(Stroke. 2000;31:688.)
© 2000 American Heart Association, Inc.
Original Contributions |
Significance of Acute Multiple Brain Infarction on Diffusion-Weighted Imaging
From the Departments of Neurology and Radiology (K-H.C.), Seoul National University College of Medicine (Korea).
Correspondence to Jae-Kyu Roh, MD, Department of Neurology, Seoul National University Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Korea. E-mail rohjk{at}snu.ac.kr
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Abstract |
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Background and Purpose—Diffusion-weighted imaging (DWI) is superior to conventional MRI in identification of small new ischemic lesions and discrimination of recent infarcts from old ones. Thus, this technique is useful in the detection of acute multiple brain infarcts (AMBI). We sought to determine the frequency and the topographical and etiologic patterns of AMBI detected on DWI.
Methods—We studied 329 consecutive ischemic stroke patients who underwent DWI and MRI/MR angiography within 4 days of stroke onset. AMBI was defined as noncontiguous high signal intensities on DWI in >1 vascular territory. Stroke mechanism was determined according to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST).
Results—We detected AMBI in 95 patients (28.9%). AMBI in anterior circulation was found in 62 cases: in 1 hemisphere in 42 (group A) and in bilateral hemispheres in 20 (group B). Twenty-two patients had AMBI in the posterior circulation (group C) and 11 in both anterior and posterior circulations (group D). The most frequent cause of stroke was large-artery atherosclerosis in groups A (33/42), B (9/20), and C (15/22) (P=0.02) and cardioembolism in group D (6/11) (P=0.02). Elevated fibrinogen or hematocrit was significantly associated with group B (P=0.01). In 9 patients in groups B and D, anatomic variations of anterior or posterior cerebral arteries or patent posterior communicating artery contributed to AMBI.
Conclusions—Different topographical patterns of AMBI are associated with different vascular pathologies and stroke mechanisms. Hemorheologic abnormality or vascular anatomic variations may be contributing factors in the pathogenesis of AMBI in bilateral cerebral hemispheres or in both anterior and posterior circulations.
Key Words: cerebral infarction • magnetic resonance imaging, diffusion-weighted • rheology • stroke, acute
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Introduction |
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Several studies have addressed the issue of multiple brain infarcts and attempted to correlate them with the underlying mechanisms and causes.1 2 3 4 5 However, the data on the frequency and etiology of multiple brain infarcts are still controversial, primarily because of differences in the methods used in the various studies. One important subgroup of multiple brain infarcts is composed of simultaneous infarcts. Bogousslavsky1 identified double infarcts in 1 cerebral hemisphere in 2% of the patients and acute multiple brain infarcts (AMBI) involving the anterior circulation in 5%,4 which were mostly caused by embolic mechanisms. Bernasconi et al3 reported the frequency of AMBI in the posterior circulation to be 11%. However, these data were mainly based on CT or MRI scans, and AMBI may be commonly overlooked when systematic MRI is not utilized. Furthermore, "silent" infarctions are not uncommon, and their frequency revealed by CT is reported to be 10% to 38%.6 7 8 Most silent infarcts were small and/or located in brain areas likely to leave the patient asymptomatic in the event of acute cerebral infarction,9 which may go undetected by conventional MRI.
Diffusion-weighted imaging (DWI) is sensitive to acute cellular injury in cerebral ischemia and can be used to detect ischemic lesions within the first few hours.10 The superiority of DWI relative to conventional MRI permits easier detection of small new ischemic lesions and differentiation of recent infarcts from old ones or nonspecific white matter high signal intensities.11 12 13 14 15 16 17 Thus, AMBI, which may be difficult to appreciate on conventional MRI, may be evident with DWI. Multiple brain infarcts on DWI have been recently studied, but the study considered old infarcts as well as recent ones.5 The purpose of our study was to determine the frequency and clinical, topographical, and etiologic patterns of AMBI detected on DWI.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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We considered 329 consecutive patients (209 males and 120 females; mean age, 62.3±10.9 years; age range, 16 to 88 years) with ischemic stroke who were admitted to our Stroke Unit from July 1997 to June 1999 and underwent both conventional MRI and DWI during the acute stage (within 4 days of stroke; the apparent diffusion coefficient was persistently reduced during this time window).15
Clinical Evaluation
All patients underwent systematic investigations, including
complete blood cell count, blood chemistry, lipid profiles, coagulation
abnormalities, urinalysis, chest roentgenogram, ECG, CT scan, MRI, and
MR angiography. In selected patients, transthoracic and
transesophageal echocardiography,
including a microbubble test, transcranial Doppler, and
catheter angiography, were also performed.
Risk factors included hypertension (blood pressure >160/90 mm Hg on 2 separate occasions), hypercholesterolemia (cholesterol concentration >6.216 mmol/L or LDL cholesterol >4.144 mmol/L), diabetes mellitus, regular cigarette smoking, myocardial ischemia, arrhythmia, valvular heart disease, a family history of stroke or ischemic heart disease, and a history of vascular disease or migraine.
The potential stroke mechanisms were determined according to the classification of the Trial of Org 10172 in Acute Stroke Treatment (TOAST)18 : (1) large-artery atherosclerosis, (2) cardioembolism, (3) small-artery occlusion, (4) other determined etiologies, or (5) undetermined etiology.
The topography of infarcts was determined with reference to the maps establishing anatomic correspondence with dominant arterial territories proposed by Tatu et al.19 20 The diagnosis of AMBI was defined as multiple recent infarcts demonstrated on DWI. Infarcts had to include noncontiguous regions of abnormality on DWI that were present in >1 vascular territory. Uninterrupted lesions visible in contiguous territories were considered a single lesion and were excluded. The arterial territories were divided for the anterior circulation as follows: internal carotid artery (ICA), anterior cerebral artery (ACA), superior division of the middle cerebral artery (MCA), inferior division of the MCA, perforating branches of the MCA, medullary branches of the MCA, and anterior choroidal artery. The arterial territories for the posterior circulation were superficial posterior cerebral artery (PCA), perforating branch of PCA, basilar artery (BA), superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA), and posterior inferior cerebellar artery (PICA).
On the basis of the topographical patterns of AMBI, we divided patients into 4 categories: group A, patients with AMBI in 1 cerebral hemisphere in the anterior circulation; group B, patients with AMBI in the bilateral cerebral hemispheres in the anterior circulation; group C, patients with AMBI in the posterior circulation; and group D, patients with AMBI in both the anterior and posterior circulations.
MRI Evaluation
All patients underwent conventional MRI and DWI on a 1.5-T
system with echo-planar imaging capability (Signa Horizon, Echospeed;
General Electric Medical Systems). Conventional MRI consisted of
transverse T2-weighted sequences (repetition time [TR], 4000 ms; echo
time [TE], 98 ms; 3 excitations) and sagittal T1-weighted sequences
(TR, 450 ms; TE, 10 ms; 2 excitations) with 5-mm-thick slices. DWI was
obtained in the transverse plane with a single-shot, echo-planar,
spin-echo pulse sequence with TR of 6500 ms, TE of 107 ms, 1
excitation, and 2 b values (0 and 1000
s/mm2). The diffusion-gradient pulse duration was
31 ms, with a gradient separation of 33 ms and a gradient strength of
2.16 G/cm. Diffusion gradients were applied simultaneously
along the 3 axes (x, y, z).
The criteria for the diagnosis of acute infarction on DWI included the following16 : (1) focal bright high signal intensities; (2) a location or configuration not thought to represent the normal anisotropy of diffusion; and (3) a location or configuration not thought to represent a magnetic susceptibility artifact (ie, typically seen near the interfaces between the brain and air-filled paranasal sinuses).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Ninety-five (28.9%) of the total 329 patients had AMBI. Sixty-two of them were men, and 33 were women. Their mean age was 64.0±10.0 years, ranging from 38 to 88 years.
Advantages of DWI
DWI was superior to conventional MRI in 43 patients (45.3%). DWI
demonstrated additional ischemic lesions not seen on
conventional MRI in 34 patients. Eighteen of these showed a single
infarct on conventional MRI. DWI discriminated recent infarcts from old
ones or nonspecific periventricular high signal intensities
in 12 patients.
Frequency of AMBI
AMBI in the anterior circulation was found in 62 patients (28.8%)
of 215 with anterior circulation ischemic strokes. Forty-two
had AMBI in the unilateral hemisphere, and 20 had AMBI in the bilateral
hemispheres. AMBI in the posterior circulation was found in 22 patients
(21.4%) of the 103 with posterior circulation ischemic stroke.
Eleven patients had AMBI in both the anterior and posterior
circulations.
AMBI in 1 Cerebral Hemisphere in the Anterior Circulation (group
A, n=42)
Five patients had superficial AMBI, involving the superior and
inferior leptomeningeal territories of the MCA.
Thirty-seven patients had superficial and deep AMBI. Twenty-five of
these patients had AMBI involving the territories of the perforating
and leptomeningeal branches of the MCA (Figure 1
). Five patients had multiple
border-zone (cortical and internal) infarcts. Seven patients had
superficial MCA territory infarcts, 2 of which were associated with
internal border-zone infarct, 2 with MCA perforator and internal
border-zone infarct, 1 with ACA territory deep infarct, 1 with anterior
choroidal infarct, and 1 with medullary branch infarct.
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The potential cause of stroke was large-artery
atherosclerosis in 33 patients (MCA disease [>50%
stenosis or occlusion] in 16, ICA disease [>50%
stenosis or occlusion] in 15, and aortic arch plaque in 2) and
cardioembolism in 7 patients (Table 1).
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Twenty-six patients had a first-ever stroke. All of these patients showed unilateral hemispheric symptoms or signs. Six patients had a lacunar infarct in the territory of the perforating branch of the MCA and additional infarcts in the territory of the superficial MCA. In 3 of these patients, the infarct located in the superficial territories was not evident on conventional MRI.
AMBI in the Bilateral Cerebral Hemispheres in the Anterior
Circulation (Group B, n=20)
In 13 patients AMBI involved the superficial and deep territories.
It was associated with large-artery atherosclerosis in
8, cardioembolism in 3, and undetermined etiology in 2
of these patients. In 7 patients AMBI involved the bilateral deep
territories. It was associated with small-artery occlusion in 5 of
these patients, large-artery atherosclerosis in 1, and
other determined etiology (syphilitic vasculitis) in 1 (Table 2).
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Among 9 patients with large-artery atherosclerosis as a
stroke mechanism, 4 had malignancy (gastrointestinal cancer in 3 and
prostatic cancer in 1) (Figure 2), 7 had
elevated fibrinogen level, and 1 had polycythemia (hematocrit >0.5).
Among 5 patients with bilateral small-artery occlusion, 3 had elevated
fibrinogen level and 1 had polycythemia.
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Five patients had AMBI in the territories of the unilateral MCA and/or
ACA and contralateral ACA. All of them had a common ACA trunk for the
bilateral ACA territories (Figure 3).
Three of these patients had carotid disease (unilateral in 1 and
bilateral in 2), and the other 2 had cardiac sources of embolism.
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Unilateral ICA or MCA disease was the only underlying vascular
pathology in 2 patients. One of them with MCA disease had a malignancy
(Figure 2
), and the other with ICA disease had bilateral ACAs
supplied by a common ACA trunk.
In 14 patients experiencing stroke for the first time, 8 presented with unilateral hemispheric symptoms or signs, while the other 6 showed bilateral hemispheric dysfunction.
AMBI in the Posterior Circulation (Group C, n=22)
AMBI involved the cerebellum and PCA territory in 6 patients; the
brain stem and PCA territory in 4; the bilateral cerebellum in 4; the
perforator zone and leptomeningeal branch of PCA in 3; the cerebellum,
brain stem, and PCA territory in 2; the bilateral thalami in 2; and the
cerebellum and brain stem in 1. The acute infarcts were most frequently
located in the territory of the PCA (18 infarcts in the superficial PCA
territory and 12 infarcts in the territory of the perforating branch of
the PCA), followed by the PICA territory (n=16), the SCA territory
(n=8), the AICA territory (n=5), and the territory of the perforating
branch of the BA (n=3).
The stroke mechanism was large-artery atherosclerosis
in 15 patients (vertebral artery disease in 6, BA disease in 4, PCA
disease in 3, and PICA disease in 2 with bilateral PICA territory
infarcts), cardioembolism in 6, and other determined
etiology (stroke after catheter angiography) in 1 (Table 3).
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AMBI in the Anterior and Posterior Circulations (Group D,
n=11)
Six patients presented with posterior circulation stroke
syndrome, 2 with anterior circulation stroke syndrome, and the other 3
with both anterior and posterior circulation stroke syndromes.
Cardioembolism was presumed to be the cause of stroke
in 6 patients, large-artery atherosclerosis in 3, and
other determined etiologies in 2 (stroke after catheter angiography in
1 and isolated central nervous system angiitis in the other) (Table 3).
The posterior communicating artery was patent in 3 patients: 2 with
large-artery atherosclerosis and 1 with
cardioembolism. Fetal-type PCA on the right side was
evident in 1 patient (Figure 4) with AMBI
in the temporoparietal and occipital lobes on the right side. A diffuse
aortic arch plaque was presumed to be the source of the embolism.
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Stroke Mechanisms According to Topographical Patterns
Large-artery atherosclerosis was the most frequent
cause of stroke in groups A, B, and C (57/84) compared with group D
(3/11) (P=0.016, Fisher’s exact test) (Table 3).
Cardioembolism was the most frequent in group D (6/11)
compared with groups A, B, and C (16/84) (P=0.017, Fisher’s
exact test). Small-artery occlusion was exclusively associated with
group B (5/20) compared with groups A, C, and D (0/75)
(P=0.0003, Fisher’s exact test).
Hemorheologic Abnormalities
Elevated fibrinogen or hematocrit levels were significantly
associated with AMBI in the bilateral cerebral hemispheres in the
anterior circulation. Thirteen patients (65%) in group B showed
abnormal hemorheologic findings, while 25 of 75 patients (33.3%) with
AMBI in other topographical distributions showed these same findings
(P=0.02, 
2 test). With the
exception of patients with cardioembolism, the
association remained significant (12/17 in group B versus 18/56 in
groups A, C, and D) (P=0.01, 2
test).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In our study AMBI detected on DWI represented >25% of ischemic strokes, which is higher than that of previous studies.3 4 The frequency of AMBI may have been underestimated before the era of DWI. The results from another recent study using DWI were different from ours; 19 (13.4%) of a total of 142 patients had acute multiple infarcts.5 The patients in their study underwent DWI within 15 days of stroke onset, and there is a possibility that DWI missed some of the acute ischemic lesions.11
Our results suggest that MCA (38%) as well as ICA (36%) disease are the main causes of AMBI in 1 hemisphere in the anterior circulation. This finding is in contrast with the findings of Western studies, in which the prevalence of ICA stenosis or occlusion was approximately 75% in patients with double infarcts in 1 hemisphere,1 and ICA disease and cardioembolism explained approximately 60% of acute multiple infarctions in the anterior circulation.4 This discrepancy may be a result of a high prevalence of intracranial arterial disease in Asians.21 The topography of AMBI in 1 hemisphere in the anterior circulation was also different from the previous study.1 The most common topographical pattern in our study was superficial leptomeningeal and perforator zones of MCA (59.5%, 25/42), while Bogousslavsky1 reported the superior and inferior MCA leptomeningeal pattern to be the most common (approximately 50%). We believe that this difference also lies in the high prevalence of MCA disease in our patients. MCA disease might cause intra-arterial embolization to the distal MCA territory, even though it is unclear whether MCA perforator infarcts were due to thrombotic or intra-arterial embolic processes. In 3 patients who had a lacunar infarct in the territory of the perforating branch of the MCA, the superficially located infarcts on DWI were not evident on conventional MRI. This suggests that these superficial infarcts were asymptomatic. In each of these patients, either the proximal ICA or the heart was the embolic source. This supports the hypothesis that local small-artery disease does not explain all small infarcts in the territory of the deep perforators.22 23
One third of the patients with AMBI in the anterior circulation had bilateral infarcts. Bogousslavsky et al4 found AMBI in the bilateral hemispheres in 25% of anterior circulation ischemic strokes that were associated with embolisms, usually arising from the heart. On the contrary, the main causes of stroke in this group in our study were large-artery atherosclerosis, followed by small-artery occlusion and cardioembolism. Small-artery occlusion was the main cause of bilateral deep cerebral infarcts.
It should be emphasized that bilateral or unilateral large-artery disease or small-artery occlusion may be associated with acute infarcts in both cerebral hemispheres. Although the factors that determine contemporary infarcts are unknown, we believe that hyperviscosity may be an important contributory factor. Grotta et al24 demonstrated a negative correlation between either hematocrit or serum fibrinogen levels and cerebral blood flow in stroke patients. Harrison et al25 found a direct correlation between elevated hematocrit levels and the size of cerebral infarction. An elevated hematocrit was also reported to be associated with the occurrence of watershed infarction distal to ICA occlusion.26 27 Elevated hematocrit or fibrinogen levels were significantly associated with bilateral cerebral infarction in patients with large-artery atherosclerosis or small-artery occlusion in this study.
Malignancy was exclusively associated with bilateral cerebral infarcts in our case series. A malignancy-associated hypercoagulable state may result from the production of coagulation promoters by the cancer.28 Atherosclerosis is not as common a cause of symptomatic cerebrovascular disease in patients with cancer as it is in the general population because severe atherosclerosis is less frequent in patients who die from cancer than in others.29 On the contrary, a retrospective analysis suggested that conventional large-artery atherosclerosis was the most common cause of cerebral ischemia in adult cancer patients.30 Although our patients with malignancy had severe large-artery disease, it seems likely that hypercoagulability may somehow contribute to multiple infarction in these patients.
We found AMBI in the posterior circulation in 21.4% of the cases of
posterior circulation ischemic stroke, which is more frequent
than the findings of a previous report.3 However, this
discrepancy lies in the different interpretations of the definition of
AMBI in the posterior circulation. We focused on the
arterial trees, while Bernasconi et al3
emphasized topographical patterns and defined AMBI in the posterior
circulation as the involvement of 
2 of the 3 main sequential segments
of the posterior circulation, as defined in the New England Medical
Center classification.31 32 Thus, they classified
infarction involving the superficial and deep PCA territory or
bilateral infarcts in the thalamoperforate territory as a single
lesion. Nonetheless, we found similar results in that embolisms from
arterial or cardiac sources were the main etiologies of
AMBI in the posterior circulation. In our study the most common
locations of AMBI were the territories of the PCA, PICA, and SCA.
Several other studies have shown that occlusion of the PCA, PICA, SCA,
or distal BA is usually embolic, with in situ atherosclerotic disease
being more uncommon.33 34 35
Approximately 10% of the patients in our study had multiple infarcts in both the anterior and posterior circulations, suggesting that the source of embolism was more proximal than the carotid arteries. In our study >50% of the patients in group D had a cardiac source of embolism. We found that the frequency of AMBI in the anterior and posterior circulations in our patients was lower than that in a previous Western study.4 This may be due to the lower incidence of cardiac-origin embolism in our country.36 37
On the other hand, ICA disease can cause simultaneous infarcts in the anterior circulation and PCA territory, because PCA may originate from the ICA (fetal-type of PCA) in up to 25% of cerebral hemispheres.38 39 Anterior circulation stroke may also be associated with steno-occlusive disease in the posterior circulation, because the posterior communicating artery is patent in nearly 67% of anatomic dissections.40 AMBI in the territories of both ACAs can also occur because a single artery supplies both medial aspects of the hemispheres in 18% of the normal population.41 Nine of the 31 patients in groups B and D in our study had multiple infarcts due to these kinds of anatomic variation.
This study contains a few limitations. First, simultaneity of multiple infarcts remains uncertain. Because we considered patients who underwent DWI within 4 days after stroke onset, we cannot exclude the possibility that multiple ischemic episodes occurred during this short period. Second, we did not consider other hemorheologic data, including factors V and VII, platelet aggregation and adhesion, or erythrocyte aggregation and flexibility.42
In conclusion, our findings emphasize the heterogeneity of the topographical and etiologic aspects of acute multiple brain infarction. Different topographical patterns are associated with different vascular pathologies and stroke mechanisms. DWI allows the identification of ischemic lesions that previously went undetected. This suggests that early identification of multiple infarcts with the use of DWI may provide early clues to stroke mechanism and guide therapeutic options in the acute phase of stroke.
Received October 18, 1999; revision received December 9, 1999; accepted December 9, 1999.
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Y. Ueno, K. Kimura, Y. Iguchi, K. Shibazaki, T. Inoue, N. Hattori, and T. Urabe Mobile Aortic Plaques Are a Cause of Multiple Brain Infarcts Seen on Diffusion-Weighted Imaging Stroke, September 1, 2007; 38(9): 2470 - 2476. [Abstract] [Full Text] [PDF]
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L. H. Bonati, A. Kessel-Schaefer, A. Z. Linka, P. Buser, S. G. Wetzel, E.-W. Radue, P. A. Lyrer, and S. T. Engelter Diffusion-Weighted Imaging in Stroke Attributable to Patent Foramen Ovale: Significance of Concomitant Atrial Septum Aneurysm Stroke, August 1, 2006; 37(8): 2030 - 2034. [Abstract] [Full Text] [PDF]
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M. Jauss, T. Wessels, S. Trittmacher, J. Allendorfer, and M. Kaps Embolic Lesion Pattern in Stroke Patients With Patent Foramen Ovale Compared With Patients Lacking an Embolic Source Stroke, August 1, 2006; 37(8): 2159 - 2161. [Abstract] [Full Text] [PDF]
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 T. Wessels, C. Wessels, A. Ellsiepen, I. Reuter, S. Trittmacher, E. Stolz, and M. Jauss Contribution of Diffusion-Weighted Imaging in Determination of Stroke Etiology AJNR Am. J. Neuroradiol., January 1, 2006; 27(1): 35 - 39. [Abstract] [Full Text] [PDF]
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 L. E. Allport, M. W. Parsons, K. S. Butcher, L. MacGregor, P. M. Desmond, B. M. Tress, and S. M. Davis Elevated hematocrit is associated with reduced reperfusion and tissue survival in acute stroke Neurology, November 8, 2005; 65(9): 1382 - 1387. [Abstract] [Full Text] [PDF]
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 S. Koch, M. Amir, A. A. Rabinstein, Y. Reyes-Iglesias, J. G. Romano, and A. Forteza Diffusion-Weighted Magnetic Resonance Imaging in Symptomatic Vertebrobasilar Atherosclerosis and Dissection Arch Neurol, August 1, 2005; 62(8): 1228 - 1231. [Abstract] [Full Text] [PDF]
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M. J. Alberts, R. E. Latchaw, W. R. Selman, T. Shephard, M. N. Hadley, L. M. Brass, W. Koroshetz, J. R. Marler, J. Booss, R. D. Zorowitz, et al. Recommendations for Comprehensive Stroke Centers: A Consensus Statement From the Brain Attack Coalition Stroke, July 1, 2005; 36(7): 1597 - 1616. [Abstract] [Full Text] [PDF]
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K. Saito, H. Moriwaki, H. Oe, K. Miyashita, K. Nagatsuka, S. Ueno, and H. Naritomi Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images AJNR Am. J. Neuroradiol., April 1, 2005; 26(4): 809 - 814. [Abstract] [Full Text] [PDF]
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 V Caso, K Budak, D Georgiadis, B Schuknecht, and R W Baumgartner Clinical significance of detection of multiple acute brain infarcts on diffusion weighted magnetic resonance imaging J. Neurol. Neurosurg. Psychiatry, April 1, 2005; 76(4): 514 - 518. [Abstract] [Full Text] [PDF]
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T. Wessels, C. Rottger, M. Jauss, M. Kaps, H. Traupe, and E. Stolz Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes Stroke, April 1, 2005; 36(4): 757 - 761. [Abstract] [Full Text] [PDF]
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D.-W. Kang, L. L. Latour, J. A. Chalela, J. A. Dambrosia, and S. Warach Early and late recurrence of ischemic lesion on MRI: Evidence for a prolonged stroke-prone state? Neurology, December 28, 2004; 63(12): 2261 - 2265. [Abstract] [Full Text] [PDF]
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S. Koch, A. A. Rabinstein, J. G. Romano, and A. Forteza Diffusion-Weighted Magnetic Resonance Imaging in Internal Carotid Artery Dissection Arch Neurol, April 1, 2004; 61(4): 510 - 512. [Abstract] [Full Text] [PDF]
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S. T. Engelter, S. G. Wetzel, E. W. Radue, M. Rausch, A. J. Steck, and P. A. Lyrer The clinical significance of diffusion-weighted MR imaging in infratentorial strokes Neurology, February 24, 2004; 62(4): 574 - 580. [Abstract] [Full Text] [PDF]
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D.-W. Kang, J. A. Chalela, M. A. Ezzeddine, and S. Warach Association of Ischemic Lesion Patterns on Early Diffusion-Weighted Imaging With TOAST Stroke Subtypes Arch Neurol, December 1, 2003; 60(12): 1730 - 1734. [Abstract] [Full Text] [PDF]
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K. Kang, K. Chu, D.-E. Kim, S.-W. Jeong, J.-W. Lee, and J.-K. Roh POEMS Syndrome Associated With Ischemic Stroke Arch Neurol, May 1, 2003; 60(5): 745 - 749. [Abstract] [Full Text] [PDF]
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D.-W. Kang, K. Chu, S.-B. Ko, S.-J. Kwon, B.-W. Yoon, and J.-K. Roh Lesion Patterns and Mechanism of Ischemia in Internal Carotid Artery Disease: A Diffusion-Weighted Imaging Study Arch Neurol, October 1, 2002; 59(10): 1577 - 1582. [Abstract] [Full Text] [PDF]
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R. P. Gerraty, M. W. Parsons, P. A. Barber, D. G. Darby, P. M. Desmond, B. M. Tress, and S. M. Davis Examining the Lacunar Hypothesis With Diffusion and Perfusion Magnetic Resonance Imaging Stroke, August 1, 2002; 33(8): 2019 - 2024. [Abstract] [Full Text] [PDF]
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A. B. Singhal, M. A. Topcuoglu, and F. S. Buonanno Acute Ischemic Stroke Patterns in Infective and Nonbacterial Thrombotic Endocarditis: A Diffusion-Weighted Magnetic Resonance Imaging Study Stroke, May 1, 2002; 33(5): 1267 - 1273. [Abstract] [Full Text] [PDF]
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K. Chu, D.-W. Kang, D.-E. Kim, S.-H. Park, and J.-K. Roh Diffusion-Weighted and Gradient Echo Magnetic Resonance Findings of Hemichorea-Hemiballismus Associated With Diabetic Hyperglycemia: A Hyperviscosity Syndrome? Arch Neurol, March 1, 2002; 59(3): 448 - 452. [Abstract] [Full Text] [PDF]
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K. Chu, D.-W. Kang, H.-J. Kim, Y.-S. Lee, and S.-H. Park Diffusion-Weighted Imaging Abnormalities in Wernicke Encephalopathy: Reversible Cytotoxic Edema? Arch Neurol, January 1, 2002; 59(1): 123 - 127. [Abstract] [Full Text] [PDF]
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K. Chu, D.-W. Kang, B.-W. Yoon, and J.-K. Roh Diffusion-Weighted Magnetic Resonance in Cerebral Venous Thrombosis Arch Neurol, October 1, 2001; 58(10): 1569 - 1576. [Abstract] [Full Text] [PDF]
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K. Kimura, K. Minematsu, M. Koga, R. Arakawa, M. Yasaka, H. Yamagami, K. Nagatsuka, H. Naritomi, and T. Yamaguchi Microembolic Signals and Diffusion-weighted MR Imaging Abnormalities in Acute Ischemic Stroke AJNR Am. J. Neuroradiol., June 1, 2001; 22(6): 1037 - 1042. [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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D. G. Darby, M. W. Parsons, P. A. Barber, S. M. Davis, J.-K. Roh, and D.-W. Kang Significance of Acute Multiple Brain Infarction on Diffusion-Weighted Imaging Response Stroke, September 1, 2000; 31 (9): 2266 - 2278. [Full Text] [PDF]
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