(Stroke. 2000;31:1318.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the Departments of Neuroradiology (P.D.S., O.J., J.B.F., S.H., O.P., H.R., K.S.) and Neurology (P.D.S., T.S., S.S., W.H.), University of Heidelberg Medical School, Heidelberg, Germany.
Correspondence to Peter D. Schellinger, MD, Neurologische Universitaetsklinik, Im Neuenheimer Feld 400, D 69120 Heidelberg, Germany. E-mail Peter_Schellinger{at}med.uni-heidelberg.de
| Abstract |
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MethodsStroke MRI (diffusion- and perfusion-weighted imaging [DWI and PWI, respectively], magnetic resonance angiography, and T2-weighted imaging) was performed before, during, or after thrombolysis and on days 2 and 5. We assessed clinical scores (National Institutes of Health Stroke Scale [NIHSS], Scandinavian Stroke Scale [SSS], Barthel Index, and Rankin scale) at days 1, 2, 5, 30, and 90. Furthermore, we performed volumetric analysis of infarct volumes on days 1, 2, and 5 as shown in PWI, DWI, and T2-weighted imaging.
ResultsTwenty-four patients received rtPA within a mean time interval after symptom onset of 3.27 hours and stroke MRI of 3.43 hours. Vessel occlusion was present in 20 of 24 patients; 11 vessels recanalized (group 1), and 9 did not (group 2). The baseline PWI lesion volume was significantly larger (P=0.008) than outcome lesion size in group 1, whereas baseline DWI lesion volume was significantly smaller (P=0.008) than final infarct size in group 2. Intergroup outcome differed significantly for all scores at days 30 and 90 (all P<0.01). Intragroup differences were significant in group 1 for change in SSS and NIHSS between day 1 and day 30 (P=0.003) and for SSS only between day 1 and day 90 (P=0.004).
ConclusionsStroke MRI provides comprehensive prognostically relevant information regarding the brain in hyperacute stroke. Stroke MRI may be used as a single imaging tool in acute stroke to identify and monitor candidates for thrombolysis. It is proposed that stroke MRI is safe, reliable, and cost effective; however, our data do not prove this assumption. Early recanalization achieved by thrombolysis can save tissue at risk if present and may result in significantly smaller infarcts and a significantly better outcome.
Key Words: magnetic resonance imaging, diffusion-weighted magnetic resonance imaging, perfusion-weighted recanalization thrombolysis
| Introduction |
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However, the need remains for a stroke imaging tool that is fast, has a sufficiently high sensitivity for detecting both intracerebral hemorrhage (ICH) and ischemia within the first 6 hours, can identify the tissue at risk if present, and shows occlusion of major arteries at the base of the brain. The advent of new MRI techniques such as perfusion- and diffusion-weighted imaging (PWI and DWI, respectively) has revolutionized diagnostic imaging in stroke.5 6 7 8 9 10 11 12 It is presumed that the difference (mismatch) between abnormal areas on DWI and PWI (with PWI>DWI) represents the ischemic tissue at risk, which is potentially salvageable.8 11 13 Several investigators have found a significant correlation of DWI and PWI changes with follow-up T2-weighted imaging (T2WI) changes as well as with neurological outcome as assessed by the National Institutes of Health Stroke Scale (NIHSS) and the Barthel Index (BI).5 6 7 8 11 14 These authors conclude that different infarct patterns can be identified by means of DWI and PWI in hyperacute stroke, which may allow a more rational selection of therapeutic strategies based on the presence or absence of tissue at risk. However, all these studies suffer from a small number of patients investigated in the relevant time window for therapeutic intervention, absence of a sufficiently standardized stroke MRI protocol, and lack of patients treated with rtPA, with the exception of one study, which reports 6 rtPA patients in whom stroke MRI was performed 2.66 hours, on average, after thrombolytic therapy.15 The purpose of the present study was to assess the feasibility of stroke MRI in the initial evaluation and follow-up monitoring of patients with hyperacute ischemic stroke who received intravenous thrombolytic therapy.
| Subjects and Methods |
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Imaging and Clinical Assessment
All patients were examined with a state-of-the-art CT scanner
(PQ 2000, Picker) and immediately thereafter with a 1.5-T whole-body MR
imager (EDGE, Picker) equipped with enhanced gradient hardware for echo
planar imaging (EPI). For the MRI examination, we used a circular
polarized head coil. We performed stroke MRI on days 1 (initial scan),
2, and 5 (day 5 without PWI). The stroke MRI protocol included an axial
T2-weighted fast spin echo sequence, an axial fluidattenuated
inversion recovery EPI sequence, an axial isotropic DWI spin echo EPI
sequence (b=0, 333, 666, and 1000
s/mm2), time-of-flight magnetic resonance
angiography (MRA), and PWI with an axial T2-weighted gradient echo EPI
sequence (40 data sets during and after injection of 25 mL Gd-DTPA
[Magnevist, Schering AG] with a power injector [5 mL/s]). Mean
transit time (MTT) is defined as the quotient of cerebral blood volume
divided by cerebral blood flow (CBF). Perfusion maps were calculated
from the concentration time curves as the normalized first moment of
the concentration time curve, ie, the time that divides the area
under the concentration curve (relative cerebral blood volume)
into 2 equal parts (relative MTT or time to
midpoint).16 Quantitative CBF
measurement17 was not performed because of the requirement
of extensive postprocessing and thus nonavailability for bedside use.
Because quantitative CBF measurements and thus MTT were not available,
we chose the unspecific term "perfusion map" instead of MTT map.
The complete stroke MRI protocol takes 15 minutes, and an additional 5
to 10 minutes are necessary for patient positioning and transfer.
Postprocessing of the MRIs was performed by using commercial image
analysis software and a workstation (Picker VISTAR). All
neuroimaging studies were cross-read by staff neuroradiologists.
Infarct volumes were measured in a semiautomatic fashion: We outlined
manually the lesion volume, multiplied it by the slice thickness, and
added up the slice volumes. To define the initial infarct volume, we
used the images acquired with the strong DWI sequence
(b=1000 s/mm2). The location and size
of the tissue at risk were determined on the basis of perfusion maps
generated from PWI, whereas the final infarct volume was determined on
day 5 according to T2WI. We defined a volume ratio of PWI/DWI >1.2
(ie, the PWI lesion being at least 20% larger than the DWI lesion) as
a relevant perfusion-diffusion mismatch that indicated the presence of
tissue at risk. Furthermore, we calculated the difference between PWI
and DWI volumes as an absolute measure of tissue at risk. Initial and
follow-up vessel status were assessed by MRA, with MRA on day 2 used to
evaluate persisting arterial occlusion or
recanalization. Group assignment was retrospective.
Patients with vessel occlusion that was subsequently recanalized were
arbitrarily assigned to group 1, and those with no subsequent
recanalization were assigned to group 2. Those
patients who had no anterior territory stroke (patient 24, posterior
cerebral artery occlusion) or no vessel occlusion at all were assigned
to group 3. We assessed clinical data at days 1, 2, 5, 30, and 90 by
use of NIHSS,3 SSS,18 BI,19
and MRS.20 We defined a favorable outcome as NIHSS
2,
SSS
54, BI
95, and MRS
1. All clinical scores were obtained by a
senior neurology resident or a stroke fellow, who were video-trained
and certified for application of the NIHSS.21
Statistical Analysis
For statistical analysis, we used a standard software
package (StatView 4.5, Abacus Concepts). Demographic data, time
intervals of examinations and onset of rtPA infusion, and descriptive
statistics of scores are given as mean or median values with SD and
range. Spearman rank correlation was used to determine the correlation
between lesion volumes and neurological scores. Because our data are
not normally distributed, we used nonparametric tests
(Mann-Whitney U test and Wilcoxon signed rank test)
to determine whether there were significant differences between initial
and follow-up lesion volumes, scores, and interindividual differences
in morphological and functional outcome between those patients with
successful recanalization of the occluded vessel
(group 1) versus those without recanalization
(group 2). The group differences regarding the localization of vessel
occlusion was assessed by a Fisher exact test.
| Results |
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Seven patients each presented with either a proximal or a
distal MCA main stem occlusion, 4 had an MCA branch occlusion, and 2
had a distal internal carotid artery (ICA) occlusion according to the
initial MRA. All but 1 of these 20 patients had an abnormal initial DWI
scan and a perfusion-diffusion mismatch (ie, tissue at risk, PWI/DWI
>1.2) of >20% (mean 8.07%, range 0.81% to 29.9%). In the 1
patient with an initial proximal MCA occlusion but without PWI/DWI
mismatch (patient No. 11) the occluded vessel recanalized during the
MRI examination between MRA and PWI, as shown by Doppler ultrasound
immediately after MRI. He had a good outcome, with only a minimum
facial weakness left at day 90 (NIHSS 1, SSS 56, BI 100, and MRS 1). In
11 (55%) of 20 patients, vessels recanalized after rtPA according to
follow-up MRA on day 2. We thus divided the 20 patients into 2 groups:
group 1 (n=11) consisted of the patients with
recanalization (Figure 1
), and group 2 (n=9) consisted of those
without recanalization (Figure 2
). The mean time interval for delivery
of rtPA was greater in group 2 than in group 1 (3.72±1.13 hours and
2.76±1.48 hours, respectively), although this difference did not reach
statistical significance (P=0.13, Mann-Whitney U
test). The initial clinical deficit was higher in group 2 (median NIHSS
15 versus 10 in group 1, median SSS 19 versus 28 in group 1), which was
not due to a higher proportion of left hemispheric infarctions and thus
worse disability scores in group 2 versus 1 (7 and 4 versus 6 and 3),
and did not reach statistical significance (P=0.11 for NIHSS
on day 1 and P=0.063 for SSS on day 1, Mann-Whitney
U test). Also, there was no difference between groups 1 and
2 regarding the proportion of proximal (ICA and proximal MCA mainstem)
and distal (distal MCA main stem and branches) occlusions
(P=0.65, Fisher exact test). There was a considerable
difference in the mean values of mismatch (PWI/DWI) between group 1
(26.27) and group 2 (8.13); however, the median values were fairly
similar (3.65 versus 4.73), and neither the difference of PWI/DWI nor
of PWI-DWI between groups 1 and 2 was statistically significant
(P=0.97 and P=0.305, Mann-Whitney U
test). Also, baseline DWI and PWI lesion volumes did not differ between
groups 1 and 2 (P=0.102 and P=0.23 by
Mann-Whitney U test).
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Two patients (Nos. 15 and 17) experienced a symptomatic
secondary hemorrhage after treatment with rtPA, which was
identified on day-2 stroke MRI. One late death occurred in each group
between days 30 and 90, 1 because of pulmonary embolism
(patient 4) and the other due to cardiopulmonary failure
(patient 15). See Table 1
for
demographic data, time windows, and day-1, day-30, and day-90 scores.
See Table 2
for baseline and outcome
lesion sizes, mismatch ratio, and PWI-DWI volume difference.
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Analysis of Intragroup and Intergroup Outcome
All neurological scores and outcome scales differed significantly
between groups 1 and 2 on day 30 (NIHSS, SSS, BI, and MRS,
P
0.004; Mann-Whitney U test). There was a
slight decrease in statistical significance between groups 1 and 2 on
day 90 (NIHSS, SSS, BI, and MRS, P
0.008; Mann-Whitney
U test). Within group 2, SSS and NIHSS from day 1 and day 30
or 90 did not differ significantly. In group 1, however, there was a
significant difference between the neurological scores on day 1 and day
30 (SSS and NIHSS, P=0.003). The difference between NIHSS on
day 1 and day 90 barely missed statistical significance
(P=0.0505) because of the 1 deceased patient with a formal
NIHSS of 42 points (death is not coded in the NIHSS). The difference
between day-1 and day-90 SSS was still highly significant
(P=0.004).
Correlation and Difference of Initial and Follow-Up Infarct
Volumes
The day-1 PWI lesion volumes of either group did not correlate
with day-2 lesion volumes on DWI or with day-5 lesion volumes on T2WI
(all r<0.6, all P=NS; Spearman). Day-1 DWI
volumes and day-2 DWI volumes did not correlate at all in group 2,
whereas lesion volumes on day 1 (DWI) and day 5 (T2WI) were
significantly different (P=0.008, Wilcoxon), with
day-5 T2WI always being larger. In group 1, DWI volumes on days 1 and 2
correlated significantly (r=0.697, P=0.037;
Spearman). There also were significant correlations for DWI on day 2
(P=0.0038, r=0.964) and PWI on day 2
(P=0.045, r=0.708) with T2WI on day 5 in group 1
but not in group 2. Day-1 PWI and day-5 T2WI volumes differed
significantly in group 1 (P=0.008, Wilcoxon);
however, day-1 DWI and day-5 T2WI volumes did not (P=0.155,
Wilcoxon). There was no relationship between lesion size and
recanalization.
Correlation and Difference of Absolute Infarct Volumes With
Outcome
In group 2, lesion volumes on days 1, 2, and 5 did not correlate
with any outcome score, nor did the day-1 DWI lesions in group 1.
However, DWI volume on day 2 and even more T2WI volume on day 5
correlated in group 1 with all outcome scales except the BI (day-2
DWI/NIHSS, P<0.01 and r=0.88; day-5
T2WI/NIHSS, P=0.006 and r=0.88; day-5 T2WI/SSS,
P<0.01 and r=0.68; and day-2 DWI and day-5
T2WI/MRS, P<0.05 and r=0.71). There was neither
a correlation between PWI lesion on any day with any score in any group
nor a correlation of mismatch ratio or absolute mismatch volume and any
outcome score in any group. See Table 3
for summary of group data and statistical analysis.
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| Discussion |
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The need for an all-round diagnostic tool with which all the important pathophysiological aspects of hyperacute stroke can be investigated is evident. Such a method must answer 5 decisive questions: (1) Where and how large is the actual area of irreversible ischemic brain damage? (2) How old is the infarction? (3) Is there tissue at risk, and how much tissue is at risk? (4) Is there a vessel occlusion, and where is it? (5) Is there an intracerebral hemorrhage or another underlying nonischemic disease? Presently, the decision to initiate intravenous rtPA treatment is based on clinical findings and CT scanning. The reported diagnostic yield of CT within 3 hours after symptom onset is low (50% to 70%).1 7 24 25 DWI may delineate infarcted brain tissue in <1 hour after symptom onset, probably within minutes,26 although there is cumulating evidence that in the very early stage of stroke, there may be reversible DWI changes.27 PWI and DWI reveal the ischemic tissue potentially at risk.8 We would like to stress, however, that PWI renders only relative information regarding CBF and that the volumetric difference of DWI and PWI does not directly represent the penumbra, which is a more complex pathophysiological concept of the presence of a nonfunctional but potentially salvageable area of brain tissue.28 A PWI/DWI mismatch may, however, reflect the ischemic penumbra to a certain extent and therefore make it possible to pragmatically estimate the size of tissue at risk of irreversible infarction. MRA can reliably assess the cerebral vessel status.29 The utility of MRI to demonstrate hyperacute primary ICH is still a matter of controversial discussion. It has been shown that susceptibility-weighted images, such as the T2-weighted source images of PWI, allow a definitive diagnosis of ICH within the first hours of stroke.30 Although hyperacute subarachnoid hemorrhage is difficult to detect on MRI,31 certain sequences seem to be promising32 ; however, the clinical presentation of subarachnoid hemorrhage rarely mimics that of acute ischemic (or hemorrhagic) stroke. Stroke MRI as a single diagnostic tool provides critical data that have the potential to guide therapeutic decisions in hyperacute stroke patients.
Of course, a single-center study with 24 patients cannot provide meaningful statements as to cost-effectiveness. It seems reasonable, though, that by eliminating the need for CT and Doppler ultrasound in the initial evaluation of acute stroke patients, stroke MRI may indeed be more cost-effective. In all of our patients, the necessary information was available initially and at follow-up. The data are consistent with the pathophysiological understanding of vessel occlusion, the presence or absence of tissue at risk, and the morphological and clinical outcome, which ultimately depends on timely vessel recanalization or permanent occlusion. Stroke MRI cannot determine in which patients vessel occlusion will persist and in which patients vessel recanalization will occur (no imaging modality can answer this question at present), although recanalization rates tend to be lower with more proximal vessel occlusions (carotid T and proximal MCA), an observation also made in patients treated with intra-arterial thrombolysis.33 However, we speculate that stroke MRI can answer the critical questions of who may profit from recanalization, in whom recanalization should be achieved by all means, and in which patients there is no tissue at risk or no ischemic disease at all but only an excessive risk of hemorrhage due to thrombolytic therapy. The utility of stroke MRI, although not proven yet by analysis of predefined parameters in a prospective study, is likely to be the early identification of those patients in whom the outcome and final infarct size, ultimately the patients fate, have not yet been determined.
Presumably, the reason for any therapeutic effect of rtPA is
recanalization of the occluded artery. The true
recanalization rate of intravenous rtPA
in ischemic stroke is not known presently but is estimated
to be
50%. In addition, there may be a substantial number of early
spontaneous recanalizations. Older nonrandomized
studies with small numbers of patients report
recanalization rates of 25% to 50% for
intravenous thrombolysis33 34
but >90% when the agent is given
intra-arterially.35 An
intra-arterial thrombolysis study using
prourokinase randomized 180 patients and showed a
recanalization rate of 67%.25
However, the intravenous rtPA trials, including ECASS I and
II, NINDS, and Alteplase Thrombolysis for Acute
Noninterventional Therapy in Ischemic Stroke (ATLANTIS), did
not assess whether clinical improvement depended on initial vessel
occlusion with subsequent recanalization after
thrombolytic therapy or on the rate of spontaneous
vessel reopening. Our group of patients, in which a
recanalization rate of 55% was seen after
intravenous thrombolysis, is too small to
give a reliable estimate of the true recanalization
rate after intravenous thrombolysis.
Although the level of significance decreased for all outcome scales
from day 30 to day 90 because of 1 death after pulmonary
embolism in group 1, intergroup and intragroup comparisons demonstrate
a significant benefit of recanalization. Patients
without recanalization had a significant increase
in infarction size from day 1 to day 5 (P=0.008), and the
difference between lesion volumes in groups 1 and 2 was highly
significant on day 2 (P=0.015) and even more on day 5
(P=0.006). There also were significant correlations for DWI
on day 2 (P=0.0038 and r=0.964) and PWI on day 2
(P=0.045 and r=0.708) with T2WI on day 5 in group
1 but not in group 2, indicating further infarct dynamics and
progressive infarct growth even after 24 hours in patients with
persisting vessel occlusion.
Interestingly, the presence of tissue at risk and thus a potential for
infarct growth was bound to a vessel occlusion in all our patients.
This finding is consistent with the observation of other
authors involving a smaller group of patients.36 A larger
patient cohort, however, is needed to render sufficient evidence for
this observation. On rare occasions, a good collateral flow may result
in a good clinical outcome, despite persisting vessel occlusion (Figure 3
). Our findings strengthen the
hypothesis that early lysis of an obliterating thrombus by rtPA with
subsequent recanalization of a major cerebral
artery is the basis for an improved clinical outcome in many patients.
This event can be monitored effectively by stroke MRI. Furthermore,
baseline stroke MRI renders relevant information that may allow the
identification of ideal candidates for thrombolytic
therapy and also the identification of those patients who are not. On
the basis of stroke MRI criteria, we suggest that patients who are most
suitable for thrombolytic therapy are likely to be
those who present with a proximal vessel occlusion in the anterior
cerebral circulation and tissue at risk of infarction as defined by DWI
and PWI. Additionally, our data suggest that
recanalization should be achieved by aggressive
means in these patients, because a persisting vessel occlusion is
associated with large infarcts and an unfavorable clinical outcome.
|
The recently published study by Marks et al15 reports 12 patients with early stroke MRI within 3 hours to 5 hours. Six of their 12 patients received rtPA at 1.95 hours, on average, after stroke onset (range 51 minutes to 2.75 hours). The mean time interval between rtPA infusion and stroke MRI was 2.66 hours (range 1.75 to 4.17 hours), with all MRI examinations being performed after thrombolytic therapy was initiated. Five of the 6 rtPA patients had smaller PWI than DWI volumes, suggesting early recanalization.15 An important next step is an rtPA case-control study in which patients are matched for demographic factors, initial stroke severity, time windows, and stroke MRI criteria, such as vessel occlusion, DWI lesion size, and diffusion-perfusion mismatch. However, our cohort of 51 acute ischemic stroke patients imaged within 6 hours after symptom onset with stroke MRI presently lacks a sufficient number of non-rtPA patients for matching.
The present study also has some limitations: The fact that stroke MRI was performed in 8 patients after initiation of thrombolysis is an important point that has to be addressed. PWI findings can be significantly altered if performed 1 to 2 hours after thrombolytic therapy as a consequence of partial or complete recanalization. Although 4 of these 8 patients were imaged within 30 minutes and another 3 were imaged within 1.5 hours after rtPA bolus administration, we cannot exclude an effect of rtPA at that point. One patient did not have an occlusion but a lacunar infarction, most probably of microangiopathic origin. Seven of 8 patients had a vessel occlusion according to the baseline MRA (1 distal ICA, 3 proximal M1, 2 distal M1, and 1 M2 occlusions), so that at least complete recanalization had not occurred yet. All but 1 of these 7 patients had a PWI-DWI mismatch; the 1 patient experienced recanalization between the assessment of MRA and PWI. Marks et al15 deducted recanalization after thrombolytic therapy from clinical improvement and a lack of PWI-DWI mismatch in their patients. This speculation would be unnecessary if MRA were performed at baseline in their study. Another point of criticism in the present study is the rather late assessment of recanalization by day-2 MRA. Reperfusion within the first few hours after stroke may be much more important than late reperfusion. One may assume, however, that the patients in whom vessels did not recanalize within 8 to 10 hours after stroke onset were those with a persistent occlusion and a poor outcome as opposed to those who experienced early recanalization and thus saved a more or less large area of tissue at risk. Late reperfusion at a time point when there is no longer any tissue at risk is not of use for the patient and may even cause harm via reperfusion injury and symptomatic parenchymal hemorrhage. On the other hand, a recent subgroup analysis of ECASS II data showed that late reperfusion may be associated with a better outcome than no reperfusion,37 and even after 6 to 8 hours, a salvageable tissue at risk as shown by DWI and PWI may still be present (Schellinger et al, unpublished data, 2000). Also, there was a statistical trend toward a significant difference in baseline NIHSS and SSS scores, with those patients in the nonrecanalization group (group 2) having more severe strokes. Baseline DWI and PWI lesion volumes were slightly but not significantly larger. This may, in part, account for the better outcomes in group 1 at days 30 and 90 and thus lead to a bias in favor of recanalization. We believe that this trend is at least partially due to the slightly larger number of left hemispheric infarctions and more proximal occlusions in group 2. This reflects the experience that recanalization rates are lower in more proximal MCA or carotid T occlusions33 and that moderately severe left as opposed to right hemispheric infarctions show a median difference in stroke severity of 5 NIHSS points.38 Thus, the natural course of patients with proximal and left-sided vessel occlusions is worse than that of others. On the other hand, they may constitute a subgroup of patients that profit most from recanalization. Stroke MRI may be useful to identify those patients not suitable for thrombolysis because of extensive infarctions39 and those with large infarctions and a tissue at risk still present, which might be saved by more aggressive therapeutic means.40 41 42
In addition to a higher diagnostic and prognostic potential, stroke MRI is feasible and appears to be safe and reliable in patients with hyperacute hemispheric ischemia. When stroke MRI is available, time-consuming diagnostic efforts with different modalities are not needed, because the vascular status is reliably assessed, and the presence or absence of ICH can be determined. The findings on stroke MRI are consistent with the general understanding of stroke pathophysiology and predict morphological as well as functional outcome. Early recanalization has the potential to save tissue at risk if present and thus may lead to smaller infarctions and a better neurological outcome. We believe that the utility of stroke MRI is implicit, because it can define the patient target group for thrombolytic therapy and monitor thrombolysis in acute ischemic stroke and is suitable for follow-up evaluation of stroke patients.
| Acknowledgments |
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Received September 8, 1999; revision received March 16, 2000; accepted March 16, 2000.
| References |
|---|
|
|
|---|
2.
Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von
Kummer R, Boysen G, Bluhmki E, Hoexter G, Mahagne MH, et al.
Intravenous thrombolysis with recombinant
tissue plasminogen activator for acute
hemispheric stroke: the European Cooperative Acute Stroke Study.
JAMA. 1995;274:10171025.
3.
The National Institute of Neurological Disorders, and
Stroke rt-PA Stroke Study Group. Tissue plasminogen
activator for acute ischemic stroke. N
Engl J Med. 1995;333:15811587.
3. Clark WM, Wissman S, Albers GW, Jhamandas JH, Madden KP, Hamilton S. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset. The ATLANTIS study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA.1999;282:20192026.
4.
Fagan SC, Morgenstern LB, Petitta A, Ward RE, Tilley
BC, Marler JR, Levine SR, Broderick JP, Kwiatkowski TG, Frankel M, et
al. Cost-effectiveness of tissue plasminogen
activator for acute ischemic stroke: NINDS rt-PA
Stroke Study Group. Neurology. 1998;50:883890.
5. Warach S, Dashe JF, Edelman RR. Clinical outcome in ischemic stroke predicted by early diffusion-weighted and perfusion magnetic resonance imaging: a preliminary analysis. J Cereb Blood Flow Metab. 1996;16:5359.[Medline] [Order article via Infotrieve]
6. Warach S, Boska M, Welch KM. Pitfalls and potential of clinical diffusion-weighted MR imaging in acute stroke. Stroke. 1997;28:481482.
7.
Sorensen AG, Buonanno FS, Gonzalez RG, Schwamm LH, Lev
MH, Huang Hellinger FR, Reese TG, Weisskoff RM, Davis TL, Suwanwela N,
et al. Hyperacute stroke: evaluation with combined multisection
diffusion-weighted and hemodynamically weighted
echo-planar MR imaging. Radiology. 1996;199:391401.
8.
Tong DC, Yenari MA, Albers GW, M OB, Marks MP, Moseley
ME. Correlation of perfusion- and diffusion-weighted MRI with NIHSS
score in acute (<6.5 hour) ischemic stroke.
Neurology. 1998;50:864870.
9. Moseley ME, Wendland MF, Kucharczyk J. Magnetic resonance imaging of diffusion and perfusion. Top Magn Reson Imaging. 1991;3:5067.
10. Mintorovitch J, Moseley ME, Chileuitt L, Shimizu H, Cohen Y, Weinstein PR. Comparison of diffusion- and T2-weighted MRI for the early detection of cerebral ischemia and reperfusion in rats. Magn Reson Med. 1991;18:3950.[Medline] [Order article via Infotrieve]
11.
Barber PA, Darby DG, Desmond PM, Yang Q, Gerraty RP,
Jolley D, Donnan GA, Tress BM, Davis SM. Prediction of stroke outcome
with echoplanar perfusion- and diffusion-weighted MRI.
Neurology. 1998;51:418426.
12. Bahn MM, Oser AB, Cross DT III. CT and MRI of stroke. J Magn Reson Imaging. 1996;6:833845.[Medline] [Order article via Infotrieve]
13. Jansen O, Schellinger PD, Fiebach JB, Hacke W, Sartor K. Early recanalization in acute ischemic stroke saves tissue at risk defined by MRI. Lancet. 1999;353:20362037.[Medline] [Order article via Infotrieve]
14. Lovblad KO, Baird AE, Schlaug G, Benfield A, Siewert B, Voetsch B, Connor A, Burzynski C, Edelman RR, Warach S. Ischemic lesion volumes in acute stroke by diffusion-weighted magnetic resonance imaging correlate with clinical outcome. Ann Neurol. 1997;42:164170.[Medline] [Order article via Infotrieve]
15.
Marks MP, Tong D, Beaulieu C, Albers G, de Crespigny A,
Moseley ME. Evaluation of early reperfusion and IV rt-PA therapy using
diffusion- and perfusion-weighted MRI. Neurology. 1999;52:17921798.
16. Heiland S, Benner T, Reith W, Forsting M, Sartor K. Perfusion-weighted MRI using gadobutrol as a contrast agent in a rat stroke model. J Magn Reson Imaging. 1997;7:11091115.[Medline] [Order article via Infotrieve]
17.
Rempp KA, Brix G, Wenz F, Becker CR, Gückel
F, Lorenz WJ. Quantification of regional cerebral blood flow and volume
with dynamic susceptibility contrast-enhanced MR imaging.
Radiology. 1994;193:637641.
18.
Scandinavian Stroke Study Group. Multicenter trial of
hemodilution in ischemic stroke. Stroke. 1985;16:885890.
19. Mahoney FI, Barthel DW. Functional evaluation: the Barthel Index. Md Med J. 1965;2123:6165.
20. Rankin J. Cerebral vascular accidents in people over the age of 60: prognosis. Scott Med J. 1957;2:200215.[Medline] [Order article via Infotrieve]
21. Lyden P, Brott T, Tilley B, Welch KM, Mascha EJ, Levine S, Haley EC, Grotta J, Marler J. Improved reliability of the NIH Stroke Scale using video training: NINDS TPA Stroke Study Group. Stroke. 1994;25:22202226.[Abstract]
22. Koroshetz WJ, Gonzalez G. Diffusion-weighted MRI: an ECG for brain attack? Ann Neurol. 1997;41:565566.[Medline] [Order article via Infotrieve]
23.
Powers WJ, Zivin J. Magnetic resonance imaging in acute
stroke: not ready for prime time. Neurology. 1998;50:842843.
25.
Furlan A, Higashida R, Wechsler L, Gent M, Rowley H,
Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, Silver F, Rivera F.
Intra-arterial prourokinase for acute ischemic stroke. The PROACT II
study: a randomized controlled trial. Prolyse in Acute Cerebral
Thromboembolism. JAMA. 1999;282:20032011.
26. Conturo TE, McKinstry RC, Aronovitz JA, Neil JJ. Diffusion MRI: precision, accuracy and flow effects. NMR Biomed. 1995;8:307332.[Medline] [Order article via Infotrieve]
27. Moseley M. Pathophysiologic basis of diffusion and perfusion-weighted imaging. In: 25th International Stroke Conference; February 1012, 2000; New Orleans, La.
28. Ginsberg MD, Pulsinelli WA. The ischemic penumbra, injury thresholds, and the therapeutic window for acute stroke. Ann Neurol. 1994;36:553554.[Medline] [Order article via Infotrieve]
29. Jansen O, Heiland S, Schellinger P. Neuroradiological diagnosis in acute ischemic stroke: value of modern techniques. Nervenarzt. 1998;69:465471.[Medline] [Order article via Infotrieve]
30.
Schellinger PD, Jansen O, Fiebach JB, Hacke W, Sartor
K. A standardized MRI stroke protocol: comparison with CT in hyperacute
intracerebral hemorrhage. Stroke. 1999;30:765768.
31.
Busch E, Beaulieu C, de Crespigny A, Moseley ME.
Diffusion MR imaging during acute subarachnoid
hemorrhage in rats. Stroke. 1998;29:21552161.
32. Wiesmann M, Mayer TE, Medele R, Brueckmann H. Diagnosis of acute subarachnoid hemorrhage at 1.5 Tesla using proton-density weighted FSE and MRI sequences. Radiologe.. 1999;39:860865.[Medline] [Order article via Infotrieve]
33.
von Kummer R, Holle R, Rosin L, Forsting M, Hacke W.
Does arterial recanalization improve
outcome in carotid territory stroke? Stroke. 1995;26:581587.
34.
Mori E, Yoneda Y, Tabuchi M, Yoshida T, Ohkawa S,
Ohsumi Y, Kitano K, Tsutsumi A, Yamadori A. Intravenous
recombinant tissue plasminogen activator in
acute carotid artery territory stroke. Neurology. 1992;42:976982.
35. Zeumer H, Freitag HJ, Zanella F, Thie A, Arning C. Local intra-arterial fibrinolytic therapy in patients with stroke: urokinase versus recombinant tissue plasminogen activator (r-TPA). Neuroradiology. 1993;35:159162.[Medline] [Order article via Infotrieve]
36.
Rordorf G, Koroshetz WJ, Copen WA, Cramer SC, Schaefer
PW, Budzik RF Jr, Schwamm LH, Buonanno F, Sorensen AG, Gonzalez G.
Regional ischemia and ischemic injury in patients with
acute middle cerebral artery stroke as defined by early
diffusion-weighted and perfusion-weighted MRI. Stroke. 1998;29:939943.
37.
von Kummer R, Berrouschot J, Barthel H, Hesse S, Dieler
C, Schneider D. The effect of early and late brain tissue reperfusion
on infarct volume. Stroke. 2000;31:275. Abstract.
38.
Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L.
Early clinical and radiological predictors of fatal brain swelling in
ischemic stroke. Stroke. 1999;30:287292.
39.
Hacke W, Schwab S, Horn M, Spranger M, De Georgia M,
von Kummer R. Malignant middle cerebral artery territory
infarction: clinical course and prognostic signs. Arch
Neurol. 1996;53:309315.
40.
Schwab S, Schwarz S, Spranger M, Keller E, Bertram M,
Hacke W. Moderate hypothermia in the treatment of patients with severe
middle cerebral artery infarction. Stroke. 1998;29:24612466.
41. Schwab S, Rieke K, Krieger D, Hund E, Aschoff A, von Kummer R, Hacke W. Craniectomy in space-occupying middle cerebral artery infarcts. Nervenarzt. 1995;66:430437.[Medline] [Order article via Infotrieve]
42.
Schwab S, Steiner T, Aschoff A, Schwarz S, Steiner HH,
Jansen O, Hacke W. Early hemicraniectomy in patients with complete
middle cerebral artery infarction. Stroke. 1998;29:18881893.
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