434

The Syndrome of Unilateral Tuberothalamic Artery
Territory Infarction
J U U E N BOGOUSSLAVSKY, M . D . ,

FRANCO REGLI, M . D . ,

AND G I L A S S A L ,

M.D.

SUMMARY The study of 3 personal cases and 5 published cases of unilateral infarct limited to the
territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other
thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes
may be present but remain mild. The patients are apathetic, show perseverations and may be disoriented.
In left-sided infarcts, transcortkal aphasia, verbal and visual memory impairment and sometimes acalculia
are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe
motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and
dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain
may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating
artery, which often receives its supply from the carotid system, further justifies considering unilateral
tuberothalamic infarcts as a syndrome.
Stroke Vol 17, No 3, 1986

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THE CLINICAL SYNDROMES of thalamic infarction in the territory of the thalamogeniculate pediclel~*
and in the territory of the posterior thalamo-subthalamic paramedian artery2-3> 5~i are well recognized. Infarcts in the tuberothalamic artery territory have occasionally been reported,9"12 but they have not been
specifically studied and no attempt has been made to
differentiate their clinical picture from that of the other
paramedian thalamic infarcts. We have studied neurologicaliy and neuropsychologically three patients with
a unilateral infarct limited to the tuberothalamic artery
territory confirmed on CT scan. The presence of certain findings characteristically associated with the absence of other findings suggests that this type of thalamic infarct can be recognized.
Methods and Patients
We diagnosed tuberothalamic artery infarction from
the CT scan pictures, according to the topographic
description of Percheron.13 All 3 patients were examined by at least 3 neurologists and 1 neuropsychologist. A comprehensive battery of tests was done in
patients 1 and 3, and a partial battery was administered
to patient 2, because of marked speech disturbances
and impaired cooperation. The following evaluation
was done: orientation to time and place, spontaneous
speech, verbal fluency, naming (Boston naming
test14), repetition of isolated, or series (3-5 items) of,
phonemes or words and sentences (3-15 words), auditory comprehension (Token test15), writing (spontaneous, dictation), reading (words, non-words, text, summary of text meaning), dichotic listening test, oral and
written calculation, bucco-linguo-facial praxias, limb
(symbolic, imitation) praxias, constructional praxia
(spontaneous drawing of a cube, Rey complex Figure"), Benton Facial Recognition test17 and other visual gnosia tests (Ghent,18 Poppelreuter,19 Columbia20),
From the Department of Neurology and the Center of Neurophysiology. Centre HospitalierUniversitaire Vaudois, Lausanne, Switzerland.
Address correspondence to: Dr. Julien Bogousslavsky, Department
of Neurology, CHUV, 1011 Lausanne, Switzerland.
Received June 3, 1985; revision # 1 accepted August 29, 1985.

orientation on a map of Switzerland, right-left discrimination, evocation of recent and remote events,
verbal learning (Hebb's recurring digits,2122 Rey Auditory Learning16), visual learning (Corsi's Block-tapping,22 delayed reproduction of Rey Complex Figure16), Wisconsin Card Sorting test,23 Stroop test,24
Luria's conflicting tasks, sequential rhythms and sequential geometrical figures,23 and a nonverbal intelligence test (Raven progressive matrices26).
Case 1
A 45-year-oldright-handedhousewife was admitted
after she suddenly experienced dizziness, vomiting,
numbness in the right side of the face, clumsiness of
therighthand and speech disturbances. Her past history revealed episodes of hypoglycemia and migraine,
and she was treated with estrogens for primary ovarian
insufficiency. She was suffering from familial type IV
hypercholesterolaemia, and had a strong family history of coronary heart disease on her father's side.
On neurological examination, the visual fields, the
optic fundi, the pupils and oculomotricity were normal. A slight light touch hypoesthesia involving the
right side of the face down to the C2 dermatome was
present, without involving the mouth and tongue, and
with symmetrical corneal reflexes. An "emotional"
right facial weakness was present, with normal contraction on command but droop of the lips on the right
side when smiling. The taste and the remainder of the
cranial nerves were normal. There was a slight downward drift of the right upper limb on the stretched arm
test performed with the eyes closed, but no objective
weakness could be demonstrated, and the tone, tendon
and cutaneousreflexeswere normal. The coordination
of all four limbs and the gait were normal. However,
the patient tended to lose her balance when trying to
jump on the right leg. Tactile, temperature, pain, postural and vibratory sensation were preserved, with normal graphesthesia, stereognosis and topoesthesia. Her
blood pressure was 110/70 mm Hg with aregularpulse
(80/min). No bruit was heard on the neck or precordium, and the general examination was normal.

SYNDROME—UNILATERAL INFARCT TUBEROTH ALAMIC ARTERY TERRTTORY/Bogousslavsky et al

435

Neuropsychological Examination

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The patient was well-oriented in time and space. She
complained of concentration difficulty and memory
disturbances. Her spontaneous speech was quantitatively reduced, with short sentences (5 words maximum) and slowed output. Occasional phonemic paraphasias were present ("anassin" instead of "assassin")
and less frequently, semantic paraphasias ("clock" instead of "watch"). Naming was impaired (46/76, Boston naming test) and verbal fluency was reduced (14
names of animals in 9 minutes). The dichotic listening
test did not show any asymmetry. Verbal comprehension (31/36, Token test) was only mildly impaired,
despite slowness of answering. The repetition of isolated, or series (up to 5) of, phonemes and words and
of sentences (up to 15 words) was normal. Words,
non-words, and text reading were normal. Spontaneous writing was reduced but without paragraphia or
syntaxic disturbances. Writing on dictation was unimpaired. Oral calculation was markedly impaired, even
for simple arithmetical operation (0/6), with tendency
to perseverate. Written calculation was similarly impaired, with loss of the arithmetical programs for addition, subtraction, multiplication and division. Spontaneous drawing of a cube was preserved, although
slowed. Bucco-linguo-facial praxias were normal, and
limb praxias did not show any significant disturbance
(4/4 on symbolic gestures, 5/6 on imitation gestures).
Visual and visuo-spatial gnosias were normal (Ghent:
35/36, Columbia: 10/12, orientation on a geographic
map). Marked difficulties were present on evocation of
recent events, and visual as well as verbal learning
difficulties were present (Hebb's recurring digits:
maximal span of 5, failure of span + 1 learning; Corsi's Block-tapping: maximal span of 5, failure of span
+ 1 learning). Perseverations were present on execution of Luria's conflicting tasks, sequential rhythms
and sequential geometrical figures. On Stroop test,
naming was markedly slowed (1 '48", 1 mistake, 7
autoconnections) compared with word reading (1'3").
EKG and Standard blood and urine tests were normal. An EEG did not show any abnormality. A CT
scan performed 4 days after admission showed an isolated lucency in the anterior paramedian part of the left
thalamus, suggesting a recent infarct in the territory of
the tuberothalamic artery (fig. 1).
Case 2
A 74-year-old right-handed, hypertensive man was
admitted after he suddenly experienced speech disturbances, followed a few hours later by mild right-sided
weakness. On examination, visual acuity, visual
fields, ocular movements and pupils were normal. Op-1
tic fundi revealed moderate retinal vascular sclerosis.
Facial, buccal and lingual sensation were preserved,
with symmetrical corneal reflex. A slight "emotional"
right-sided facial paresis was present, with symmetrical contraction on command. The taste and the remainder of the cranial nerves were normal. The strength
was normal and symmetrical in the four limbs, but on
the stretched arm test, there was a slow drift with

FIGURE 1. Case 1, CT scan. Small infarct in the anterior part
of the left thalamus.

pronation tendency of the right arm. Fine motility of
thefingerswas slowed on the right, and the tone of the
right arm and leg was slightly increased, without tendon reflexes asymmetry or abnormality. Abdominal
reflexes were present and plantar reflexes were downgoing. Coordination was normal in the four limbs,
except moderate dysdiadochokinesia in the right upper
limb. The gait was normal. Tactile, temperature, pain,
postural and vibratory sensations were normal and
symmetrical, with normal 2-point discrimination,
graphesthesia, stereognosia and absence of sensory extinction. Blood pressure was 160/100, but general examination was normal for his age.
Neuropsychological Examination
The patient was well-oriented in time and place. A
detailed neuropsychological assessment was not possible, because of the marked disturbances of language.
Spontaneous speech was moderately reduced, with
slowed output and shortened sentences (8 words maximum). Phonemic and semantic paraphasias were present, as well as preservations and occasional neologisms, with preserved syntax and absence of
dysarthria. The frequency of the paraphasias rendered
the patient's speech very difficult to understand. Naming was impaired (17/76, Boston naming test). Production of automatic series (days of the week, months)
was preserved in anterograde order, but paraphasias
and perseverations appeared in retrograde order. Verbal fluency was reduced (4 names of animals in three
minutes), with perseverations. The dichotic listening

436

STROKE

test did not disclose any left-right ear asymmetry. Verbal comprehension was moderately impaired (25/36
Token test), and the repetition of isolated, or series (up
to 5) of, phonemes or words and of sentences (up to 15
words) was fully preserved. The reading of a text was
normal, although slow, but his account of the story
showed appearance of numerous paraphasias, perseverations, and neologisms. Spontaneous writing
showed paragraphias and neologisms, with preserved
copying. Writing on dictation was impaired, with
paragraphias and perseverations of letters and words.
Spelling of words was disturbed (2/5). Oral calculation
was impaired (1/5). Written calculation showed preservation of addition and subtraction, but multiplication
and division were impaired. Spontaneous drawing of a
cube was normal. Bucco-linguo-facial praxias were
preserved and limb praxias (symbolic and imitation)
showed only occasional perseverations with autocorrection. Visual gnosias were preserved (Ghent: 33/36,
Poppelreuter: 3/4), with preserved orientation on a
geographic map. Learning of series of visual and verbal items was markedly impaired but was not quantified, because the patient did not cooperate well
enough. Evocation of recent or remote events was disturbed by the speech disturbances. On execution of
Luna's conflicting orders, sequential rhythms and sequential geometrical figures, perseverations appeared,
with selfcorrection attempts and refusal to continue the
tests.
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Standard blood and urine tests were normal. EKG
showed moderate ischemic changes with left ventricular hypertrophy. A CT scan performed 2 days after
admission showed an isolated lucency in the anterior

FIGURE 2.

VOL 17, No

3, MAY-JUNE

1986

aspect of the thalamus on the left side, suggesting a
recent infarct in the tuberothalamic artery territory
(fig. 2).
Case 3

A 68-year-old insulin dependent diabetic righthanded man suddenly experienced transient blurring of
vision with persisting left-sided weakness and feeling
of intense fatigue. On admission, visual acuity was
moderately decreased in both eyes (right: 0.5; left: 0.7)
with diabetic retinopathy on optic fiindi examination.
The visual fields were full, but left-sided extinction
appeared on bilateral simultaneous stimulation. The
pupils and ocular movements were normal. Light
touch and pain sensation were slightly decreased in the
left side of the face, with a decreased left cornea]
reflex. A slight lower facial paresis was present, either
on voluntary or emotional contraction. Bilateral hypoacusis was present, but the remainder of the cranial
nerves showed no abnormality. The strength and tone
were normal in the 4 limbs, but the right arm drifted
slowly downward and pronated on the stretched arm
test. The fine movements of the fingers were slightly
slowed on the left side, with dysdiadochokinesia and
moderate imprecision on finger-to-nose movements.
No hypermedia or rebound phenomenon were found.
The tendon reflexes were decreased distally in the 4
limbs. Abdominal reflexes were decreased on the left
side. The left plantar reflex was upgoing, but was
flexor on the right. Tactile, pain and temperature sensations were slightly decreased on the left side of the
body, with a tendency to extinction on simultaneous
bilateral stimulation, but with normal graphesthesia

Case 2, CT scan. Infarct of the anterolateral (A) and polar (B) part of the left thalamus.

SYNDROME—UNILATERAL INFARCT TUBEROTH ALAMIC ARTERY TERRITORYIBogousslavsky et al

and stereognosis. Vibratory and postural sensations
were decreased distally in the 4 limbs, with some degree of imbalance on Romberg's manoeuvre and tandem gait. Blood pressure was 160/90 mm Hg, with a
pulse of 72/min. The general examination was unremarkable.

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Neuropsychologkal Examination
The patient was well-oriented in time and place,
with a normal level of consciousness. His spontaneous
speech showed no abnormality, with normal output.
Naming was within normal ranges (60/75 Boston naming test). The repetition of isolated, or series of, phonemes or words and of short and long sentences was
fully preserved. Auditory comprehension showed very
mild difficulties (32/36 Token test). Spontaneous writing and writing on dictation were normal, except for
neglect of the left side of the page. The reading of
words, non-words and a text was normal, with a good
oral summary of the text meaning. On dichotic listening test, left-sided extinction was prominent (right ear:
25/30, left ear 0/30 with 10/10 on monaural stimulation). Oral calculation was preserved (4/5), but written
calculation was markedly impaired (0/4) because of
loss of the correct spatial disposition of the operations
and right-sided neglect. Bucco-linguo-facial praxias
and limb (symbolic, imitation) praxias were normal.
Spontaneous drawing of a cube was impaired (loss of
perspective). Recognition of faces was preserved
(43/54, Benton test). Tests for visual gnosis showed
normal results (35/36, Ghent; 10/12, Columbia). The
copy of Rey complex figure was impaired (16 points,
centile 0). Orientation on a map was preserved, and no
right-left confusion was found. Verbal learning was

FIGURE 3. Case 3, CIscan. Infarct of the anteriorpart of the
right thalamus.

437

insufficient (Hebb's recurring digits: span of 5, failure
of span + 1 learning; 15 words of Rey: total of 22: 5-35-5-4, centile 0). Visual learning was more impaired
(Corsi's block-tapping: span of 4, failure of span + 1
learning; learning of 15 signs: total of 18: 2-3-4-5-4;
11/15 on recognition; delayed reproduction of Rey
complex figure: immediate reproduction: 6 points,
centile 0, and delayed reproduction: 2 points, centile
0). The Wisconsin card sorting test was much disturbed (0 series realized) and marked slowing was
present on the Stroop test (1'39"). The results of
the Raven PM 38 test were insufficient (15 points,
centile 0).
Standard blood and urine tests were within normal
ranges, except elevated cholesterol (8.2 mmole/1).
EKG showed a left anterior hemiblock. The CSF was
clear, wih normal proteins (390 mg/1); 1 white cell/cm3
and negative VDRL and FTA-Abs. Somatosensory
evoked potentials (median nerve stimulation) showed
an altered morphology and reduced amplitude on the
right parietal recording. A CT scan done one week
after admission showed an isolated lucency in the anterior part of the right thalamus, suggestive of an infarct
in the territory of the right ruberothalamic artery
(fig. 3).
Discussion
The ruberothalamic artery has also been called the
polar artery of the thalamus, the anterior thalamosubthalamic paramedian artery, the anterointernal optic artery, and the premamillary pedicle. 2132728 It
originates from the middle third of the posterior communicating artery, but may be absent in 30-40% of the
population,7' '3 in which case its territory is supplied by
the posterior thalamo-subthalamic paramedian artery
originating from thefirstsegment of the posterior cerebral artery (P, or basilar communicating artery.67-l3
When the ruberothalamic artery is present, it supplies
the reticular nucleus, the mamillo-thalamic tract, part
of the ventral lateral nucleus and of the dorsomedial
nucleus, and the lateral aspect of the thalamic pole,
but not the anterior nucleus.7 l3 Three other systems
supply the thalamus (fig. 4): 1) The posterior thalamo-subthalamic paramedian artery (or deep interpeduncular profunda artery,27 thalamoperforate or retromamillary pedicle2) is often unpaired and originates
from P,. It supplies the paramedian part of the upper
midbrain and of the thalamus (intralaminar nuclei, dorsomedial nucleus, internal part of the ventral posterior
nucleus);7-13 2) The thalamogeniculate pedicle originates from the posterior cerebral artery after the level
of the posterior communicating artery (P2) and includes the thalamic infero-lateral arteries and the pulvinarian inferolateral arteries.29 It supplies most of the
ventral posterior nucleus, a part of the ventral lateral
nucleus, and of the pulvinar.29 3) The posterior choroidal arteries leave the posterior cerebral artery at the
same level as the thalamogeniculate branches and separate into a mesencephalo-posteromedial system and a
hippocampo-posterolateral system,7-13 which supply
the subthalamic region, part of the substantia nigra and

STROKE

438

FIGURE 4. Schematic representation of arterial supply to the
thalamus after Lazorthes55, Schlesinger27 and Castaigne et at',
A) Lateral view, B) Dorsal view. 1: carotid siphon, 2: basilar
artery, 3: basilar communicating artery (P/), 4: posterior cerebral artery (P2), 5: posterior communicating artery, 6: tuberothalamic artery, 7: posterior thalamo-subthalamic paramedian
artery, 8: thalamo-geniculate pedicle, 9: posterior choroidal
arteries.

TABLE 1 Reported Syndromes in Unilateral Thalamic

VOL 17, No 3, MAY-JUNE 1986

of the pulvinar, and the medial and lateral geniculate
bodies. 7 ' l3
Suggestive clinical syndromes have been reported in
unilateral infarcts in these three territories (table 1).
The infarcts in the thalamogeniculate pedicle territory
are the most common ones, and typically produce a
sensory stroke which may or may not evolve towards a
Dejerine-Roussy syndrome. The infarcts in the posterior thalamo-subthalamic paramedian artery territory
are often bilateral, because this artery is often a single
branch coming off the basilar communicating artery
(butterfly-shaped infarcts13). When there are 2 arteries,
the infarct is unilateral. It typically gives rise to decreased consciousness, neuropsychological impairment, and oculomotor disturbances, sometimes delayed abnormal movements. 7 Infarcts limited to the
posterior choroidal system are very uncommon, and
seem to produce partial visual field defects.41
On the other hand, no study has been devoted to
infarcts of the tuberothalamic artery territory. We

Infarction

Territory of thalamic infarction

Origin of artery

Reported clinical features

Posterior thalamo-subthalamic
paramedian artery

Initial segment of the PCA =
basilar communicating artery
(Pi)

1 consciousness, confusion,
behavioral changes 7
asterixis 30

intralaminar nuclei

motor hemineglect 8 - 3I

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memory impairment 7 - 8
language disturbances
(dominant thalamus) 8 ' 3 2 - 3 3

DM

contralateral cerebellar
dysfunction34
faciobrachial tactile
hypoesthesia8

internal part of VPL and VPM

upgaze palsy,7- 8 vertical 1 Vi
syndrome35
Weber's & Claude's third nerve
fascicular syndromes7- M

upper mesencephalon

delayed abnormal movements 7
Thalamo-geniculate pedicle

Second segment of the PCA
(P2)

hemisensory syndromes:
Dejerine-Roussy
syndrome, 1 - 2 pure sensory
stroke, 4 cheiro (podo)
oral/pseudo radicular
variants3

VPL, VPM

motor hemineglect (nondominant thalamus) 37
contralateral cerebellar
dysfunction38

VL

ataxic hemiparesis 39

Posterior choroidal arteries

Second segment of the PCA
(P2)

language disturbances
(dominant thalamus) 40

\ VL, pulvinar

homonymous horizontal
sectoranopia41

\ lateral geniculate body

i = decreased; DM = dorsomedial nucleus; VL = ventral lateral nucleus; VPM = ventral posterior medial nucleus; VPL = ventral
posterior lateral nucleus.

SYNDROME — UNILATERAL INFARCT TUBEROTH ALAMIC ARTERY TERRYTORY/Bogousslavsky et al

could identify only 5 published cases of isolated unilateral infarcts in this territory, with CT scan and neurological and neuropsychological assessment (table 2).
Percheron13 mentioned a personal case with pathological study, but the clinical picture was unknown. Three
more cases studied by CT scan were reported,"-42 but
they had an associated infarct in the ipsilateral occipital
lobe which obscured the symptomatology. Bilateral
infarcts limited to this territory also seem to be very
rare. 4 3 ' u In the cases where the tuberothalamic artery
is absent, its territory is supplied by the posterior
thalamo-subthalamic paramedian artery and infarcts
then involve the whole paramedian area, unilaterally45
or bilaterally.46
The study of our 3 cases and of 5 published cases
with a unilateral infarct limited to the tuberothalamic
artery territory (table 2) shows that delineation of a
suggestive syndrome is possible. The onset is usually
sudden, with mild to moderate contralateral motor
weakness or clumsiness (86%). A contralateral "emotional" facial weakness with preserved voluntary contraction is frequently found, as formerly reported."
Contralateral sensory changes may occur (43%), but
involve only the superficial modalities of sensation and
remain mild. Neuropsychological dysfunction is present in 100% of the cases. The patients are withdrawn,
but not drowsy and show apathy, lack of spontaneity

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TABLE 2

439

and perseverations, especially in the cases with rightside infarction. They can be disoriented (28%). In infarcts of the dominant thalamus, speech disturbances
are associated with visuo-verbal memory impairment,
and sometimes acalculia. The language disturbances
do not seem to be different from those described in
other types of thalamic infarction involving the lateral
formation40 or the posterior paramedian area, 8 ' 32 ' 33 and
suggest transcortical aphasia: speech is reduced, with
anomia and some phonemic/semantic paraphasias and
occasionally neologisms (case 2), with slightly impaired or normal comprehension and normal repetition. The memory disturbances involve both the verbal
and visual items, with learning difficulties. In infarcts
of the non-dominant thalamus, contralateral hemispatial neglect may be prominent, with memory impairment involving mainly the visual learning and altered
visuospatial processing with constructional dyspraxia.
Since no cases with pathological verification are
available, except one with unknown symptomatology,13 clinical-anatomic correlations are limited to
speculations based on other types of thalamic infarcts
or diseases, or on electrocoagulation studies. Language disturbances in the setting of a thalamic lesion
have been attributed to involvement of the ventral lateral nucleus, 40 ' 47-49 pulvinar,40 41-49 or dorsomedial nucleus. 4050 " 53 In a case of unilateral left posterior tha-

Unilateral Infarction of the Tuberothalamic Artery Territory: Summary of Clinical Features
Sensory
changes

Onset

Neuropsychological
examination

Authors

Sex

Age Risks factors

Cohen et al 9 1980

6

62

DM

L right-sided weakness and speech
disturbances (sudden)

( + ) phonemic paraphaseas, anomia,
slight of comprehension, normal
repetition

Archer et al 10 1981

6

57

?

L transient right-sided weakness and
persisting speech disturbances
(sudden)

—

paraphasias, | of comprehension,
normal repetition, perseverations, I visual/verbal memory

Graff-Radford et al"
1984 (case 3)

6

75

HT

L subacute change of personality,
depression

-

disorientation, aspontaneity of
anomia, normal repetition,
| visual/verbal memory

Graff-Radford et al
1984 (case 5)

9

64

HT multiple
aneurysms

R left-sided weakness and hemineglect (sudden)

-

disorientation, normal language,
1 nonverbal memory, J visuospatial processing

Billeretal 1 2

6

29

lupus anticoagulant

L transient right-sided weakness and
numbness, and dysarthria,
followed by progressive
memory impairment

-

disorientation to time, | memory,
normal speech but monotone
voice, omission of words when
reading

Present study
(case 1)

9

45

hypercholesterolaemia

L dizziness, vomiting, right-sided
facial numbness and hand
clumsiness, speech disturbances
(sudden)

(+)

paraphasias, aspontaneity of speech,
anomia, normal comprehension
and repetition, I visual/verbal
memory, perseverations, acalculia

Present study
(case 2)

6

74

HT

L sudden speech disturbances
followed by right-sided
weakness

-

paraphasias and neologisms,
anomia, slight I of
comprehension, normal
repetition, | visual/verbal
memory, perseverations

Present study
(case 3)

6

68

DM

R fatigue, transient blurring of
vision, persisting left-sided
weakness (sudden)

(+)

normal language, multimodal leftsided hemineglect, constructional
apraxia, visual more than verbal
memory impairment, "frontal"
syndrome

Side

DM = diabetes mellitus; HT = hypertension; ( + ) = slight; + = marked; -

= absent; R = right; L = left; j , = decrease.

440

STROKE

lamo-subthalamic paramedian artery territory infarct,
which was pathologically studied, we found that the
language disturbances and the impairment of verbal
memory correlated well with involvement of the dorsomedial nucleus, in the absence of significant involvement of the ventral lateral nucleus, pulvinar and
mamillothalamic tract.8 In the present case, involvement of the dorsomedial nucleus also seems to correlate the best with the dysphasic and memory disturbances, because of the arterial supply topography of
the tuberothalamic artery. The mamillothalamic tract
is usually supplied by this artery13 and may also participate in the memory disturbances. Involvement of the
ventral lateral nucleus may also account for at least
some of the aphasic deficits,404749 and probably explains the occurrence of "emotional" facial paresis and
contralateral neglect in nondominant side infarction.
Contralateral neglect may also be produced by a lesion
of the intralaminar nuclei,8 but these nuclei are not
supplied by the tuberothalamic artery. The occasional
presence of only mild sensory changes indicates that
the ventral posterior nucleus is mostly spared. Initial
transient or mild contralateral weakness probably corresponds to continuous involvement of the internal
capsule by edema or pressure during the acute ischemic phase,39 and it is not similar to the severe hemiplegia produced by peduncular involvement in infarcts
of the posterior thalamo-subthalamic paramedian or
circumferential arteries,736 or to the hemiplegic syndrome of the posterior cerebral artery.54
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Many of the neuropsychological disturbances found
in this syndrome do not markedly differ from those
reported in unilateral infarcts of the posterior thalamosubthalamic paramedian artery territory, probably because of vascular supply overlap in structures like the
dorsomedial nucleus. However, infarcts of the tuberothalamic artery territory should be differentiated from
those of the posterior thalamo-subthalamic paramedian
artery territory, because they do not produce altered
consciousness, supranuclear upgaze palsy, intra-axial
third nerve palsy, severe contralateral hemiplegia or
delayed abnormal movements, as they do not involve
the intralaminar nuclei and the upper midbrain. Moreover, as the posterior communicating artery — from
where the tuberothalamic artery originates — is filled
by the internal carotid artery in as many as 40% of the
hemispheres,55 recognition of this syndrome among
the other syndromes of thalamic infarction is important, because it may occasionally be related to carotid
system disease. One case of thalamic infarction was
reported after carotid artery occlusion,56 but the configuration of the posterior cerebral artery was not described. An angiographic study of the pattern of the
circle of Willis in thalamic infarction still remains to be
done.
In summary, we believe that tuberothalamic artery
territory infarcts can be differentiated from the other
types of thalamic infarcts by their clinical aspects and
CT scan pictures. However, since no cases with clinico-anatomic correlation have yet been reported, we
think that the hypotheses advanced for the explanation

VOL 17, No

3, MAY-JUNE

1986

of the symptomatology should, for the moment, be
accepted with reservation, because they are based on
pathologic studies of other thalamic syndromes.
Addendum
Another case of unilateral left infarction in the territory of the tuberothalamic artery has been reported by
Gorelick et al (Gorelick PB, Hier DB, Benevento L,
Levitt S, Tan W: Aphasia after left thalamic infarction.
Arch Neurol 41: 1296-1298, 1984), with a detailed
analysis of speech disturbances.
Acknowledgment
We would like to thank Andrew Kertesz, MD, University of Western
Ontario, for his helpful comments on the manuscript.

References
1. Dejerine J. Roussy G: Le syndrome thalamique. Rev Neurol 14:
521-532, 1906
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