Global Aphasia Without Hemiparesis
Daniel Tranel, PhD; Jos\l=e'\Biller, MD; Hanna Damasio, MD;
Harold P. Adams, Jr, MD; Steven H. Cornell, MD

\s=b\ Three patients acutely developed
global aphasia, but did not manifest the
typical accompanying right hemiparesis.
Computed tomography and magnetic resonance imaging studies demonstrated
that the patients had two discrete left
hemisphere lesions, one in the anterior
language cortices or language-related
subcortical areas, and one in the posterior language cortices. Cerebral angiography showed that two patients had complete occlusion of the left internal carotid
artery, and the third had an intraluminal
"clot" in the supraclinoid portion of the
left internal carotid, findings suggestive
of an embolic etiology. Our cases indicate
that global aphasia without hemiparesis
predicts two discrete lesions and a particularly good recovery of speech and lan-

guage.

(Arch Neurol 1987;44:304-308)

is characterized by
fllobal aphasia
impairment of speech pro¬
severe

duction, auditory comprehension, and
repetition. Hemiplegia is considered

to be an almost constant component of
the clinical presentation.1 The pres¬
ence of

global aphasia is indicative of
a large lesion in the left perisylvian
and basal ganglia regions, an assump¬
tion supported by most studies for
which anatomical data are available.
Furthermore, the severity of global
aphasia and the size of lesion in these

Accepted for publication Oct 20, 1986.
From the Departments of Neurology, Divisions
of Behavioral Neurology (Drs Tranel and Damasio) and Cerebrovascular Diseases (Drs Biller
and Adams), and Radiology, Section of Neuroradiology (Dr Cornell), University of Iowa, Iowa
City.
Reprint requests to Department of Neurology,
University of Iowa Hospitals and Clinics, Iowa
City, Iowa 52242 (Dr Tranel).

locations

are strongly associated.25
Recently, however, it has been noted
that global aphasia can be associated
with large lesions confined to prerolandic language areas.6 8 Finally, glob¬
al aphasia may even result from two
discrete lesions, one affecting the
anterior and the other involving the
posterior left language areas.910 Van

Horn and Hawes10 described three
patients who developed global aphasia
without hemiparesis, and suggested
that this presentation was indicative
of "embolie encephalopathy." We
recently studied three patients who

acutely developed global aphasia

without hemiparesis as a result of
cerebral infarctions. These patients
were examined in both acute and
chronic stages. Our findings support
the conclusions that global aphasia
without hemiparesis predicts two dis¬
crete left hemisphere lesions; predicts
an unusually good recovery of speech
and language; and may be an indica¬
tor of an embolie etiology.
PATIENTS AND METHODS

We evaluated three patients who, as a
result of cerebral infarctions, developed
global aphasia without hemiparesis. Two
patients had computed tomography (CT)
and neuropsychologic evaluation both in
the acute phase (within 14 days of onset),
and in the chronic phase (between three
and ten months after onset), and the third
patient received these studies acutely and
again five weeks after onset. Magnetic
resonance
imaging (MRI) was also
obtained for all patients. Cerebral angiography was performed during the acute
phase of the illness.
Computed tomography was obtained

with a fourth generation scanner (Picker
1200 Sinerview). Transverse slices of 8 mm
thickness were obtained. Magnetic reso¬
nance imaging was obtained using a scan¬
ner (Picker 0.5 Tesla Superconducting
Magnetic Resonance Scanner). Anatomical

Downloaded From: by a Thomas Jefferson University User on 06/24/2018

localization was obtained by analysis of CT
and MRI according to the standard proce¬
dures of the Division of Behavioral

Neurology's Neuroimaging Laboratory,
University of Iowa, Iowa City. Patient
identification in the films was masked.

Investigators blind to the patients' behav¬
ioral status selected the appropriate tem¬
plate system for plotting the abnormal
images and charted the position of those
images on a standard template protocol.11
A transparency containing the boundaries
of neural units of interest, in both gray-

and white-matter structures, was then
superimposed on the chart. Damage was
assigned to the units that contained the
abnormal images.
A complete neuropsychologic evaluation
included assessment of intellectual func¬
tioning (Wechsler Adult Intelligence
Scale—Revised), verbal and visual memo¬
ry, perception, and orientation. Testing
was conducted over several short sessions,
commensurate with the patients' ability to
cooperate and attend. Some tests were
omitted or truncated, as necessitated by
the patients' condition. Speech and lan¬
guage were assessed with the Multilingual
Aphasia Examination12 and the Boston
Diagnostic Aphasia Examination.15 Em¬
phasis was placed on the most salient
parameters of speech and language,

including fluency, articulation, naming,
repetition, comprehension, and reading
and writing.
REPORT OF CASES

Case 1.—After an evening of heavy alco¬
hol consumption and subsequent vomiting,
a

37-year-old right-handed man suddenly

became unable to speak, except for saying
"yes" and "goddamn." He complained of
"numbness" of the right side of the face.
Neurologic examination showed a discrete
right facial weakness and a minimal right
pronator drift (both of which resolved
completely by the third day after onset).
Strength was otherwise normal. Tendon
reflexes were slightly brisker in the right
upper extremity. Plantar responses were
normal. Computed tomography showed

asymmetry of the lateral ventricles, but no

focal area of abnormal attenuation was
seen. Angiography demonstrated an intraluminal filling defect in the supraclinoid
portion of the left internal carotid artery.
During the next three days, the patient
was noted to utter only a few poorly artic¬
ulated words. Comprehension of conversa¬
tional speech was restricted to very simple
commands. He could not name, repeat,
read, or write. Six days after onset, CT
with contrast enhancement showed two
well-defined areas of infarction in the left
hemisphere, one anterior (frontal lobe)
and one posterior (parietal lobe). The ante¬
rior lesion involved the most superior part
of the frontal operculum (area 44), and
extended into the premotor region immedi¬
ately above (area 6). The posterior lesion
involved part of the supramarginal gyrus
(area 40), as well as the inferior part of the
superior parietal lobule (areas 7 and 5). It
extended inferiorly to involve the most
posterior portion of the superior temporal

gyrus (posterior area 22).

Comprehensive neuropsychologic evalu¬
ation was completed within two weeks of
the ictus. The patient continued to have
severely nonfluent speech. He had virtual¬
ly no spontaneous speech production. In
response to questions, he attempted to
communicate. However, utterances were
restricted to a few grunts and to one or two
unintelligible phonemes. He was unable to
name in either the visual, auditory, or
tactile modalities. Repetition was not pos¬
sible. He could follow simple commands
and showed some preservation of aural and
reading comprehension of simple words
and short phrases; however, aural and
reading comprehension of more complex
material was severely defective. He was
severely agraphic, and had gestural aprax¬
ia. Nonverbal abilities, such as visual per¬
ception and two- and three-dimensional
constructional praxis, were normal.
Magnetic resonance imaging obtained
five months after onset showed two dis¬
crete lesions in the left hemisphere, in the
same locations as described before (Fig 1).
At this time, follow-up neuropsychologic
evaluation revealed remarkable recovery
of speech and language (Table). His speech
remained slightly effortful, but he pro¬
duced sentences of normal length, and
there were no paraphasias. As shown in
Table, nearly all formal linguistic func¬
tions had improved to the normal range.
Case 2.—A 52-year-old right-handed
man suddenly developed right-sided focal
seizures and an inability to speak. On
admission to the hospital, he was alert and
oriented. He did not produce any intelligi¬
ble speech, but answered questions by nod¬
ding. He was able to follow a few very
simple commands. He had mild right cen¬
tral facial paresis, and slight pronator
drift on the right. There were no other
signs of motor weakness. Tendon reflexes
were slightly brisker in the right upper
extremity and right knee. Plantar
responses were normal. He had frequent
episodes of right facial twitching. By the
seventh day after onset, the facial weak¬
ness and pronator drift had disappeared.
Computed tomographic scans obtained

Fig 1.—Magnetic resonance imaging scan of patient 1 obtained five months after onset with
T2-weighted image. Note two distinct areas of increased signal in left hemisphere.

Speech and Language Characteristics of Patients 1 and 2
Patient 2

Patient 1

Characteristic

Acute

Severely

Speech

nonfluent;
reduced

Chronic

Fluent,

nonparaphasic

to "yes"

and a

Acute

Chronic

Severely

Essentially

two

fluent with
occasional

profanities

paraphasias

nonfluent;

profanity
Language

Naming*

0/30

2/30

8/14

Sentence

repetition*
Aural

1/18

8/18

comprehension*
Token test*

33/44

Readingt

4/10

Writing*

Severely

9/10

Severely
defective

defective
Gestural praxis

Severely
defective

Controlled oral
word

association

*

*

Multilingual Aphasia Examination.
tBoston Diagnostic Aphasia Examination.

Downloaded From: by a Thomas Jefferson University User on 06/24/2018

Normal

Moderately

Normal

defective

Severely
defective

Moderately
defective

long history of poorly controlled
arterial hypertension and severe cerebral
vascular disease. According to relatives, he
began to evidence changes in behavior and
mental status three years previously, with
a gradual diminution of activities and
mental acuity, and eventual retirement
from work. In retrospect, these changes
probably reflect the cumulative effect of
multiple ischemie events; however, at no
time did he show evidence of focal motor or
sensory deficits. He then developed an
acute onset of difficulty speaking, which
prompted admission to our service.
On admission, he showed severe global
aphasia. The remainder of the neurologic
examination was normal. Computed
tomography performed three days after
onset showed multiple infarcts located in
the left posterior temporoparietal region,
left basal ganglia, left prefrontal region,
right corona radiata, and right posterior
infracalcarine area. These lesions were
also seen on MRI obtained the same day.
Cerebral angiography performed five
days after the onset of symptoms showed
complete occlusion of the left internal
carotid artery. The left middle cerebral
artery filled through the ophthalmic col¬
laterals. Branch occlusions of the angular
and posterior parietal branches of the left
middle cerebral artery were also noted.
Neuropsychologic testing was conducted
ten days after admission. His speech was
severely nonfluent, and he showed pro¬
found deficits in most aspects of linguistic
functioning. He did produce some short
utterances of two or three words. These
contained paraphasse errors, but no signif¬
icant articulatory disturbance. Naming
and repetition were not possible. He
showed marked impairment of aural and
reading comprehension, even for simple
material such as single words and short
phrases. He was agraphic, with frequent
paragraphic errors especially when copy¬
ing written text.
Five weeks later, he showed slightly
improved speech fluency. He produced
longer utterances with frequent paraphasic errors, but continued to have little suc¬
cess in naming, repetition of short sen¬
tences, or comprehension of verbal materi¬
al. Also, he showed moderate compromises
in areas of nonverbal, visuospatial cogni¬
tive functioning. These deficits, less severe
than those in the verbal sphere, were inter¬
preted as due to the right hemisphere
man had a

Fig 2.—Magnetic resonance imaging scan of patient 2 obtained two days after onset with
T2-weighted image. Note two distinct areas of increased signal in left hemisphere.
the day of onset showed a lesion in the
parietal region, and an ill-defined area of
possible infarct in the left frontal lobe.
Electroencephalography demonstrated
rare, left frontal high amplitude and
rhythmic delta paroxysms. Cerebral angiography showed complete occlusion at the
origin of the left internal carotid and a
small residual stump. The left middle cere¬
bral artery filled through retrograde flow
from the ophthalmic artery. It did not
receive collateral flow from the right inter¬
nal carotid or from the posterior circula¬
tion.

Magnetic resonance imaging performed

at this time showed two discrete lesions in
the left hemisphere (Fig 2). A frontal-lobe
lesion involved the most anterior and supe¬
rior portion of the frontal operculum (area
45 and white matter undercutting area 44),
and extended into prefrontal areas 46 and
9. The other lesion was in the parietal lobe,
and involved the inferior and posterior
portions of the inferior parietal lobule
(areas 40 and 39).
Laboratory evaluation of speech and lan¬
guage was started the day after the event,
and continued for several days. It revealed
severe impairments in nearly all aspects of
speech and language. Spontaneous speech
was limited to only two words, both pro-

fanities. Even these were uttered with
extreme effort and frequent initial stutter¬
ing. The patient could not name or repeat.
He had severe alexia and agraphia, and
gestural apraxia of the right arm. Compre¬
hension was limited to very simple, onestep commands (eg, "make a fist"). He also
showed constructional apraxia and im¬
paired right-left discrimination. Visual
perception was relatively intact. He
improved slightly during the first week in
the hospital, the most notable recovery
taking place in the domain of comprehen¬
sion of conversational speech.
Follow-up neuropsychologic evaluation
ten months after the stroke showed excel¬
lent recovery of speech and language (Ta¬
ble). He had occasional pauses and wordfinding difficulties in spontaneous speech,
but formal linguistic assessment demon¬
strated normal or near-normal levels of
performance in most areas tested. Com¬
puted tomography performed at this time
showed a well-defined frontal lobe lesion
in the same area as described before, but
extending higher into prefrontal regions in
the dorsolateral sector (areas 9 and 8). The
parietal lobe lesion was visible as an area
of atrophy in the inferior parietal lobule
(areas 40 and 39).
Case 3.—A 51-year-old right-handed

Downloaded From: by a Thomas Jefferson University User on 06/24/2018

lesions.
Computed tomography performed at

this time showed three distinct areas of
infarcì in the left hemisphere (Fig 3). One
was in the dorsolateral prefrontal cortex
(areas 46, 9, 8). Another was in the basal
ganglia, and involved the head of the cau¬
date nucleus, part of the anterior limb of
the internal capsule, and the paraventricular white matter. The third was in the
posterior portion of the superior temporal
gyrus (posterior area 22 and 37) and the
inferior parietal lobule (areas 40 and 39).
A neuropsychologic follow-up examina¬
tion was performed four months after the
initial event. His speech at this time was
essentially fluent, although there were fre¬
quent pauses and hesitations. Paraphasias

common, especially in spontaneous
speech and naming tasks. He remained
unable to name (nearly all paraphasic
responses) or repeat, but aural and reading
comprehension were significantly im¬
proved. There were also very significant
improvements in gestural and construc¬
tional praxis. Although nearly all of his
scores continued to fall in the "impaired"
range, he generally showed a very good
profile of recovery of verbal communica¬
tion abilities, relative to the severe global
aphasia he manifested acutely.
were

COMMENT

Our patients acutely developed a
syndrome of global aphasia without
the expected hemiparesis, caused by

cerebral infarction. The lesions asso¬
ciated with global aphasia can vary in
both extent and location. There is,
however, a strong association between
the typical clinical picture of global
aphasia and involvement of the entire
left perisylvian region. These lesions
result from a large infarction in the
territory of the left middle cerebral
artery. Damage involves all or most of
the areas known to be related to
speech and language: the frontal operculum (areas 44 and 45), the posterior
half of the superior temporal gyrus
(areas 41, 42, and posterior area 22),
the posterior region of the middle and
inferior temporal gyri (area 37), the
supramarginal and angular gyri (ar¬
eas 40 and 39), and deep structures,
including the basal ganglia and insu¬
la. Commonly, damage involves part
of the motor cortices, or the subcortical white matter where corticobulbar
fibers cross, or both. Thus, global
aphasia and right-sided motor deficits
typically occur together, although the
latter may be relatively transient in a
few cases.14
Our cases, however, had two dis¬
crete lesions. One of these was in
anterior language cortices or in the
subcortical gray-matter areas known
to be related to language dysfunc¬
tion,1516 and one was in the posterior
language cortices. The primary motor
cortices were intact. A similar local¬
ization of lesions in a case of global
aphasia was noted previously in a
description from this laboratory.9
The pathological events that lead to
such double and discrete areas of
damage are of special interest. Van
Horn and Hawes10 described three
patients who developed global aphasia
without hemiparesis, all of whom had
two separate lesions in the left hemi¬
sphere. The authors concluded that
this clinical picture was indicative of
an "embolie encephalopathy." Our
cases are also consistent with the
notion of an embolie pathophysiology.

Fig 3.—Magnetic resonance imaging scan of patient 3 obtained five weeks after onset without
contrast. Note three distinct areas of low density in left hemisphere.

Two patients had complete occlusion
of the left internal carotid artery, and
the third had an intraluminal "clot"
in the supraclinoid portion of the left
internal carotid artery.
A final point of importance is the
issue of recovery. Poor recovery from
global aphasia is a ubiquitous finding
in extant research.51721 A comparison
between recoveries from different
types of aphasia shows that patients
with global aphasia invariably fare
the poorest.18·20·21 Sarno and Levita19
noted that the greatest changes in the
evolution of global aphasia may occur
between the sixth and 12th months
after onset. Nevertheless, these
patients remained severely defective
in communication skills 12 months
after onset, and were still classified as
global aphasies. Intensive speech

Downloaded From: by a Thomas Jefferson University User on 06/24/2018

therapy does not appear to signifi¬
cantly improve this poor recovery.18'9
In sharp contrast, the three cases
described here showed very good
recovery of speech and language. This
was particularly evident in patients 1
and 2, in whom speech became fluent,
repetition became normal, and aural
comprehension only showed deficits
with complex material. Agraphia and
gestural apraxia also resolved. Pa¬
tient 3 also improved substantially,
although not as completely. By ten
months after onset, none of the three

patients continued to meet diagnostic
criteria for global aphasia. Patients 1
and 2 showed only minimal signs of
residual aphasia, not sufficient to
qualify for formal classification;
patient 3 could be classified as having
a residual Broca's aphasia.

It is interesting to speculate as to
the possible reasons for this unchar¬
acteristic recovery. A major differ¬
ence between our patients and the
traditional patient with global apha¬
sia is the extent of involvement of

language-related areas. Typically, as
elaborated above, there is extensive
destruction of most of the perisylvian
and basal ganglia regions, including
the frontal operculum, posterior supe¬
rior temporal gyrus, inferior parietal

lobule, insula, and motor cortices.
However, our patients had only cir¬

cumscribed involvement of some of
these areas. Thus, although the initial
insults rendered these areas suffi¬

ciently dysfunctional to produce a pic¬
ture of global aphasia, the amount of
undamaged language-related territo¬
ry probably allowed for this otherwise
unusually complete recovery of speech
and language.
In short, the presentation of global

aphasia without hemiparesis predicts

two discrete lesions in the anterior

and posterior left hemisphere lan¬

guage areas, possibly of an embolie
etiology. This syndrome also seems to

indicate the possibility of an unusual¬
ly good recovery of verbal communica¬
tive abilities.
This study was supported in part by National
Institute of Neurological and Communicative
Diseases and Stroke (Bethesda, Md) grant POI
NS 19632.

References
1. Geschwind N: Current concepts: Aphasia. N
Engl J Med 1971;284:654-656.
2. Benson DF, Geschwind N: The aphasias and
related disturbances, in Baker AB, Baker LH
(eds): Clinical Neurology. New York, Harper &
Row Publishers Inc, vol 1, 1971.
3. Naeser MA, Hayward RW: Lesion localization in aphasia with cranial computed tomography and the Boston Diagnostic Aphasia Examination. Neurology 1978;28:545-551.
4. Naeser MA, Hayward RW, Laughlin SA, et
al: Quantitative CT scan studies in aphasia: I.
Infarct size and CT numbers. Brain Lang 1981;
12:140-164.
5. Kertesz A, Harlock W, Coates R: Computer
tomographic localization, lesion size, and prognosis in aphasia and nonverbal impairment. Brain

Lang 1979;8:34-50.
6. Mazzocchi F, Vignolo LA: Localization of
lesions in aphasia: Clinical-CT scan correlation
in stroke patients. Cortex 1979;15:627-653.
7. Basso A, Lecours AR, Moraschini S, et al:
Anatomical correlations of the aphasias as

defined

through computerized tomography:
Exceptions. Brain Lang 1985;26:201-229.
8. Vignolo LA, Boccardi E, Caverni L: Unexpected CT-scan findings in global aphasia. Cortex
1986;22:55-69.
9. Damasio H: Cerebral localization of the

aphasias, in Sarno MT (ed): Acquired Aphasia.
Orlando, Fla, Academic Press Inc, 1981, pp 27\x=req-\

50.
10. Van Horn G, Hawes A: Global aphasia
without hemiparesis: A sign of embolic encepha-

lopathy. Neurology 1982;32:403-406.
11. Damasio H: A computed tomographic
guide to the identification of cerebral vascular

territories. Arch Neurol 1983;40:138-142.
12. Benton AL: Multilingual Aphasia Examination. Iowa City, Department of Neurology,
University of Iowa, 1976.
13. Goodglass H, Kaplan E: The Assessment of
Aphasia and Related Disorders. Philadelphia,
Lea & Febiger, 1972.
14. Ferro JM: Global aphasia without hemi-

paresis. Neurology 1983;33:1106.

Downloaded From: by a Thomas Jefferson University User on 06/24/2018

15. Damasio AR, Damasio H, Rizzo M, et al:
Aphasia with nonhemorrhagic lesions in the
basal ganglia and internal capsule. Arch Neurol
1982;39:15-20.
16. Naeser M, Alexander MP, Helm-Esta-$
brooks N, et al: Aphasia with predominantly
subcortical lesion sites. Neurology 1982;39:2-14.
17. Yarnell P, Monroe P, Sobel L: Aphasia

outcome in stroke: A clinical

neuroradiological

correlation. Stroke 1976;7:516-522.
18. Sarno MT, Levita E: Recovery in treated
aphasia in the first year post-stroke. Stroke 1979;
10:663-670.
19. Sarno MT, Levita E: Some observations on
the nature of recovery in global aphasia after
stroke. Brain Lang 1981;13:1-12.
20. Kertesz A, McCabe P: Recovery patterns
and prognosis in aphasia. Brain 1977;100:1-18.
21. Demeurisse G, Demol O, Derouck M, et al:
Quantitative study of the rate of recovery from
aphasia due to ischemic stroke. Stroke 1980;
11:455-458.