Clinical and Neuroimaging Findings in Thalamic Territory

Infarctions: A Review
Shuo Li , Yogesh Kumar, Nishant Gupta , Ahmed Abdelbaki, Harpreet Sahwney, Anil Kumar, Manisha Mangla,
Rajiv Mangla
From the Department of Radiology, Yale New Haven Health Bridgeport Hospital, Bridgeport, CT (SL, AA, HS); Department of Radiology, Columbia University at Bassett
Healthcare, Cooperstown, NY (YK); Department of Radiology, Columbia University Medical Center, New York, NY (NG); Division of Neurology, Department of Internal
Medicine, Great Plains Health, North Platte, NE (AK); Department of Radiology, State University of New York (SUNY) Upstate Medical University, Syracuse, NY (MM, RM);
Department of Public Health and Preventive Medicine, State University of New York (SUNY) Upstate Medical University, Syracuse, NY (MM); and Department of Radiology,
University of Rochester, Rochester, NY (RM).

ABSTRACT
The thalamus is a part of the diencephalon, containing numerous connections between the forebrain and subcortical structures.
It serves an important function as a relay center between the cerebral cortex and the subcortical regions, particularly with
sensory information. The thalamus also plays a major role in regulating arousal and the levels of awareness. Distinct vascular
distribution of the thalamus give rises to different syndromic presentation of thalamic nuclei infarcts. The clinical records and
available imaging studies of patients with confirmed thalamic territory infarcts on magnetic resonance imaging (MRI) at the
University Hospital of Rochester were reviewed and analyzed. This analysis was then used to provide an effective summary of
thalamic vascular anatomy, the clinical symptoms, and syndromes associated with strokes in the affected territories. Specifically,
we review the syndromes associated with classic vascular territories, including the anterior, paramedian, inferolateral, and
posterior thalamic nuclei, that are supplied by the polar (tuberothalamic), paramedian, inferolateral (thalamogeniculate), and
posterior choroidal arteries, respectively. In addition, we will also review the variant thalamic territories and associated infarction
syndromes of the anteromedian, central, and posterolateral territories. This review article is aimed to better the clinical and
radiologic understanding as well as the diagnosis of classic and variant thalamic territory infarcts. This article will also briefly
touch on the recovery of function after thalamic infarcts.

Keywords: CT, MRI, thalamic infarct, thalamic infarct syndrome.

Acceptance: Received November 21, 2017. Accepted for publication January 18, 2018.

Correspondence: Address correspondence to Shuo Li, Department of Radiology, Yale New Haven Health Bridgeport Hospital, Bridgeport, CT. E-mail:
dr.shuo.li@gmail.com; shuo.li@ynhh.org.
Acknowledgements and Disclosure: There is no external funding for this manuscript.
All authors have indicated they have no financial relationships relevant to this article to disclose.
All authors have indicated they have no potential conflicts of interest to disclose.
The authors would like to thank the Imaging Sciences Graphics Department at University of Rochester for their assistance in the preparation of this
manuscript.

J Neuroimaging 2018;00:1-7.
DOI: 10.1111/jon.12503

Overview of Thalamus Anatomy
The thalamus is a part of diencephalon, the caudal (posterior)
part of the forebrain that contains the thalamus, epithalamus,
hypothalamus, third ventricle, and pituitary gland.1 Thalamus
has numerous connections and relays the information between
the forebrain and subcortical structures. It is connected to the
hippocampus via the mammillary tract and fornix, the cerebral
cortex via the cerebrocortical radiations, and the spinal cord
via the spinothalamic and spinocerebellar tracts.2,3
and ventral anterior nuclei transmit the motor signals, with
evidence to suggest that the dominant ventrolateral thalamus
is also involved in language processing.6 The somatosensory
information is transmitted via the ventral posterior lateral
and ventral posteromedial thalamic nuclei.7 The medial
dorsomedial nucleus is associated with autonomic functions
and emotions. The symptoms of thalamic infarction are varied,
and can include vertical gaze palsy, memory impairment, and
confusion.

Overview of Thalamic Functions Blood Supply of the Thalamus

The thalamus serves as the relay center, particularly for the
sensory system (all except the olfactory) between the cerebral
cortex and the subcortical regions. The thalamus plays a major
role in regulating arousal, the levels of awareness, and activity.
Damage to the thalamus can also lead to permanent coma.4 The
functions of the thalamic nuclei are described briefly below.
The medial and lateral geniculate nuclei are involved with
visual and auditory function.5 The pulvinar and lateral dorso-
medial nuclei are involved with visual functions. Ventrolateral
The thalami receive their blood supply from both anterior and
posterior circulations, with several known variations. The thala-
moperforator arteries arise from the anterior circulation usually
supply the anteroinferior aspects of the thalami and midbrain.
The posterior circulation supplies the remaining portion of the
thalami. The medial aspects of the thalami and the midbrain
are supplied by branches arising from the P1 segments of the
posterior cerebral artery (PCA). The lateral and superior as-
pects of the thalami are supplied with branches arising from P2

Copyright ◦ 2018 by the American Society of Neuroimaging

C 1
 thalamic arterial territories stemming from the posterior circu-
lation, which originates from the PCA. Although infarcts in the
anterior thalamic territory account for about 12% of all thala-
mic infarcts, very few reports exist for isolated anterior thalamic
infarcts.9 These involve the anterior nuclei, which receive pro-
jections from the mammillothalamic tract and are connected to
the anterior limbic system.8 Anatomy and imaging findings of
anterior thalamic infarcts are illustrated in Figure 3.

Fig 1. Artist’s rendition of various arteries supplying the thalamus

(adapted from Schmahmann8 with permission). P-com = posterior
communicating artery; P1 = segment of the posterior cerebral artery
(PCA) prior to the P-com; P2 = segment of the PCA distal to the
P-com to the posterior margin of the midbrain; P3 = segment of the
PCA distal to the posterior margin of the midbrain.

segments of the PCAs. The arterial supply of the thalamus is

illustrated in Figure 1.

Classical Thalamic Vascular Territories

The classical thalamic territories were classified according
to their arterial supply: anterior, paramedian, inferolateral,
and posterior. These are supplied respectively by the po-
lar (tuberothalamic), paramedian, inferolateral (thalamogenic-
ulate), and posterior choroidal arteries (Fig 2).8

Thalamic Infarcts and Clinical Syndromes
Anterior Thalamic Infarcts
Anatomy
The anterior thalamic territories are supplied by the tuberotha-
lamic arteries (also known as the anterior thalamosubthalamic
paramedian arteries), which originate from middle third of the
posterior communicating (P-com) artery. This varies from other
Fig 3. Schematic diagram of lateral (A) and dorsal (B) views of
tuberothalamic artery infarction. MR image (C) shows the appear-
ance of a classical tuberothalamic artery infarction on the left side
(small green circle) and anteromedian territory (large blue circle) on
right side. CT image (D) in a patient with bilateral chronic tuberotha-
lamic artery infarction (double-headed blue arrow). VA = ventral an-
terior; VL = ventral lateral; DM = dorsomedial; IL = intralaminar
nuclear complex; VP = ventral posterior; P = pulvinar. Figures A and
B were adapted with permission from Schmahmann.8

Fig 2. Schematic diagram of lateral view (A) and dorsal view (B) of four major thalamic arteries and the nuclei they irrigate (adapted from
Schmahmann8 with permission). VA = ventral anterior; VL = ventral lateral; DM = dorsomedial; IL = intralaminar nuclear complex; VP =
ventral posterior; P = pulvinar; LGB = lateral geniculate body; PCA = posterior cerebral artery; ICA = internal carotid artery; P-com = posterior
communicating artery.

2 Journal of Neuroimaging Vol 00 No 0 xxxx 2018

 Clinical Syndrome

The clinical syndrome of anterior thalamic infarct is character-

istic, with the principal manifestation being severe and wide-
ranging neuropsychological deficits. The patients can exhibit
changing levels of consciousness in the early stages of anterior
thalamic infarction, and can appear withdrawn.
Persistent personality changes are seen in the later course
of the disease, which include disorientation in time and place,
euphoria, lack of insight, apathy, and lack of spontaneity. Lack
of emotional concern may be prominent.10
Severe problem in perseverance and increased sensitiv-
ity to interference can present in anterior thalamic infarcts,
giving patients an appearance of wandering thoughts. Addi-
tionally, the patients tend to have improper superimposition
of temporally unrelated information, dubbed palipsychism by
Ghika-Schmid and Bogousslavsky.9 Another common find-
ing in anterior thalamic infarct is the impairment of antero-
grade memory, consistent with previously reported amnesia
after thalamic lesions with involvement of the mammillothala-
mic tract.9,11 Aphasia is also a constant finding with high fre-
quency of hypophonia and dysarthria.9 Interestingly, transcor-
tical aphasia appears to only be associated with left-sided
lesions.12

Paramedian Artery Infarction

Anatomy

The paramedian thalamic arteries arises from the P1 section of

the PCA, with infarcts in the paramedian territory accounting
for about 35% of all thalamic infarcts.8 The configurations of
the origin of the paramedian arteries varies greatly, and were
classified into three types by Percheron as described below.13,14
Anatomy and imaging findings of paramedian artery infarction
are illustrated in Figure 4.

Variants Paramedian Thalamic Artery Origin
Type I: This is the most common variant of the paramedian
thalamic arteries. In this variant, the origins are symmetrical,
with each paramedian thalamic artery arising from their corre-
sponding P1 segments of the PCA.13
Type II: This variant is asymmetric in arrangement and has
two subtypes. Type IIa presents with both paramedian arteries
arising from the same PCA but having separate origins. Type
IIb is the so-called artery of Percheron, with a single perfo-
rating vessel arising from one of the P1 segments, which then
subdivides into two separate paramedian thalamic arteries. This
single arterial trunk supplies the bilateral paramedian thalami
and rostral midbrain. Occlusion of this artery results in bilateral
thalamic and mesencephalic infarctions.8,10,15,16
Type III: The third variant is again a symmetric arrange-
ment, with an arcade of perforating branches arising from the
P1 segments of both PCAs, which subsequently give rise to the
paramedian thalamic arteries.13
These variants are illustrated in Figure 5.
Clinical Symptoms
The clinical syndromes of paramedian thalamic infarcts de-
pend on the type of vascular arrangement, and can involve
unilateral or bilateral infarcts. Bilateral paramedian infarcts
Fig 4. Schematic diagram of lateral (A) and dorsal (B) views of
paramedian artery infarction. Diffusion-weighted MR image (C) of a
patient with bilateral classical paramedian artery infarction (red ar-
rows). Axial T2-weighted MR image (D) of a patient with paramedian
artery infarction (yellow arrow). Coronal T2-weighted MR image (E) of
a patient with paramedian artery infarction (green arrow). CT image
(F) of a patient with bilateral chronic tuberothalamic artery infarction
(blue double headed arrow). VA = ventral anterior; VL = ventral lat-
eral; DM = dorsomedial; IL = intralaminar nuclear complex; VP =
ventral posterior; P = pulvinar. Subparts A and B were adapted with
permission from Schmahmann.8
presents as a unique syndrome, discussed in a separate section
below.
In unilateral paramedian thalamic infarcts, the early stages
demonstrates impairment of arousal with decreased as well as
fluctuating level of consciousness, which can last for hours to
days. In the long term, mood and behavioral changes per-
sists. These include agitation, aggression, disorientation, apa-
thy, and prostration. Speech and language impairments is also
seen which is characterized by hypophonia and dysprosody,
with frequent perseveration and markedly reduced verbal
fluency.13
When the tuberothalamic artery is absent, the paramedian
artery may assume that territory as well, and thus infarction in
this vascular territory can be devastating.10

Li et al: A Review of Thalamic Infarcts 3


Fig 5. Artist drawing of variant anatomy of the paramedian artery.
(A) Type I, the most common variant, with small perforators arising
from P1 segment of posterior cerebral artery (PCA). (B) Type IIa,
both paramedian arteries arise from the same PCA. (C) Type IIb,
the artery of Percheron, with a single common trunk arising from the
PCA, supplying both thalami. (D) Type III, a variant with an arcade
connecting the paramedian arteries, allowing for communication and
collateral flow. Subparts A, B, C, and D were adapted with permission
from Schmahmann.8
Bilateral Paramedian Infarction (Artery of Percheron
Infarction)
Anatomy
Bilateral infarctions in the paramedian artery territories may
occur in type IIb variant, or occlusion of the artery of Percheron.
This type of infarct may result in an acutely ill and severely
impaired patient.17 Imaging findings of bilateral paramedian
infarction are illustrated in Figure 6.
Clinical Features
There has long been a well-recognized clinical syndrome due
to bilateral paramedian thalamic artery infarcts. This syndrome
is rare, however, making up approximately .7% of all ischemic
strokes, with the most common cause being small vessel disease,
followed by cardioembolism.18
The clinical features of bilateral paramedian thalamic in-
farcts consists of four elements: (1) disorder of vigilance such
as stupor or coma; (2) amnesia with a marked tendency to
confabulate; (3) changes in instinct and mood, generally with
a mixture of irritability, and apathy or chronically presenting
with bad moods; and (4) vertical gaze paresis, with possible
absence of vertical saccadic and pursuit movements.19,20 Other
findings such as disorientation, confusion, and akinetic mutism
have also been reported.21 The neurologic deficits and hyper-
somnia can recover in most patients, though cognitive deficits
4 Journal of Neuroimaging Vol 00 No 0 xxxx 2018
Fig 6. T2 fluid-attenuated inversion recovery image (A), in a 79-
year-old female patient found unresponsive, shows subtle hyper-
intense signal intensity in the median portions of both thalami.
Diffusion-weighted image (B) in same patient shows bright signal in-
tensity in the medial portions of the thalamus. The apparent diffusion
coefficient image (C) in the same patient shows restricted diffusion
suggestive of acute infarction, with a region of interest measurement
placed over the area of infarction, as denoted by the small green
circle. MR angiography (D) shows normal appearance.
such as anterograde and retrograde memory deficit and apathy
tend to be severe and persistent.18
Inferolateral (Thalamogeniculate) Artery Infarction
Anatomy
The inferolateral arteries, also known as thalamogeniculate ar-
teries, are composed of 5–10 arteries that arise from the P2
branch of the PCA just after the level of the posterior commu-
nicating artery. Infarcts in the inferolateral territory account for
about 45% of all thalamic infarcts, and consist of three main
groups: the medial geniculate, principal inferolateral, and in-
ferolateral pulvinar arteries.8 Anatomy and imaging findings of
inferolateral (thalamogeniculate) artery infarction are illustrated
in Figure 7.
Clinical Symptoms
Patients with inferolateral thalamic (thalamogeniculate) artery
infarction presents with the thalamic syndrome, which was ini-
tially described by the French neurologist Dejerine.22 The most
prominent feature of this syndrome is the intense pain unre-
lieved by analgesics, which may be related to separation of
the thalamus from cortical inhibition.23 The thalamic pain syn-
drome typically has a delayed onset, though it may also present
acutely. Approximately 80% of patients with a compromise
of this vascular territory present with this syndrome, with an
apparent preference for right thalamic infarcts.22 Other com-
ponents of the thalamic syndrome includes sensory loss and
impaired extremity movement. Loss of sensory modality may
involve all modalities such as touch and temperature, though
not necessarily all seen in the same patient. A combination of
sensory loss and ataxic hemiparesis is strongly suggestive of the
thalamic syndrome.3,21 Additionally, pure sensory syndrome
with a loss of all modalities of sensation, particularly when the
distribution is face-arm-leg, are highly suggestive of inferolateral
Fig 7. Schematic diagram of lateral (A) and dorsal (B) views of infer-
olateral (also referred to as the thalamogeniculate) artery infarction.
Axial T2-weighted images (C and D) and diffusion-weighted image
(E) in a patient with right inferolateral artery infarction. VA = ventral
anterior; VL = ventral lateral; DM = dorsomedial; IL = intralaminar
nuclear complex; VP = ventral posterior; P = pulvinar. Subparts A
and B were adapted with permission from Schmahmann.8
(thalamogeniculate) artery infarction. Some patients with the
pure sensory syndrome can also develop delayed pain and/or
dysesthesia.24
Foix and Hillemand described a finding of flexed and
pronated hand, with the thumb tucked under other fingers in
inferolateral thalamic infarcts, which they termed the “thalamic
hand.”25 More complex behavioral syndromes have not been
reported with inferolateral thalamic infarcts.8 Language impair-
ment and aphasia is only occasionally reported in inferolateral
thalamic infarcts.26
Posterior Choroidal Artery Infarction
Anatomy
The posterior choroidal arteries also arise from the P2 segment
of the PCA, similar to the inferolateral (thalamogeniculate) ar-
teries. The posterior choroidal arteries are also a group of small
vessels, with one to two branches arise adjacent to the origin
of the posterior communicating (PCOM) artery, and one to six
branches from the distal P2 segment of the PCA.8 Anatomy
and imaging findings of posterior choroidal artery infarction
are illustrated in Figure 8.
Clinical Symptoms
Currently, there are limited number of reports of infarcts in-
volving the posterior choroidal artery. In a study of 20 patients
with posterior choroidal artery infarcts, Neau et al. found that
in lateral posterior choroidal artery infarcts, the most common
manifestations includes homonymous quadrantanopsia with
possible hemisensory loss. Transcortical aphasia and memory
disturbances may also present. They suggest that a homony-
mous horizontal sectoranopia is a rare but particularly sugges-
Fig 8. Schematic diagram of lateral (A) and dorsal (B) views of pos-
terior choroidal artery infarction. T2 (C) and fluid-attenuated inversion
recovery (D) images show right thalamic infarct in posterior choroidal
territory. VA = ventral anterior; VL = ventral lateral; DM = dorso-
medial; IL = intralaminar nuclear complex; VP = ventral posterior; P
= pulvinar; LGB = lateral geniculate body. Subparts A and B were
adapted with permission from Schmahmann.8
tive finding of lateral posterior choroidal artery infarcts. Medial
posterior choroidal artery infarct is characterized by eye move-
ment disorder that is not particular to thalamic infarcts, and is
relatively more infrequent.27 A delayed complex hyperkinetic
motor syndrome that includes ataxia, rubral tremor, dystonia,
myoclonus, and chorea, termed the “jerky dystonic unsteady
hand,” was also observed in a small subset of patients.8,27
Variant Thalamic Territories and Associated
Syndromes
In addition to the traditional vascular territories described
above, which included the anterior, paramedian, inferolateral
(thalamogeniculate), and posterior arteries, there are also three
variant vascular distribution of the thalamus. These variants are:
anteromedian, central, and posterolateral territories, as grouped
by their anatomic location within the thalamus.
Anteromedian Territory
Anatomy
The anteromedian territory, as implied by the name, is formed
by combining the traditional anterior and paramedian terri-
tories. Specifically, it combines the posterior portion of the
anterior territory, and the anterior portion of the paramedian
territory.10
Clinical Syndrome
The dominant feature of anteromedian territory infarcts are the
severe neuropsychological disturbances, which is more severe
when the infarcts are bilateral.
Li et al: A Review of Thalamic Infarcts 5
 Severe anterograde amnesia is a common feature of antero-
median territory infarcts. This feature is particularly prominent
when involving the anteromedian thalamic structures, such as
the dorsomedian nuclei, intralaminar nuclei, and the internal
medullary lamina. This is in contrast from prior reports that
found amnesia required involvement of the mammillothalamic
tracts.10,28,29
Contrary to infarcts restricted to the anterior territory, pa-
tients with anteromedian territory infarcts do not exhibit issues
with perseverance. Instead, the main behavior change in antero-
median infarct is a severe loss of self-activation, with require-
ment of constant external stimulation. Characteristics of lin-
guistic troubles after anteromedian infarcts were word-finding
difficulties, reduced fluency, and denomination. Decreased con-
sciousness is less frequently found in anteromedian territory
infarcts.10
Vertical gaze palsy has been reported in isolated antero-
medial territory infarcts, postulated to be due to involvement
of frontocortical fibers that may be decussating in the medial
thalamus.30
Central Territory
Anatomy
The central territory corresponds to the thalamic center, with
involvement of parts of all four adjacent classic territories.10
Clinical Syndrome
Infarct of the central territory is rare. The clinical syndrome of
central territory infarct reflects the involvement of adjacent nu-
clei. In the four patients observed by Carrera et al., hypesthesia
is a common feature due to involvement of the medial portion
of the ventroposterolateral nucleus (VPL).10
Anterograde amnesia and short-term memory impairment
were also reported in central territory infarcts, and more se-
vere than in anteromedian territory infarcts. However, because
central territory infarcts can involve the adjacent nuclei of the
classic territories, memory deficits of central territory infarcts
are typically seen when involving the anterior portion of the
central territory, overlapping with the anteromedian territory.31
Posterolateral Territory
Anatomy
The posterolateral territory is formed by combining the poste-
rior portion of the inferolateral territory and the anterior portion
of the posterior territory.10
Clinical Syndrome
An unusual finding in posterolateral territory infarct is the find-
ing of impaired cognition. Aphasia is also seen in infarcts of
this territory, with impaired repetition that resembles cortical
motor aphasia, and differs from aphasia due to anteromedian
or central territory infarcts.10
Executive dysfunction may also be seen, more commonly
with the left thalamic involvement, because of the disruption of
thalamo-cortical fibers.
Sensory impairment is also a major feature which can be
explained by the localization of the VPL in this area of the tha-
lamus. Dystonic posture and hemihypesthetic ataxic hemipare-
sis should raise concern for posterolateral territory infarcts.10
6 Journal of Neuroimaging Vol 00 No 0 xxxx 2018
A single case of Holmes tremor has been reported one year
after posterolateral thalamic infarct.32
Recovery of Function
The prognosis after thalamic infarction is generally regarded as
good, when compared to infarcts of the cerebral cortex or other
subcortical structures. This refers to low incidence of mortality
after infarct with good recovery of motor deficits. The presence
of ventricular extension, however, portends a more guarded
prognosis.33 Although there are persistent cognitive and psy-
chiatric manifestations of thalamic infarcts, particularly those
involving tuberothalamic or paramedian artery infarcts, there
lacks longitudinal analysis. Therefore, the incidence of cogni-
tive impairment, mood alteration, and personality changes after
thalamic infarcts are not known.8
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