J Neurosurg 48:570-574, 1978

Aphasia and left thalamic hemorrhage
ARDEN F. REYNOLDS, JR., M . D . , A. BASIL HARRIS, M.D.,
GEORGE A. OJEMANN, M.D., AND PAUL T. TURNER, M . D .

Department of Neurological Surgery, University of Washington, Seattle, Washington,
and Division of Neurological Surgery, University of New Mexico, Albuquerque, New
Mexico
Left thalamic hemorrhage as a cause of aphasia has not been widely recognized.
Large thalamic hemorrhages cause coma, making speech examination impossible;
smaller thalamic hemorrhages were difficult to document until recent diagnostic advances. Nine cases of thalamic hemorrhage with aphasia have been described in the
literature. This report presents four additional cases. These patients had acute onset of
aphasia, supranuclear paralysis of upward gaze, right hemisensory deficits, and mild
right hemiparesis. Three of the four patients responded to ventriculostomy drainage
with rapid clearing of the supranuclear paralysis of upward gaze, and two later required placement of permanent ventricular shunts. After 1 year, two patients exhibited
no clinically detectable speech malfunction and the other two were severely aphasic.
The hemiparesis, hemisensory deficits, and ocular pareses all cleared. These cases are
discussed with respect to present models of the role of the thalamus in speech.
KEY WORDS
9 aphasia
9 thalamus
9 hemorrhage
ventriculostomy - Parinaud's syndrome

LTHOUGH a thalamic effect on speech
has been postulated, 6,18 spontaneous
thalamic lesions causing acute aphasia have been considered an unusual occurrence. In large part this can be attributed
to the coma which confounds detailed speech
testing. Nine cases of thalamic hemorrhage
and two cases of hemorrhagic infarction
associated with speech abnormalities have
been reported in the literature? ,5,1~ Four additional cases of left thalamic hemorrhage are
the subject of this report. The patients
presented with aphasia,
supranuclear
paralysis of conjugate vertical gaze, rightsided sensory deficits, and minor right-sided
m o t o r deficits. This constellation of symptoms was initially attributed to thalamic
hemorrhage by Fisher, s and reiterated in
detail in reviews of the role of thalamus in
speech, lo,14

A

570

9

Case Reports

Case 1
This 25-year-old right-handed man noted
during intercourse the acute onset o f leftsided h e a d a c h e and an awareness of
decreased perception of all senses on the right
side of the body. On examination he had a
fluent aphasia with anomia and perseveration, supranuclear paralysis of upward gaze,
right sixth nerve paresis, and right supranuclear facial paresis. The pupils were equal
and reactive. There was decreased perception
of touch, pinprick, position, and vibration on
the right side of the body including the face,
and a moderate right hemiparesis. Deep tendon reflexes were symmetric and plantar
responses were flexor.
Retrograde femoral arteriography revealed
an abnormal arterial blush in the region of

J. Neurosurg. / Volume 48 /April, 1978

Aphasia and left thalamic hemorrhage
the left pulvinar. An electroencephalogram
(EEG) demonstrated pronounced delta activity over the left hemisphere with epileptiform discharges. Technetium-99 cerebral
blood flow study and brain scan were normal.
Ventriculography revealed that the floor ot
the trigone of the left lateral ventricle was
irregular and elevated, and the fluid contained 42,500 red blood cells (RBC)/cu mm.
The patient became more alert, and the upward gaze paresis resolved immediately after
placement of a ventriculostomy catheter. The
posterior third ventricle failed to fill as demonstrated by both pneumoencephalography
and positive contrast (Conray-60) ventriculography. The diagnosis was left posterior
thalamic hemorrhage due to cryptic arteriovenous malformation.
One month later there was a minimal central seventh nerve paresis and decreased
graphesthesia in the right hand. The right
hemiparesis had cleared. Repeat Conray ventriculography showed absence of the
scalloped floor of the left lateral ventricle,
and the posterior third ventricle now was well
filled. Following the ventriculogram, the
patient's anomia transiently returned and the
right central facial paresis worsened for 12
hours.
Eight months after the initial event,
neurological examination was normal.
Repeat left vertebral and carotid arteriograms were normal. A Reitan psychological
test battery was administered 1 year following
the initial episode, and the patient still
demonstrated a mild degree of aphasia. In addition, his right hand performance was
slightly impaired in comparison to his left
hand during complex manipulations.
Case 2

This 39-year-old man was admitted with
confusion, aphasia, and right-sided paresis.
He was being treated for diabetes mellitus of
adult onset and hypertension. The patient was
alert with a nonfluent aphasia. He intermittently followed commands. Cranial nerve
examination revealed conjugate downward
deviation of the eyes which failed to move
above the horizontal meridian. There was
nystagmus on right lateral gaze. There was no
response to visual field threat from the right.
There were right fifth, twelfth, and central
seventh nerve pareses. Sensory examination
J. Neurosurg. / Volume 48 / April, 1978

revealed decreased perception of touch and
pain on the right side including the face.
Motor examination revealed a fluctuating
right hemiparesis. Deep tendon reflexes were
symmetrically depressed and the right plantar
response was extensor.
A brain scan was normal and an EEG
showed symmetric delta waves. Arteriography revealed flattening and a 5 mm left-toright shift of the internal cerebral vein.
Conray ventriculography revealed thinning of
the posterior third ventricle with elevation
and lateral deviation of the floor of the left
lateral ventricle at the region of the trigone.
The ventricular fluid contained 39,000
RBC/cu mm. The patient's aphasia, paralysis
of upward gaze, right sensory deficit, and
right hemiparesis failed to improve, despite
external ventriculostomy drainage for 5 days.
His neurological examination 8 weeks later
was unchanged and he was transferred to a
chronic care facility.
Case 3

This 51-year-old right-handed hypertensive woman had the acute onset of
headache, emesis, and shortly became unresponsive. On examination she was hypertensive, unresponsive to verbal commands,
and had fixed conjugate downward deviation
of the eyes which failed to move above the
horizontal meridian. Lumbar puncture
showed bloody cerebrospinal fluid (CSF) with
600,000 RBC/cu mm. Respirations were of
Cheyne-Stokes type.
On external ventriculostomy, the initial
pressure was 400 mm CSF above the brow.
The ventricular fluid was bloody. With ventricular drainage the patient improved over
the next 5 hours and could speak but was
dysphasic. A retrograde femoral arteriogram
showed flattening and left-to-right shift of the
internal cerebral vein. Paralysis of upward
gaze cleared after 3 days of ventricular
drainage. The external ventriculostomy was
removed 5 days after admission, and the
patient became progressively more obtunded.
A ventriculoatrial shunt was placed 4 days
later, and her level of consciousness returned
to normal.
The patient was contacted 1 year later and
refused to return for neuropsychological
testing or examination. However, she denied
any language, sensory, or motor difficulties.
571

A. F. R e y n o l d s , Jr., e t al.

FIG. 1. Case 4. Computerized tomography
scan. A large clot can be seen limited to the left
thalamus except for a small extension into the third
ventricle.

Case 4

This 44-year-old Navajo silversmith
acutely developed a dysphasia, supranuclear
paralysis of upward gaze, right hemiparesis,
and right sensory deficit. A computerized
tomography (CT) scan revealed a left
thalamic hemorrhage with rupture into the
posterior third ventricle (Fig. 1). He became
progressively obtunded, and an external ventriculostomy was placed. An EEG showed left
posterior delta activity. An arteriogram
revealed an apparent vascular glioma, limited to the thalamus, as the etiology of the
hemorrhage.
Supranuclear paralysis of upward gaze
cleared after ventriculostomy drainage was
started. He underwent a course of radiation
therapy for the presumed glioma. The rightsided sensory and motor deficits markedly
improved over the first week, but the aphasia
remained unchanged. The patient's level of
consciousness deteriorated after removal of
the ventriculostomy, so a ventriculoperitoneal shunt was placed. The patient's
neurological function was stable for the 4
months of follow-up study; severe aphasia
and mild right-sided sensory and motor
deficits remained.
572

Discussion
In the syndrome of left thalamic hemorrhage as described by Fisher, 6 three cardinal
features were emphasized: 1) the predominance of sensory deficits over motor deficits;
2) the presence of ocular motor disturbances,
with vertical gaze being impaired by medial
thalamic lesions; and 3) the presence of
dysphasia, with perseveration being prominent. All of our patients showed all of these
features.
The diagnosis was confirmed in our
patients by arteriography in three, ventriculography in two, and CT scan in one.
Thalamic hemorrhage produces typical
changes in each of these diagnostic studies.
The arteriographic changes include shift of
the internal cerebral vein from side to side
and sometimes posterior superior displacement. Lateral displacement of the basilar vein
was present in one patient. A small cryptic
arteriovenous malformation was present in
another.
Changes evident in the ventriculogram included elevation and irregularity of the floor
of the third portion of the lateral ventricle.
The posterior third ventricle was irregular
and poorly filled. These filling deficits were
thought to represent clot in the posterior third
ventricle. The CT scan showed a blood density mass in the left thalamus with third ventricular clot.
The management of left thalamic hemorrhage would seem to be best accomplished as
follows. When the diagnosis is suspected on
clinical grounds, it should be confirmed by
CT scan. Then, if the patient has a depressed
level of consciousness, supranuclear paralysis
of upward gaze, or hemiparesis, a trial of ventriculostomy drainage seems indicated. Two
of our patients, Cases 3 and 4, eventually required a permanent ventricular shunt system.
Supranuclear paralysis of upward gaze in
these patients probably reflects pressure from
the hematoma on the quadrigeminal plate.
The depressed level of consciousness could
reflect pressure on the reticular activating
system. Hemipareses are probably due to
pressure on the internal capsule, since only
one of the five cases that came to autopsy had
extension of the hematoma into the internal
capsule. 4,5,1~Thus, ventriculostomy may serve
to decompress the quadrigeminal plate, the
reticular activating system, and the internal
capsule.
J. Neurosurg. / Volume 48 / April, 1978

Aphasia and left thalamie hemorrhage
The finding of speech disturbance without a
cortical lesion is not well known. The
evidence for a language deficit without cortical lesions is twofold. First, autopsy data
from patients with left thalamic hemorrhage
and aphasia have been reported in five instances. These patients did not have cortical
lesions. The speech disturbance has been
characterized as fluctuating widely, 1~ with a
paucity of spontaneous speech, occasional
nonsense syllables, 1~ and as a fluent anomia
with perseveration? 4
The second evidence for the role of the left
thalamus in speech is from observations on
patients undergoing t h a l a m o t o m y , where no
lesion in speech cortex was made. Acute
dysphasia has been reported at clinical examination in 34% to 42% of patients after left
t h a l a m o t o m y ? ,19 Pathologically, the lesions
in those patients who evidenced dysphasia
were confined to the left ventrolateral nucleus
or globus pallidus, s,ls The incidence of the
dysphasia f r o m dorsomedial thalamotomies,
even in left brain, was much less frequent, one
in 90. 20 W i t h f o r m a l l a n g u a g e testing,
Ojemann 1" found anomic errors in 62% of
patients 48 hours after left ventrolateral
lesions. This was significantly m o r e frequent
than before o p e r a t i o n , or a f t e r right
t h a l a m o t o m y . These errors consisted of misnamings and perseverations.
Several m e c h a n i s m s have been proposed to
explain the role of thalamus in speech. It has
been suggested that speech disturbances
reflect a general deterioration of neural function with thalamic lesions. 3,7,uaa Evidence
against this view comes from our Cases 1, 3,
and 4, where the generalized deficits cleared
with ventriculostomy while the speech deficits
remained. Additionally, speech disturbances
seem to be associated primarily with the left
thalamus, and not the righP 4 and even there,
in a rather discrete a r e a ? T M The speech disturbances with thalamic lesions do not seem
to be identical to any of those described with
cortical lesions. Lesions characteristic of thalamic speech deficits include wide fluctuation
in performance, with fluent speech containing widely extraneous perseverations? ,1~
These thalamic speech deficits also differ
from those seen with " c o n d u c t i o n " aphasia,
which follows disturbance of a subcortical
fiber tract system running through the insula
from the posterior t e m p o r a l association area
to Broca's area. 2 Patients with conduction

J. Neurosurg. / Volume 48 / April, 1978

aphasia are unable to repeat auditory input.
All four of our patients could repeat auditory
input.
M o r e recently, it has been proposed that
the left thalamus is involved in attention
mechanisms that are i m p o r t a n t to storage
and retrieval of verbal items from both shortterm and long-term verbal m e m o r y . 12-15
These mechanisms can be altered by electrical
stimulation of the left ventrolateral t h a l a m u s
where stimulation during input enhances later
recall, and enhances the accuracy of naming
items presented during stimulation in a preexisting a p h a s i a ? T M Difficulties in focusing
attention and associated problems with recent
memory would seem a likely explanation for
the wide fluctuation in the p e r f o r m a n c e and
the apparent perseverative intrusion of unrelated verbal material, 9 the h a l l m a r k s of
"thalamic" language disturbances. Left
thalamic mechanisms also seem to be involved in coordinating the m o t o r aspects and
the respiratory substrate of speech?* D a m a g e
to these mechanisms m a y also be i m p o r t a n t
in some of the more severe output deficits
with thalamic lesions, as in our Case 2.1
References
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91:619-638, 1968
2. Benson DR, Sheremata WA, Bouchard R, et
al: Conduction aphasia. A clinicopathological
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3. Brown JW: Language, cognition and the
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1970
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A. F. Reynolds, Jr., et al.
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18. Samra K, Riklan M, Levita E, et al: Language
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This research was supported by NIH Research
Grant NS-05211 awarded by the National Institute
of Neurological and Communicative Disorders and
Stroke.
Dr. Harris and Dr. Ojemann are affiliates of the
Child Development and Mental Retardation
Center, University of Washington.
Address reprint requests to: Arden Reynolds,
M.D., Division of Neurosurgery, University of
New Mexico, 915 Stanford Drive N.E., Albuquerque, New Mexico 87131.

J. Neurosurg. / Volume 48 / April, 1978