(Stroke. 1999;30:1591-1597.)
© 1999 American Heart Association, Inc.
Original Contributions |
Diffusion- and Perfusion-Weighted MRI
The DWI/PWI Mismatch Region in Acute Stroke
From the Department of Neurology (T.N.-H., H.-J.W., M.S., R.J.S., H.-J.F.) and Institute of Diagnostic Radiology (H.-J.W., F.W., U.M.), Heinrich-Heine University, Düsseldorf, Germany, and the Department of Radiology, Stanford University (T.N.-H.), Stanford, Calif.
Correspondence to Dr Tobias Neumann-Haefelin, Department of Radiology, Stanford University, Lucas MRS Center, MC: 5488, Stanford, CA 94305. E-mail tnh{at}s-word.stanford.edu
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Abstract |
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Background and Purpose—Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are relatively new MR techniques increasingly used in acute stroke. During the first hours of stroke evolution, the regions with abnormal perfusion are typically larger than the DWI lesions, and this mismatch region has been suggested to be "tissue at risk." The aim of this study was to evaluate the PWI/DWI mismatch region in acute stroke patients and find parameters indicative of both infarct progression and functional impairment.
Methods—Twenty patients with nonlacunar ischemic stroke
were imaged with DWI, PWI, and conventional MRI within 24 hours of
symptom onset and after 1 week; in addition, the European Stroke Scale
(ESS) score was recorded. With PWI, the volumes of regions with
"time-to-peak" (TTP) delays of 
2, 4, 6, 8, and 10 seconds were
measured; these volumes were compared with the acute DWI lesion
volumes, final infarct size, and ESS score.
Results—In 80% of patients the acute DWI lesion was surrounded
by regions with abnormal TTP delays (PWI>DWI lesion). A TTP delay of
6 s in the mismatch region was found to be associated with lesion
enlargement between the initial and follow-up MRI scans. Lesions
increased in 9 of 12 patients (75%) in whom the area with TTP delay
6 s was larger than the DWI lesion, but they increased in only 1 of 8
(12.5%) of the remaining patients, in whom the area with a TTP delay
6 s was smaller than the DWI lesion. The volume of the regions with
TTP delays of 4 s correlated better with ESS
(r=-0.88, P<0.001) than other PWI (or
DWI) volumes, which indicated that a TTP delay of 
4 s might be the
threshold for functional impairment of brain tissue.
Conclusions—Only patients with severe perfusion deficits in the
PWI/DWI mismatch (TTP delays of 6 s) are at high risk of lesion
enlargement. Functionally, more moderate perfusion deficits (TTP delays
4 and <6 s) appear to also contribute to the acute clinical deficit.
Key Words: diffusion • magnetic resonance imaging • penumbra • perfusion • stroke, acute
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Introduction |
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The new MR techniques of diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are rapidly becoming integral parts of the diagnostic workup in the acute stroke setting. With DWI it is possible to identify severely ischemic brain regions within minutes to hours after stroke onset.1 2 3 A decrease in the apparent diffusion coefficient of water (ADC), apparent as hyperintensity on DW images, indicates a restriction in the diffusional movement of water and is believed to result from energy failure and subsequent cytotoxic edema.1 4 DWI abnormalities typically evolve into infarction in humans, and it has been suggested that the DWI abnormality corresponds to the ischemic core.5 PWI, on the other hand, provides information on the hemodynamic status of the tissue and can detect impaired perfusion in both the ischemic core and the surrounding brain regions, thereby complementing the information derived from DWI.3 6 7
During the first hours of stroke evolution, regions with abnormal perfusion (as assessed with PWI) are typically larger than the DWI lesions.8 9 10 11 12 It has been postulated that this mismatch region reflects the ischemic penumbra, ie, the functionally impaired "tissue at risk" surrounding the irreversibly damaged ischemic core. Typically, the ischemic penumbra is partially recruited into the ischemic core during the first hours after symptom onset.13 14 15 16 This process might be prevented pharmacologically and has therefore become the focus of intense interest.
In support of the hypothesis that the PWI/DWI mismatch reflects tissue
at risk is the observation that a PWI>DWI lesion is associated with
subsequent infarct enlargement.8 10 However, because PWI
is very sensitive in detecting perfusion deficits, the PWI/DWI mismatch
region may comprise not only tissue at risk but also hypoperfused
tissue with cerebral blood flow (CBF) values above the critical
viability thresholds.3 From both animal experiments and
human PET studies, it is well known that the flow thresholds are 10
and 15 to 20 mL/100 g per minute for structural injury and functional
impairment, respectively (average normal CBF 50 mL/100 g per
minute).13 17 18 19 PWI, however, has been shown to be
sensitive enough to detect perfusion deficits in patients with
occlusive internal carotid artery (ICA) disease20 but
without symptoms at the time of the scan, which indicates that PWI can
detect even relatively mild hypoperfusion states.
Thus, to determine the functional relevance and the risk for subsequent structural injury, it would be necessary to know the severity of the perfusion deficit within the PWI/DWI mismatch region. PWI—as it is performed in most centers—is, however, only semiquantitative. Calculating absolute CBF values, although theoretically possible, is not yet widely applied, in part because it requires time-consuming postprocessing as well as operator intervention to determine the arterial input function. In most previous stroke studies only relative measurements of various hemodynamic parameters (bolus arrival time or time to peak [TTP], mean transit time, and relative CBV and CBF) were analyzed; in fact, the perfusion deficits were mostly assessed qualitatively,8 ie, the volume of the total PWI lesion was measured without differentiating between different degrees of ischemia.
In this prospective study we used a simple and rapid semiquantitative method of analyzing PWI abnormalities to assess both the extent of the PWI lesion and the severity of the perfusion deficits in the PWI/DWI mismatch region. The method requires minimal operator intervention and can be easily applied in the acute stroke setting.
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Subjects and Methods |
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Patients
Between January and November 1998, we consecutively enrolled 20 patients at our stroke center. The inclusion criteria were focal neurological deficit of sudden onset with persisting symptoms at the time of the acute MR study, acute MRI study within 24 hours after symptom onset, and stable general medical status. The exclusion criteria were history of major stroke or other disabling neurological disease prior to the index event, subcortical lacunar stroke, and nonischemic conditions. Patients receiving rtPA (4 patients) or anticoagulation were eligible for the study; however, none of the patients received investigational drugs. Informed consent was obtained from all patients included in the study or from their close family members. The study was approved by the local ethics committee.
All patients enrolled in the study were imaged within 24 hours of symptom onset. Follow-up scans were obtained at 6 to 10 days (and in 1 patient at 14 days). Three clinical scores (European Stroke Scale, Rankin scale, and Barthel Index) were recorded at the time of the acute imaging study and at follow-up by a neurologist experienced in stroke management. Although similar results were obtained for all correlations between these 3 clinical scores and MR lesion volumes, only the results obtained with the ESS are presented due to the obviously nonlinear relationship between the other scores and lesion volumes. All strokes were classified by vascular territory and stroke mechanism according to the Trial of Org 10172 in Acute Ischemic Stroke (TOAST) study criteria.21
Imaging Protocol
The MR measurements were performed on a 1.5-T clinical
whole-body MR scanner (Siemens Magnetom Vision) equipped with a
gradient overdrive, using the standard head coil. The acute study
included a conventional T2-weighted axial turbo spin-echo sequence
(T2WI), an axial diffusion-weighted single-shot echo planar sequence
(DWI), and an axial echo planar perfusion-weighted sequence (PWI).
Total scan time for the acute protocol (including scout and MRA) was
20 minutes. The follow-up study consisted of the T2 sequence and
DWI.
The T2 sequence contained 20 slices (thickness 5 mm) with an interslice gap of 1.5 mm and a field of view (FOV) of 240 mm with a matrix of 345x512 pixels. Each of the 20 axial slices obtained with spin-echo DWI (slice thickness 5 mm, interslice gap 1.5 mm, TE 103 ms, FOV 240 mm, and matrix 96x128) was acquired with b values of 0 and 1000 s/mm2; the high b value DWI measurements were performed with diffusion gradients in the 3 orthogonal (x, y, z) directions in space. The perfusion study (gradient echo, 12 slices, slice thickness 5 mm, interslice gap 1.5 mm, TE 54 ms, FOV 240 mm, and matrix 128x128) consisted of 40 T2*-weighted measurements obtained at intervals of 2 s. The contrast agent (15 mL Gd-DTPA) was injected at the time of the fourth scan at a rate of 5 mL/s.
Postprocessing and Image Analysis
For postprocessing the data were transferred to a Sun
UltraSparc1 workstation. With DWI a trace diffusion-weighted image was
calculated by averaging the images obtained with diffusion weighting in
the x, y, and z directions using
inhouse software; in addition, ADC maps were calculated from the DWI
data. PWI data were computed pixel by pixel to create TTP) maps. (TTP
refers here to the time between the first T2*-weighted measurement and
the bolus peak.) Other parameter maps (relative regional
CBV [rCBV] and bolus amplitude) were also routinely calculated but
not used in this analysis, because the volume of the perfusion
deficits was usually considerably more difficult to delineate on these
maps than on the TTP maps.
The DWI and PWI lesion volumes were measured by 2 independent observers. The average of the lesion volumes determined by the 2 observers was used for further analysis. DWI lesion volumes were determined by manually tracing the edge of the hyperintense signal on each slice of the trace DWI scans obtained at b=1000 s/mm2. The areas of hyperintensity were summed and multiplied with the slice thickness plus interslice gap to calculate the volume of the DWI abnormality.
For the calculation of the perfusion deficit volumes, the TTP maps were
modified with use of the contralateral MCA territory as reference
tissue (see Figure 1
); the average TTP
value obtained for this reference region was subtracted from the
unmodified TTP map. Using this simple method, we were able to generate
maps that depicted areas of pathological bolus delay, ie, bolus delay
beyond the normal delay in unaffected tissue. To calculate the
reference TTP value we always defined an area of the size depicted in
Figure 1 using a slice at approximately the same high
ventricular level. The mean difference between the TTP
values determined for the reference regions by the 2 observers was
0.3 s (range 0.0 to 1.2 s), indicating that the interobserver
error introduced by selecting the reference regions is minimal. In
addition, to get an estimate of how much selecting different slice
levels would influence the reference TTP value, we measured the average
TTP of contralateral regions at different slice levels. When selecting
regions similar in size to our reference region, the TTP delays were
found to not differ by >1 s in individual patients.
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We then determined the PWI lesion volumes by systematically measuring
the volumes of the regions with TTP delays of >0, 2, 4, 6, 8,
and 10 s in all patients. The interobserver reliability
(r) values for measuring these volumes were 0.89 (TTP delays
>0 s), 0.87 (TTP delays 2 s), 0.90 (4 s), 0.96 (6 s), 0.99 (8
s), and 0.99 (10 s), compared with 0.99 for DWI and 0.97 for T2WI
lesion measurements. The volumes of the regions with abnormal
perfusion determined with this method were compared with the volumes of
the acute DWI lesion, the final infarct size (T2WI at follow-up), and
the acute neurological scores (ESS).
Statistical Analysis
Results are presented as mean±SD unless stated
otherwise. When analyzing the change in infarct size we considered
(T2WI lesion at follow-up >1.05xacute DWI lesion) as indication of
infarct growth. The mean acute PWI volumes were compared with the mean
DWI volume with use of ANOVA and subsequently Dunnett's procedure for
multiple comparisons against a single "control" group (DWI lesion
volume). For correlations between the PWI/DWI lesion volumes and ESS
scores, Pearson's product moment correlation coefficient was used
with Bonferroni correction for multiple comparisons.
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Results |
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Thirty patients fulfilled our primary inclusion criteria, but 10 of these were retrospectively excluded due to the following exclusion criteria: subcortical lacunar stroke (n=3), other nonischemic neurological diseases (n=5), and insufficient PWI quality due to severe patient motion during data acquisition (n=2). We therefore analyzed the results of 20 patients with nonlacunar ischemic stroke (for demographic data see Table 1
); all of these 20 patients had
received our complete MR stroke protocol within 24 hours after symptom
onset (mean 8.8 hours, range 1 to 23 hours) as well as the follow-up
study.
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Acute DWI revealed at least 1 lesion in all 20 patients included in the study; the mean±SD DWI lesion volume was 32.7±33.7 mL for all patients investigated in the study. With acute PWI we were able to identify regions with an abnormal TTP delay in 18 of 20 patients when using the contralateral MCA territory as reference tissue. In 4 of 20 patients (including the 2 patients without a perfusion deficit) the region with a TTP delay was smaller than the DWI lesion, indicating that partial or complete reperfusion had occurred before the acute MR study. In the other 16 of 20 patients the PWI lesion was larger than the DWI lesion, ie, these patients had an area with a positive PWI/DWI mismatch when the TTP maps were used to calculate the PWI lesion volumes.
The severity of ischemia was not homogenous within the PWI/DWI
mismatch area of the 16 patients with a positive mismatch. The DWI
lesion (ischemic core) was typically surrounded by regions with
progressively less pronounced TTP delays (see Figures 1
and 2). The average size of this PWI/DWI
mismatch region was 132.8±69.4 mL (in comparison, mean DWI lesion
volume was 33.0±32.7 mL). The fractions of the total mismatch volume
(100%) with TTP delays of 2 s, 4 s, 6 s, and 8 s were
63±42%, 31±30%, 15±23%, and 3±19%, respectively, whereas the
area with a TTP delay of 10 s was smaller than the mean DWI lesion
volume.
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The risk of infarct growth was clearly related to the degree of the TTP
delay in the PWI/DWI mismatch region (Figure 3). When evaluating all patients with a
positive PWI/DWI mismatch (n=16), infarct size increased in 9 of 16
(56%) compared with 10 of 20 (50%) for the total study population.
Infarct size increased in 9 of 12 patients (75%) with a severe
perfusion deficit in the PWI/DWI mismatch region (TTP delay 6 s). On
the other hand, none of the patients with TTP delays of 
4 s in the
mismatch region showed an increase in infarct size (n=4). Lesion size
increased, however, in 1 patient without a detectable perfusion deficit
at acute PWI. In total, lesion size increased, therefore, in 1 of 8
patients (12.5%) with 1 of the following 3 patterns: PWI>DWI lesion
(but TTP delays of 4 s in the mismatch), PWI<DWI lesion, and no
perfusion deficit. The difference between the patients with TTP delays
6 s in the mismatch region and those without was also obvious when
comparing the changes in lesion size between the acute DWI study and
follow-up T2WI (Figure 4). Lesion
size increased on average 25% (absolute change, mean 8.3±11.1 mL;
percentage given is percent change of the mean) in the former group
(P<0.05) but decreased (nonsignificantly) in the latter
group by -13% (absolute change, mean –4.1±13 mL), with the
difference between the 2 groups statistically significant at
P<0.05.
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Finally, to assess the functional relevance of the different TTP delays
in the PWI/DWI mismatch region, we correlated the PWI lesion volumes
obtained with the different TTP thresholds with the acute neurological
deficit as assessed with the ESS (see Table 2). Overall, acute PWI lesion volumes
correlated better with ESS score than DWI lesion volumes. When
analyzing the correlations between the TTP volumes and acute ESS score,
the volume of the region with a TTP delay of 4 s correlated best with
acute ESS, particularly when the patients with a positive mismatch were
analyzed independently. In patients with PWI<DWI lesions, the
functional impairment was probably mainly due to the DWI lesion. With
TTP delays of 6 s, the correlations with ESS became weaker again,
indicating that some functionally affected areas were no longer
included in the PWI measurements.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In this study we analyzed the PWI/DWI mismatch region in acute stroke with a relatively simple semiquantitative method for assessing the perfusion deficits. The currently most widely used form of PWI in acute stroke patients is "bolus-tracking" of the first pass of a paramagnetic contrast agent, which was also used here. Different functional maps (TTP, mean transit time [MTT], peak amplitude, and relative rCBV and rCBF) can be generated on a pixel-by-pixel basis from the raw data. The TTP maps (or the MTT maps), where a bolus delay indicates abnormal perfusion, are often used for volumetric analyses because the perfusion deficits tend to be most distinct on these maps. The absolute TTP values, however, are difficult to compare between individuals, because the time between the intravenous injection and the arrival of the bolus in the cerebral arteries varies between different patients. Our approach to circumvent this problem was to generate "bolus delay" maps; this is simply achieved by subtracting the bolus arrival time of unaffected contralateral tissue. If done in a standardized fashion, the interobserver agreement of this method is good, requires minimal postprocessing, and is feasible in the acute stroke setting.
With this approach we were able to separate areas within the PWI/DWI
mismatch region with mild (TTP delay of <4 s), moderate (TTP delay 4
s and <6 s), and severe (TTP delay 6 s) perfusion deficits. Our
classification (mild, moderate, severe) is based on the following
findings: severe perfusion deficits (TTP delays of 6 s) in the
mismatch region were associated with subsequent lesion enlargement, and
TTP delays of 4 s (including severe and moderate perfusion deficits)
were found to correlate highly significantly with functional impairment
(ESS). The latter finding indirectly indicates that areas with TTP
delays of <4 s (mild perfusion deficit) did not contribute to the
clinical deficit. On average, only 31% of the total mismatch region
had TTP delays of 4 s, which indicates that—in contrast to the
ischemic penumbra—large parts of the PWI/DWI mismatch are not
"at risk" on hemodynamic grounds.
The ischemic penumbra was initially defined in animal studies as the region surrounding the irreversibly damaged ischemic core with flow rates between 2 critical thresholds, those of electrical and membrane failure, which translates into functional impairment but not structural injury.17 More recently, it has been suggested that the penumbra be defined as the region of constrained blood flow in which energy metabolism is preserved (in contrast to the ischemic core)13 or as tissue with transiently disturbed metabolism and recurrent anoxic depolarizations.22 Often, however, the term is used in a broader sense to characterize ischemically affected but still viable tissue surrounding the irreversibly damaged ischemic core with "uncertain chances for recovery or infarction."14 16
As in previous DWI/PWI studies, we operationally defined the DWI lesion as the ischemic core. Although acute DWI lesions are highly correlated with final infarct size in humans,9 10 23 24 25 there is compelling evidence from animal studies4 that DWI changes are potentially reversible for a limited time period. In transient focal ischemia models, regression of DWI abnormalities has been reported to occur after up to 60 minutes of ischemia. In rodents the periphery of the DWI lesion (ADC 90% of control values) was found to have preserved energy metabolism (normal ATP levels but increased lactate levels) even at 2 hours of middle cerebral artery (MCA) occlusion, which indicates that a small outer rim of the DWI lesion was still viable at that time.26 In humans, on the other hand, reversal of DWI abnormalities has not been shown convincingly. However, it was previously noted (as also observed in our study) that acute DWI lesions can be larger than the final infarct.6 8 10 This phenomenon may be due to a true reversal of the DWI abnormality at the periphery of the lesion, but other factors, such as vasogenic edema at the acute time point (and later resolution) or tissue atrophy prior to the follow-up scan, are difficult to exclude. In summary, it is likely that DWI slightly overestimates the ischemic core region and that a minor fraction of the DWI lesion extends into the ischemic penumbra.
Our study adds to previous PWI/DWI studies8 9 10 11 12 in acute
stroke by emphasizing the importance of quantifying the severity of the
perfusion deficits within the mismatch region. With our
semiquantitative approach, we were able to identify a high-risk group
with TTP delays of 6 s in the PWI/DWI mismatch region. In this
subgroup of patients (TTP delay 6 s in mismatch region), 75% of
lesions increased in size, compared with 12.5% in the subgroup without
a TTP delay of 6 s. Infarct size increased only in 1 patient in the
latter group (n=8); because this patient (patient 16 in Table 1)
deteriorated clinically before the follow-up scan and had no PWI lesion
on the initial scan, we believe that lesion enlargement was due to a
secondary ischemic event. With respect to the high-risk group,
it is important to mention that we were unable to predict infarct
growth with certainty. Even in some patients (n=2) with TTP delays of
10 s in the mismatch region, final infarct size did not exceed the
initial DWI lesion. The most likely explanation for this phenomenon is
that spontaneous thrombolysis occurred shortly after
the acute scan and "rescued" the severely ischemic tissue
in these patients.
Schlaug et al5 used a different approach to define tissue at risk for infarct progression. They operationally defined the ischemic penumbra as tissue with reduced perfusion surrounding the DWI lesion, which became infarcted between the initial and the follow-up scan. With this definition they restricted their analysis a priori to a region with a very high risk. They found that the MTT was increased by a mean of 73% and that rCBV was increased by 29% in this region, while in the core both rCBF and rCBV were decreased and MTT extremely prolonged. Others found that the rCBV lesions exceeded the DWI lesions in size but were substantially smaller than the MTT lesions.3 27 When TTP maps are used (as in this study), the total mismatch is probably of a size similar to that with MTT maps, but no systematic comparison between TTP and other relative parameter maps (MTT, rCBV, rCBF, and peak bolus) has been reported for acute stroke patients; it is therefore still difficult to directly compare the results of these studies.
The main advantages of using TTP maps to visualize the perfusion deficits are that they are easy to generate, time required for postprocessing is minimal, and abnormal regions can be easily identified and delineated. With rCBV and rCBF maps, the borders of the lesions are often less distinct than on the TTP (or MTT) maps. This is partially due to the lack of differences between gray and white matter on the latter maps; these differences are, however, prominent on rCBF and rCBV maps and can potentially obscure subtle changes, particularly those at the gray matter–white matter junction.27 However, there are also notable limitations to the TTP maps. The TTP is only an indirect measure of tissue perfusion, and TTP delays may occur in patients with high-grade ICA stenosis without acute stroke. Therefore, use of TTP maps only qualitatively (ie, differentiating between normal and abnormal tissue perfusion) can lead to a substantial overestimation of the region at risk in acute stroke patients with high-grade ICA stenosis. In our opinion this problem can be (at least partially) overcome by quantifying the degree of the TTP delay in the mismatch region as proposed here. However, this issue needs to be addressed in a future systematic study comparing the PWI exams (and TTP delays in particular) of acute stroke patients with and without ICA stenosis.
Recently, 2 groups28 29 30 reported methods of measuring absolute CBF (and CBV) in both healthy volunteers and patients with carotid artery stenosis (without acute stroke). Both techniques require determination of the arterial input function and subsequent deconvolution techniques. Until now, these techniques have not been validated in a sufficient number of stroke patients; in addition, because they require a high degree of operator intervention as well as relatively time-consuming postprocessing, it is unclear whether they are feasible in acute stroke, where time is a critical factor. Possibly, other PWI techniques, such as arterial spin tagging,31 may eventually prove to be useful in acute stroke because they are potentially quantitative, but there are still technical problems to be overcome.
Finally, our results add further evidence to the notion that
functionally affected tissue surrounds the DWI lesions. PWI lesion
volumes were previously found to correlate better than DWI lesion
volumes with the acute neurological deficit;10 in our
study the best correlation was found between the volume with TTP delays
of 4 s and ESS score. This indirectly indicates that tissue with TTP
delays of 4 s is functionally impaired, thereby contributing to the
patients' clinical symptoms. Assuming that this hypothesis is correct,
the functionally impaired region would be on average more than twice
the size of the DWI lesion. However, only a relatively small fraction
of this region becomes recruited into the final infarct. Because PWI
lesions typically regress with time, it is possible that a substantial
proportion of the clinical recovery typically seen within the first few
days after stroke results from a shrinkage of the mismatch region, as
suggested previously,10 which would also be in line with
existing PET data.18
In summary, our study focused on the PWI/DWI mismatch region in acute stroke patients. We have shown that it is possible to identify patients (through severe perfusion deficit in the mismatch region) at high risk of lesion enlargement. Large parts of the mismatch region, however, appear not to be at risk, even though they may contribute to functional impairment. If our data can be confirmed in a larger patient sample, it may become possible to select specific therapies for individual patients based on the hemodynamic status of their PWI/DWI mismatch region.
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Acknowledgments |
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This study was supported by SFB 194 (A9/A13), by the Ernst and Bertha Grimmke-Stiftung (Drs Neumann-Haefelin and Siebler), and by a grant from the Deutsche Forschungsgemeinschaft (Ne569/2-1). The authors would like to express their gratitude to A. de Crespigny and M.E. Moseley for helpful comments on the manuscript and to E. Rädisch for technical assistance.
Received March 9, 1999; revision received May 10, 1999; accepted May 10, 1999.
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K. Flemming, S. Ulmer, B. Duisberg, A. Hahn, and O. Jansen MR Spectroscopic Findings in a Case of Alpers-Huttenlocher Syndrome AJNR Am. J. Neuroradiol., September 1, 2002; 23(8): 1421 - 1423. [Abstract] [Full Text] [PDF]
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A. E. Hillis, R. J. Wityk, P. B. Barker, N. J. Beauchamp, P. Gailloud, K. Murphy, O. Cooper, and E. J. Metter Subcortical aphasia and neglect in acute stroke: the role of cortical hypoperfusion Brain, May 1, 2002; 125(5): 1094 - 1104. [Abstract] [Full Text] [PDF]
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F. Calamante, D.G. Gadian, and A. Connelly Quantification of Perfusion Using Bolus Tracking Magnetic Resonance Imaging in Stroke: Assumptions, Limitations, and Potential Implications for Clinical Use Stroke, April 1, 2002; 33(4): 1146 - 1151. [Abstract] [Full Text] [PDF]
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 T. Baumann, R. Petsch, G. Fesl, and R. Niessner Flow and Diffusion Measurements in Natural Porous Media Using Magnetic Resonance Imaging J. Environ. Qual., March 1, 2002; 31(2): 470 - 476. [Abstract] [Full Text] [PDF]
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U. Junghans, R. J. Seitz, A. Ritzl, H.-J. Wittsack, G. R. Fink, H.-J. Freund, and M. Siebler Ischemic brain tissue salvaged from infarction by the GP IIb/IIIa platelet antagonist tirofiban Neurology, February 12, 2002; 58(3): 474 - 476. [Abstract] [Full Text] [PDF]
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J. Fiehler, M. Foth, T. Kucinski, R. Knab, M. von Bezold, C. Weiller, H. Zeumer, and J. Rother Severe ADC Decreases Do Not Predict Irreversible Tissue Damage In Humans Stroke, January 1, 2002; 33(1): 79 - 86. [Abstract] [Full Text] [PDF]
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K. Yamada, O. Wu, R. G. Gonzalez, D. Bakker, L. Ostergaard, W. A. Copen, R. M. Weisskoff, B. R. Rosen, K. Yagi, T. Nishimura, et al. Magnetic Resonance Perfusion-Weighted Imaging of Acute Cerebral Infarction: Effect of the Calculation Methods and Underlying Vasculopathy Stroke, January 1, 2002; 33(1): 87 - 94. [Abstract] [Full Text] [PDF]
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F. Calamante, V. Ganesan, F.J. Kirkham, W. Jan, W.K. Chong, D.G. Gadian, and A. Connelly MR Perfusion Imaging in Moyamoya Syndrome: Potential Implications for Clinical Evaluation of Occlusive Cerebrovascular Disease Stroke, December 1, 2001; 32(12): 2810 - 2816. [Abstract] [Full Text] [PDF]
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C. Oppenheim, C. Grandin, Y. Samson, A. Smith, T. Duprez, C. Marsault, and G. Cosnard Is There an Apparent Diffusion Coefficient Threshold in Predicting Tissue Viability in Hyperacute Stroke? Stroke, November 1, 2001; 32(11): 2486 - 2491. [Abstract] [Full Text] [PDF]
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V. N. Thijs, A. Adami, T. Neumann-Haefelin, M. E. Moseley, M. P. Marks, and G. W. Albers Relationship between severity of MR perfusion deficit and DWI lesion evolution Neurology, October 9, 2001; 57(7): 1205 - 1211. [Abstract] [Full Text] [PDF]
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F. Caramia, A. Santoro, P. Pantano, E. Passacantilli, G. Guidetti, A. Pierallini, L. M. Fantozzi, G. P. Cantore, and L. Bozzao Cerebral Hemodynamics on MR Perfusion Images before and after Bypass Surgery in Patients with Giant Intracranial Aneurysms AJNR Am. J. Neuroradiol., October 1, 2001; 22(9): 1704 - 1710. [Abstract] [Full Text] [PDF]
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R. Bruening, M. Dichgans, C. Berchtenbreiter, T. Yousry, K. C. Seelos, R. H. Wu, M. Mayer, G. Brix, and M. Reiser Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy: Decrease in Regional Cerebral Blood Volume in Hyperintense Subcortical Lesions Inversely Correlates with Disability and Cognitive Performance AJNR Am. J. Neuroradiol., August 1, 2001; 22(7): 1268 - 1274. [Abstract] [Full Text] [PDF]
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 I. A. Staroselskaya, C. Chaves, B. Silver, I. Linfante, R. R. Edelman, L. Caplan, S. Warach, and A. E. Baird Relationship Between Magnetic Resonance Arterial Patency and Perfusion-Diffusion Mismatch in Acute Ischemic Stroke and Its Potential Clinical Use Arch Neurol, July 1, 2001; 58(7): 1069 - 1074. [Abstract] [Full Text] [PDF]
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M. W. Parsons, Q. Yang, P. A. Barber, D. G. Darby, P. M. Desmond, R. P. Gerraty, B. M. Tress, and S. M. Davis Perfusion Magnetic Resonance Imaging Maps in Hyperacute Stroke : Relative Cerebral Blood Flow Most Accurately Identifies Tissue Destined to Infarct Stroke, July 1, 2001; 32(7): 1581 - 1587. [Abstract] [Full Text] [PDF]
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C. Nasel, A. Azizi, A. Wilfort, R. Mallek, and E. Schindler Measurement of Time-to-peak Parameter by Use of a New Standardization Method in Patients with Stenotic or Occlusive Disease of the Carotid Artery AJNR Am. J. Neuroradiol., June 1, 2001; 22(6): 1056 - 1061. [Abstract] [Full Text] [PDF]
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K. Szabo, R. Kern, A. Gass, J. Hirsch, and M. Hennerici Acute Stroke Patterns in Patients With Internal Carotid Artery Disease : A Diffusion-Weighted Magnetic Resonance Imaging Study Stroke, June 1, 2001; 32(6): 1323 - 1329. [Abstract] [Full Text] [PDF]
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C. B. Grandin, T. P. Duprez, A. M. Smith, F. Mataigne, A. Peeters, C. Oppenheim, and G. Cosnard Usefulness of Magnetic Resonance-Derived Quantitative Measurements of Cerebral Blood Flow and Volume in Prediction of Infarct Growth in Hyperacute Stroke Stroke, May 1, 2001; 32(5): 1147 - 1153. [Abstract] [Full Text] [PDF]
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D. C. Tong, A. Adami, M. E. Moseley, and M. P. Marks Prediction of Hemorrhagic Transformation Following Acute Stroke: Role of Diffusion- and Perfusion-Weighted Magnetic Resonance Imaging Arch Neurol, April 1, 2001; 58(4): 587 - 593. [Abstract] [Full Text] [PDF]
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O. Wu, W. J. Koroshetz, L. Ostergaard, F. S. Buonanno, W. A. Copen, R. G. Gonzalez, G. Rordorf, B. R. Rosen, L. H. Schwamm, R. M. Weisskoff, et al. Predicting Tissue Outcome in Acute Human Cerebral Ischemia Using Combined Diffusion- and Perfusion-Weighted MR Imaging Stroke, April 1, 2001; 32(4): 933 - 942. [Abstract] [Full Text] [PDF]
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P. Pantano, D. Toni, F. Caramia, A. Falcou, M. Fiorelli, C. Argentino, L. M. Fantozzi, and L. Bozzao Relationship between Vascular Enhancement, Cerebral Hemodynamics, and MR Angiography in Cases of Acute Stroke AJNR Am. J. Neuroradiol., February 1, 2001; 22(2): 255 - 260. [Abstract] [Full Text] [PDF]
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M. Koenig, M. Kraus, C. Theek, E. Klotz, W. Gehlen, and L. Heuser Quantitative Assessment of the Ischemic Brain by Means of Perfusion-Related Parameters Derived From Perfusion CT Stroke, February 1, 2001; 32(2): 431 - 437. [Abstract] [Full Text] [PDF]
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E. COMMITTEE OF THE ASITN Intraarterial Thrombolysis: Ready for Prime Time? AJNR Am. J. Neuroradiol., January 1, 2001; 22(1): 55 - 58. [Full Text] [PDF]
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J. O. Karonen, Y. Liu, R. L. Vanninen, L. Østergaard, P. L. Kaarina Partanen, P. A. Vainio, E. J. Vanninen, J. Nuutinen, R. Roivainen, S. Soimakallio, et al. Combined Perfusion- and Diffusion-weighted MR Imaging in Acute Ischemic Stroke during the 1st Week: A Longitudinal Study Radiology, December 1, 2000; 217(3): 886 - 894. [Abstract] [Full Text]
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T. Back, J. G. Hirsch, K. Szabo, and A. Gass Failure to Demonstrate Peri-Infarct Depolarizations by Repetitive MR Diffusion Imaging in Acute Human Stroke Stroke, December 1, 2000; 31(12): 2901 - 2906. [Abstract] [Full Text] [PDF]
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V. N. Thijs, M. G. Lansberg, C. Beaulieu, M. P. Marks, M. E. Moseley, and G. W. Albers Is Early Ischemic Lesion Volume on Diffusion-Weighted Imaging an Independent Predictor of Stroke Outcome? : A Multivariable Analysis Stroke, November 1, 2000; 31(11): 2597 - 2602. [Abstract] [Full Text] [PDF]
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K. Krueger, H. Kugel, M. Grond, A. Thiel, D. Maintz, and K. Lackner Late Resolution of Diffusion-Weighted MRI Changes in a Patient With Prolonged Reversible Ischemic Neurological Deficit After Thrombolytic Therapy Stroke, November 1, 2000; 31(11): 2715 - 2718. [Abstract] [Full Text] [PDF]
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S. L. Keir and J. M. Wardlaw Systematic Review of Diffusion and Perfusion Imaging in Acute Ischemic Stroke Stroke, November 1, 2000; 31(11): 2723 - 2731. [Abstract] [Full Text] [PDF]
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C. Nasel, A. Azizi, A. Veintimilla, R. Mallek, and E. Schindler A Standardized Method of Generating Time-to-peak Perfusion Maps in Dynamic-susceptibility Contrast-enhanced MR Imaging AJNR Am. J. Neuroradiol., July 1, 2000; 21(7): 1195 - 1198. [Abstract] [Full Text] [PDF]
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T. Neumann-Haefelin, H.-J. Wittsack, G. R. Fink, F. Wenserski, T.-Q. Li, R. J. Seitz, M. Siebler, U. Modder, and H.-J. Freund Diffusion- and Perfusion-Weighted MRI : Influence of Severe Carotid Artery Stenosis on the DWI/PWI Mismatch in Acute Stroke Stroke, June 1, 2000; 31(6): 1311 - 1317. [Abstract] [Full Text] [PDF]
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H.-J. Wittsack, A. Ritzl, G. R. Fink, F. Wenserski, M. Siebler, R. J. Seitz, U. Modder, and H.-J. Freund MR Imaging in Acute Stroke: Diffusion-weighted and Perfusion Imaging Parameters for Predicting Infarct Size Radiology, February 1, 2002; 222(2): 397 - 403. [Abstract] [Full Text] [PDF]
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