211
Changes of Blood Flow in the Cerebral Cortex
After Subcortical Ischemic Infarction
Else H0jer-Pedersen, MD, and Ole Fritz Petersen, MD
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The two-dimensional xenon-133 inhalation method was used to measure cortical blood flow in
16 patients with small subcortical ischemk infarcts and in 10 patients with larger cortical
infarcts in the chronic phase of stroke. An abnormal hemispheric asymmetry of blood flow was
seen, not only in patients with cortical infarcts, but also in those with subcortical infarcts. In the
patients with subcortical infarcts, focal areas of reduced cortical blood flow were seen in the
symptomatic hemisphere remote from the tissue destruction, usually including part of the
noninfarcted frontoparietal cortex. The cortical dysfunction may have contributed to the
clinical manifestations including aphasia, which was present in 14 of the 16 patients with
subcortical lesions. (Stroke 1989;20:211-216)
M
easurements of regional cerebral blood
flow (rCBF) with the two-dimensional
xenon-133 inhalation technique,1 calculated as the initial slope index (ISI),2 reveal the
perfusion in the outermost part of the brain,
mainly the cortex. Minor infarcts situated deep in
the brain, with no cortical extension and covered
by a layer of apparently normal brain parenchyma,
may be expected not to influence the rCBF findings. To test this suggestion, we analyzed the
results of rCBF measurements as to global and
focal changes in a group of patients with subcortical infarcts and compared the rCBF findings with
those in a group of patients with cortical infarcts
and in a group of controls. rCBF was measured
during the chronic phase of stroke, when the
changes of blood flow have stabilized3-6 and the
uncoupling of cerebral blood flow and metabolism
seen in the acute postinfarct period has
disappeared.7
Subjects and Methods
Our study comprised 26 patients with symptoms
of unilateral cerebral ischemia in the carotid territory. We included only patients in whom computed
tomography (CT) confirmed the presence of nonhemorrhagic cerebral infarcts. Sixteen patients had
deep cerebral infarcts without cortical involvement
(Figure 1); in the remaining 10 patients the infarcts
From the Departments of Neurology and Radiology, Odense
University Hospital, Odense, Denmark.
Supported in part by the Foundation of Laegevidenskabens
Fremme.
Address for correspondence: Else H0jer-Pedersen, MD, Department of Neurology, Bispebjerg Hospital, Bispebjerg Bakke 23,
DK-2400 Copenhagen, Denmark.
Received November 25, 1987; accepted August 30, 1988.
affected the cortex and underlying structures (Figure
2). The size of the infarcts was estimated by
multiplying the length by the width of the hypodense lesion in the slice showing the largest area.
This product was multiplied by the depth, summed
across the several slices showing the lesion. The
size of the infarcts is indicated in Table 1. CT
scanning was performed using third-generation
scanners a mean of 46 (range 4-216) days after the
onset of the ischemic symptoms.
Table 1 summarizes the patient data and clinical
findings. Fifteen of the 16 patients with subcortical
infarcts had left hemisphere lesions, and among the
15, 14 were aphasic in the acute stage. All 16
patients with subcortical stroke were right-handed;
three had hypertension. The clinical evaluation in
the chronic stage took place when rCBF was measured, a mean of 113 (range 27-228) days after the
onset of the symptoms. At that time all 26 patients
were independent in activities of daily living.
We also measured rCBF in 23 normal healthy
volunteers (controls) after informed consent was
obtained. The volunteers were 29-70 (mean 51)
years old and had no brain disorders, hypertension,
or diabetes by history.
rCBF was measured in both patients and controls
using the xenon-133 inhalation technique1-2 on a
Novo Cerebrograph with 16 scintillation detectors
for each side of the head, with the collimator tubes
perpendicular to the brain surface. The system has
been described in detail elsewhere.8 During the
measurements the subjects were lying in a quiet
room, resting, with their eyes covered and their
ears plugged. Paco2 was estimated from recordings on a capnograph of end-tidal CO2 concentrations during the investigations and was found to be
212
Stroke
Vol 20, No 2, February 1989
The rCBF data were analyzed as to hemispheric
asymmetry and focal abnormalities. Hemispheric
asymmetry was quantified as the difference between
the mean hemispheric ISI values in the asymptomatic and symptomatic hemispheres. Focal changes
were defined as ISI values of two or more adjacent
detectors in a hemisphere differing from the ISI
values of the corresponding detectors in the other
hemisphere by >7.2%, a difference that was not
exceeded in any of the 23 controls in this study. The
absolute hemispheric rCBF values were not evaluated because of the variability with age and other
physiologic conditions.1011
Statistical analyses were performed with the paired
and unpaired / tests.
Results
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Controls
rCBF in the two hemispheres was almost identical, in accordance with other investigations812; the
difference between the right and left mean hemispheric ISI values was nonsignificant (mean difference 0.1, SD 0.7, p<0.3), which means that a
hemispheric difference of ^1.5 is abnormal with a
confidence level of <5%. rCBF values were correlated with age, and a significant decline of blood
flow with advancing age was found, as has been
reported previously13 and in accordance with other
studies.1415 Therefore, our results in these controls
were considered to be representative of normality.
15
13
16
FIGURE 1. Schematic representation of appearance on
computed tomogram of subcortical infarcts in 16 patients in
ascending order of size ofinfarct cavity. Slice with largest
lesion is shown. Patient number beneath each slice.
within normal limits. Mean arterial blood pressure
was measured by auscultation after rCBF was
measured. The rCBF values were calculated as the
Patients With Subcortical Infarcts
Hemispheric asymmetry ranged from -0.9 to 4.2
(mean 1.6, SD 1.5) (Table 2); the mean difference
between hemispheres was highly significant
(p<0.005). The greatest hemispheric asymmetries
appeared in four of the five patients with the largest
lesions on CT. This tendency of increasing hemispheric asymmetry with increasing infarct size was
not analyzed statistically because of the small number of patients and the inexactness of infarct size
measurements.
FIGURE 2. Schematic representation of appearance on computed tomogram of cortical infarcts
in 10 patients in ascending order of size of
infarct cavity. Slice with largest lesion is shown.
In Patients 24 and 30, slices nearer top of head
showed cortical involvement. Patient number
beneath each slice.
26
27
28
29
30
Hjjer-Pedersen
and Petersen
CBF in Subcortical Infarction
213
TABLE 1. Summary of CUnkal Data and Findings at Computed Tomography in 26 Patients With Symptoms of Unilateral Cerebral Ischemia
Neurologic manifestations
Acute
Pt/sex/age
Subcortical infarcts
l/M/61
2/F/45
3/M/61
4/M/58
5/M/49
6/M/55
7/M/58
8/M/45
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9/F/50
IO/F/49
ll/M/38
12/M/49
13/F/32
14/M/67
15/M/62
167M/53
Mean 52
Cortical infarcts
21/M/37
22/F/46
23/M/6O
24/F/58
25/M/59
26/M/5I
27/M/67
28/M/42
29/M/59
3O/F/52
Mean 53
R hemiparesis
R hemiparesis/esthesia, slight
motor aphasia
R hemiparesis, mixed
motor/sensory aphasia
R hemiparesis, aphasia
R hemiparesis, slight motor
aphasia
R hemiparesis, slight motor
aphasia
L hemiparesis
R hemiparesis, slight motor
aphasia
Mixed motor/sensory aphasia
Mixed motor/sensory aphasia
R hemiparesis, mixed
motor/sensory aphasia
R severe hemiparesis/esthesia,
mixed motor/sensory aphasia
R hemiparesis, R hemianopsia;
mixed motor/sensory aphasia
R hemiparesis, mixed
motor/sensory aphasia
R paresis of arm, motor aphasia
R paresis of arm, motor aphasia
L
L
L
L
hemiparesis/esthesia
hemiparesis
central facial palsy
paresis and apraxia of hand,
motor aphasia
R dyscoordination of arm
R hemioaresis/esthesia. mixed
motor/sensory aphasia
L severe paresis/esthesia of
hand
L hemiparesis
R dyscoordination of hand,
motor aphasia
L hemiparesis
Computed tomography
Chronic
Infarct size (cm3)
Days from onset
Slight constructional apraxia
None
1
1
46
216
None
1
70
None
R slight paresis of arm
1
2
13
30
Slight motor aphasia
2
31
L slight hemiparesis
None
5
5
72
90
Moderate motor aphasia
Slight motor aphasia
None
8
8
9
35
83
24
R slight hemiparesis/esthesia, slight
mixed motor/sensory aphasia
R slight paresis of arm, slight
motor aphasia
Slight motor aphasia, agraphia
9
14
10
37
14
10
None
None
18
18
7
8
8
49
L slight hemiesthesia
None
L slight central facial palsy
L slight paresis and apraxia of
hand, slight motor aphasia
R dyscoordination of arm
R slieht hemiDaresis/esthesia.
moderate motor aphasia,
acalculia
L moderate paresis of hand
9
16
18
18
5
65
60
16
35
37
58
II
41
24
None
None
45
4
48
52
L moderate paresis of arm
48
117
32
41
Pt, patient; age in years; M, male; F, female; R, right; L, left.
Fourteen patients had focal areas of decreased
rCBF in the symptomatic hemisphere, usually involving at least part of the frontal region (Table 2, Figure
3). As seen in Figure 1, no infarct in these patients
affected the frontal cortex.
In two of these 14 patients an ipsilateral focal area
with increased rCBF was also seen. In Patient 3 a
small temporo-occipital area was localized adjacent
to the frontal low-flow area, which presented an ISI
value 10.3% higher than that of the corresponding
area in the asymptomatic hemisphere. In Patient 5 a
frontal area adjacent to the frontoparietal low-flow
area had an ISI value 7.5% higher than that on the
other side. In both patients the rCBF examinations
were performed >2 months after the stroke, and the
patients were clinically stable. They appeared slightly
demented, being slow, with difficulties in concentrating and memorizing. Patient 3 had been healthy
previously, whereas Patient 5 suffered multiple transient ischemic attacks (TIAs) before his stroke.
214
Stroke Vol 20, No 2, February 1989
<Cortical Blood Flow in 26 Patients With Symptoms of
Unilateral Cerebral Ischemia
TABLE 2.
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Hemispheric
Pt
asymmetry
Subcortical infarcts
1
2.3
2
1.6
0.4
3
4
2.0
5
0.4
6
0.9
7
-0.6
8
0.2
9
1.6
10
0.8
11
1.3
12
4.2
13
14
3.4
3.9
15
-0.9
3.9
16
1.6±1.5*
Mean±SD
Cortical infarcts
21
1.4
22
23
24
25
3.5
0.8
1.3
2.4
26
2.3
27
28
29
30
Mean±SD
2.8
0.8
3.3
1.6
2.0±1.0t
Focal low-flow area
in symptomatic
hemisphere
Focal %
difference in
low-flow
area
Frontal and temporal
Frontal and parietal
Frontal
Frontal
Frontoparietal
Frontal
None
Parieto-occipital
Frontal and parietal
Frontotemporal
Frontoparietal
Frontal and
parieto-occipital
Frontoparietal
Frontotemporal and
parietal
None
Frontotemporo-occipital
10.7
9.5
10.4
15.3
9.1
12.0
Frontal and
temporo-occipital
Frontoparietal
Frontotemporal
Frontoparietal
Frontal and
temporo-occipital
Tempo roparietooccipital
Frontoparietal
Frontal and parietal
Frontotemporo-occipital
Frontoparietal
8.6
7.5
12.0
14.6
16.2
14.1
14.1
18.5
16.2
14.8
11.7
12.0
13.2
16.7
16.2
14.2
16.5
11.7
Hemispheric asymmetry, initial slope index of asymptomatic
hemisphere minus that of symptomatic hemisphere.
•1y><0.005, p<0.001, significant difference between hemispheres by paired / test.
In Patients 7 and 15 no focal abnormalities were
present, and the differences of ISI between hemispheres were within the limits seen in the controls.
Patients With Cortical Infarcts
Hemispheric asymmetry was present, with the
lower ISI in the symptomatic hemisphere. The
difference between hemispheres ranged from 0.8 to
3.5 (Table 2); the mean difference (2.0±1.0) was
highly significant (p<0.001). Hemispheric asymmetry tended to be more pronounced than with subcortical infarcts; however, this was not significant
22—
27
3. Schematic representation of appearance on
blood flow maps of area of decreased cortical blood flow
in symptomatic hemisphere in (top) two patients with
subcortical infarcts (Patients 6 and II) and in (bottom)
two patients with cortical infarcts (Patients 22 and 27).
FIGURE
Focal areas of reduced rCBF in the symptomatic
hemisphere were observed in all 10 patients (Table
2), and two typical cases are illustrated in Figure 3.
Comparison of the blood flow maps and the CT
scans revealed consistent changes on the whole.
In Patients 23 and 28 the blood flow maps showed,
adjacent to the low-flow areas, focal areas with
increased rCBF compared with the asymptomatic
hemisphere. In Patient 23 an area with 16.7% higher
ISI was localized in the occipital region, and in
Patient 28 an area with 10.4% higher ISI was seen
frontal to the frontal and parietal low-flow area. The
rCBF assessments had been performed >2 months
after the stroke, at a time when the patients had
made a good recovery and did not appear demented.
Patient 23 had been healthy previously, whereas
Patient 28 had one TIA 16 months before his stroke.
Discussion
Our results suggest that subcortical infarction
causes significant hemispheric asymmetry of blood
flow in the cerebral cortex as measured by the
two-dimensional xenon-133 inhalation method after
the acute stage of stroke. Hemispheric asymmetry
appeared to be of the same magnitude as that seen
in cortical infarcts, although subcortical infarcts
were smaller. Remote focal areas of decreased
rCBF in the ipsilateral cortex, predominantly in the
frontoparietal region, were present with the subcortical infarcts in 14 of 16 patients.
Distant reductions of rCBF (diaschisis) have been
described in acute stroke in studies performed before
the introduction of CT.16-22 Only a few studies
report the influence of discrete subcortical infarcts
on rCBF recorded by the two-dimensional clearance technique in chronic stroke. Takano et al23
studied the effect of small, deep hemispheric infarcts
in the subacute-chronic stage on the ipsilateral cortical circulation using the xenon-133 intracarotid
injection technique; a focal area of hypoperfusion
around the central sulcus was observed in all 10
patients studied, whereas no information was given
on hemispheric asymmetry due to the method used.
In another study24 using the xenon-133 intracarotid
injection technique, rCBF was recorded in 10
Hjjer-Pedersen and Petersen CBF in Subcortical Infarction
Downloaded from http://stroke.ahajournals.org/ by guest on June 16, 2017
patients with subcortical lesions on CT, and large
low-flow areas were observed in five patients,
whereas rCBF was normal in the other five; however, the recordings were performed in the acute
stage, an average of 2 days after the stroke, in
contrast to the chronic static lesions in our study.
Three-dimensional methods based on positron
emission tomography (PET) have shown an area of
depressed rCBF larger than that of the anatomic
infarct on CT.7-2526 Remote effects were noted in
both the acute and the chronic postinfarction
periods.27 In patients with lacunar infarcts in the
internal capsule or the basal ganglia, PET images
showed decreased rCBF in the frontoparietal cortex
ipsilateral to the lesion. Decreased rCBF in chronic
lesions was coupled with decreased rate of metabolism. In unilateral chronic vascular thalamic lesions,
a significant metabolic hemispheric asymmetry at
the expense of the affected side has been demonstrated, and furthermore, a tendency of a regional
pattern of cortical hypometabolism was observed.28
A reduction in blood flow matched that in metabolism. Ourfindings,obtained with much less advanced
equipment, appear to support the PET results. A
study using single-photon emission computed tomography (SPECT) in a series of 16 patients with
unilateral subcortical hemorrhagic or ischemic stroke
demonstrated a significantly greater reduction of
cortical blood flow in eight patients with aphasia
and neglect than in eight patients without neuropsychological deficits.29 rCBF in that study was measured both during a very acute phase (<24 hours)
and up to 33 (average 15) days after the stroke in
contrast to our study in which we measured rCBF
not earlier than 27 (mean 113) days after the onset of
symptoms. The different time schedule makes comparison of the rCBF results in the two studies
difficult due to changes of rCBF from the acute to
the chronic phase in stroke. 36 However, a concordant finding was cortical hypoperfusion in patients
with aphasia and subcortical infarcts.
In addition to focal areas of low rCBF, focal areas
of relatively increased rCBF were seen in four of
our 26 patients. Areas of increased blood flow,
luxury perfusion, and relative or absolute hyperemia have been described in acute stroke. 33031
However, our patients were in a chronic phase after
stroke, without any clinical evidence of deterioration at the time rCBF was measured. The focal
areas gave a spotty appearance to the blood flow
maps, as with multi-infarct dementia.8 Two of the
four patients were slightly demented but the other
two were not. It appears difficult to draw any firm
conclusion from our data on these four patients.
CT findings in cerebrovascular disease have been
correlated with neuropathologic findings,32 and it
was very difficult to detect accurately on CT small
infarcts of <5 mm largely because of the limitations
in the efficiency of the CT scanner. Therefore,
independent small infarcts in the cortex may have
been present in our patients, contributing to the
215
rCBF abnormalities in subcortical lesions. However, it appears that this alone may not explain our
findings of a hemispheric asymmetry of the same
magnitude in these patients as in the patients with
rather large cortical infarcts.
Several reports have been published recently on
the clinical effects of subcortical stroke on "higher
cortical functions" such as language, cognition,
practic functions, and aphasia; cognitive deficits
and apraxia have been described in deep cerebral
lesions.33-38 Fourteen of our 16 patients with subcortical infarcts were aphasic in the acute stage.
Several mechanisms responsible for the observed
symptoms have been proposed in the literature:
compression of adjacent structures, disconnection
of strategic efferent and afferent fiber tracts of the
cortex, and damage to basal ganglia gray matter;
reduction of cortical blood flow and metabolism
may contribute, also. It is unknown if these changes
are secondary to deafferentation, with adjustment
of blood flow to reduced metabolic activity. However, these changes do show that the cortex is
involved and dysfunctional in subcortical tissue
destruction, which may explain why some clinical
manifestations resembled cortical symptoms. In
some of our patients blood flow abnormalities were
present after the symptoms had disappeared, which
may mean that rCBF measurements give more
subtle information on regional function than clinical
evaluation and may demonstrate the complexity of
clinical recovery. Further studies may give important information on pathophysiology and recovery
in subcortical stroke.
Acknowledgments
We thank the staff of the CBF laboratory for
assistance with the rCBF measurements. Dr.
Enevoldsen is thanked for permission to use the
cerebrograph.
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KEY WORDS • cerebral blood flow • cerebral infarction •
xenon
Changes of blood flow in the cerebral cortex after subcortical ischemic infarction.
E Højer-Pedersen and O F Petersen
Stroke. 1989;20:211-216
doi: 10.1161/01.STR.20.2.211
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Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1989 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628
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