vascularization, cognitive impairment, paramedian thalamus territory,
speech disorder, vertical gaze palsy

Background

Correspondence: Paola Caruso
Department of Clinical Neurology,
University of Trieste, Ospedale di
Cattinara, Strada di Fiume, 447 34149
Trieste, Italy
Tel +39 040 399 4569
Fax +39 040 4284
Email caruso.paola1983@libero.it

The thalamus and midbrain have a complex blood supply with a large number of feeding arteries. The arterial supply of the thalamus and midbrain consists of a complex
arterial network involving the anterior and posterior cerebral circulation. The anterior
and inferior midbrain and thalami are supplied mostly by the internal carotid artery,
while the medial, lateral, and posterior territories are irrorated from the vertebrobasilar
system. In recent decades, according to pathological data, the following four territories
for thalamic vascularization were identified: tuberothalamic, paramedian, inferolateral,
and posterior choroidal arteries. The paramedian arteries normally supply the medial
ventral thalami, hypothalamus, and subthalamic–mesencephalic junction and derive
from the proximal segment of the posterior cerebral artery.1,2
In addition to the paramedian thalamic territory, the paramedian thalamic arteries supply the following medial areas of the upper brainstem: the interpeduncular
nucleus, the decussation of the superior cerebellar peduncles, the medial part of the
red nucleus, the third and fourth cranial nerve nuclei, and the anterior portion of the
periaqueductal gray matter.3
Thalamic stroke accounts for 11% of vertebrobasilar infarcts. Strokes limited to
paramedian territories account for ~22–35% of all thalamic infarcts, usually due to
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http://dx.doi.org/10.2147/VHRM.S119395

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Caruso et al

cardioembolism. Paramedian arteries (arising from the P1
section of the posterior cerebral artery on both sides) supply
dorsomedian nucleus (divided into anteromedial magnocellular and posterolateral parvocellular mediodorsal nuclei that
receive projections from the amygdala and are connected to
the prefrontal cortex and ventral pallidum) and the intralaminar nuclei (central lateral, centromedian, and parafascicular;
the intralaminar nuclei are divided into the caudal part and the
rostral part that project to the orbitofrontal and mediofrontal
cortices, the motor and premotor cortex, and the internal
globus pallidus).4–6
Consequently, occlusion of the artery of Percheron causes
a bilateral paramedian thalamic infarction with or without
midbrain infarction. Additional involvement of the anterior
thalamus is uncommon.
Regarding the origin of the paramedian artery, it is known
that in one-third of human brains, the vessel originates from
a single pedicle named the type B artery of Percheron. In
these cases, stroke affects both paramedian thalamic regions
and may lead to a complex clinical syndrome (~0.1–2% of
all ischemic strokes; Figure 1).7
The artery of Percheron may be visualized with CT or
MR angiography. However, diagnosis of Percheron artery
infarction is often made in the late stage. Successful recanalization of the artery of Percheron with thrombolysis has
been described.
In the majority of cases, clinical features include varying
levels of decreased consciousness, neuropsychological and
memory impairment, and vertical gaze palsy. Oculomotor
disturbances, hemiplegia, cerebellar ataxia, and movement
disorders have also been described.8
The goal of this article is to report a case where the diagnosis of an infarction due to an occlusion of the Percheron
artery has been made directly and not retrospectively as
usually appears.
A

Case presentation
We describe the case of a 52-year-old well-fit Caucasian
female who was admitted to our emergency department
because of a sudden onset of decreased consciousness and
speech disorder. Written informed consent was received from
the patient for this study. The first neurological examination
revealed a Glasgow Coma Scale score of 8 and a National
Institutes of Health Scale Score of 13.
When deeply stimulated, she could only open her eyes,
verbal communication was absent, and she was not able to
perform any command, and on cranial nerve examination,
vertical gaze palsy was detected, while no other motor deficits
could be identified. Blood examinations excluded a possible
metabolic, toxic, infective, endocrine, or iatrogenic etiology
of the comatose state.
Brain CT scan examination was immediately obtained,
and no acute lesions could be seen; a filling defect of the
P1 segment of the left posterior cerebral artery was only
described, and the radiologist could not identified the posterior communicant left artery (Figure 2).
However, taking into account all the symptoms and
considering the possibility of an acute stroke, intravenous
thrombolysis was performed resulting in a slow improvement
of her clinical condition in the next days, although the confusion state, disorientation, slurred speech, and oculomotor
disorder persisted.
On the next day, thrombolysis brain CT and MRI scans
were performed that showed bilateral thalamic lesions in the
paramedian territory (Figure 3).
During recovery, duplex ultrasound of trial sequential
analysis and transcranial doppler ultrasound and transesophageal echocardiography were performed that revealed a patent
foramen ovale with spontaneous passage of contrast bubbles
from the right auricle to the left cavities, which could probably be the cause of embolism.
B

T

PCOM

PA
PCA
BA

Figure 1 (A) Schematic representation of the affected thalamic nuclei in this case compared to an axial diffusion-weighted magnetic resonance image of the same patient.
The black line limits the area of infarction in both paramedian regions. (B) Schematic representation of the artery of PA, T, BA, PCA, and PCOM.
Abbreviations: PCOM, posterior communicating artery; BA, basilar artery; CM, centromedian; CL, central lateral; MD, dorsomedialis; Pf, parafascicularis; PA, percheron;
PCA, posterior cerebral artery; Pv, paraventricular; T, thalamus.

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A

Complex neurological symptoms in bilateral thalamic stroke
B

Figure 2 Brain angio CT scan’s coronal view (A) and axial view (B).
Note: Performed in the emergency department, showing no parenchymal lesions
or main vessel obstruction: brain CT scan examination showed only a filling defect
of the P1 segment of the left posterior cerebral artery (A).

A

B

Figure 3 (A) Brain CT scan axial view, performed after thrombolysis showing
ischemic stroke in the paramedian territory of both thalami. (B) MRI axial view
seq T2.

The first neuropsychological exam showed deficits on
attention and memory task changes in behavioral were found,
like impulsive behavior, also deficit in executive function were
found, anosoagnosia and slowness in executive functions.
After a week, the patient was discharged to home with a
diagnosis of a bilateral thalamic stroke in cardioembolism.
After 3 months, she was evaluated again and memory and
behavioral impairment could be still detected. She was not
able to go back to her work.

Discussion
First described in 1973, the artery of Percheron is a rare
anatomical variant where a single thalamic perforating artery
arises from the proximal posterior cerebral artery (P1 segment) between the basilar artery (BA) and the posterior communicating artery and supplies the rostral mesencephalon and
both paramedian thalami. If this artery becomes occluded,
bilateral paramedian thalamic infarction occurs. Proximal
embolism is thought to be the most common e­ tiology of
stroke in this territory with this variant. Asymmetric thalamic
involvement is seen in two-thirds of cases, and midbrain
infarction is present in over half.9
Vascular Health and Risk Management 2017:13

Conventional vascular imaging does not routinely demonstrate these tiny perforating vessels. Hypoplastic or absent
P1 segments are more likely to be seen with this variant.
Lazzaro et al identified four patterns of ischemic infarctions
when the Percheron artery is occluded. Approximately 43% of
their cases presented infarction of both paramedian thalami and
midbrain, and in 38% of cases, only damage to paramedian
thalami was detected. In ~14% of patients, the damage involved
the anterior thalamic nuclei in addition to paramedian thalami
and upper midbrain. The least common pattern (5%) was ischemic damage of the bilateral paramedian and anterior thalami;
the midbrain was spared in these cases. Moreover, in their
work, the “V” sign for the diagnosis of Percheron artery was
described; a fluid-attenuated inversion recovery (FLAIR) and
diffusion weight imaging sequences in 67% of cases of artery
of Percheron infarction with midbrain involvement were found,
and this sign supports the diagnosis when present. The “V” sign
appears as a distinct pattern of V-shaped hyperintensity on axial
FLAIR and/or diffusion weight imaging along with the pial
surface of the midbrain adjacent to the interpeduncular fossa.10
Although bilateral ischemic lesions can be seen on MRI,
differential diagnoses include inflammatory, infectious,
and neoplastic illnesses; particularly, venous infarction and
neoplastic lesion do not follow a particular arterial territory.
However, more often, diagnosis is only clinical; actually,
patients with bilateral paramedian thalamic lesions may
develop altered sensorium, vertical gaze palsy, and memory
impairment. Sudden onset of altered eye movements with partial/complete limitation of vertical gaze, loss of convergence,
bilateral internuclear ophthalmoplegia, pseudopalsy of the
abducens nerve, and intolerance to light are the characteristics; pupils are frequently abnormal, and pupil size varies
depending on the involvement of the Edinger–Westphal
nucleus or oculomotor fascicles, descending sympathetic
fibers, or some combination of these structures.11–13 Dysarthria, altered consciousness, and motor paresis should alert
the clinician to the possibility of ischemia of posterior circulation territory, including the BA. Severe cognitive impairment,
amnesic syndrome, and executive dysfunction impairment
can occur, which can still be present some months after
presentation. Behavioral problems with inappropriate social
conduct, apathy, and flattened emotions are also described.14,15
Recently, Arauz et al,16 in a study of 15 consecutive
patients with a Percheron artery infarct, described the following seven main clinical patterns: 1) mental status disturbance;
2) behavioral amnesic impairment (confusion, agitation,
apathy, or disinhibition); 3) aphasia or dysarthria including
any component of language component or slurred speech;
4) ocular movements; 5) motor deficits; 6) cerebellar signs;
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Caruso et al

and 7) other symptoms that are not previously reported (such
as hypersomnia, tremors, seizures, and hyperthermia).
The large number of variants of the blood supply in the
posterior cranial fossa (especially regarding the presence
and size of P1 segments, which give rise to the paramedian
arteries) might show that the artery of Percheron is not such
an infrequent variant and is most underdiagnosed. The characteristic artery of Percheron infarction may occur in 0.1–2%
of all ischemic strokes and in 4–18% of all thalamic strokes.
Stroke due to PA artery occlusion should be suspected
in every patient with acute onset of symptoms related to
posterior circulation deficit. Diagnosis is firstly clinical,
acute neuroimaging may not help in diagnosis, main clinical
signs include vertical gaze palsy, alteration in consciousness
and cognition. If possible intravenous thrombolysis should
be performed, although the intraarterial approach has been
described with successful exit.

Disclosure
The authors report no conflicts of interest in this work.

References

1. Carrera E, Michel P, Bogousslavsky J. Anteromedian, central and
posterolateral territory infarcts: three variant types. Stroke. 2004;
35(12):2826–2834.
2. Schmahmann J. Vascular syndromes of the thalamus. Stroke. 2003;
34(9):2264–2278.
3. Lamot U, Ribaric I, Popovic KS. Artery of Percheron infarction: review
of literature with a case report. Radiol Oncol. 2015;49(2):141–146.

4. Castaigne P, Lhermitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen O.
Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann Neurol. 1981;10(2):127–148.
5. Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke.
1988;19(9):1083–1092.
6. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes,
etiology, and prognosis. Neurology. 1988;38(6):837–847.
7. Saez de Ocariz M, Nader J, Santos J, Bautista M. Thalamic vascular
lesions. Risk factors and clinical course for infarcts and hemorrhages.
Stroke. 1996;27(9):1530–1536.
8. Cassourret G, Prunet B, Sbardella F, Bordes J, Maurin O, Boret H.
Ishemic stroke of the artery of Percheron with normal initial MRI: a
case report. Case Rep Med. 2010;2010:425734.
9. Percheron G. Arteries of the human thalamus: II. Arteries and paramedian thalamic territory of the communicating basilar artery. Rev Neurol
(Paris). 1976;132(5):309–324.
10. Lazzaro NA, Wright B, Castillo M, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol.
2010;31(7):1283–1289.
11. Thurtell MJ, Halmagyi GM. Complete ophthalmoplegia an unusual
sign of bilateral paramedian midbrain-thalamic infarction. Stroke.
2008;39(4):1355–1357.
12. Amin OSM, Shwani SS, Zangana HM, Hussein EMH, Ameen NA.
Bilateral infarction of paramedian thalami: a report of two cases of
artery of Percheron occlusion and review of the literature. BMJ Case
Rep. 2011;2011.
13. Turner J, Richardson T, Kane I, Vundavalli S. Decreased consciousness:
bilateral thalamic infarction and its relation to the artery of Percheron.
BMJ Case Rep. 2014;2014.
14. Jiménez Caballero PE. Bilateral paramedian thalamic artery infarcts:
report of 10 cases. J Stroke Cerebrovasc Dis. 2010;19(4):283–289.
15. Margolin E, Hanifan D, Berger MK, Ahmad OR, Trobe JD, Gebarski SS.
Skew deviation as the initial manifestation of left paramedian thalamic
infarction. J Neuroophthalmol. 2008;28(4):283–286.
16. Arauz A, Paino-Rodriguez HM, Vargas-Gonzalez JC, et al. Clinical
spectrum of artery of Percheron infarct: clinical-radiological correlations. J Stroke Cerebrovasc Dis. 2014;23(5):1083–1088.

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