982
Young Adult Stroke: Neuropsychological
Dysfunction and Recovery
Jose M. Ferro, MD, and Manuela Crespo, MD
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Etiology, neuropsychological deficits, aphasia type, and recovery were retrospectively studied in
254 young adults with stroke. Cardiac embolism was the most common cause of stroke in
patients younger than 40, while atherosclerosis was the most frequent etiology among those aged
41-50 years. In 166 aphasic patients, Broca's aphasia was the most common while Wernicke's
and transcortical aphasias were rare. Compared with an older aphasic population, young
patients had significantly more nonfluent aphasias and fewer comprehension deficits. These
differences were related to stroke localization: the majority of infarcts localized by computed
tomography in 37 patients involved either the entire middle cerebral artery territory or its
superior or deep branches, explaining the preponderance of nonfluent aphasia. Prognosis of
aphasia in our patients was better than has been reported for non-age-selected aphasia
populations. Roughly one third of our patients recovered completely, one third improved, and
one third had an unresolved language deficit. Complete recovery and significant improvement
were observed even > 6 months after stroke. In some patients, recovery was much better than
might have been predicted from lesion site and size depicted on computed tomograms. (Stroke
1988;19:982-986)
S
troke in young adults represents only a small
fraction (approximately 4%) of strokes in
North America1-3 and most western European countries; much higher rates have been reported from developing countries.4-5 The causes of
cerebral infarction in young adults have been thoroughly reviewed in recent comprehensive publications 16 ; however, only a few studies7-8 have been
devoted to prognostic factors and profiles of functional recovery from stroke in this age group. No
study describes neuropsychological deficits and their
rate of recovery.
This article is a retrospective review of young
adults with strokes who were evaluated in our unit
during 14 years, with emphasis on neuropsychological sequelae and outcome.
Subjects and Methods
We reviewed the files of 254 patients aged 15-50
years referred to the Language Research Laboratory, Centro de Estudos Egas Moniz, between
January 1972 and February 1986 for evaluation of
neuropsychological deficits caused by hemispheric
stroke. There were 120 men and 134 women; 102
From the Language Research Laboratory, Centro de Estudos
Egas Moniz and Stroke Clinic, Department of Neurology, Hospital de Santa Maria (M.C.) and University of Lisbon (J.M.F.),
Lisbon, Portugal.
Address for reprints: Jose' M. Ferro, Centro de Estudos Egas
Moniz, Hospital de Santa Maria, 1600 Lisbon, Portugal.
Received August II, 1987; accepted March 24, 1988.
were <40 years old and 152 were between 41 and 50
years of age.
The diagnosis of stroke and its etiology were
based on clinical and laboratory data obtained after
reviewing hospital records and were confirmed by
appropriate imaging procedures in most cases (computed tomography [CT scan], cerebral angiography,
two-dimensional echocardiography). The anatomic
distribution of the infarct was investigated in 69
patients for whom CT data were available. The
involved vascular territories were localized according to the guidelines of Damasio,9 Ringlestein et
al, l 0 andZulch."
Neuropsychological evaluation was performed in
the first month after stroke for 142 patients, between
the second and third month for 36 patients, and
after 6 months for 54 patients. The comprehensive
neuropsychological battery included four subtests
for aphasia; a 22-item version of the token test12;
and tests of alexia; agraphia; buccofacial, limb, and
constructional apraxia12; and hemispatial neglect.13
Diagnosis and classification of aphasia were based
on numerical taxonomic criteria according to scores
on the aphasia subtests.14
Patients evaluated more than once were classified
as follows: completely recovered, test scores
improved to the normal range; improved, change to
a less severe type of aphasia; stabilized, no change
in the type of aphasia based on the evaluations
performed; or recurrent stroke during follow-up.
Ferro and Crespo Young Adult Stroke
15 - 30 years
31 - 40 years
983
4 1 - 5 0 years
FIGURE 1. Pie graphs of eti-
ology of strokes in young adults
between ages 15 and 30 (left),
31 and 40 (center), and 41 and
50 years (right).
Cardiac Embolism
Atherosclerosis
•
Pregnancy, oral anticonceptive
E3 Other
etiologies
Non-atherosclerotic vasculopathies
LJ Unknown
Hematologic Diseases
O Intracerebral hemorrhage
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Results
Following the guidelines of Hart and Miller,1
patients were grouped into eight etiologic categories
(Figure 1): cerebral atherosclerosis (89 patients),
cardiac embolism (78 patients including 54 with
valvular heart disease), intracerebral hemorrhage
(21 patients), vasospasm (14 patients), strokes occurring during puerperium, pregnancy, or due to oral
contraceptives (9 patients), hematologic diseases (5
patients), nonatherosclerotic cerebral vasculopathy
(8 patients), and unknown etiology (39 patients).
Etiology of stroke in the two younger age groups
(15-30 years, 31-40 years) were almost identical. In
the older patients (41-50 years), cardiac embolism
was less frequent, although not significantly so
(*2 = 3.43,p<0.10).
Among the 234 patients with left-hemisphere
lesions, 165 (71%) were aphasic, 121 (65% of 186
literates) were alexic, and 148 (76% of 195 literates)
had a writing disturbance. Buccofacial apraxia (82
patients, 40%) was more common than limb apraxia
(44 patients, 22%); 83 patients (41%) had constructional apraxia. Since patients were referred to our
laboratory mainly because of speech problems,
only 20 patients with right-hemisphere strokes were
tested. Of these, eight had hemispatial neglect and
five showed constructional apraxia. Crossed aphasia (aphasia due to right-hemisphere lesion in a
right-handed person) was found only once.
Table 1 shows the distribution of aphasia type
among the 166 young adults with stroke in relation
to the overall population with aphasia due to stroke
evaluated at our unit during that period. Broca's
aphasia was significantly (x2 = 15.07, p<0.001) more
common while Wernicke's (x 2 = 8.66, p<0.005) and
transcortical sensory aphasia (^ 2 = 6.41, p<0.25)
were significantly less frequent among young adults.
Fluent aphasia and aphasias with comprehension
deficits were less common in young patients than in
the overall stroke population (x2= 13.07, p<0.001
and x2 = 26.4, p<0.001; respectively). Figure 2 shows
that this pattern is valid for all the young age
groups.
Among the 69 patients who had CT, 32 were
excluded: 21 for technical reasons (artifacts, poorly
defined lesion boundaries, report but no CT print
available) that precluded detailed anatomic localization; two had a normal CT scan, and nine had
intracerebral hemorrhages. Infarct location on the
remaining 37 CT scans is depicted in Table 2
according to the involved vascular territories. The
more common patterns consisted of large infarcts of
the entire middle cerebral artery (MCA) territory (7
patients), involvement of the superior division of
the MCA (9 patients), and deep lesions corresponding to the lenticulostriate territory or to a watershed
infarct between the cortical and subcortical circulations (10 patients). Parietal branches of the MCA
were involved in a few cases, while temporal infarcts
due to occlusion of the inferior division of the MCA
were uncommon.
Of the 69 patients who underwent CT, 26 were
aphasic. Two had deep striatocapsular hemorrhages
causing mixed transcortical and conduction aphaTABLE 1. Stroke in Young Adults 15-50 Years Old: Type of
Aphasia
Young
Type of aphasia
Nonfluent aphasias
Global
Broca's
Transcortical motor
Transcortical mixed
Fluent aphasias
Wernicke's
Transcortical sensory
Conduction
Anomic
Total aphasias
Total strokes
adults
Total
%
60
54
7
6
310
159
44
19
34*
16
24
13
2
10
14
166
254
141
50
38
70
837
1551
*t$p<0.001, 0.005, 0.025, respectively.
25
9t
4t
26
20
20*
16
984
Stroke Vol 19, No 8, August 1988
1001
30 years
n - 29
C
31Z
481
TM
0%
TMX
01
W
10Z
TMX
3Z
u
8Z
TS
OZ
A
71
C
3Z
100Z
31 - 40 years
n - 40
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•
•
C
38Z
B
TM
351
3Z
TS
37.
A
87.
c
5Z
FlGURE 3. Example of disparate results between lesion
site and size on computed tomogram and aphasia in
young adult with stroke: large middle cerebral artery
infarct produced only mild conduction aphasia.
c
tal infarct causing only dysarthria, and the other was
a 42-year-old woman with a massive MCA infarct
producing a mild transcortical motor aphasia.
Follow-up examinations were given to 64 (39%)
of the 166 aphasic patients. Among these 64, 19
(30%) recovered completely and 21 (33%) improved;
21 (33%) were stabilized and 3 patients (5%) had a
recurrent stroke (Table 3). Although significant
improvement and complete recovery were more
common during the first 6 months, some aphasic
patients improved or even recovered fully later.
Among 44 patients first seen in the acute period
(the first month after stroke) (follow-up mean 11.79,
range ±9.59 months), there were no significant differences (#2 = 0.14, not significant) in outcome among
the three age groups (Table 4).
100Z
41 - 50 years
n - 98
Hi
^1
•mm
c
37Z
B
27*
TM
6Z
TMX
5Z
W
8Z
TS
A
1Z
9Z
n
• qui Z - 4.90. p < 0 . 5
FIGURE 2. Bar graphs of type of stroke aphasia in
different age groups. G, global; B, Broca's; TM, transcortical motor; TMX, transcortical mixed; W, Wernicke's; TS, transcortical sensory; A, anomic; C, conduction.
sias. Among the 26 patients with CT-demonstrated
infarcts, 19 had nonfluent aphasias (14 global, 3
Broca's, 2 transcortical motor) and five had fluent
aphasias (2 conduction, 2 anomic, 1 Wernicke's).
Except for two cases (parietal infarctions causing
Broca's and global aphasia), nonfluent speech was
always associated with either prerolandic, subcortical, or massive MCA infarcts. One patient with
Wernicke's aphasia had a temporoparietal lesion.
The two patients with anomic aphasia had prerolandic and subcortical infarcts. The two patients with
conduction aphasia had large lesions with an uncommon localization for that type of aphasia (Figure 3).
Among patients with nonfluent speech, two had less
severe aphasias than would have been predicted by
their lesion site and size on CT. One patient was a
45-year-old man with a large cortico-subcortical fron-
Discussion
Our series is a retrospective review collected
over several years, during which period new imaging and diagnostic tools were introduced into clinical practice enabling a better understanding of stroke
type and etiology. These facts strongly limit the
interpretation of our data on stroke etiology. However, our results are quite comparable to published
data,1-8 except for a higher rate of cardiac embolism
as a result of rheumatic valvular heart disease. This
finding reflects the fact that rheumatic valvular
heart disease is still rather common in Portugal.15
The localization of cerebral infarcts is strongly
related to their pathophysiology. Emboli tend to
involve the MCA territory, lodging at its bifurcation
or trifurcation or occluding its frontal, opercular, or
parietal branches. Carotid thrombosis can produce
Ferro and Crespo Young Adult Stroke
TABLE 2.
985
Stroke in 37 Young Adults 15-50 Years Old: lnfarct Localization by Computed Tomography
Vascular territory
No. patients
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Middle cerebral artery
Superior division + inferior division + lenticulostriate arteries
Superior division + inferior division
Superior division
Superior division + anterior cerebral artery
Superior division + lenticulostriate arteries
Superior division + angular artery
Lenticulostriate arteries + angular artery
Lenticulostriate arteries + watershed infarct
Lenticulostriate arteries
Watershed infarct
Terminal territory + watershed infarct
Terminal territory + watershed infarct (middle and anterior cerebral arteries)
Posterior parietal artery
Angular artery
Inferior division + angular artery
Inferior division
Watershed infarct (middle and anterior cerebral arteries)
Choroidal anterior artery + lenticulostriate arteries
Choroidal anterior artery
Watershed infarct (middle and posterior cerebral arteries)
Posterior cerebral artery
Posterior cerebral artery (bilateral)
•27 (65%)
2 \ 10
2
1
1
1
2
I
2
2
1
1
2
2
2
6 (12%)
Watershed infarct, superficial and deep circulation.
massive MCA, watershed, or terminal territory
infarcts. Lacunes involve mainly deep structures
such as the thalamus and internal capsule. Changes
in infarct localization with age are rarely mentioned
in the literature. Our data indicate that in young
adults, infarcts most commonly involve either the
entire MCA territory, its superior division and
branches, or the lenticulostriate or terminal zones.
In general, temporal infarcts causing Wernicke's
aphasia are believed to be of embolic origin.16
However, in this age group temporal infarcts were
infrequent, indicating that emboli rarely lodge in the
MCA inferior division. Age-related changes in
embolus size, cardiac output, and collateral blood
flow might explain this finding. In young adults, a
large embolus stopping at the stem of the MCA
makes the uncollateralized lenticulostriate territory
vulnerable to infarction. When emboli lodge in the
MCA bifurcation, the territory supplied by the
TABLE 3.
angular and temporal arteries may escape ischemia
through leptomeningeal anastomoses from the posterior cerebral artery.17
Several researchers have found that patients with
Broca's aphasia were significantly younger than
those with Wernicke's aphasia.18-23 According to
Eslinger and Damasio,23 that difference could be
due to 1) changes in stroke loci with age; 2) cumulative effects of mental decline associated with
aging plus damage to language areas regardless of
stroke locus; 3) age-related changes in the anatomic
and physiologic mechanisms underlying language
function, such that regardless of lesion location,
certain aphasia types might become more prevalent
with age; or 4) better recovery from comprehension
deficit in younger adults, thereby leading to a
decreased prevalence of Wernicke's aphasia.
Our results clearly indicate that locus of stroke is
the major cause of age-related changes in aphasia
Stroke in Young Adults 15-50 Years Old: Aphasia Evolution in 64 Patients
Follow-up period
Evolution
Completely recovered
Improved
Stabilized
Recurrent stroke
3 mo
(« = 37)
8
10
19
3
6 mo
(n = 28)
6
7
15
1 yr
("=33)
>1 yr
Overall
(n = 64)
3
8
22
1
2
10
19
21
21
3
Evolution defined in text. Data are number of patients.
Reference values (%)
Kertesz20
Ferro'2
14
22
22
55
31
56
986
Stroke
Vol 19, No 8, August 1988
TABLE 4. Stroke in 44 Young Adults 15-50 Years Old: Aphasia
Evolution During First Month After Stroke
Age (yr)
Evolution
Completely recovered
Improved
Stabilized
Recurrent stroke
41-50
<30
31-40
(n = 19) Total
(» = 9)
No. % No. % No. % (JV=44)
2 22 5 31 6 32
13
2 22 5 31 7 36
14
4 45 4 25 6 32
14
1 11 2 13 0
3
0
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type. In fact, the large number of nonfluent aphasias
in young adults is the neuropsychological counterpart of the predominance of prerolandic and subcortical infarcts in this age group. Our data suggest
that the third and fourth explanations of Eslinger
and Damasio may also influence the different distribution of aphasia type with age. In fact, aphasia
types characterized by impairment of comprehension, whether nonfluent (global) or fluent (Wernicke's, transcortical sensory), were less frequent
in our young patients, indicating that comprehension deficits are either less prevalent or have a
superior recovery in young adults.
A few patients provided exceptions to the classic rules of lesion location in aphasia. In two
patients, postrolandic lesions produced nonfluent
aphasias, while in four other patients, a more
severe aphasia would have been expected from the
lesion size.
Our series points out that young adults generally
have a favorable prognosis, with lack of improvement demonstrated in only 33%. Improvement of
aphasia in this age group is clearly superior to that
indicated in the literature on recovery (78% and
56%, respectively). 12 - 20 Moreover, significant
changes in aphasia type and severity were observed
even several months after onset, showing that recovery continues into the chronic period, a finding rare
in older patients.20 Although some changes in aphasia features with age can possibly be related to
modifications in the neural network subserving language, most changes are secondary to a different
localization of cerebral infarcts with age. These
changes are related to differences in etiology and
other as yet not clearly established factors, such as
different embolus size or route.
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KEY WORDS • cerebrovascular disorders • young adults
cognition disorders • aphasia
Young adult stroke: neuropsychological dysfunction and recovery.
J M Ferro and M Crespo
Stroke. 1988;19:982-986
doi: 10.1161/01.STR.19.8.982
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