BRAIN

AND

LANGUAGE

19,

306-316 (1983)

Aphasia following a Right Thalamic Hemorrhage
ANDREW L. CHESSON, JR.
Louisiana

State University
Medical
Center and The Veterans
Administration
Medical
Center,
Shreveport

A left-handed patient with a right thalamic hemorrhage and disordered speech
is described. Sequential examinations and aphasia testing were done during a lyear follow-up period and the results are reported. This case supports those
authors who have described characteristics they feel are helpful in diagnosing
disordered speech associated with thalamic lesions. Paucity of speech, reduced
voice volume, anomia, some paraphasia, and severe dysgraphia were present,
but comprehension and repetition were relatively preserved. She showed modest
improvement with time. This case also confirms that thalamic involvement in
speech is a dominant, rather than a specifically left hemispheric function.

INTRODUCTION
The role of the thalamus in disorders of speech has been discussed
and debated in the recent literature (Bugiani, Conforto, & Sacco, 1969;
Cappa & Vignolo, 1979; Ciemins, 1968, 1970; Riklan & Cooper, 1975).
Some authors feel the disordered speech may not represent a true aphasia.
Thalamic lesions in association with disordered speech have been reported
with tumors (Arseni, 1958; Cheek & Taveras, 1966; Smyth & Stern,
1938), abscesses (Panchal, Parikh, & Karapurkar,
1974), and vascular
lesions (Bugiani, Conforto, & Sacco, 1969; Cappa & Vignalo, 1979; Ciemins,
1968, 1970; Fazio, Sacco, & Bugiani, 1973; Mohr, Watters, & Duncan,
1975; Reynolds, Harris, Ojemann et al., 1978; Reynolds, Turner, Harris
et al., 1979). Vascular cases which have been well documented as limited
to the thalamus have been hemorrhagic in nature (Ciemins, 1970; Samarel,
Wright, Sergay et al., 1976), although the possibility of hemorrhagic
infarction in two cases has been suggested (Mohr et al., 1975). Data
regarding the role of the thalamus in speech has also been presented
The patient secretarial assistance of Nell Butts and Jerry Morse and the neuropsychological
testing assistance performed by Pat Caskey and Ron Goebel, Ph.D., are acknowledged
and appreciated. Please send requests for reprints to Dr. Andrew L. Chesson, Department
of Neurology, LSU Medical Center, P.O. Box 33932, Shreveport, LA 71130.
306
0093-934X183 $3.00
Copyright
All rights

Q 1983 by Academic Press, Inc.
of reproduction
in any form reserved.

THALAMIC

HEMORRHAGE

AND

APHASIA

307

from cases of thalamic stimulation (Cappa & Vignolo, 1979; Ojemann,
1977; Fedio & Van Buren, 1975) and from surgically induced thalamic
lesions (Darley, Brown, & Swenson, 1975; Riklan & Levita, 1970; Ciemins,
1970; Guiot, Hertzog, Rondot et al., 1961; Waltz, Riklan, Stellar et al.,
1966; Bell, 1968). Several authors have concluded that thalamic involvement
with speech is a left hemispheric function (Cappa & Vignolo, 1979;
Reynolds et al., 1978; Reynolds et al., 1979; Riklan & Cooper, 1975),
although this is not accepted by others.
I have been unable to find a previously reported case of a right sided
thalamic hemorrhage producing documented aphasia. The purpose of
this paper is to report such a case, to provide additional evidence that
a thalamic lesion can produce a persisting speech deficit, and to describe
the results of testing such a patient at intervals during a l-year period
following her thalamic hemorrhage.
CASE REPORT

A 71-year-old, left-handed, black female with a ninth grade education
was admitted to the Louisiana State University Medical Center. Her past
medical history was significant only for 5 years of intermittently
treated
hypertension. On the morning of admission, while walking into church,
she experienced a sudden onset of weakness involving her left arm and
leg. She complained of nausea but denied headache, loss of consciousness,
or visual disturbance. Her family described that she spoke very little
and when she responded “her words didn’t come out right.” As she
was brought to the hospital from an outlying community she was noted
to become sleepy.
The patient was lethargic but easily arousable to verbal stimuli. She
was oriented to name, location, month, and year. Her speech was sparse,
hoarse sounding, reduced in volume, and mildly dysarthric. She had little
spontaneous speech but answered direct questions. Her level of attentiveness fluctuated, but she was sufficiently alert to follow verbal commands. Occasional verbal paraphasic errors were present in her responses
(i.e., “winder” instead of clasp, in requesting her watch to be removed).
Bedside aphasia testing revealed intact comprehension
for multistage
commands and fair preservation of repetition. Naming was impaired for
common objects, their component parts, colors, and body parts. Rightleft orientation,
one- and two-digit calculations, and drawing were all
impaired. Writing was illegible.
Cranial nerve examination
revealed small, minimally reactive pupils.
In the resting position her eyes were conjugately deviated downward
and to the left of midline. Extraocular movements were full horizontally
but upgaze was absent and downgaze moderately limited. Lateral gaze
produced horizontal nystagmus. A left hemianopic field cut was suspected
by threat testing. A moderately severe left hemiparesis was present with
arm and leg involvement greater than the facial weakness. Reflexes were

308

ANDREW

L. CHESSON,

JR.

mildly hyperactive on the right. Plantar response was flexor on the right
and extensor on the left. Sensory testing revealed loss of pain and to a
lesser extent touch and vibration on the left, including the face and trunk.
An electroencephalogram
revealed moderate amounts of right sided,
irregular, polymorphic,
low-voltage delta activity, most prominent in the
posterior frontal and the temporal regions. A CT scan with and without
contrast enhancement was performed and revealed a hemorrhage in the
right thalamus. Follow-up scans performed 16 days later are also seen
in Fig. 1.
The patient underwent aphasia testing using the aphasic screening test
from the Halstead-Reitan
neuropsychological
test battery at 3 and 12
days and 6 and 12 months after the onset of symptoms. These results
and the findings on serial neurologic examinations are described below.
Selected results are noted in Fig. 2 and Table 1.

FIG. 1. These unenhanced CT scans. at the level of maximal extent of the hemorrhage,
were performed on the 1st and 17th days posthemorrhage. Contrast enhancement performed
with the second scan revealed no areas of enhancement beyond the area of the original
hemorrhage. No additional lesions were visualized.

THALAMIC

HEMORRHAGE

AND

APHASIA

309

Clinically,
by the third day the patient was beginning to show signs
of improvement
and increasing alertness. Pupils were larger and more
briskly reactive to light. Nystagmus and ocular movement limitations
remained. Her hemiparesis and reflex asymmetry was unchanged but the
facial weakness was less pronounced. The first of the aphasia series was
administered. A portion of the results are shown for comparison purposes
in Table 1. She could name only two of six simple objects, repeat three
of five words or phrases, and read virtually only single letters. When
attempting to read words or phrases she read one letter at a time. Double
digit subtraction and single digit multiplication
were correct only in one
of seven attempts. Other portions of the testing revealed left sided perceptual neglect, constructional apraxia and left-right confusion regarding
commands and instructions. Her hand writing was severely dysgraphic
and her drawings unrecognizable (Fig. 2).
Ten days later, by bedside testing, her language was clearly better,
with a more normal voice volume. Ocular motility revealed some remaining
upgaze limitation.
Nystagmus had substantially diminished and a field

FIG.

I-Continued.

310

ANDREW

L. CHESSON,

JR.

FIG. 2. Examples of the patient’s ability to copy a square (top) and an old-fashioned
key (bottom) at 3 days, 12 days, 6 months, and 12 months following a thalamic hemorrhage.

cut was no longer demonstrable. The motor weakness and hemisensory
loss remained unchanged. Formal aphasia testing showed significant improvement in her use and comprehension of language symbols. Changes
in naming, repetition, and reading ability are noted in Table I. Her Ieftsided perceptual difficulty had also substantially decreased. Her handwriting
and drawing continued to be severely impaired.
At 6 months, neurologic examination revealed normal extraocular motility, symmetric and reactive pupils, and no field cut or nystagmus. A
moderate hemiparesis remained with leg and arm weakness being equal
and more severe than facial weakness. The left-sided sensory loss remained
and the hyperreflexia included sustaining clonus at the left ankle. The
aphasia battery showed continued improvement in expressive language,
as well as in drawing and writing skills. Some dyslexic errors remained
but reading skills were better. There continued to be mild spelling and
naming errors (Table 1). The handwriting had become recognizable and
readable but with some dysgraphic errors still present. Some constructional
apraxia persisted but the drawings were beginning to be recognizable
(Fig. 2). At her l-year follow-up the neurological examination
showed
no significant change over the preceding 6 months. Aphasia testing revealed
some mild improvements
in spelling and reading but some erroneous
responses continued to be present. Handwriting was still dysgraphic and
her drawings continued to reveal some evidence of impairment. The level
of naming errors remained essentially as it was 6 months earlier. On
confrontation naming and in conversational speech she continued to have
difficulty with naming which resulted in pauses, some generalization and
naming errors (i.e., watch winding stem was called “catch,”
a cloth
watch band was called “chain,”
button called “hooker,”
etc.).
The findings on neurologic examination in patients with thalamic hem-

THALAMIC

HEMORRHAGE

AND

APHASIA

311

orrhage have clinically localizing value. Fisher’s summary of findings in
this disorder included predominance of sensory over motor deficits, ocular
motor disturbances, small sluggish pupils, and significantly reduced alertness or even coma (Fisher, 1959). The ocular motor disturbances can
include impairment of conjugate vertical gaze and often downward deviation
of the eyes at rest. Fisher also noted a global dysphasia seen in dominant
hemisphere lesions. Ciemins (1970) reported two additional cases with
mixed aphasia and with autopsy findings of localized hemorrhage in the
left thalamus. He concluded that “lesions in the dominant thalamus, and
most particularly
in the posterior portion, may produce aphasia,” and
that the aphasia is of a mixed motor and receptive type. Benson (1979),
in his recent book, concluded that thalamic lesions producing speech
abnormalities
appear to be quite rare but have been described with some
increasing frequency. Reports have most often involved hemorrhages
(Bugiani et al., 1969; Cappa & Vignolo, 1979; Ciemins, 1968, 1970; Fazio
et al., 1973; Mohr et al., 1975; Reynolds et al., 1978; Reynolds et al.,
1979; Samarel et al., 1976) but have also included tumors (Arseni, 1958;
Cheek & Taveras, 1966; Smyth & Stern, 1938), abscesses (Panchal et
al., 1974), and possibly hemorrhagic infarcts (Mohr et al., 1975).
Some authors have, however, debated the existence of a specific type
of aphasia associated with lesions restricted to the thalamus (Brown,
1974; Van Buren, 1975) and explanations for altered speech have included
the concept that acute brain lesions involving a particular region can
cause more extensive disturbances than accounted for by the local lesion
alone (phenomenon of diaschisis) (Samarel et al., 1976). Other explanations
have included: compression and edema affecting the adjacent temporal
lobe pathways (Van Buren, 1975; Horenstein, Chung, & Brenner, 1978;
Mohr et al., 1975), decreased alertness mimicking speech disturbances,
and the possibility of an undetected cortical lesion located in one of the
more classical speech areas.
Reports from series of postoperative thalamic lesions, performed as
treatment of movement disorders, have also reviewed changes in speech
patterns. Reduced voice volume which improves in the immediate postoperative period but which may persist when lesions involve the dominant
hemisphere have been described (Bell, 1968; Hermann, Turner, Gillingham
et al., 1966). Other authors have noted the occurrence of postoperative
dysarthria and dysphasia (Bell, 1968; Waltz et al., 1966; Ojemann, 1977;
Fedio & Van Buren, 1975; Ojemann & Ward, 1971). Bell (1968) reported
reduced verbal output and disturbances in rhythm modulation
which
occurred despite normal repetition, characteristics he felt indicated an
expressive rather than receptive type of dysphasia.
Hemispheric
dominance in patients with aphasia is unclear in many
reports. Bell’s (1968) data and literature review suggests dysphasia only
occurred after operation on the left hemisphere. However, one of their

312

ANDREW

L. CHESSON,

JR.

six 2
+
s..e..v..e..n
s..e..e...t..e...
d..o..e
g..e...female,
feminine

+

trying
+
+

The dog can’t
see
-

+

six 27

t

he is a friendly
small uh.. .of
dog shows

He is a friendly
animal, a.. .a..
former washer
of dog shows

+
+
+
+

phonetically close
+

phonetically close
+

+
+
+
+

+
+

+
+

Note. Comparison data for selected portions of the aphasia testing done 3 days to I year after the thalamic hemorrhage. +, Indicates correct
response; - indicates no response.
‘I May reflect some element of perseveration as the request to spell “square” had shortly preceded naming of these two objects.

He is a friendly animal,
a famous winner of
dog shows

Reading
I six 2
MGW
seven
See the black dog

Repeating
Triangle
Massachusetts
Methodist, Episcopal
He shouted the
warning
Seven

W

w

m

8
E

fz

ii
E

$

314

ANDREW

L. CHESSON,

JR.

possibly left-handed patients, who was excluded from statistical analysis,
had dysphasia which could have possibly been due to a hemorrhage
around a cryogenic lesion in the right thalamus. Hermann (1966) noted
dysphasia in right-handed patients occurred only after a left-sided lesion.
Based on conclusions drawn from thalamic stimulation studies and postoperative thalamotomy
data, as well as their own cases, some authors
have gone as far as describing a specific left hemispheric thalamic function
for speech (Reynolds et al., 1978; Reynolds et al., 1979). Most other
authors who support the concept of thalamic aphasia are more traditional,
and advocate a dominant hemisphere thalamic speech function. Although
this latter approach would be consistent with that expected from other
types of aphasia, right-sided lesions producing a thalamic aphasia are
not documented.
The data in this report, concerning a right thalamic
lesion producing a persisting aphasia in a left-handed patient, supports
the concept of dominant hemisphere localization.
Those authors who advocate a more specific type of “thalamic aphasia”
have reported that in spontaneously occurring cases a constellation of
features such as paucity of speech, fading voice volume, anomia, perseveration, and neologisms occur, while comprehension and word repetition
remain intact (Reynolds et al., 1979). Cappa and Vignolo (1979) reported
decreased spontaneous speech, relatively preserved repetition, varying
degrees of impairment
of auditory comprehension,
marked inertia, and
grossly defective writing. Benson (1979) described near mutism with
eventual change to verbose, paraphasic jargon output and anomia which
is often severe but with relatively preserved comprehension and repetition.
He emphasized a generally transient time course of these deficits.
The present case provides support for those who advocate a more
specific type of “thalamic aphasia” with characteristics different from
Broca’s and Wernicke’s aphasia. The preservation of repetition, while
helping to differentiate this from conduction aphasia, suggests similarities
to transcortical motor and sensory dysphasias. This would not be surprising
if retained repetition is a feature of a lesion which leaves an intact
perisylvian language core. The preserved repetition would seem to imply
preserved phonemic elements of language while the associated dysphasia
suggests an impairment of semantic levels of language (Cappa & Vignolo,
1979).
The persistence of some of this patient’s deficits for greater than a
year after onset would be against the suggestion advocated by some that
the aphasia in thalamic lesions is a transient deficit due to associated
swelling in the area near the hemorrhage. This case would also support
the speech dysfunction characteristics mentioned by others as being
related to thalamic lesions including reduced spontaneous speech, low
voice volume, severe dysgraphia, anomia that is frequently initially severe
but shows rapid improvement,
and relatively good preservation of com-

THALAMIC

prehension and repetition.
showed early improvement.

315

HEMORRHAGE

AND APHASIA

In this patient

these latter two deficits also

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for Parkinson’s