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.

References 1.

2.

Brant-Zawadzki M, Weinstein P, Bartowski H, Moseley M. MR imaging and spectroscopy in clinical and experimental cerebral ischemia: a review. AJNR 1987; 8:39-48.

Laub GA, Kaiser with gradient Tomogr 1988;

3.

4.

5.

6.

7.

8.

Masaryk

WA.

rephasing. 12:377-382.

TJ, Modic

In-

tracranial circulation: preliminary clinical results with three-dimensional (volume) MR angiography. Radiology 1989; 171:793799. Mattle HP, Wentz KU, Edelman RR, et al. Cerebral venography with MR. Radiology 1991; 178:453-458.

Edelman

RR, Mattle

HP, O’Reilly

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LR, Melski

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Wentz KU, Liu C, Zhao B. Magnetic resonance imaging of flow dynamics in the cirdc of Willis. Stroke 1990; 21:56-65. Edelman RR, Mattle HP, Atkinson DJ, et al. Cerebral blood flow: assessment with dynamic contrast-enhanced T2*weighted MR imaging at 1.5 T. Radiology 1990; 176: 211-220. Rosen BR, Belliveau JW, Chien D. Perfusion imaging by nuclear magnetic resonance. Magn Reson Q 1989; 5:263-281.

MohrJP,

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MR angiography J Comput Assist

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diseases JW, et al. chelates

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pafor

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11.

be essential.

in acute stroke a major problem

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Classification of cerebrovascular III. Stroke 1990; 21:637-676. Villringer A, Rosen RB, Belliveau Dynamic imaging with lanthanide

in normal

to

efficient

manner (24). Last, further work is needed to allow quantification of blood volumes and flow with MR imaging, and positron emission tomography

National

Communicative

techniques

not yet widely available, come this limitation and screen

9.

on T2-weighted clinical local-

23.

24.

BockJC, Sander B, HierholzerJ, et al. Regional cerebral blood flow by gadoliniumDTPA bolus tracking. In: Book of abstracts: Society of Magnetic Resonance in Medicine 1991. Berkeley, Calif: Society of Magnetic Resonance in Medicine, 1991; 117. Moseley ME, Mintorovitch J, Cohen Y, et al. Early detection of ischemic injury: comparison of spectroscopy, diffusion-, T2-, and magnetic susceptibility-weighted MRI in cats. Acta Neurochir Suppl (Wien) 1990; 51:207-209. Moseley ME, KucharczykJ, Mintorovitch J, et al. Diffusion-weighted MR imaging of acute stroke: correlation with T2-weighted and magnetic susceptibility-enhanced MR imaging in cats. AJNR 1990; 11:423-429. White DL, Wendland MF, Aicher KP, Tzika AA, Moseley ME. Susceptibility-enhanced echo-planar MRI: detection of regional ccrebral ischemia in rat brain. In: Book of abstracts: Society of Magnetic Resonance in Medicine. Berkeley, Calif: Society of Magnetic Resonance in Medicine, 1990; 57. Brant-Zawadzki M, Pereira B, Weinstein P, et al. MR imaging of acute experimental ischemia in cats. AJNR 1986; 7:7-11. Mano I, Levy RM, Crooks LE, Hosobuchi Y. Proton nuclear magnetic resonance imaging of acute experimental cerebral ischemia. Invest Radiol 1983; 17:345-351. Buonanno FS, Pykett IL, Brady TJ et al. Proton NMR imaging in experimental cerebral ischemic infarction. Stroke 1983; 14: 178-184. Levy RM, Mano I, Brito A, et al. NMR imaging of acute experimental cerebral ischemia: time course and pharmacologic manipulations. AJNR 1983; 4:238. Sipponen J, Kaste M, Ketonen L, et al. Serial nuclear magnetic resonance (NMR)

imaging in patients with cerebral infarction. J Comput Assist Tomogr 1983; 7:585. Ogata J, Yutani C, Imakita M, et al. Hemonrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke. Stroke 1989; 20:876-883. McNamara MT. Brant-Zawadzki MB, Berry I, et al. Acute experimental cerebral ischemia: MR enhancement using Gd-DTPA. Radiology 1986; 158:701-705. Elster AD, Moody DM. Early cerebral infarction: gadopentetate dimeglumine enhancement. Radiology 1990; 177:627-632.

LeBihan

D, Turner

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Comparison of two approaches to real-time brain perfusion MR imaging: IVIM-EPI and magnetic susceptibility induced contrast enhanced EPI. In: Book of abstracts: Society of Magnetic Resonance in Medicine 1990. Berkeley, Calif: Society of Magnetic Resonance in Medicine, 1990; 317.

R21Iin1i-,

#{149} “7

Acute cerebral ischemia: evaluation with dynamic contrast-enhanced MR imaging and MR angiography.

Dynamic contrast-enhanced T2-weighted magnetic resonance (MR) imaging and MR angiography (MRA) were used to evaluate cerebral blood volume and the int...
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