| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Department of Neurology (G.R., W.J.K., S.C.C., L.H.S., F.B.,
A.G.S., G.G.) and Division of Neuroradiology (W.A.C., P.W.S., R.F.B.),
Massachusetts General Hospital, Boston.
Correspondence to Guy Rordorf, MD, Department of Neurology, Massachusetts General Hospital, BLK 1291, Fruit St, Boston, MA 02114. E-mail rordorf{at}helix.mgh.harvard.edu
Methods—Seventeen patients seen within 12 hours of onset of MCA
stroke had MR angiography, standard MRI, and PWI and DWI MRI. PWI maps
were generated by analysis of the passage of
intravenous contrast bolus through the brain. Cerebral
blood volume (CBV) was determined after quantitative analysis
of PWI data. Volumes of the initial DWI and PWI lesion were calculated
and compared with a final infarct volume from a follow-up imaging study
(CT scan or MRI).
Results—Group 1 (10 patients) had MCA stem (M1) occlusion by MR
angiography. DWI lesion volumes were smaller than the volumes of CBV
abnormality. In 7 patients the final stroke volume was larger or the
same, and in 3 it was smaller than the initial CBV lesion. Group 2 (7
patients) had an open M1 on MR angiography with distal MCA stroke. In 6
group 2 patients, the initial DWI lesion matched the initial CBV
abnormality and the final infarct.
Conclusions—Most patients with M1 occlusion showed progression of
infarction into the region of abnormal perfusion. In contrast, patients
with open M1 had strokes consistent with distal branch
occlusion and had maximal extent of injury on DWI at initial
presentation. Application of these MRI techniques should
improve definition of different acute stroke syndromes and facilitate
clinical decision making.
Accurate clinical discrimination between different patterns of MCA
stroke is difficult, and new MRI techniques promise to improve
diagnosis of the extent and location of infarct in the emergency
setting. DWI has been shown to be sensitive to early ischemic
injury in the brain,2 3 while alteration in blood
flow can be appreciated with PWI.4 Combined
DWI/PWI permits new pathophysiological insight in
the setting of acute stroke4 5 because it allows
regional assessment of both ischemic and irreversibly damaged
or infarcted brain tissue. We used these new tools to map early
regional infarction and ischemia in patients with MCA stroke.
We hypothesize that whereas the pattern of ischemia and
infarction depends on the site of the obstructed vascular lesion,
DWI/PWI techniques allow a prediction of final infarct size along a
continuous scale.
As reported,4 our acute stroke protocol MRI
includes sagittal T1, axial T2, proton density of fluid-attenuated
inversion-recovery imaging (FLAIR), DWI, circle of Willis
two-dimensional phase-contrast MRA, postgadolinium T1, and PWI. MRI is
performed with the use of a General Electric Signa 1.5-T MRI unit with
an echo-planar retrofit from Advanced NMR Systems. The protocol
requires approximately 30 minutes.
Our DWI technique samples the entire diffusion tensor. The technique
consists of six high–b value single-shot images at each slice
position, each corresponding to diffusion measurement in a given
direction, followed by a single low–b value image. The high b value we
use is 1221 s/mm2; the low value is 3
s/mm2. A summary of the parameters is
as follows: repetition time, 6 seconds; echo time, 118 milliseconds;
matrix, 256x128; field of view, 40x20 cm; slice thickness, 6 mm;
interslice gap, 1 mm. The complete seven-image tensor acquisition
requires 42 seconds; we typically acquire three repetitions to improve
the signal-to-noise ratio, which results in a total imaging time of 126
seconds. Generation of isotropic (tensor trace) DWI occurs off-line on
a networked workstation (Sparcstation 20, Sun Microsystems) and
requires 5 to 10 minutes for data transfer and computation.
Qualitative perfusion imaging is obtained by performing spin-echo
echo-planar imaging during the rapid intravenous injection
of 0.2 mmol/kg of gadodiamide or
gadopentetate.4 We obtained 51 single-shot
echo-planar images (repetition time, 1500 milliseconds; echo time, 75
milliseconds) in each of 10 slices for a total of 510 complete images
acquired in 77 seconds, or 46 single-shot echo-planar images in each of
11 slices for 506 complete images acquired in 69 seconds. Data were
then transferred to a workstation for further analysis.
Perfusion scans were analyzed for regional abnormalities on the
rCBV maps, as previously described.4
Two-dimensional phase-contrast angiography was performed. Imaging of
three 10-mm-thick sections through the region of the circle of Willis
was performed, with an encoding velocity of 80 cm/s.
Lesion volume was calculated with a planimetric technique for DWI, T2,
and PWI scans and the follow-up study.4 The
outline of the abnormality was first obtained with the use of a
semiautomated segmentation technique in a commercial image
analysis package (Alice; Hyden Image Processing). The outlined
abnormality was then modified by a research assistant to fit the lesion
by eye in each slice independently. These were then confirmed or
corrected by a neuroradiologist and a neurologist. The area of the
abnormality on each section was multiplied by the section thickness
plus the gap between slices to obtain a volume measurement. All MRI
techniques were performed in the same section plane and location to
minimize volume-averaging errors.
The distribution of the abnormality on the acute DWI and CBV maps and
on the follow-up studies was categorized as involving one or more of
the following territories: deep lenticulostriate territory; anterior
cerebral artery/MCA territory watershed (supraventricular
white matter of the centrum semiovale and cortical borders
between the anterior cerebral artery and MCA territories); MCA superior
and/or inferior division; or small surface branch.
Statistical analyses were done with the use of the
Wilcoxon test for categorical variables and linear
regression analysis for continuous variables.
We were able to separate the patients into two groups based on the MRA
results. Ten patients (group 1) had M1 occlusion by MRA, and 7 patients
(group 2) had a normal-appearing flow signal in the M1 segment on MRA.
In all group 1 patients the final infarction volume was larger
(Table
There was no difference in the mean initial DWI lesion size
between groups 1 and 2 (49.7±20 versus 15.1±16
cm3; P>0.15). Between groups 1 and 2
there were significant differences in the size of the initial CBV
abnormality (83.3±16 versus 8.1±20 cm3;
P<0.005) and the size of the final stroke (108.6±22 versus
23.9±27 cm3; P<0.003). Both the
initial DWI abnormality and the initial CBV size correlated
significantly with final stroke size
(r2=.74 and .84, respectively;
P<0.0001 for both), with a better correlation for the
initial CBV abnormality. It should be noted that final stroke size was
always measured on a scan 3 to 7 days (mean, 6 days) after the initial
event, and the contribution of ischemic edema to stroke volume
is unknown. The T2 abnormality appeared to match the DWI abnormality in
all cases by this time. None of the included cases had clinically
evident malignant brain edema or major mass effect on imaging. However,
some contribution of ischemic edema to the stroke volume
measurement on the follow up scan is likely. A third image at or around
2 weeks from onset would be required to detect and measure this
effect.
There were three different patterns of DWI/PWI in acute MCA stroke in
patients with an occluded MCA stem (group 1). Two patients (patients 5
and 8) had early complete MCA territory infarction (Figure 1
Five patients in group 2 had a cortical branch stroke with matching DWI
and PWI abnormalities (patients 1, 6, 12, 16, and 17) (Figure 4
PWI and DWI can depict focal cerebral ischemia and irreversible
ischemic injury, respectively, in the very early stages of
stroke, earlier than can be depicted with conventional CT or
MRI.4 We4 and
others5 have reported that the region of
infarcted tissue as demonstrated by the initial DWI abnormality can
enlarge into a larger volume of brain hypoperfusion demonstrated by
decreased rCBV on the initial perfusion scans. The mismatch between the
region of hypoperfusion (larger) and the region of diffusion
abnormality (smaller) may predict those patients at risk for infarct
enlargement.4 5
Human ischemic stroke is a heterogeneous entity
caused by a variety of pathophysiological
mechanisms with different profiles and outcomes.9
MCA territory infarction is the most common arterial
territory affected in major stroke syndromes. We demonstrate for the
first time using functional MRI methods that MCA stroke can be
classified into clinically and
pathophysiologically important different
subtypes on the basis of MRA, PWI, and DWI.
In our study patients with M1 occlusion usually showed progression of
infarction into a larger region of abnormal perfusion in the hours or
days after initial presentation. These patients had a
mismatch between the extent of early infarction (DWI abnormal) and
extent of early ischemia (PWI abnormal). We were able to
demonstrate in this group that the early CBV abnormality is slightly
better than the DWI abnormality as a predictor of final infarct size.
Patients with these radiological characteristics may represent
the group most likely to benefit from reperfusion therapy. One subgroup
of the patients with MCA occlusion had early stroke injury limited to
the poorly collateralized lenticulostriate territory (Figure 3
In contrast to group 1, patients with flow-related signal enhancement
in the MCA stem and stroke location and size consistent with
distal branch occlusion were found to have maximal extent of regional
injury on their initial study (matched DWI/CBV) (Figure 4
The appearance of the MCA stem on MRA provides indirect information and
can help to predict final infarct size. These new functional MRI
techniques can directly measure parameters in an individual
patient that not only predict final infarct size but, by demonstrating
mismatch between ischemia (regions of rCBV abnormality) and
already injured tissue (regions of abnormality on DWI), define possible
salvageable tissue.4 5
The ability to demonstrate the extent of the ischemic penumbra,
defined as ischemic brain tissue at risk for infarct but still
potentially recoverable,10 11 is crucial because
it constitutes the target for early therapy. It is also crucial to
recognize those patients who have already sustained the maximal extent
of ischemic injury and do not have brain tissue at risk for
further infarct to avoid exposing them to the potential risks of
thrombolysis and neuroprotective agents.
In conclusion, combined DWI and PWI in the acute setting can help to
identify brain tissue already injured or ischemic and still at
risk for infarction. With the help of these new imaging techniques, the
pattern of acute MCA stroke can be defined more clearly. This
information may help us to more accurately select those patients who
should receive thrombolytic and neuroprotective
therapies.
Received November 21, 1997;
revision received February 16, 1998;
accepted February 16, 1998.
© 1998 American Heart Association, Inc.
Original Contributions
Regional Ischemia and Ischemic Injury in Patients With Acute Middle Cerebral Artery Stroke as Defined by Early Diffusion-Weighted and Perfusion-Weighted MRI
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and Purpose—We sought to
map early regional ischemia and infarction in patients with
middle cerebral artery (MCA) stroke and compare them with final infarct
size using advanced MRI techniques. MRI can now delineate very early
infarction by diffusion-weighted imaging (DWI) and abnormal tissue
perfusion by perfusion-weighted imaging (PWI).
Key Words: middle cerebral artery • stroke • magnetic resonance imaging • diffusion-weighted imaging • perfusion-weighted imaging
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The MCA is the artery
most commonly affected in human strokes. There is considerable
variability in the extent and location of infarction in patients with
embolic MCA territory stroke. Two major patterns
emerge1 : (1) occlusion of the MCA stem with (a) a
large infarct involving both the deep territory supplied by
lenticulostriate penetrator vessels and the cortex supplied by the
major divisions of the MCA or (b) readily available adequate
leptomeningeal collateral flow, in which case the cortex survives but
the deep territory supplied by the poorly collateralized M1 penetrators
proceeds to infarction, or (2) an open MCA stem with emboli that pass
distal to the origin of the penetrators. Infarction may involve only
the territory supplied by a single division or a small cortical branch.
Functional outcome and treatment decision should depend on which of the
above patterns are operative.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Patients who had symptoms and signs of an MCA territory stroke
between July 1994 and April 1996 and had an acute stroke protocol MRI
within 12 hours from the onset of their deficit were analyzed.
Seventeen consecutive patients were identified. Nine of these 17
patients were previously described in an initial report on DWI/PWI in
acute stroke.4 Patients underwent MRI 1.5 to 10
hours after the onset of symptoms. The initial diagnosis of MCA
territory infarct was confirmed in all 17 patients by the acute MRI as
well as on follow-up clinical and imaging examinations. In all 17
patients DWI and PWI depicted distinct abnormalities in the acute phase
that predicted infarction location on follow-up conventional CT and/or
MRI done 3 to 7 days later. All patients were treated in a similar
fashion, including the use of intravenous anticoagulation.
Anticoagulation was started before the DWI/PWI was performed.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Seventeen consecutive patients with symptoms and signs of an MCA
territory stroke underwent the acute stroke protocol MRI between July
1994 and April 1996. 
) than the initial DWI lesion. In 6
of 10 patients the lesion size more than doubled. Initial DWI lesion
volumes were smaller than the volume of CBV abnormality in all but 3
patients (patients 4, 8, and 15). Final infarct volume was smaller than
the initial CBV abnormality in 3 patients (patients 3, 7, and 9) and
was of similar size in 2 (patients 5 and 11). In the remaining 5
patients the final stroke volume exceeded the initial CBV lesion
volume. In 3 of the group 2 patients (Table) the initial DWI lesions
matched the final infarct size (patients 1, 12, and 17), and in 2
(patients 6 and 16) the final infarct sizes were close to the volumes
of the initial DWI lesions. In 1 patient (patient 6) the stroke size
was so small that the apparent shrinkage in size could be related to
measurement variability since slice position was not identical on the
follow-up scan. Only 1 patient (patient 14) had a major increase in
stroke size (Table). This patient likely had a second vascular event
after his initial DWI and PWI scans. The first scan showed a superior
division territory abnormality, whereas the follow-up study showed a
complete MCA and posterior cerebral artery stroke.
View this table:
[in a new window]
Table 1. Acute DWI and CBV Lesion Volume Compared With Infarct Size on
Follow-up Scan and Correlation With Vascular Lesion ). Five patients had extensive
ischemia with progressive infarction starting in the
peri-insular region (group 1; patients 2, 4, 10, 11, and 15) (Figure 2). Three patients had MCA flow
obstruction with DWI abnormalities in the lenticulostriate territory
and cortical ischemia on PWI but never developed evidence of
cortical injury (group 1; patients 3, 7, and 9) (Figure 3).
View larger version (126K):
[in a new window]
Figure 1. Early large MCA infarction. A 53-year-old man
underwent imaging 3 hours after the onset of left hemiparesis. The MRI
shows a normal T2-weighted sequence, whereas the DWI demonstrates a
large area of ischemic injury (arrow). The CBV map shows an
area of abnormal perfusion only slightly larger than the DWI
abnormality (arrow). MRA demonstrates an occlusion of the right MCA
stem (arrow). The follow-up head CT scan shows an infarction (arrow)
consistent with the area of abnormal perfusion seen on the CBV
map.
View larger version (125K):
[in a new window]
Figure 2. Progressive cortical infarction. A 62-year-old man
had sudden onset of dense right hemiplegia 7 hours before his MRI
study. The T2 sequence shows only a subtle increase in signal in a
gyral pattern, whereas the DWI map shows an ischemic injury
(arrow) mostly located in the insular and peri-insular cortex. The CBV
map demonstrates a perfusion abnormality (arrow) much larger than the
DWI abnormality. MRA demonstrates a left MCA stem occlusion (arrow). In
the follow-up MRI the stroke has expanded beyond the initial area of
perfusion abnormality (arrow).
View larger version (116K):
[in a new window]
Figure 3. MCA flow obstruction with lenticulostriate injury
and cortical ischemia without injury. A 72-year-old woman was
seen 2.5 hours after the onset of left hemiparesis. The T2 maps are
normal, whereas the DWI sequence (arrow) shows an area of
ischemic injury located in the deep white matter. The CBV maps
demonstrate an area of abnormal perfusion involving cortical branches
of the right MCA territory (arrow). The follow-up scan shows that the
stroke (arrow) is limited to the area seen as abnormal on the initial
DWI study, while the rest of the left MCA territory is now
normal. ), while one patient had
ischemia in both MCA divisions with abnormal DWI initially
limited to one division; on the following scan the territory of the
spared division was recruited into the infarct (patient 13).
View larger version (118K):
[in a new window]
Figure 4. Cortical branch stroke with matching DWI and
perfusion abnormality. A 75-year-old man presented to our
emergency department 4 hours after the acute onset of mutism. His
initial MRI study is shown. The T2-weighted image is normal, whereas a
matching abnormality consistent with ischemic injury is
seen on the DWI and CBV maps (arrows). MRA shows an open MCA stem
bilaterally (arrow). The follow-up head CT scan done 4 days later
confirms the presence of the stroke (arrow), which is
consistent with the abnormality seen on the initial DWI and CBV
maps.
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
After cerebrovascular occlusion the transition from reversible
ischemia to irreversible damage is a process that occurs at a
variable rate dependent on the degree of
ischemia.6 7 Recent positron emission
tomography8 and functional
MRI5 studies have reported that potentially
viable tissue persists in some ischemic stroke patients in the
peri-infarct region for the first 24 to 48 hours after stroke onset. A
technique that could delineate irreversibly damaged tissue from
ischemic but viable brain would greatly assist present and
future treatment decisions that involve thrombolytic or
neuroprotective drugs. 
). In
such patients, cortical regions demonstrated abnormal PWI but normal
DWI. The ischemic cortex in such patients may or may not
survive, depending on the degree and duration of ischemia, and
constitutes ischemic brain at risk. Other patients showed an
early ischemic injury in the peri-insular cortex, which then
spread into other cortical areas (Figure 2). The peri-insular cortex
may be especially susceptible because of relatively poor collateral
flow since it is located most distal to the leptomeningeal collaterals.
A third group of patients with MCA occlusion presumably without
collateral flow had rapid evolution of infarction in the entire
territory of ischemia (Figure 1). This
heterogeneity could also, at least in part, relate to
the duration of occlusion and timing of spontaneous
recanalization. Although extension of infarction
appears to play a major role in enlargement of the region of injury,
the contribution of ischemic edema leading to overestimation of
final stroke size or tissue loss leading to underestimation needs to be
further investigated. ). Unless
neuroprotective or reperfusion agents can be shown to reverse DWI
abnormalities, then in these patients, as well as in those with M1
occlusion and rapid evolution of DWI injury path through the entire
ischemic territory, such therapies may not be justified.
Selected Abbreviations and Acronyms
CBV
=
cerebral blood volume
DWI
=
diffusion-weighted imaging
MCA
=
middle cerebral artery
MRA
=
magnetic resonance angiography
PWI
=
perfusion-weighted imaging
rCBV
=
regional cerebral blood volume
Acknowledgments
This study was supported by a grant from the National Stroke
Association (to Dr Cramer).
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  M. Kawata, M. Sekino, S. Takamoto, S. Ueno, S. Yamaguchi, K. Kitahori, H. Tsukihara, Y. Suematsu, M. Ono, N. Motomura, et al. Retrograde cerebral perfusion with intermittent pressure augmentation provides adequate neuroprotection: Diffusion- and perfusion-weighted magnetic resonance imaging study in an experimental canine model J. Thorac. Cardiovasc. Surg., October 1, 2006; 132(4): 933 - 940. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. S. Kim, D. H. Lee, C. W. Ryu, J. H. Lee, C. G. Choi, S. J. Kim, and D. C. Suh Multiple Cerebral Microbleeds in Hyperacute Ischemic Stroke: Impact on Prevalence and Severity of Early Hemorrhagic Transformation After Thrombolytic Treatment. Am. J. Roentgenol., May 1, 2006; 186(5): 1443 - 1449. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R.G. Gonzalez Imaging-guided acute ischemic stroke therapy: From "time is brain" to "physiology is brain". AJNR Am. J. Neuroradiol., April 1, 2006; 27(4): 728 - 735. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Seitz, S. Meisel, P. Weller, U. Junghans, H.-J. Wittsack, and M. Siebler Initial Ischemic Event: Perfusion-weighted MR Imaging and Apparent Diffusion Coefficient for Stroke Evolution Radiology, December 1, 2005; 237(3): 1020 - 1028. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Ay, W. J. Koroshetz, M. Vangel, T. Benner, C. Melinosky, M. Zhu, N. Menezes, C. J. Lopez, and A. G. Sorensen Conversion of Ischemic Brain Tissue Into Infarction Increases With Age Stroke, December 1, 2005; 36(12): 2632 - 2636. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Fiehler, K. Knudsen, G. Thomalla, E. Goebell, M. Rosenkranz, C. Weiller, J. Rother, H. Zeumer, and T. Kucinski Vascular Occlusion Sites Determine Differences in Lesion Growth from Early Apparent Diffusion Coefficient Lesion to Final Infarct AJNR Am. J. Neuroradiol., May 1, 2005; 26(5): 1056 - 1061. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Kucinski, D. Naumann, R. Knab, V. Schoder, S. Wegener, J. Fiehler, A. Majumder, J. Rother, and H. Zeumer Tissue at Risk Is Overestimated in Perfusion-Weighted Imaging: MR Imaging in Acute Stroke Patients without Vessel Recanalization AJNR Am. J. Neuroradiol., April 1, 2005; 26(4): 815 - 819. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Feng, C. L. Dumoulin, S. Dashnaw, R. D. Darrow, R. L. DeLaPaz, P. L. Bishop, and J. Pile-Spellman Feasibility of Stent Placement in Carotid Arteries with Real-time MR Imaging Guidance in Pigs Radiology, February 1, 2005; 234(2): 558 - 562. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.-K. Lee, D. I. Kim, S. Y. Kim, D. J. Kim, J. E. Lee, and J. H. Kim Reperfusion Cellular Injury in an Animal Model of Transient Ischemia AJNR Am. J. Neuroradiol., September 1, 2004; 25(8): 1342 - 1347. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Liu, J. O. Karonen, R. L. Vanninen, J. Nuutinen, A. Koskela, S. Soimakallio, and H. J. Aronen Acute Ischemic Stroke: Predictive Value of 2D Phase-Contrast MR Angiography--Serial Study with Combined Diffusion and Perfusion MR Imaging Radiology, May 1, 2004; 231(2): 517 - 527. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H.-C. Koennecke Editorial Comment--Challenging the Concept of a Dynamic Penumbra in Acute Ischemic Stroke Stroke, October 1, 2003; 34(10): 2434 - 2435. [Full Text] [PDF]
|
|
|
|
|
|
R. E. Latchaw, H. Yonas, G. J. Hunter, W. T.C. Yuh, T. Ueda, A. G. Sorensen, J. L. Sunshine, J. Biller, L. Wechsler, R. Higashida, et al. Guidelines and Recommendations for Perfusion Imaging in Cerebral Ischemia: A Scientific Statement for Healthcare Professionals by the Writing Group on Perfusion Imaging, From the Council on Cardiovascular Radiology of the American Heart Association Stroke, April 1, 2003; 34(4): 1084 - 1104. [Full Text] [PDF]
|
|
|
|
|
|
P. D. Schellinger, J. B. Fiebach, W. Hacke, and J. Rother Imaging-Based Decision Making in Thrombolytic Therapy for Ischemic Stroke: Present Status Stroke, February 1, 2003; 34(2): 575 - 583. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. W. Schaefer, G. J. Hunter, J. He, L. M. Hamberg, A. G. Sorensen, L. H. Schwamm, W. J. Koroshetz, and R. G. Gonzalez Predicting Cerebral Ischemic Infarct Volume with Diffusion and Perfusion MR Imaging AJNR Am. J. Neuroradiol., November 1, 2002; 23(10): 1785 - 1794. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ishikawa, K. Yokoyama, T. Kuroiwa, and K. Makita Apparent diffusion coefficient mapping predicts mortality and outcome in rats with intracerebral haemodynamic disturbance: potential role of intraoperative diffusion and perfusion weighted magnetic resonance imaging to detect cerebral ischaemia Br. J. Anaesth., October 1, 2002; 89(4): 605 - 613. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Fiehler, M. von Bezold, T. Kucinski, R. Knab, B. Eckert, O. Wittkugel, H. Zeumer, and J. Rother Cerebral Blood Flow Predicts Lesion Growth in Acute Stroke Patients Stroke, October 1, 2002; 33(10): 2421 - 2425. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Mullins, P. W. Schaefer, A. G. Sorensen, E. F. Halpern, H. Ay, J. He, W. J. Koroshetz, and R. G. Gonzalez CT and Conventional and Diffusion-weighted MR Imaging in Acute Stroke: Study in 691 Patients at Presentation to the Emergency Department Radiology, August 1, 2002; 224(2): 353 - 360. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Wintermark, M. Reichhart, O. Cuisenaire, P. Maeder, J.-P. Thiran, P. Schnyder, J. Bogousslavsky, and R. Meuli Comparison of Admission Perfusion Computed Tomography and Qualitative Diffusion- and Perfusion-Weighted Magnetic Resonance Imaging in Acute Stroke Patients Stroke, August 1, 2002; 33(8): 2025 - 2031. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. U. Harrer and C. Klotzsch Second Harmonic Imaging of the Human Brain: The Practicability of Coronal Insonation Planes and Alternative Perfusion Parameters Stroke, June 1, 2002; 33(6): 1530 - 1535. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. W. Muir Heterogeneity of Stroke Pathophysiology and Neuroprotective Clinical Trial Design Stroke, June 1, 2002; 33(6): 1545 - 1550. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. N. Fink, M. H. Selim, S. Kumar, B. Silver, I. Linfante, L. R. Caplan, and G. Schlaug Is the Association of National Institutes of Health Stroke Scale Scores and Acute Magnetic Resonance Imaging Stroke Volume Equal for Patients With Right- and Left-Hemisphere Ischemic Stroke? Stroke, April 1, 2002; 33(4): 954 - 958. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. J. Perkins, E. Kahya, C. T. Roque, P. E. Roche, G. C. Newman, and S. Warach Fluid-Attenuated Inversion Recovery and Diffusion- and Perfusion-Weighted MRI Abnormalities in 117 Consecutive Patients With Stroke Symptoms Editorial Comment Stroke, December 1, 2001; 32(12): 2774 - 2781. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
S. Ishikawa, K. Yokoyama, T. Kuroiwa, and K. Makita Evolution of cerebral ischaemia induced by thromboembolism in rats detected by early sequential MR imaging Br. J. Anaesth., September 1, 2001; 87(3): 469 - 476. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. W. Albers Advances in intravenous thrombolytic therapy for treatment of acute stroke Neurology, September 1, 2001; 57(90002): S77 - 81. [Abstract] [Full Text]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
G. Rordorf, W. J. Koroshetz, M. A. Ezzeddine, A. Z. Segal, and F. S. Buonanno A pilot study of drug-induced hypertension for treatment of acute stroke Neurology, May 8, 2001; 56(9): 1210 - 1213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.J. Kelly, E.T. Hedley-Whyte, J. Primavera, J. He, and R.G. Gonzalez Diffusion MRI in ischemic stroke compared to pathologically verified infarction Neurology, April 10, 2001; 56(7): 914 - 920. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. G. Lansberg, V. N. Thijs, M. W. O'Brien, J. O. Ali, A. J. de Crespigny, D. C. Tong, M. E. Moseley, and G. W. Albers Evolution of Apparent Diffusion Coefficient, Diffusion-weighted, and T2-weighted Signal Intensity of Acute Stroke AJNR Am. J. Neuroradiol., April 1, 2001; 22(4): 637 - 644. [Abstract] [Full Text]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
P. W. Schaefer, P. E. Grant, and R. G. Gonzalez Diffusion-weighted MR Imaging of the Brain Radiology, November 1, 2000; 217(2): 331 - 345. [Abstract] [Full Text]
|
|
|
|
|
|
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]
|
|
|
|
|
|
C. Oppenheim, Y. Samson, R. Manai, T. Lalam, X. Vandamme, S. Crozier, A. Srour, P. Cornu, D. Dormont, G. Rancurel, et al. Prediction of Malignant Middle Cerebral Artery Infarction by Diffus |