Steven
Warach,
MD,
PhD
#{149} Wei
Li, MD
#{149} Michael
Ronthal,
Mb BCh
#{149} Robert
R. Edelman,
MD
Acute Cerebral Ischemia: Evaluation with Dynamic Contrast-enhanced MR Imaging and MR Angiography’
Dynamic
contrast-enhanced
M
T2*
weighted magnetic resonance (MR) imaging and MR angiography (MRA) were used to evaluate cerebral blood volume and the intracranial arterial system in 34 patients within 48 hours after the onset of cerebral ischemia.
In 24 of the patients, an abnormality identified on T2-weighted images corresponded
to the
deficit.
Intracranial
strated
occlusions
acute
clinical
MRA
demon-
or severe
lesions
early
vessels,
MR.
stenosis
or obstruction,
nance
(MR),
Radiology
17.1214
contrast 1992;
ischemia, 17.124 #{149} Cerebral 17.781
angiography display major tails in stroke
With
stenoses
in the
13.781, 15.781 #{149} Cerebral blood blood vessels, #{149} Magnetic reso-
enhancement
therapy noninvasive
ology
182:41-47
Brookline 30,
Ave. revision
1991;
ceived
September
Address ,
R.R.E.),
RSNA,
reprint 1992
Beth
Israel
Boston, MA requested
requests
Hospital,
02215. Received July 19; revision
16; accepted
can
for
acute and
cerebral readily
useful. Dynamic MR imaging has
September
to R.R.E.
Thirty-six
evaluate
cerebral
Contrast-enhanced like positron
MR emission
a
used
to
(6). un-
hancement seen in cerebral tions of various ages were The results suggested that
infarcpresented. decreased
330 May re23.
We have
applied
contrast-en-
hanced MR imaging and MRA in a series of patients with acute cerebral ischemia. Our goal was to compare enhancement patterns on dynamic
MR images giograms ischemia.
with
findings
in the
evaluation
on MR anof cerebral
not complete cooperation;
and dynamic contrast-enMR imaging. These patients 19 women and 15 men (age
37-93
years).
Patients
ther
a random
nor
medical
completed spin-echo
all three MR imag-
were
inrange,
selected
systematic
in nei-
manner,
was a bias toward clinical deficits and
al-
patients more
sta-
conditions.
The patients were studied 2-48 hours after the onset of deficits attributable to focal cerebral ischemia. Four of these patients had a stuttering course before a ered
worsening,
the stroke
which
onset.
was
In the
consid-
other
pa-
tients, the approximate time from stroke onset, rounded off to the nearest hour, was measured from the time that the patient or an observer first noticed the deficit.
Patients
were
to en-
symp-
MRA,
clear-cut
ier to perform in an emergency setting. In a previous report (6), the technique and normal patterns of dycorresponding were deof dynamic
and
ing,
though there with greater
umes (7). An important practical issue is that MR imaging is much more widely available than positron emission tomography and, in general, eas-
enhancement blood volume and features
signs
ischemia of less than were referred for
34 patients of the study:
hanced cluded
cannot be used to quantify blood volume or flow; it can, however, provide an assessment of relative blood vol-
namic cerebral scnibed,
with
therefore, aspects
ble
imaging, tomography,
METHODS
study. Two patients could the study because of poor
cerebral vasculacould prove
hemodynamics
patients
toms of focal cerebral 48 hours in duration
ischemia, available
contrast-enhanced recently been
AND
Patients
be used to anatomic dewithout the
blood volume associated with cerebral infarctions could be identified with this technique; angiographic correlation, however, was not available, and the number of acute cases was lim-
Harvard Medical School and the Dcof Neurology (SW., MR.) and Radi-
(W.L.,
(MRA) vascular patients,
method for assessing ture and hemodynamics
ited. From partments I
PATIENTS
imag-
material, provide flow in the circle of Willis (2-5). the advent of thrombolytic
dynamics
clinical course. By providing information about hemodynamics not available with conventional Ti- or T2-weighted images, MRA and dynamic MR imaging could prove helpful in describing the pathophysiologic characteristics of stroke and in guiding early therapeutic intervenlion. Index terms: Brain, Cerebral angiography,
(MR)
ing is highly sensitive in detecting morphologic changes associated with stroke (1). In addition, MR
need for injection of contrast and further refinements can functional information about
of major vessels supplying the area of infarction in 16 of these patients, and decreased blood volume correlated well with MRA abnormalities. Infarcts less than 2 cm in diameter were not reliably shown with MRA or blood volume studies. Correlation between lesions seen with MRA and decreased blood volume in acute infarcts was good, and both techniques demonstrated
resonance
AGNETIC
the
who
considered time
awoke
with
their
to have
their
deficit
of awakening;
thus,
for
deficit from
some,
the
onset of noticeable deficit may have succeeded the actual onset of ischemia by hours. The vascular localization and presumptive mechanism tenmined by
clinical
of the a neurologist
criteria
In some
of the
zodiazepines,
or haloperidol
plete
the study.
MR MR
(8,9) and
the MR findings.
patients,
sedation
with
was
Patient
in the
ben-
mepeni-
required
to corn-
characteristics
are
Table.
Studies imaging
MR imaging tems,
were destandard
diphenhydramine,
dine,
summarized
ischemia using
Iselin,
was
system NJ) and
performed
(Siemens standard
with a 1.5-T Medical Syshardware.
Abbreviations: BBB = blood-brain barrier, MRA = MR angiography, ROI = region of interest, SE = spin echo, SEM = standard error of the mean.
41
The patients were studied with (a) standard TI- and T2-weighted spin-echo (SE) imaging, (b) MRA of the circle of Willis and its major branches, (c) dynamic contrast-enhanced MR imaging, (d) delayed Ti-weighted and
contrast-enhanced
(e) follow-up
after
stroke
weighted
2-li
For some
cases,
images-enhanced
hanced-and/or
follow-up of poor
tion,
medical
Case Sex
(y)
I
M
28
2 3
M
73
M F F
88 72 86
M
82
8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32
F M M M F M F F F F M F M F F F M F F M F F M M M F
33
F
34
F
68 73 80 62 37 85 89 73 87 93 79 44 72 72 81 93 40 62 80 70 66 89 68 69 65 87 84 89
days
TI-
images
were
patient
instability,
4 5
coopera-
or withdrawal
6 7
of
consent. Images
obtained
tion
of contrast
with
standard
the
material
TI-
sequences.
were time
before
Typical
administra-
were
and
acquired
T2-weighted
imaging
SE
parameters
600/15 (repetition time msec/echo msec) for TI-weighted images and
2,000-2,500/40,
90 for
T2-weighted
double-
echo images. Section thickness was 5 mm, field of view was 23 cm, the acquisition matrix was 256 x 192, and one or two excitations
were
MRA
used.
of the
circle
formed with time-of-flight sated
of Willis
a standard technique.
gradient-echo
with
typical
20#{176} flip
was
sequence
angle,
per-
three-dimensional A flow-compen-
imaging
was
used
parameters
slab
thickness
of 40/7, of 40-50
mm,
32 or 64 partitions, one or two slabs, 256 x 256 acquisition matrix, and a field of view of 21 cm.
tamed
Angiographic
from
the
mum-intensity
After MR
was
pnoaches
exist
Several
performing
after administration For instance, fast
quences FLASH
Ti-weighted
ap-
dynamic of a contrast gradient-echo se-
with inversion prepulses [Siemens] sequence) allow
strongly
images
(Turbo-
to be
manifested intensity
as an on these
increase images.
a T2*weighted
weighted) During
the
sequence
first
dimeglumine
pass
brain,
the
short-
T2* results in a loss of signal intensity (10). Our initial experience with these two techniques in healthy subjects superior
for the
contrast-to-noise
T2*weighted
method
was
used
for
T2* weighting
was
pulse
echo
As previously
spoiled
fast
all
stroke
sequence
low-angle
studies.
with with
level
of the
tient
(case
The
delay;
25 images
images dynamic
L pons
NA
L P L F T P L F T P Negative Negative Negative Old R P L F R pons Negative L cerebellum Negative RBG Negative R T P BG R T P R insula Old and new R F, P. BG Negative L P. BG, IC Negative Negative L pontomes L pons R pons R thalamus Negative L P R 0, thalamus L F Bilateral pons R F T P
Negative Positive Positive Negative Negative Negative Positive Positive Negative Negative Negative Negative Negative Negative Positive Positive Positive Positive Positive Negative Positive Negative Negative Positive Positive Positive Positive Negative Positive Positive Positive Positive Positive
were
within
Committee
the on
was
Spin-echo
time image
were
explain matched small
images
were
of an acute the clinical the clinical
deficit. deficit
a positive study. The ( < 1 cm in diameter)
of clinical
deficits
examined
infarction
to an
acute ificity
would
An infarct that was consid-
presence infarct
suggesting
of a in cases
involvement
both
dynamic
seen
as a decrease
the
a pixel-by-pixel an
gadopentetate
venously by means of manual injection for approximately 5 seconds, followed by a saline flush. Variability in timing of the
The angiographic images were exammed for evidence of occlusion or severe stenosis in a vessel that supplied the terntory that was symptomatic. When an an-
injection
giographic
42
and
#{149} Radiolocrv
20 mL of gadopentetate (469 NJ)
patient
mg/mL; Berlex was administered
stability
Laboraintra-
occasionally
lesion
was
suspected,
confin-
tensity
images image on
studies
the
specwere
ternin de-
were
analyzed The
intensity
signal
obtained
di-
by dividing,
before
dimeglumine
on
In addition,
created basis,
image
the
for and nor
was performed by disMR images in a cine of contrast material was
obtained an
found
quantitatively.
images.
were
sup-
No false-
evaluated
in signal
T2*weighted
territory
outside
and
qualitative analysis playing the dynamic loop. The passage
and images
sensitivity not assessed,
lesions
MR
comedeficit
spin-echo
relevance
qualitatively
on
images
were
of clinical
on
obtained,
dimeglumine tories, Wayne,
four
on
im-
considered
lesion
The
MRA
study.
were
approximately
spin-echo
were clinical
lesion
vision
After
on
acute
infarctions. of MRA
The
for
that
voids
of the angiognaphic
that fell within the vascular plied by the artery in question. positive results of MRA were
tory tail.
Analysis
inspection
at MRA
of a large vascular territory (eg, middle cerebral artery) was considered a negative
acquired.
R P
of the
if the vascular
positive sponded
pa-
on
flow
Findings
parenchymal
in one
performed
of the hospital Investigations.
and
ages.
Conventional
performed
based partitions
images
on T2that, to the
deficit.
was
individual
at a single-section to the level of
abnormality or, lacking
was
mation MR
suspected
ered
no intenimage
Enhanced
=
I).
studies
field was
with
L
clinical
angiography
Data
a
technique
17 cm. Imaging 2.8 seconds per
artery,
most prominent weighted images
evidence
x
Dynamic
T2-weighted
Mid basilar Negative L ICA L MCA NA Negative Negative Post R MCA L ICA Negative Negative Negative Negative Negative Negative Prox R MCA R ICA R MCA branch Post L MCA R ICA Negative L ICA Negative NA Basilar Basilar Negative R PCA Negative L ICA Negative Negative Basilar R ICA
2 4 5 6 6 6 7 7 7 8 8 8 9 10 11 ii 12 12 13 16 18 19 21 22 22 24 33 36 38 39 40 42 48 48
were acquired corresponding
used with 35/25, a 10#{176} flip angle, one excitation, section thickness of 8 mm, acquisition matrix of 256 x 80, and a rectangular of view of 23 approximately
MRA
a gra-
a long
described, shot
quality, cephalic
guidelines Clinical
so this
obtained
dient-echo
time.
ratio
sequence,
Spin-Echo
(h)
artery, BC = basal ganglia. F = frontal lobe, IC = internal capsule, ICA = inleft, MCA = middle cerebral artery. mid = middle, NA = not of acceptable 0 = occipital lobe, P = parietal lobe, PCA = posterior cerebral artery, pontomes = pontomesenjunction, post = posterior division, prox = proximal, R = right, T = temporal lobe.
carotid
location
ened
showed
of MR Imaging
= basilar
Note-Basilar ternal
images
can be used. the
and MR
Examination
led to fewer contrast-enhanced available for analysis. The
of gadopentetate
through
by Type
is
in brain signal As an alterna-
(susceptibility-
pulse
Onset
of Ischemia
between
ac-
in as little as I second. Enhancewith gadopentetate dimeglumine
quired ment
tive,
contrast-enhanced
performed.
for
ob-
a maxi-
algorithm.
dynamic
imaging
were
by using
projection
MRA,
imaging agent.
images
partitions
Age
No.
or unen-
omitted
because
Findings Interval
imaging,
SE imaging
onset.
of Cases
Summary
intensity passage
of
by signal
in-
during
passage; appropriate thresholding scaling factors were used. In division ages, regions of large signal change
January
its and im(lange
1992
blood volume) nal intensity, signal
appear whereas
change
as areas regions
appear
of high sigwith little of low sig-
as areas
nal intensity.
the
Dynamic
MR
positive sion
findings
if, on images,
focal
increase
ment
was
tissue
either
were the
area
an
seen
to surrounding to the
din-
ical deficit. Region-of-interest (ROI) measurements of signal intensity, usually including at least 25 pixels, were performed in the area
of the stroke (as determined with T2weighted images). The ROIs were over cerebrocortical gray matter in the cases of cortical infarcts and over mixed gray and matter
in thalamic
infarcts.
Care
was
the
over
large
ROl
and
taken
brain
stem
to avoid
vessels
placing
or areas
of hem-
omnhage; when static gadolinium-enhanced Ti-weighted images were available, these were used to avoid placing an
ROl over areas
of breakdown
of the
blood-brain barrier (BBB). The ROI for a control region of presumably normal brain tissue was placed over a matching contralateral area, except for case 33, an extensive
bilateral
control
pontine
infarct,
was
unaffected
region
periphery
of the
estimated
to be the
2.8
infarct.
seconds-the
in which
Transit
time
the
tissue
duration
of each
image)
the
time
to peak
for
the
ues of the dimeglumine
first
control
re-
pass of gadopentetate in the first seven images
ten appearance proximately
i9.6
images many
chosen because images were
at least analyzed
The
fR2*dt
each
were enhanced
patient.
viously
has
of contrast seconds.
been
blood
tissue
Analysis
(ii).
parameter shown
to cerebral
areas
subject paired
of brain
were t tests.
to be
volume
images
the
fashion. lesion
tissue
within
performed
with
eral
days,
Volume
182
#{149} Number
of their 21) had
new
evidence
dysfunction. complete
of gb-
Of resolution
deficits and three (cases 13, 15, mild persistent deficits and of small ( < 1 cm in diame-
evidence ten) lesions that low-up imaging icit. Two patients
corresponded to their lasting (cases
symptomatic
8 and
ischemia
at fobdef19) had
in an area
of old infarction: The patient in case 8 had a transient ischemic attack, while the one in case 19 had extension of an old infarct. Ti-weighted gadoliniumenhanced images and follow-up imhelped
signal
to differentiate
and
chronic
intensity
less
acute,
infarcts.
abnormality
images
extensive
The on
appeared
in patients
T2-
lower
and
studied
within the first 24 hours than in those studied later. For example, in cases 3 and 4 (Fig 1), the area of abnormality on T2-weighted images (at 5 and 6 hours, respectively) appeared as a subtler increase in T2 signal intensity relative to surrounding tissue than that on images obtained at later times (eg,
case
MR
Angiograms
34) (Fig
2).
that in
pre-
proportional
brain was
angiograms were of satisfactory in 32 of 34 subjects. Patient motion degraded image quality so severely in two cases (cases 5 and 24) that the data were unusable. In the remainder, major branches of the cir-
per-
Statistical and nor-
the same two-tailed
cle
of Willis
smaller
were
always
branches
as well. Figure MR angiogram women with
ness
in her
Arterial
within
complete
clinical
were
shown
usually
3 illustrates in case ii, a presumed
and
shown
a normal that of a small car-
diogenic embolus from an infected valve to a distal branch of the anterior division of the right middle cerebral artery, which caused a slight weak-
In 24 of the 34 cases, the farct corresponding to the icit at the time of study was on T2-weighted SE images. one of the 10 patients with had,
initial
quality
Images
SE studies
nerve coro-
MR
apseven
RESULTS Spin-Echo
facial during
af-
in healthy
of all
formed in a nonblinded comparisons between
mal
material, The first
21) had
weighted
gion. The T2* rate change (J*) was computed as -ln (S,/S,)/TE, where ln = natural log, S, = precontrast signal intensity, and S = signal intensity at time t,. The area under the curve for R2* (fR2*dt) was computed as the sum of the zR2* val-
ipsilateral occurred
bal hemispheric these, three had
subacute, of
a one-and-a-half
artery atherectomy. That lesion have been missed owing to secsampling. Of the nine patients resolving deficits and negative SE images, six (cases 5-7, 13, 15,
ages
from the pnecontrast image to the peak reduction in signal intensity (maximal enhancement). The difference in time to peak signal reduction was computed by subtracting the time to peak for the lesion minus
nary may tion with initial
was
(in increments
caused
which
at the
time
that
and
palsy,
in enhance-
corresponding
pons
syndrome
or divi-
of unambiguous
relative
area
considered
original
or decrease
in an
white
resolution of their deficits. The patient in case 29 had a persistent deficit from a presumptive small embolic lesion in
hours
or near 1
area of inclinical defidentified All but negative or sev-
complete
ses
that
left
upper
occlusions corresponded
manifestations
were
the basilar artery in three patients, stem of the middle cerebral artery two and one
case
middle portion was identified i, that
pontine
infarct
Dynamic
stud-
suggestive
a
of oc-
Contrast-enhanced
Studies In all 16 cases
of acute
lesions
seen
at MRA, qualitative evidence of a besion was seen by inspecting the images of the dynamic study. Fifteen lesions displayed decreased enhancement, and one (case 27) showed increased enhancement in a thabamic infarct with stenosis of the posterior cerebral artery. Analysis revealed significantly bower fiR2*dt in the lesion relative
to the
control
tissue.
For
all 16
cases, mean fR2*dt (± standard error of the mean [SEM]) was 0.021 ± 0.006 for the lesion and 0.039 ± 0.006 for control regions, with a mean difference of 0.0i8 ± 0.004; paired t (df15) = 4.12 (P < .001). For the 12 cases of cerebrocorticab infarcts, the gray matter mean fR2*dt ± SEM was 0.023 ± 0.008 for the lesion and 0.041 ± 0.008 for control regions, with a mean difference of 0.018 ± 0.005; paired t (df1) = 3.81 (P = .003). The mean time to drop in peak signal intensity was 12.95 seconds ± 0.80 for control regions and 16.98 seconds ± 1.43 in the area of the lesion. Thus, the mean time to peak signal intensity reduction was delayed in the besion by 4.03 seconds ± 1.45; paired t (df15) = 2.79 (P = .014). In the gray matter of the 12 cases of cerebrocorticab infarcts, the mean time to peak
signal reduction was delayed lesion by 4.67 ± 1.67 seconds, t (df11)= 2.80 (P = .017). mean
to the
ischemic
the
identified
with
ond
entire
as early symptoms. internal
of the
the
intensity sample
period
the nal sity
4a illustrates
signal
MRA in 17 cases. Acute lesions were identified at MRA in 16 of these cases as 5 hours after the onset of These lesions affected the carotid artery in six patients,
man
the onset of sudden With SE imaging,
clusion of the perforating branches of the basilar artery was identified. Conventional angiography confirmed the presence of stenosis of unclear cause in the middle of the basilar artery, which had also been seen at angiography iO years earlier.
Figure
steno-
of the basilar with MRA in
of a 28-year-old
ied 2 hours after right hemiparesis.
extremity.
or severe
and the branch in four patients, the posterior cerebral artery in patient. In addition, focal stenosis
in the artery
left
the in
peak
over
duction
reduction
in signal
the
curve
the
of statistical
and
paired
versus
area of the lesion, intensity is greater, is less,
in the
of
time
for
i9.6-sec-
analysis.
For
the overall sigthe magnitude
in signal time
intensity
to peak
intenre-
is delayed. Radiology
#{149} 43
0
10
20
30
SEcONDS
e. Figure
1. Case
farction
in the
Figure subset
4b is the of patients
4. Six-hour-old infarct in the left middle-cerebral-artery distribution. (a) T2-weighted image shows subtle changes of early inleft temporal and panietal lobes. (b) MR angiogram demonstrates occlusion of the Ml segment of the left middle cerebral artery. (c) Calculated dynamic enhanced image demonstrates the area of blood volume decrease more clearly and more extensively than do the SE images. (d) Static enhanced Ti-weighted image demonstrates vascular enhancement in branches of the left middle cerebral artery. (e) Experimental curve of signal intensity versus time after injection of contrast material for this patient.
data
were
same curve for that (n = 12) in whom
available
during
onds, by which time ymptotically approach trast levels. Because transit time through
28 sec-
curves asthe preconof the delayed the lesion, the
were
however, still The
reached mean
performed
the
on
difference
statistical difference
and the paired (P = .039). 44 #{149} Radiology
of MR
and Dynamic Studies
Angiograms
Contrast-enhanced
the
greater time the analysis is carried, the less will be the magnitude of difference in mean fR2*dt. If the anabysis
Comparison
that
subset,
would
have
significance: is 0.015 ± .006,
t (df11) = 2.35
Figures
1 and
2 illustrate
spondence of vascular blood volume defects.
the
corre-
lesions and Case 34 (Fig
is that of an 89-year-old atrial fibrillation who
woman was studied
2)
with 48
hours after the onset of a dense left hemiparesis and left-sided neglect attributed to a cardiogenic embolus.
The
MR studies
of the
right
MRA,
markedly
dynamic
showed
internal
an occlusion
carotid
reduced
enhancement
artery
and
delayed
throughout
at
the right hemisphere, and an infarct in the right frontal, panietab, and temporab lobes (Fig 2). The middle cerebrab, anterior cerebral, and anterior communicating arteries were absent from the right side (Fig 2b). Examination of individual partitions showed trace carotid flow that stopped in the supraclinoid portion of the carotid artery; this finding did not show up well on the processed angiogram. The fR2*dt value was 0.020 on the side of the occlusion and 0.055 on the nonmal side. Figure 1 illustrates an example in which the lesion is more easily appre-
January
1992
a.
b.
Figure age
2. Case
shows
artery.
large
with
of contrast
34.
cerebral
no
signal
infarct intensity
enhancement.
middle
cerebral
the
hemisphere.
left
Forty-eight-hour-old in in
There
artery.
right
The order
the the
frontal,
c.
hemispheric parietal,
circulation
is decreased
and
of the
blood
of the images
infarct temporal
right
volume
is from
due
internal
carotid
artery.
(c)
area
of the
stroke
the
the upper
of the
right
middle
(b) MR angiogram
lobes.
within
hancement branches tery. The
to occlusion
left down.
series
and
delayed
pattern
typical of acute infarcts of the middle cerebral ar-
versus time for this patient in Figure le. The contrast
between
the
normal
and
lesion
Figure
3. Case 11. Normal-result MR angiogram obtained in a 37-year-old woman with a presumed small embolus from an infected heart valve to a small distal branch of the right middle cerebral artery. The woman had normal results of a blood volume study.
The perfusion extensive than
in the large
is
tissue
images. branches
the
the left middle
Ml
segment
of the
left middle
ce-
rebral artery. Dynamic contrast-enhanced MR imaging (Figure ic) demonstrated a barge defect throughout the left middle cerebral arterial distribution. Figure id shows vascular enVolume
182
#{149} Number
1
of cases
were
normal
definite and/or
despite
lesion on T2-weighted
tient after
3,
temporal
of a
study The
4 hours aphasia
hemianopsia. in the left panietal
lobes
was
MRA demonstrated of the
presence
dynamic images.
in case 2 was studied the onset of a fluent
right homonomous evolving infarct
and
the
posterior
cerebral
seen
a 65-year-old
man
40 hours after demonstrated cerebral artery
in blood
to the
volume
infarct
seen
weighted images (fR2*dt on the side of the lesion
come-
on T2was 0.006
and
0.026
in
contralateral cortex). Case 32 was that of an 87-year-old woman with a presumed cardiogenic embobus to the anterior division of the left middle cerebral artery. When studied 42
hours after the the infarct was T2-weighted
were
onset of symptoms, well demonstrated
images.
normal,
Results
although
dynamic
enhanced
tatively in the
apparent lesion and
of
a defect images
(fR2*dt 0.051
on
MRA on
was
quali-
was 0.044 in contralateral
cortex). The other cases involving a lesion seen on T2-weighted images
pa-
but normal findings lesions smaller than
Some
cases
and
lesions
less
An
however,
at MRA were of 2 cm in diameter.
(eg, cases
25, 26, 28, 30) of
than
in diameter,
may
2 cm
be associated
with
MRA lesions.
on SE
patent division
artery,
right
throughout
atrial fibrillation and infarction in the right and thabamus; the pre-
a decrease
sponding
16, and 20. Routine computed tomography (CT) in this patient was normal 2 hours after the onset of the stroke but showed an acute infarct in the left middle cerebral arterial distribution at 24 hours. Follow-up MR studies were unobtainable. In seven patients, MRA findings
ciated on the dynamic contrast-enhanced images than on spin-echo images. The patient (case 4) was a 72year-old woman who presented with sudden onset of a dense right hemiparesis, right visual field neglect, and nightwand neglect. T2-weighted images (Fig la) showed early changes of an evolving infarct in the left frontal, panietal, and temporal lobes. MRA (Fig ib) demonstrated an occlusion of
31 involved
patterns
of the
time
bral artery. MR study the onset of symptoms a patent right posterior
but
defect apthe area of
infarcts
shows
branches
over
carotid
sumed mechanism was a cardiogenic embobus to the right posterior cere-
abnormality on T2-weighted images. This more apparent and extensive change by perfusion imaging was also
found
images
distal
is seen
Case
SE im-
of the internal
division
of the
with new-onset a hemorrhagic occipital lobe
is greater on the dynamic enhanced images than on the SE images, rendening the lesion more apparent on
the former. pears more
of six
filling
in
(a) T2-weighted
occlusion
of enhancement
fR2*dt value was 0.052 in the normal parietab lobe versus 0.000 in the lesion. The experimental curve of signal intensity illustrated
artery.
demonstrates
Sequential
A normal
cerebral
In no
case
was
a lesion
MRA or dynamic of
the
vessel presumed to be involved. The blood volume study appeared bilaterably symmetric (the fR2*dt value was 0.024 in the lesion and 0.026 in contralaterab cortex).
when images. studied which
weighted
a lesion
found
enhanced
was
not
found
The patient in case 2 hours after stroke time subtle increases
images
finding confirmed ous appearance
were
at
imaging
on SE 1 was onset, by on T2-
present,
a
by the unambiguof the infarct on folRa1”1””
S
L1
bow-up hours.
clinical section
SE images obtained at 46 It is unfortunate that incorrect localization bed to incorrect selection for dynamic en-
hanced
imaging
dynamic was not
120
at 2 hours
and
that
through
the
infarct
imaging performed.
I-
0
z
110 0)
z
LU
z
DISCUSSION
z
Arterial occlusions in areas of a large acute stroke were demonstrated at MRA. In addition, we found good qualitative and quantitative comrelalion between MRA occlusions in acute cerebral ischemia and both blood volume decreases and transit time delays at dynamic MR imaging. Both of these techniques allowed identification of lesions that matched the abnormality and clinical deficit seen at T2weighted imaging. A blood volume defect or delay in peak signal reduc-
tion may therefore dence of a vascular fR2*dt for normal this
sample
agrees
well
be taken as evilesion. The mean gray matter in
of stroke
patients
with
previously
the
ported mean value a sample of healthy
studied
with
the
identical
thus demonstrating the technique across
100
z
0
0)
(0
r-
0
method
10
20
30
SECONDS
SECONDS
b.
Figure
4.
through
(a) Experimental
the period
signal
intensity
curve
of mean
of quantitative
versus
within
time
the
contrast
for the
stroke,
with
enhancement
dy-
tunity to image such an early lesion, is likely that the dynamic contrast-
study
it. This
would
hypothesis
the
with
show
showing
photon
emission
a match
CT,
of hypo-
and
hyper-
perfusion in 34 of 35 cases. The two cases of mismatch between MRA and blood volume testing (ie, unambiguous lesions at blood volume
testing
without
at MRA) cardiogenic
than
detectable cases
were
two
embolus
40 hours
occlusions of presumed
studied
after
stroke
Thus,
the embobus may have broken up by the time of the study. This hypothesis is supported by repeated MRA and blood volume studies, performed
days that may
later in a subset of these show that blood volume persist after a vessel has
recanalized M, Edelman
subjects, defects become
(Warach 5, Li W, Ronthab RR, unpublished data,
images
onset
thus,
the
siveby
earliest
infarcts
area
of infarct
more
extensive
hanced Whether
in stroke,
of acute
creases, 46
particularly
Radiology
#{149}
would and
be expected distal de-
decreased
blood
as 2 hours
of patients;
of infarction
MRA
imaging the first
im-
information and to show occlusions
to
on static
sample and
excbu-
dynamic-en-
may be possible few hours. Among
(eg, was
case more
on the
images than the greater
only our
4; Fig 1), the apparent
dynamic
question
becomes
considering
important
therapeutic since
stroke
large
vessel
occlusion
cardiogenic
studies
embolus
and
hemorrhage
is restored pressure arterial
of the embolus.
wall
following
the
Altemna-
of meningeal
eral vessels perfusing to the occlusion has
mod-
after
at normal or to a previously
ischemic
opening
animal
occurs
breakup
as a cause tion (21). dynamic
is a of our
of hemorrhage within the either initially or on follow-up It has been suggested from
blood flow high blood
tively,
of
infarctions (21). Five
cobbat-
the artery distal been suggested
of hemorrhagic The techniques contrast-enhanced
transformaof MRA and blood
volume imaging have the potential to allow study of such questions directly in vivo with repeated studies and use of pmesaturation pulses to examine collateral circulation (5).
per-
within the vessel and breakdown of the BBB, can be seen after administration of gadopentetate dimeglumine
in
intervention
successful
with
characteristransformations
On images, caused
abnormality in the first hours after an arterial occlusion reflects an ischemic penumbra of potentially salvageable tissue at risk is unknown. This
infarct,
of mean
for 28 seconds.
and
en-
on SE images. extent of the
areas
els that
failure
as early
detection
with
hanced within
MRA
T2-weighted
imaging and hemodynamic
in our
with
postmortem
(15).
after
mality
on
but
lesion
curve
available
presumed
images.
After ictus, the earliest reported onset of visible changes on T2-weighted images varies from 30 minutes to hours (16-20). The changes tend to increase in the first 24 hours. We have seen increased signal intensity on T2-
fusion
is evident
imaging,
hyperacute
SE images
1991). The studies of Mosebey et ab (13,14) have demonstrated perfusion deficits within minutes after experimental occlusion of the middle cerebral amtery in cats at times when no abnorages. Dynamic MR can directly provide
MR
the
weighted
more
onset.
enhanced
were
pathophysiobogic
patients had
by
for all 16 patients
of hemorrhagic
from
results of animal studies that show immediate detection of blood volume abnormalities with dynamic contrast-
time
cardiogenic embolic matter of controversy it
of subjects. This technique as applied to stroke has also been reported by Bock et ab (i2) to be correlated with the results of blood flow evaluation single
tics
demonstrate
is supported
data
The
immedi-
(6),
versus
(b) Experimental
in whom
ictus in humans as webb. we have not had the oppor-
enhanced
intensity
(19.6 seconds).
12 patients
in
the reliability of different samples
signal
analysis
ately after Although
matter (0.036)
BRAIN
a.
namic
me-
LESION
90
volume
(0.041)
for gray subjects
z
treatment
thrombolytic
therapy such as tissue pbasminogen activator likely should be initiated as early as possible (eg, within the first few hours after the neurobogic event).
(22,23).
conventional Ti-weighted SE some enhancement of strokes, by pooling of contrast material
Static
Ti-weighted
SE images
can be helpful in subacute strokes, but in acute strokes, only indirect signs are present, such as pooling of gadopentetate dimeglumine within a yessel that
is occluded.
Gadopentetate
dimeglumine is not an ideal blood volume agent, since it is distributed into both the intravascular and interstitiab
the
compartments.
BBB and
interstitial
Breakdown
leakage January
of
in 1992
subacute
strokes
are
reasons
for
en-
hancement of gray and white matter on static Ti-weighted SE images. The patterns of contrast enhancement on dynamic T2*weighted images are different from those on static Ti-weighted images in that they show a predominantly cortical enhancement. The pattern on dynamic T2*weighted images likely represents increased cortical blood volume. The T2*weighted images seem to be insensitive to gradual leakage of contrast agent into the interstitium, presumabby because a high concentration of gadopentetate dimeglumine is needed to cause a distortion in magnetic susceptibility and, thereby, a decrease in signal intensity. Indeed, Ti effects on the dynamic T2* weighted images were negligible. The proportional relationship of R2* to tissue
however,
concentration,
may
be altered by breakdown in the BBB, since this relationship is dependent on the contrast agent being completely intravascular. Therefore, areas of BBB breakdown cannot be quantitatively compared with areas of intact
BBB. We
tried
to avoid
this
problem
by avoiding ROI placement over areas of BBB breakdown. MRA was able to show major vascuban occlusions acutely in 16 subjects, but failed to show small branch occlusions even when both dynamic and T2-weighted images showed a lesion. This failure is likely an effect of limited spatial resolution. Further improvements in the angiographic techniques, such as half-Fourier transform to reconstruct full echoes from asymmetrically sampled echoes and small integrated gradient and madio-frequency coils with increased peak gradient amplitudes, may help to overcome this problem. Finally, significant drawbacks of the dynamic imaging technique must be mentioned. First, the magnetic field distortion produced by the bolus of gadopentetate dimeglumine extends over several millimeters, resulting in a potentially confusing decrease in the signal intensity of cerebrospinal fluid within the ventricles and over the cerebral convexities. Second, only a single section can be imaged with high temporal resolution. This limitation can bead, as in our case 1, to incorrect section selection because of failure to immediately recognize
Volume
182
#{149} Number
I
early, images
subtle and
ization. such
changes erroneous
Newer
imaging
as echo-planar
imaging,
the
entire
brain
though
10.
will overbe needed in an
correlation
will
Patient motion tients was not dynamic studies data acquisition,
poorer
because but did
quality
SE images
of the fast result in
in some
13.
and
cases.
we have
demon-
strated that in acute stroke, distinctive patterns of signal intensity change can be shown with a dynamic con-
trast-enhanced and major tectabbe
with
MR imaging occlusions
vessel
MRA.
14.
method, are de-
Functional
infor-
15.
mation about the microcircubation is provided that is not available with conventional static MR imaging. Additional studies are needed to determine the potential prognostic value of 16.
dynamic imaging and MR angiography in acute stroke and to determine
their value in planning early therapeutic intervention, such as thrombolytic
therapy.
17.
#{149}
18.
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R21Iin1i-,
#{149} “7