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Relationship Between Magnetic Resonance Arterial Patency and Perfusion-Diffusion Mismatch in Acute Ischemic Stroke and Its Potential Clinical Use
Irina A. Staroselskaya, MD;
Claudia Chaves, MD;
Brian Silver, MD;
Italo Linfante, MD;
Robert R. Edelman, MD;
Louis Caplan, MD;
Steven Warach, MD, PhD;
Alison E. Baird, FRACP, PhD
Arch Neurol. 2001;58:1069-1074.
ABSTRACT
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Background In patients with acute ischemic stroke the magnetic resonance (MR) perfusion-diffusion
mismatch pattern (perfusion lesion at least 20% larger than the lesion on
diffusion-weighted imaging) may indicate ischemically threatened but viable
tissue. To our knowledge, the relationship of this MR pattern to serial changes
in MR angiography (MRA) has not been reported.
Objectives To investigate the relationship between MRA changes and patterns of
diffusion-weighted imaging and perfusion abnormalities and to determine if
the information obtained could be used in clinical management.
Methods The MR studies of 35 patients who had undergone sequential multimodality
MR imaging studies within the first 4 days of stroke were reviewed. All lesions
were in the internal carotid artery territory distribution. Magnetic resonance
angiographies were read by 2 observers blinded to the clinical data.
Results During the first 24 hours a perfusion-diffusion mismatch was present
in 22 (92%) of the 24 patients with an MRA arterial occlusive lesion. (At
this time 5 [46%] of the 11 patients with a normal MRA [P = .006] also had a mismatch.) Two to 4 days after stroke, of these
22 patients resolution of the mismatch occurred in 8 (87%) of 9 patients with
recanalization on MRA compared with 5 (39%) of 13 patients without arterial
recanalization (P = .03). Resolution of mismatch
occurred in 3 (60%) of 5 patients with a normal MRA and a mismatch at the
first time point.
Conclusions Concordance between MRA and the MR perfusion-diffusion mismatch pattern
provides supportive evidence for an arterial vascular basis for this MR signature
in acute stroke. Discordance between MRA lesions and mismatch may result from
arterial branch occlusions undetected by MRA or from an alternate mechanism
for the mismatch. The MR imaging patterns identified extend our understanding
of the pathophysiology of stroke and may contribute to the improvement of
stroke management in the future.
INTRODUCTION
OVER THE PAST decade new magnetic resonance imaging (MRI) techniques
have become available providing new opportunities for the investigation of
stroke. These include diffusion-weighted imaging (DWI), which provides a measure
of cellular injury and cytotoxic edema, MR perfusion imaging, and MR angiography
(MRA). Application of these methods might identify particular pathophysiological
patterns and stroke subtypes against which more specific therapies could be
targeted.1, 2
In previous MRI studies it has been shown that tissue at risk for enlargement
of the ischemic lesion may exist when the area of ischemic injury on DWI is
surrounded by a larger area of hypoperfusion as measured by the mean transit
time map.3, 4, 5, 6, 7, 8, 9, 10
Since this pattern of tissue abnormalities may indicate ischemic, but potentially
salvageable, tissue, it could form a template for therapeutic trials.2, 8, 11 However, not all of
the DWI lesion may be irreversibly injured and not all of the hypoperfused
tissue may be at risk.
The clinical and angiographic correlates of changes in MR perfusion
and diffusion lesions have not been clearly defined or the optimal usage determined.
We hypothesized that during the first 24 hours of stroke an arterial lesion
seen on MRA would commonly be associated with a perfusion-diffusion mismatch,
while patients with a normal MRA would not have a mismatch. We also hypothesized
that reopening of the artery on MRA at 2 to 4 days would more commonly correlate
with resolution of the perfusion-diffusion mismatch.
PATIENTS AND METHODS
PATIENTS
All eligible patients in the Stroke MRI database (1993-1999) at the
Beth Israel Deaconess Medical Center, Boston, Mass, were identified and included
in the study. Inclusion criteria for the study were that (1) patients had
undergone 2 MRI studies during the acute phase of stroke, the first one during
the first 24 hours and the second at 2 to 4 days, and (2) the lesions were
in the distribution of the internal carotid artery territory. Patients with
lacunar stroke were excluded from this study. The time from the onset of stroke
was backdated to when the patient was last known to have no neurologic deficit.
Enrollment in other trials of new therapies did not exclude patients from
inclusion in this study. Three patients had received recombinant tissue plasminogen
activator therapy.
MAGNETIC RESONANCE IMAGING
Magnetic resonance DWI was obtained using the methods described in our
previous articles.3, 12 All studies
were performed using a 1.5-T MR whole-body system (Siemens AG, Erlangen, Germany),
the Vision system or its prototype. Diffusion-weighted imaging used multislice,
single-shot, echo-planar imaging with b values between 0 and 1000 s/mm2. Perfusion imaging used a dynamic first pass bolus tracking of gadolinium
diethylenetriamine penta-acetic acid and a multislice gradient echo-planar
sequence with the following parameters: echo time, 60 milliseconds; repetition
time, 2 seconds; field of view, 260 cm; acquisition matrix, 128 x 128
pixels, and slice thickness, 7 mm with no gaps. Twelve slices were acquired
at exactly the same position as on DWI. Head and neck MRAs were performed
for all patients. Intracranial MRA used a rapid (2 minutes 39 seconds) 3-dimensional
time of flight technique obtained in the region of the circle of Willis and
was performed at the same time as DWI. A flow-compensated gradient-echo sequence
was used with imaging parameters of 40/7 milliseconds (ie, repetition time,
40 milliseconds; echo time, 7 milliseconds); flip angle, 20°; slab thickness,
40 to 50 mm; acquisition matrix, 256 x 256 pixels; and field of view,
21 cm. Neck MRAs were performed within 24 hours of DWI.
DATA ANALYSES
The dynamic perfusion series was processed on a pixel-by-pixel basis
to produce a variety of maps related to cerebral blood volume and tissue perfusion.
The relative mean transit time map was calculated from the first moment to
the peak in the deltaR2* fitted curves.12 It
was found that this image provided the most distinct perfusion defect border
as previously described3, 12 as
well as providing the maximum anatomical extent of the perfusion abnormality.12 For data analyses the volumes of the DWI and relative
mean transit time map lesions were used. The lesion volumes had been measured
twice by observers (I.A.S.) blinded to the clinical data, with an interobserver
reliability of r>0.95. The accuracy of volumetric
measurements at our center has been validated in a phantom stroke model described
by Laubach et al.13
The MRAs were read by 2 observers (I.A.S. and A.E.B.) blinded to the
clinical data. All MRA lesions were identified as occlusive or stenotic. If
there was an initial disagreement, a final decision was reached by consensus.
The following definitions were used. An abnormality on MRA, whether stenotic
or occlusive, was denoted an arterial lesion. A perfusion-diffusion mismatch
was defined as a perfusion lesion (as measured on the relative mean transit
time map) at least 20% larger than the DWI lesion volume. The 20% value was
a conservative measure chosen to allow for error in volumetric measurements.
The size of the mismatch was further quantitated by the following calculations.
The relative mismatch size was defined as: [(perfusion lesion volume -
DWI lesion volume)/perfusion lesion volume]. The absolute mismatch size was
calculated: perfusion lesion volume - DWI lesion volume.
STATISTICAL ANALYSES
 2 Statistics, Fisher exact tests, Mann-Whitney tests,
and 1-way analyses of variance were used for statistical analyses. A 1-sided
Fisher exact test was used when the expected cell counts in one of the cells
was below 5. P<.05 was considered statistically
significant. All values are expressed as means (±SDs).
RESULTS
Thirty-five patients fulfilled the inclusion criteria. There were 22
men and 13 women. The mean age was 67.7 ± 18.3 years (age range, 22-90
years). The mean time of the first MR study was 8.0 ± 4.8 hours (range,
2-22 hours).
FIRST 24 HOURS
In the first 24 hours MRA arterial lesions were present in 24 (69%)
of the 35 patients while no lesion was identified in the other 11 patients
(31%) (Table 1). No significant
difference was noted in the time of MR study between the 2 groups. Arterial
lesions were present in the middle cerebral artery in 14 patients, involving
the M1 segment in 10 (bilateral in one patient, middle cerebral artery and
anterior cerebral artery lesions in another patient), M2 segment in 2 patients,
and M3 segment in 2 patients. There was 1 patient with a lesion in the anterior
cerebral artery and 9 patients with lesions in the proximal internal carotid
arteries (ICAs). Two patients had additional lesions in the arteries of the
posterior circulation.
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Table 1. Relationship Between Mismatch and Arterial Lesions in the
First 24 Hours of Ischemic Stroke*
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The perfusion lesion volume was significantly larger in patients with
an arterial lesion (P<.001, Mann-Whitney test),
the mean perfusion lesion size being 112.2 ± 75.6 mL in patients with
an arterial lesion compared with 16.8 ± 25.7 mL in patients without
a lesion. In 3 patients with normal MRAs, the perfusion lesion was greater
than 30 mL, larger than might be expected from an M3 arterial branch occlusion.
Two had striatocapsular infarcts from presumed lenticulostriate arterial occlusion.
The mean DWI lesion size was larger in patients with an arterial lesion (17.2
± 21.7 mL) compared with 6.1 ± 5.3 mL in patients without an
arterial lesion, but not significantly so (P = .45,
Mann-Whitney test, Table 1).
At this time point (<24 hours after the onset of stroke) a perfusion-diffusion
mismatch was present in 22 (92%) of the 24 patients with an arterial lesion
on MRA compared with 5 (46%) of the 11 patients with a normal MRA (P = .006, 2 test; Table 1). All 9 patients with ICA lesions had a mismatch. The absolute
and relative mismatch sizes were significantly smaller in patients with a
normal MRA than in patients with an abnormal MRA. The mean relative mismatch
size was 122.4 ± 70.4 for patients with an arterial lesion compared
with 33.6 ± 31.5 (P<.005, Mann-Whitney
test) in those without. The mean absolute mismatch size was 103.9 ±
75.6 mL for patients with an arterial lesion compared with 26.2 ± 32.6
mL (P = .02, Mann-Whitney test) in those without.
The mean relative mismatch size for patients with an ICA lesion was 128.9
± 76.8.
FOLLOW-UP STUDY 2 TO 4 DAYS AFTER STROKE
By 2 to 4 days, partial or total recanalization had occurred in 9 (38%)
of the 24 patients with an arterial lesion at the first time point (Table 2). Only 1 of the 9 patients with
ICA lesions showed recanalization while 8 of the 14 patients with middle cerebral
artery lesions showed recanalization. One patient with an anterior cerebral
artery lesion did not show recanalization—a stenotic lesion at the first
time point became completely occluded at the second time point. Four of the
10 patients with M1 middle cerebral artery lesions showed recanalization while
all 4 patients with M2 and M3 lesions showed recanalization. The MRAs were
unchanged in the 11 patients with a normal MRA at the first time point.
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Table 2. Relationship Between Mismatch and Arterial Recanalization
at 2 to 4 Days*
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Of the 22 patients with an arterial lesion and a mismatch at the first
time point, on the follow-up study the mismatch had resolved in 8 (87%) of
the 9 patients with arterial recanalization compared with 5 (39%) of the 13
patients with persisting arterial lesions (P = .03,
Fisher exact test; Table 2). In
2 of the 15 patients with persisting arterial occlusion, the DWI lesion expanded
to become equivalent to the perfusion lesion, accounting for resolution of
the mismatch. Six of the 9 patients with ICA lesions still had a mismatch,
including 1 who recanalized. Two patients with ICA lesions showed resolution
of the mismatch even though the MRA was still abnormal. The perfusion-diffusion
mismatch resolved in 3 of the 5 patients with normal MRA and mismatch at the
time of the first study. In 2 cases the perfusion lesion had resolved and
in 1 the DWI lesion had evolved to become equivalent to the perfusion lesion
volume (Table 2).
The mean mismatch sizes at this time point are given in Table 2. In the one patient with recanalization and persisting mismatch,
the relative mismatch size was 47.7 compared with 110.9 ± 76.2 for
patients without recanalization and those with a normal MRA. The results are
further illustrated in Figure 1,
with images from representative cases shown in Figure 2.
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Figure 1. A, In the first 24 hours magnetic
resonance angiography (MRA) arterial lesions were present in 24 (69%) of the
35 patients. In the other 11 patients (31%) the MRA was normal. By 2 to 4
days, partial or total recanalization had occurred in 9 (38%) of the 24 patients
with an arterial lesion at the first time point. The MRAs were unchanged in
the 11 patients with normal MRA at the first time point. B, At the first time
point (<24 hours after the onset of stroke) a perfusion-diffusion mismatch
was present in 22 (92%) of the 24 patients with an arterial lesion on MRA
compared with 5 (46%) of the 11 patients with a normal MRA (P = .006, 2 test). By the time of the follow-up study
1 (13%) of the 9 patients with arterial recanalization had a persisting perfusion-diffusion
mismatch compared with 8 (57%) of the 15 patients with persisting arterial
lesion (P<.05, Fisher exact test). In 2 patients
with persisting arterial lesions, the diffuson-weighted imaging lesion had
evolved to become equivalent to the perfusion lesion volume. A perfusion-diffusion
mismatch was present in 2 (18%) of the 11 patients with normal MRA at the
follow-up time point compared with 5 of the 11 patients at the time of the
first study. In 2 cases the perfusion lesion had resolved and in 1 the DWI
lesion had evolved to become equivalent to the perfusion lesion volume.
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Figure 2. For all parts the diffusion-weighted
image (DWI) is on the left, the relative mean transit time map (MTT) is in
the center, and the magnetic resonance angiogram (MRA) is on the right of
the image. A, A 70-year-old woman was seen with right middle cerebral artery
(MCA) syndrome with fluctuating deficits. The first study was obtained at
3.5 hours (top row) and the second study at 28 hours (lower row). On the first
MRA study at 3.5 hours there was a right proximal MCA—M1-occlusion on
MRA, likely to have resulted from a cardiac source of embolism. There was
a perfusion-diffusion mismatch with the DWI lesion surrounded by a larger
area of hypoperfusion on MR perfusion imaging. On the follow-up study there
had been partial recanalization and resolution of the perfusion abnormality
and the perfusion-diffusion mismatch. This patient showed significant clinical
improvement by the time of the second study, with resolution of her motor
weakness. B, A 75-year-old woman was seen with a mild right anterior cerebral
artery (ACA) syndrome. The first study was obtained at 3 hours (top row) and
the second study at 27 hours (lower row). On the first study at 3 hours there
was an incomplete lesion in the right anterior MCA on MRA, which was likely
to have resulted from local disease. There was a perfusion-diffusion mismatch
with the DWI lesion surrounded by a larger area of hypoperfusion on MR perfusion
imaging. On the follow-up study there was a complete occlusion of the ACA
on MRA. There was a persisting mismatch and significant expansion of the DWI
lesion had occurred. The patient progressed to a full ACA clinical syndrome
by the time of the second study. C, A 51-year-old woman was seen with transient
left-sided (face and hand) numbness. The first study was obtained at 5 hours
(top row) and the second study at 3 days (lower row). On the first MR study
at 5 hours the MRA was normal. There was a perfusion-diffusion mismatch with
the DWI lesion surrounded by a larger area of hypoperfusion on MR perfusion
imaging. On the follow-up study there was persistence of the DWI lesion and
the perfusion-diffusion mismatch, although now there was also an area of perfusion
abnormality in the posterior parietal region of uncertain cause (possibly
due to embolism). D, A 78-year-old man with transient aphasia that had resolved
at the time of the initial study. The first study was obtained at 9 hours
(top row) and the second study at 3 days (lower row). On the first MR study
at 9 hours the MRA was normal as was the rMTT map image. It is likely that
reperfusion had already occurred by the time of the initial study at 9 hours,
later than the preceding examples. There was a small peripheral cortical DWI
lesion in the left posterior frontal cortex. The findings were unchanged on
the follow-up study.
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On the follow-up study DWI lesion evolution (enlargement by at least
20%) had occurred in 20 of the 24 patients with an arterial lesion at the
first time point compared with 8 of the 11 patients (P>.05)
with a normal MRA. The mean absolute difference in the DWI lesion volume was
16.0 ± 28.3 mL compared with 1.7 ± 4.87 mL, respectively (P = .01). There was insufficient data at the chronic time
points to study the effect on final infarct volume.
COMMENT
In this study, the serial changes in arterial lesions and their relation
to perfusion-diffusion mismatch as measured by multimodality MRI were examined.
The results of this investigation partially confirmed our initial hypotheses.
The frequent finding of a perfusion-diffusion mismatch with an arterial lesion
(92%) suggested an arterial vascular basis for the MR perfusion and DWI lesions
in acute stroke. Furthermore, supportive evidence for a vascular basis of
these changes exists in some cases where the mismatch disappeared with arterial
recanalization. However, we found that 5 (46%) of the 11 patients with a normal
MRA also had a mismatch at the first time point. While this finding might
result from missed small arterial lesions on MRA, such as M3 branch, more
distal, or lenticulostriate artery occlusions, in some cases it may have been
owing to altered tissue perfusion with patent arteries or to an alternate
mechanism. Therefore, although there were significant associations, the information
from MRA and MR perfusion and DWI were not entirely concordant.
In looking at the cases with discordance between MRA and the perfusion-diffusion
mismatch, a few speculations can be made. First, in the 5 patients with a
normal MRA and a perfusion-diffusion mismatch at the first time point, it
seems likely that there may have been an arterial lesion below the resolution
of the MRA as mentioned earlier. The finding of smaller perfusion lesions
in patients with a normal MRA provides support for this theory. However, local
or alternate mechanisms of tissue ischemia should not be disregarded. Cerebral
arterial occlusions cannot be detected short-term in up to 20% to 30% of stroke
patients even using conventional angiography14;
in up to 30% of patients the stroke mechanism cannot be determined.15 Perhaps in a few cases this pattern could be analogous
to syndrome X in the cardiac literature—ischemia in the presence of
normal coronary arteries—that may be attributed to microvascular disease.16 Alternatively, in some of these 5 patients and the
1 patient where the MRA showed recanalization but the mismatch remained, there
may have been a no-reflow phenomenon after recanalization.17
Conventional angiographic studies or higher resolution MRA that may provide
better arterial definition and MRI studies conducted earlier after stroke
onset might have a greater probability of detecting arterial occlusive lesions.
A comparison of the evolution of the DWI lesions between patients with and
without arterial lesions at the first time point could provide further insights.
In our study, most patients showed DWI lesion enlargement at 2 to 4 days,
but this is a time when DWI lesions are confounded by edema.
Second, in patients in whom the arterial lesion persisted but in whom
the mismatch resolved at the second time point, we suggest that (1) recruitment
of the collateral circulation could have led to restored tissue perfusion,
(2) the DWI lesion could have expanded to its maximal size so that the DWI
and perfusion lesions became congruent, or (3) there was clearing of a distal
tandem arterial lesion.
There have been several preliminary reports of the correlation between
MRA and perfusion and diffusion lesions at one time point during the first
24 to 48 hours of ischemic stroke.7, 8, 10, 18
Barber et al8 also found that a mismatch was
more likely to be present and of larger size in patients with an arterial
lesion on MRA: further, on review of their data 5 of 17 patients with a mismatch
had a normal MRA in the first 24 hours of stroke. Conversely, Rordorf et al7 did not find a significant mismatch in any of their
patients with normal MRA although the use of relative cerebral blood volumes
may explain this finding.19 In the early study
of Warach et al,20 relative cerebral blood
volumes abnormalities were found in 15 of 16 patients with arterial lesions
on MRA. Neumann-Haefelin and colleagues21, 22also
reported that patients with ICA lesions had the largest mismatches of all.
In patients undergoing thrombolysis, Schellinger et al18
reported more extensive tissue reperfusion and arterial recanalization with
recombinant tissue plasminogen activator therapy, with subsequently smaller
infarct size.
One limitation of the study is that MRA was used without confirmation
of the results by conventional angiography. Magnetic resonance angiograpy
and conventional angiography have been found to provide similar detection
rates in prior studies of ICA occlusive disease,23
although the sensitivity and specificity of MRA for intracranial vascular
lesions have not been widely tested against conventional angiography.24 Our finding of an arterial occlusion rate of 69%
in the first 24 hours is equivalent to reports from angiographic studies in
the 1980s.14, 25 Further, the pattern
of arterial recanalization and the recanalization rate on MRA of 38% by 2
to 4 days were similar to prior angiographic reports.14, 25
We acknowledge that it is possible that in some patients at the first time
point, when an arterial lesion was seen, there was already partial recanalization.
Similarly, we acknowledge that the optimal MR perfusion map for use in these
studies is a matter of current debate and that the relative mean transit time
map may overestimate the volume of the perfusion abnormality and the tissue
at risk.19, 21, 22
The results raise the question: which is the best MRI template in the
thrombolysis setting—an MRA-identified lesion or the perfusion-diffusion
mismatch?26, 27 Most prior MRI
studies have proposed that only patients with a mismatch should receive thrombolytic
therapy because they are the individuals with potentially salvageable tissue
via reperfusion2, 11 thereby minimizing
the risk to other patients. However, this proposal has been controversial
because of uncertainty over the exact pathophysiological basis of the mismatch
and because of variable clinical correlations of lesion volumes. Whether DWI
lesion evolution always represents recruitment of the penumbra, or other processes
such as delayed neuronal injury and apoptosis, is still to be determined.3
The one currently approved therapy for stroke—recombinant tissue
plasminogen activator administered intravenously within 3 hours—is believed
to work by opening large cerebral arteries occluded by thromboembolic material.26, 27 Therefore, it seems reasonable that
arterial imaging should be a best start to guide therapy (whether by MRA,
transcranial Doppler ultrasound, or by angiography). We propose that the optimal
candidate for thrombolysis is the patient with a documented arterial occlusion
and a mismatch. The Prolyse in Acute Cerebral Thromboembolism II study has
shown that when patients are highly selected on the basis of their arterial
lesion (M1 and M2 occlusions only), reperfusion can be effectively carried
out up to 6 hours after stroke.28
The optimal treatment of patients with a mismatch and normal MRA is
one of speculation. Some patients may have an arterial occlusion below the
resolution of the MRA. The prevailing thinking is that these may be amenable
to recanalization with tissue plasminogen activator therapy, although it is
acknowledged that these branch occlusions have a high and early rate of spontaneous
recanalization. In other cases, however, there may be altered tissue perfusion
and microcirculation as the basis for this change.29
Perhaps this group of patients might specifically benefit from reperfusion
therapies that might work on the microcirculation.26, 28, 30
Evaluating the mismatch with the MRA gives the following 4 ischemic
stroke patterns: abnormal MRA, mismatch; abnormal MRA, no mismatch; normal
MRA, mismatch; and normal MRA, no mismatch. These patterns may provide a more
rational approach to treatment.
CONCLUSIONS
Concordance was frequently found between changes in the putated tissue
at risk (the mismatch) and changes in arterial patency as measured by MRA.
Discordance between MRA lesions and mismatch may have resulted from arterial
branch occlusions undetected by MRA or from an alternate mechanism for the
mismatch. The 4 MRI patterns identified could provide a pathophysiological
basis that, in combination with clinical features, could lead to a more rational
approach to the management of stroke patients and the design of stroke trials.
AUTHOR INFORMATION
Accepted for publication January 22, 2001.
This investigation was supported by the Doris Duke Charitable Foundation,
New York, NY (Dr Baird).
Presented at the 51st Annual Scientific Meeting of the American Academy
of Neurology, Toronto, Ontario, April 27, 1999.
Corresponding author: Alison E. Baird, FRACP, PhD, National Institute
of Neurological Disorders and Stroke, National Institutes of Health, 36 Convent
Dr, MSC 4129, Room 4A03, Bethesda, MD 20892-4129 (e-mail: bairda{at}ninds.nih.gov).
From the Departments of Neurology (Drs Staroselskaya, Chaves, Linfante,
and Caplan) and Radiology (Dr Edelman), Beth Israel Deaconess Medical Center
and Harvard Medical School, Boston, Mass; London Health Sciences Centre, London,
Ontario (Dr Silver); and the National Institute of Neurological Disorders
and Stroke, Bethesda, Md (Drs Warach and Baird).
Corresponding author: Alison E. Baird, FRACP, PhD, National Institute
of Neurological Disorders and Stroke, National Institutes of Health, 36 Convent
Dr, MSC 4129, Room 4A03, Bethesda, MD 20892-4129 (e-mail: bairda{at}ninds.nih.gov).
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