(Stroke. 2001;32:1330.)
© 2001 American Heart Association, Inc.
Original Contributions |
Hemorrhagic Transformation of Ischemic Brain Tissue
Asymptomatic or Symptomatic?
From the Department of Neurology, University of Heidelberg (Germany) (C.B., T.S., W-R.S., W.H.); Department of Neuroradiology, University of Dresden (Germany) (R. von K.); Department of Neuroradiology, University of Rome (Italy) (M.F., L.B.); and Boehringer Ingelheim, Biberach, Germany (E.B.).
Correspondence to Christian Berger, MD, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, D-69221 Heidelberg, Germany. E-mail christian_berger{at}med.uni-heidelberg.de
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose—The term symptomatic hemorrhage secondary to ischemic stroke implies a clear causal relationship between clinical deterioration and hemorrhagic transformation (HT) regardless of the type of HT. The aim of this study was to assess which type of HT independently affects clinical outcome.
Methods—We used the data set of the European Cooperative Acute Stroke Study (ECASS) II for a post hoc analysis. All patients had a control CT scan after 24 to 96 hours or earlier in case of rapid and severe clinical deterioration. HT was categorized according to radiological criteria: hemorrhagic infarction type 1 and type 2 and parenchymal hematoma type 1 and type 2. The clinical course was prospectively documented with the National Institutes of Health Stroke Scale and the modified Rankin Scale. The independent risk of each type of HT was calculated for clinical deterioration at 24 hours and disability and death at 3 months after stroke onset and adjusted for possible confounding factors such as age, severity of stroke syndrome at baseline, and extent of the ischemic lesion on the initial CT.
Results—Compared with absence of HT, only parenchymal hematoma type 2 was associated with an increased risk for deterioration at 24 hours after stroke onset (adjusted odds ratio, 18; 95% CI, 6 to 56) and for death at 3 months (adjusted odds ratio, 11; 95% CI, 3.7 to 36). All other types of HT did not independently increase the risk of late deterioration.
Conclusions—Only parenchymal hematoma type 2 independently causes clinical deterioration and impairs prognosis. It has a distinct radiological feature: it is a dense homogeneous hematoma >30% of the ischemic lesion volume with significant space-occupying effect.
Key Words: hematoma • hemorrhagic stroke • stroke outcome • thrombolysis
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Several large, randomized, placebo-controlled trials of thrombolytic therapy in acute ischemic stroke have been conducted during the past years. Secondary hemorrhagic transformations (HT) after different types of thrombolytic therapy are frequently reported as important safety parameters in these studies, but they also occur as natural events in the evolution of a cerebral infarct.1 2 3 4 The increase of HT in the actively treated arm is often used as evidence against the treatment tested, as reported in the early streptokinase trials, with a concurrent increase of mortality and HT in the actively treated groups.5 6 7 Although the large European and American tissue plasminogen activator (tPA) trials provided evidence of a benefit in ischemic stroke patients, the fear of hemorrhagic events frequently precludes the use of thrombolysis in clinical practice. Unfortunately, previous trials addressing safety and efficacy of thrombolytic therapy in acute stroke applied different definitions for the term symptomatic hemorrhage or symptomatic hemorrhagic transformation. In the tPA trial sponsored by the National Institutes of Neurological Disorders and Stroke (NINDS),8 9 symptomatic intracranial hemorrhage was defined as "any CT-documented hemorrhage that was temporally related to deterioration in the patient’s clinical condition in the judgment of the clinical investigator," no matter how trivial the hemorrhage on the CT scan might have been. In addition, symptomatic intracranial hemorrhage attributable to study medication was defined as "symptomatic hemorrhage that occurred within 36 hours from treatment onset." In the Multicenter Acute Stroke Trial of Italy and Europe,6 7 symptomatic HT was defined as "clinical deterioration temporally related to HT documented by CT-scan or autopsy." A CT scan was regularly obtained at 5 days after stroke onset or earlier in the event of clinical deterioration. Further studies continued to apply the term symptomatic hemorrhage according to the NINDS protocol9 10 11 or without a definition.12 13
The European Cooperative Acute Stroke Study (ECASS) I and
II14 15 went in
the opposite direction and used a pure radiological, prospective
definition: HT were categorized into 4 different subtypes without
taking into consideration whether or not any hemorrhage was
associated with clinical deterioration. In addition to the pure
radiological definition, the category of symptomatic
hemorrhage was used for patients with clinical deterioration by
4 points on the National Institutes of Health Stroke Scale (NIHSS)
and with no CT findings that might have been responsible for this
deterioration other than a hemorrhage.
Fiorelli et al16 recently demonstrated on the basis of the ECASS I data that, in both the placebo and the rtPA groups, only parenchymal hematomas (PH) >30% of the infarcted area with significant space-occupying effect increased the risk of early neurological deterioration and of 3-month death. Hemorrhagic infarctions (HI) or PH with only mild space-occupying effect did not modify the risk of early neurological deterioration, death, and disability. The different clinical outcome after different subtypes of HT illustrates the difficulty in defining symptomatic hemorrhage precisely and clearly. In fact, the spectrum of HTs differs widely and may include some trivial hemorrhagic petechiae as well as PH with space-occupying effect. To determine whether any neurological deterioration is due to HT itself or due to massive infarct and ischemic edema with a coincidental HT remains crucial in thrombolysis or other stroke trials. The aim of this study on the ECASS II data set was to define specific HT that are independently associated with an increased risk of clinical deterioration or worse outcome according to the hypothesis of Fiorelli et al.16 We sought to further assess the impact of possible confounding factors on clinical deterioration in patients with HT.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The study design and primary results of ECASS II have been described in detail elsewhere.15 ECASS II was a double-blind, placebo-controlled trial evaluating safety and efficacy of 0.9 mg/kg IV recombinant tPA (rtPA) in patients presenting within 6 hours from the onset of an acute hemispheric ischemic stroke. Intravenous heparin or oral anticoagulants within the first 24 hours were not allowed.
All patients were examined with CT scan before randomization
and after 24 to 96 hours (median, 1 day; range, 0 to 4 days). Nine
patients had their follow-up scan within 24 hours of stroke onset, 643
patients between 24 and 48 hours, 128 between 48 and 72 hours, and 3
between 72 and 96 hours. An additional CT was performed after 1 week.
We used this CT for analysis in 6 patients in whom the first
follow-up CT was not available. Following the prospective ECASS
protocol, all CT scans were evaluated twice, first by the local
investigators and then independently by 3 members of the CT reading
panel. The members of the CT reading panel were blinded to treatment
allocation, any clinical events occurring after randomization, and the
reading of the local investigators and did not see follow-up scans
before evaluating the baseline CT. After the exclusion of 10 patients
(3 rtPA, 7 placebo) with CT scans of too poor quality to allow
unequivocal assessment of HT, 790 of 800 randomized patients remained
for the analysis. HT occurring on the first follow-up CT scan
after randomization were prospectively categorized according to
definitions previously
described17 18 :
HI and PH. HI type 1 (HI-1) was defined as small petechiae along the
margins of the infarct, and HI type 2 (HI-2) was defined as more
confluent petechiae within the infarcted area but without
space-occupying effect. PH type 1 (PH-1) was defined as hematoma in
30% of the infarcted area with some slight space-occupying effect;
PH type 2 (PH-2) was defined as dense hematoma >30% of the infarcted
area with substantial space-occupying effect or as any hemorrhagic
lesion outside the infarcted area (examples are shown in
Figure 1
). In cases of >1 hemorrhagic lesion on CT
scan, the worst possible HT category was assumed.
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Baseline and follow-up CT scans were obtained nonenhanced
and on the same scanner if possible. Windows and center levels were set
to optimally distinguish gray and white matter. The study protocol
recommended a window width of 80 to 100 Hounsfield units and a center
level of 30 to 40 Hounsfield units. The chairman of the CT reading
panel gathered the categorized findings from the panel members, checked
them for disagreements, disclosed disagreements to the other panel
members, and discussed each discrepant CT to achieve consensus. The
final judgments were sent to the data management center, which then was
allowed to send the follow-up scans to the members of the CT reading
panel. We defined hypoattenuation as a visible decrease in x-ray
attenuation of brain tissue compared with other portions of the same
anatomic structure or its contralateral counterpart. We categorized the
extent of hypoattenuation of the middle cerebral artery (MCA) territory
as none, 33% (small), and >33%
(large).19 20 The
total MCA territory was considered the brain volume between 2 lines
being drawn from the anterior horn of the ventricle and from the
trigonum perpendicular to the skull involving most parts of the
frontal, temporal, and parietal lobe with the exception of the
parasagittal structures. On follow-up CT scans, we measured the volume
of acute ischemic lesions by multiplying the maximum diameter
of hypoattenuation, maximum diameter perpendicular to it in the same
slice, number of slices affected, slice distance, and a conversion
factor of 0.5 using the formula for irregular volumes. In patients with
HT, the entire ischemic and hemorrhagic lesion was
measured.
From the ECASS II database, we retrieved the following
variables: age, sex, allocation to placebo/rtPA treatment, severity
of neurological deficit on admission as quantified with the NIHSS and
the Scandinavian Stroke
Scale,21 NIHSS score 24±2
hours after stroke onset, extent of initial ischemic lesion on
baseline CT scan (none, 33% of MCA territory, and >33% of MCA
territory), body temperature, blood glucose, and blood pressure at the
inclusion time. We calculated the frequencies of the different subtypes
of HT for placebo and rtPA groups. Statistical difference was tested
with the 
2 test.
To examine which of the collected variables accounted
for clinical deterioration 24 hours after stroke onset (increase in
NIHSS score by 4 between baseline and after 24±2
hours22 according to the
prospective definition used in ECASS II), for disability and death at 3
months (modified Rankin Scale score >2), and for death up to 3 months
after stroke onset, we performed a logistic regression analysis
on each of these variables. Variables with a
P>0.05 in the Wald test and
the logistic likelihood ratio test were assumed to be irrelevant for
the outcome tested and were excluded from further analysis. We
calculated the odds ratios (ORs) and 95% CIs for each HT subtype,
comparing the ORs of each level of HT with no HT. Subsequently, we
performed a multiple regression analysis including all
variables considered relevant factors from the
univariate analysis and calculated ORs for clinical
deterioration at 24 hours, disability and death after 3 months, and
death at 3 months after stroke onset. In a backward stepwise
regression, we excluded all variables from our model that did not
contribute significantly in at least 1 outcome test. The adjusted ORs
are given for all variables finally kept in the model.
Variables leading to a clear change of the ORs for HT were
considered confounding factors.
Finally, we evaluated the relationship between the frequency of PH-2 and the extent of hypoattenuation on baseline CT scan and calculated ORs for the development of PH-2. The Newman-Keuls test was applied to assess the relationship between incidence of different types of HT and the lesion volume at 24 hours. In all tests, a statistical significance was assumed for P<0.05. Analyses were performed with StatView statistical software (edition 5.0.1).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Of a total of 790 intent-to-treat patients in ECASS II, 406 patients received rtPA (0.9 mg/kg), and 384 patients were treated with placebo. In the first follow-up CT scan, significantly more HT occurred in the rtPA group: 29.5% versus 18.5% in the placebo group (Table 1
). This was mainly due to a higher incidence of
PH-2 in the rtPA group (7.6% versus 0.5%;
P<0.0001). The incidences of
HI-1, HI-2, and PH-1 were statistically not different between the
placebo and the actively treated group, although there was a clear
trend for HI-2 and PH-1 to more likely occur after
thrombolysis.
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Table 2 presents the unadjusted and adjusted risk
ratios for the 4 different types of HT and for other factors found to
contribute significantly to outcome. Sex, body temperature, and blood
pressure at the inclusion time were irrelevant for outcome and thus
were excluded from analysis. PH-2 significantly increased the
risk of early deterioration, of disability and death at 3 months, and
of death at 3 months alone. PH-1 accounted for an increased risk of
early deterioration but not of disability or death at 3 months. Thus,
outcome at 3 months was modified only by presence of PH-2 on the first
follow-up CT scan. In our search for factors contributing significantly
to outcome, we found a confounding effect of severity of stroke
syndrome at onset and of presence of hypodensity >33% on baseline CT
scan. Both were associated with an increased risk rate for disability
and death. Presence of a large hypodensity was associated with early
deterioration. Other contributing factors for outcome were age and
glucose level. Increase of age or glucose was associated with an
increased risk of disability and death at 3 months. Treatment with rtPA
led to a significantly decreased risk of disability or death after 3
months; however, its influence for early deterioration or death alone
at 3 months was insignificant.
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Figure 2 demonstrates the positive correlation between
large lesion volumes and large PH in both the actively treated and the
placebo-treated groups. In both treatment groups, the total lesion
volumes in patients with PH-2 were significantly larger than those of
all other groups, including the group without HT. Thus, the
space-occupying effect of PH-2 becomes evident.
Table 3 presents the relationship between
incidence of PH-2 and extent of hypoattenuation on baseline CT scan.
Clearly, the incidence of PH-2 is more frequent with presence of large
hypodensity on CT scan. The risk ratio of developing PH-2 with an
initially large extent of the ischemic lesion was
4.4.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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HT of a brain infarct is a major concern when thrombolysis is used in acute stroke. Frequently, HT of any type and extent found on routine follow-up CT scans is considered a serious adverse event and is often termed symptomatic hemorrhage regardless of whether a certain type of HT was really causing symptoms. In the larger thrombolysis studies, various definitions for symptomatic hemorrhage consisting of radiological and clinical criteria were applied. The NINDS tPA trial defined symptomatic hemorrhage as "any CT-documented hemorrhage that was temporally related to deterioration in the patient’s clinical condition in the judgment of the clinical investigator."8 Symptomatic hemorrhage was considered to be due to study medication if it occurred within 36 hours of treatment. It appears inconceivable that a clinical deterioration under this definition could not be merely coincidental with any HT appearing on CT scan. In fact, the deterioration could well have been the natural course of a stroke independent of the coinciding HT, especially if the HT was only a minor part of a large infarct. In a post hoc analysis by the NINDS Stroke Study Group,9 it was nevertheless stated that presence of a severe neurological deficit and clear signs of brain edema or mass effect on pretreatment CT increased the risk of symptomatic hemorrhage. Again, pure radiological criteria of different types of HT were not considered, and other factors causing clinical deterioration were ignored. Similar definitions for symptomatic hemorrhage were applied in the Multicenter Acute Stroke Trial of Italy and Europe6 7 and in recent thrombolysis surveys.10 11
In ECASS I and II, prospective radiological definitions of the 4 different subtypes of HT were applied regardless of clinical events, and CT scans with or without HT were analyzed regardless of clinical data. CT was performed at 24 hours and 7 days after symptom onset and treatment and in case of clinical deterioration. Almost all major hemorrhages were detected by the first follow-up CT. However, local investigators collecting data on neurological status might have created some unavoidable bias in that they knew the result of the CT scan and might have implemented a preconceived notion of any relationship between HT and neurological deterioration. We believe that a prospective protocol for CT scanning at predetermined dates is necessary to study the question of whether certain types of hemorrhage are associated with clinical deterioration. In our view, an early follow-up CT within 48 hours of treatment is necessary to detect hemorrhages caused by rtPA.
In this post hoc analysis of the ECASS II data set, we confirm previous results by Fiorelli et al16 that only PH >30% of the infarcted area with considerable space-occupying effect (PH-2) significantly increased the risk of early clinical deterioration and of a worse long-term outcome, including death. Other types of HT, particularly HI-1 and HI-2, were not associated with clinical deterioration. This was also true for PH-1, which at least did not increase the risk of disability or death up to 3 months after stroke onset. Thus, while these latter types of HT would have been termed symptomatic hemorrhages according to the definition of many ongoing trials, their presence might not have been responsible for deterioration. Instead, other factors such as age, initial glucose level, extent of initial hypodensity on baseline CT scan, and severity of stroke syndrome at baseline additionally contributed to clinical outcome, as described in a previous study.23 Treatment with rtPA, although associated with a higher incidence of PH-2, decreased the overall risk of disability and death at 3 months.
In particular, stroke severity and the presence of large hypodensity on the initial CT scan were associated with a significantly increased risk for disability and death up to 3 months after stroke onset. Thus, they appear as confounding factors for the influence of HT on outcome. After adjustment for these confounding factors, the risk for disability or death at 3 months was increased insignificantly after PH-2, but with respect to a long-term outcome, PH-2 independently and significantly increased only the risk of death at 3 months. HI-1 was even associated with some clinical improvement and may, at least in this early stage, indicate the effect of successful early reperfusion. Since PH-2 is of major clinical relevance or may in fact be considered hemorrhage that is most likely to be symptomatic, emphasis must be placed on the recognition of stroke patients who are more likely to develop large PH and subsequently should be excluded from thrombolysis. PH-2 occurred more frequently in patients with hypodensity >33% on early CT. These early ischemic changes identified on the pretreatment CT represent early cytotoxic edema and possibly the development of irreversible injury.24 In a study by Hamann et al,25 the presence of microscopic hemorrhages in the ischemic area has been related to a loss of cerebrovascular basal lamina integrity. Since these microscopic hemorrhages always occur within the infarcted area, particularly in the subcortical core, a large infarct volume a priori offers a larger area of lost basal lamina integrity, thus possibly leading more frequently to parenchymal hemorrhages. We were able to confirm this relationship by demonstrating a positive correlation between large lesion volume and presence of PH-2. Thus, to detect signs of early infarction on CT remains crucial, although it is questioned whether these signs can be detected reliably.26 In a previous study the interobserver agreement in assessing subtle CT signs of cerebral infarction was moderate to substantial.20 Similar results for assessment of the hypoattenuation in thirds of the MCA territory were obtained by the Alberta Stroke Programme Early CT Score (ASPECTS) study group.27 Whether general reading of CT scans can be improved by quantification and division of the MCA territory into many regions of interest remains to be confirmed in clinical practice. To date, presence of hypoattenuation larger than one third of the MCA territory on baseline CT seems to be the most simple and readily available predictor of the development of large PH.
In summary, only large PH >30% of the infarcted area with space-occupying effect (PH-2) independently modify the risk of a worse clinical outcome both early and late after stroke onset. Smaller but still homogeneous PH (PH-1) increase the risk of early deterioration but not of a worse long-term outcome. Heterogeneous, petechial HI are not associated with worse early or late outcome. Thus, the term symptomatic hemorrhage should be applied with caution because it implies a causal relationship between signs of HT found on CT and clinical deterioration. Additional factors, such as extent of the lesion, edema formation, and severity of the stroke syndrome, however, offer an explanation for a patient’s deterioration or bad outcome. In future reports dealing with safety aspects of thrombolysis, a clearer distinction between nonrelevant forms of HT and PH with risk of clinical deterioration should be made.
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Acknowledgments |
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ECASS II was supported exclusively by Boehringer Ingelheim, Biberach, Germany.
Received October 26, 2000; revision received February 21, 2001; accepted February 22, 2001.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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 R. I. Aviv, C. D. d'Esterre, B. D. Murphy, J. J. Hopyan, B. Buck, G. Mallia, V. Li, L. Zhang, S. P. Symons, and T.-Y. Lee Hemorrhagic Transformation of Ischemic Stroke: Prediction with CT Perfusion Radiology, March 1, 2009; 250(3): 867 - 877. [Abstract] [Full Text] [PDF]
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O. Y. Bang, J. L. Saver, J. R. Alger, S. H. Shah, B. H. Buck, S. Starkman, B. Ovbiagele, D. S. Liebeskind, and for the UCLA MRI Permeability Investigators Patterns and Predictors of Blood-Brain Barrier Permeability Derangements in Acute Ischemic Stroke Stroke, February 1, 2009; 40(2): 454 - 461. [Abstract] [Full Text] [PDF]
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R. G. Nogueira, W. S. Smith, and on Behalf of the MERCI and Multi MERCI Writing Com Safety and Efficacy of Endovascular Thrombectomy in Patients With Abnormal Hemostasis: Pooled Analysis of the MERCI and Multi MERCI Trials Stroke, February 1, 2009; 40(2): 516 - 522. [Abstract] [Full Text] [PDF]
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G. Seidel, H. Cangur, T. Albers, A. Burgemeister, and K. Meyer-Wiethe Sonographic Evaluation of Hemorrhagic Transformation and Arterial Recanalization in Acute Hemispheric Ischemic Stroke Stroke, January 1, 2009; 40(1): 119 - 123. [Abstract] [Full Text] [PDF]
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E. C. Henning, L. L. Latour, J. M. Hallenbeck, and S. Warach Reperfusion-Associated Hemorrhagic Transformation in SHR Rats: Evidence of Symptomatic Parenchymal Hematoma Stroke, December 1, 2008; 39(12): 3405 - 3410. [Abstract] [Full Text] [PDF]
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A-H. Cho, J. S. Kim, S.-J. Kim, S.-C. Yun, C.-G. Choi, H.-R. Kim, S. U. Kwon, D.-H. Lee, E.-K. Kim, D.-C. Suh, et al. Focal Fluid-Attenuated Inversion Recovery Hyperintensity Within Acute Diffusion-Weighted Imaging Lesions Is Associated With Symptomatic Intracerebral Hemorrhage After Thrombolysis Stroke, December 1, 2008; 39(12): 3424 - 3426. [Abstract] [Full Text] [PDF]
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J.W. Dankbaar, J. Hom, T. Schneider, S.-C. Cheng, B.C. Lau, I. van der Schaaf, S. Virmani, S. Pohlman, W.P. Dillon, and M. Wintermark Dynamic Perfusion CT Assessment of the Blood-Brain Barrier Permeability: First Pass versus Delayed Acquisition AJNR Am. J. Neuroradiol., October 1, 2008; 29(9): 1671 - 1676. [Abstract] [Full Text] [PDF]
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 L Derex and N Nighoghossian Intracerebral haemorrhage after thrombolysis for acute ischaemic stroke: an update J. Neurol. Neurosurg. Psychiatry, October 1, 2008; 79(10): 1093 - 1099. [Abstract] [Full Text] [PDF]
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O. Ozdemir, M. Bussiere, A. Leung, I. Gulka, D. Lee, R. Chan, J.D. Spence, and D. Pelz Intra-Arterial Thrombolysis of Occluded Middle Cerebral Artery by Use of Collateral Pathways in Patients with Tandem Cervical Carotid Artery/Middle Cerebral Artery Occlusion AJNR Am. J. Neuroradiol., September 1, 2008; 29(8): 1596 - 1600. [Abstract] [Full Text] [PDF]
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M. Paciaroni, G. Agnelli, F. Corea, W. Ageno, A. Alberti, A. Lanari, V. Caso, S. Micheli, L. Bertolani, M. Venti, et al. Early Hemorrhagic Transformation of Brain Infarction: Rate, Predictive Factors, and Influence on Clinical Outcome: Results of a Prospective Multicenter Study Stroke, August 1, 2008; 39(8): 2249 - 2256. [Abstract] [Full Text] [PDF]
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 B Thanvi, S Treadwell, and T Robinson Early neurological deterioration in acute ischaemic stroke: predictors, mechanisms and management Postgrad. Med. J., August 1, 2008; 84(994): 412 - 417. [Abstract] [Full Text] [PDF]
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B R Thanvi, S Treadwell, and T Robinson Haemorrhagic transformation in acute ischaemic stroke following thrombolysis therapy: classification, pathogenesis and risk factors Postgrad. Med. J., July 1, 2008; 84(993): 361 - 367. [Abstract] [Full Text] [PDF]
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J. Eggers, I. R. Konig, B. Koch, G. Handler, and G. Seidel Sonothrombolysis With Transcranial Color-Coded Sonography and Recombinant Tissue-Type Plasminogen Activator in Acute Middle Cerebral Artery Main Stem Occlusion: Results From a Randomized Study Stroke, May 1, 2008; 39(5): 1470 - 1475. [Abstract] [Full Text] [PDF]
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T. Tomsick, J. Broderick, J. Carrozella, P. Khatri, M. Hill, Y. Palesch, J. Khoury, and for the Interventional Management of Stroke II Inv Revascularization Results in the Interventional Management of Stroke II Trial AJNR Am. J. Neuroradiol., March 1, 2008; 29(3): 582 - 587. [Abstract] [Full Text] [PDF]
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N.A. Vora, R. Gupta, A.J. Thomas, M.B. Horowitz, A.H. Tayal, M.D. Hammer, K. Uchino, L.R. Wechsler, and T.G. Jovin Factors Predicting Hemorrhagic Complications after Multimodal Reperfusion Therapy for Acute Ischemic Stroke AJNR Am. J. Neuroradiol., August 1, 2007; 28(7): 1391 - 1394. [Abstract] [Full Text] [PDF]
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P. C. Lavallee, M. Mazighi, J.-P. Saint-Maurice, E. Meseguer, H. Abboud, I. F. Klein, E. Houdart, and P. Amarenco Stent-Assisted Endovascular Thrombolysis Versus Intravenous Thrombolysis in Internal Carotid Artery Dissection With Tandem Internal Carotid and Middle Cerebral Artery Occlusion Stroke, August 1, 2007; 38(8): 2270 - 2274. [Abstract] [Full Text] [PDF]
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J. L. Saver Hemorrhage After Thrombolytic Therapy for Stroke: The Clinically Relevant Number Needed to Harm Stroke, August 1, 2007; 38(8): 2279 - 2283. [Abstract] [Full Text] [PDF]
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B. M. Demaerschalk Thrombolytic Therapy for Acute Ischemic Stroke: The Likelihood of Being Helped Versus Harmed Stroke, August 1, 2007; 38(8): 2215 - 2216. [Full Text] [PDF]
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The IMS II Trial Investigators The Interventional Management of Stroke (IMS) II Study Stroke, July 1, 2007; 38(7): 2127 - 2135. [Abstract] [Full Text] [PDF]
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G. A. Christoforidis, A. Slivka, Y. Mohammad, C. Karakasis, B. Avutu, and M. Yang Size Matters: Hemorrhage Volume as an Objective Measure to Define Significant Intracranial Hemorrhage Associated With Thrombolysis Stroke, June 1, 2007; 38(6): 1799 - 1804. [Abstract] [Full Text] [PDF]
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G. Thomalla, J. Sobesky, M. Kohrmann, J. B. Fiebach, J. Fiehler, O. Zaro Weber, A. Kruetzelmann, T. Kucinski, M. Rosenkranz, J. Rother, et al. Two Tales: Hemorrhagic Transformation but Not Parenchymal Hemorrhage After Thrombolysis Is Related to Severity and Duration of Ischemia: MRI Study of Acute Stroke Patients Treated With Intravenous Tissue Plasminogen Activator Within 6 Hours Stroke, February 1, 2007; 38(2): 313 - 318. [Abstract] [Full Text] [PDF]
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P. Khatri, L. R. Wechsler, and J. P. Broderick Intracranial Hemorrhage Associated With Revascularization Therapies Stroke, February 1, 2007; 38(2): 431 - 440. [Abstract] [Full Text] [PDF]
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H. M. Shaltoni, K. C. Albright, N. R. Gonzales, R. U. Weir, A. M. Khaja, R. M. Sugg, M. S. Campbell III, E. D. Cacayorin, J. C. Grotta, and E. A. Noser Is Intra-Arterial Thrombolysis Safe After Full-Dose Intravenous Recombinant Tissue Plasminogen Activator for Acute Ischemic Stroke? Stroke, January 1, 2007; 38(1): 80 - 84. [Abstract] [Full Text] [PDF]
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M. Saqqur, C. A. Molina, A. Salam, M. Siddiqui, M. Ribo, K. Uchino, S. Calleja, Z. Garami, K. Khan, N. Akhtar, et al. Clinical Deterioration After Intravenous Recombinant Tissue Plasminogen Activator Treatment: A Multicenter Transcranial Doppler Study Stroke, January 1, 2007; 38(1): 69 - 74. [Abstract] [Full Text] [PDF]
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T. A. Tomsick 2006: A Stroke Odyssey AJNR Am. J. Neuroradiol., November 1, 2006; 27(10): 2019 - 2021. [Full Text] [PDF]
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D. Kim, R. Jahan, S. Starkman, A. Abolian, C.S. Kidwell, F. Vinuela, G.R. Duckwiler, B. Ovbiagele, P.M. Vespa, S. Selco, et al. Endovascular Mechanical Clot Retrieval in a Broad Ischemic Stroke Cohort AJNR Am. J. Neuroradiol., November 1, 2006; 27(10): 2048 - 2052. [Abstract] [Full Text] [PDF]
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M. Ning, K. L. Furie, W. J. Koroshetz, H. Lee, M. Barron, M. Lederer, X. Wang, M. Zhu, A. G. Sorensen, E. H. Lo, et al. Association between tPA therapy and raised early matrix metalloproteinase-9 in acute stroke Neurology, May 23, 2006; 66(10): 1550 - 1555. [Abstract] [Full Text] [PDF]
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 R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Circulation, March 14, 2006; 113(10): e409 - e449. [Abstract] [Full Text] [PDF]
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The IMS Study Investigators Hemorrhage in the Interventional Management of Stroke Study Stroke, March 1, 2006; 37(3): 847 - 851. [Abstract] [Full Text] [PDF]
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R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Stroke, February 1, 2006; 37(2): 577 - 617. [Abstract] [Full Text] [PDF]
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P. Trouillas and R. von Kummer Classification and Pathogenesis of Cerebral Hemorrhages After Thrombolysis in Ischemic Stroke Stroke, February 1, 2006; 37(2): 556 - 561. [Abstract] [Full Text] [PDF]
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M. E. Mullins, M. H. Lev, D. Schellingerhout, R. G. Gonzalez, and P. W. Schaefer Intracranial Hemorrhage Complicating Acute Stroke: How Common Is Hemorrhagic Stroke on Initial Head CT Scan and How Often Is Initial Clinical Diagnosis of Acute Stroke Eventually Confirmed? AJNR Am. J. Neuroradiol., October 1, 2005; 26(9): 2207 - 2212. [Abstract] [Full Text] [PDF]
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M S Mouradian, A Senthilselvan, G Jickling, J A McCombe, D J Emery, N Dean, and A Shuaib Intravenous rt-PA for acute stroke: comparing its effectiveness in younger and older patients J. Neurol. Neurosurg. Psychiatry, September 1, 2005; 76(9): 1234 - 1237. [Abstract] [Full Text] [PDF]
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D.-W. Kang, J. A. Chalela, W. Dunn, S. Warach, and NIH-Suburban Stroke Center Investigators MRI Screening Before Standard Tissue Plasminogen Activator Therapy Is Feasible and Safe Stroke, September 1, 2005; 36(9): 1939 - 1943. [Abstract] [Full Text] [PDF]
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L. H. Schwamm, E. S. Rosenthal, C. J. Swap, J. Rosand, G. Rordorf, F. S. Buonanno, M. G. Vangel, W. J. Koroshetz, and M. H. Lev Hypoattenuation on CT Angiographic Source Images Predicts Risk of Intracerebral Hemorrhage and Outcome after Intra-Arterial Reperfusion Therapy AJNR Am. J. Neuroradiol., August 1, 2005; 26(7): 1798 - 1803. [Abstract] [Full Text] [PDF]
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W. S. Smith, G. Sung, S. Starkman, J. L. Saver, C. S. Kidwell, Y.P. Gobin, H. L. Lutsep, G. M. Nesbit, T. Grobelny, M. M. Rymer, et al. Safety and Efficacy of Mechanical Embolectomy in Acute Ischemic Stroke: Results of the MERCI Trial Stroke, July 1, 2005; 36(7): 1432 - 1438. [Abstract] [Full Text] [PDF]
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 M. D. Hill, A. M. Buchan, and for The Canadian Alteplase for Stroke Effectivenes Thrombolysis for acute ischemic stroke: results of the Canadian Alteplase for Stroke Effectiveness Study Can. Med. Assoc. J., May 10, 2005; 172(10): 1307 - 1312. [Abstract] [Full Text] [PDF]
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E. Y. Kim, D. G. Na, S. S. Kim, K. H. Lee, J. W. Ryoo, and H. K. Kim Prediction of Hemorrhagic Transformation in Acute Ischemic Stroke: Role of Diffusion-Weighted Imaging and Early Parenchymal Enhancement AJNR Am. J. Neuroradiol., May 1, 2005; 26(5): 1050 - 1055. [Abstract] [Full Text] [PDF]
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L Derex, M Hermier, P Adeleine, J-B Pialat, M Wiart, Y Berthezene, F Philippeau, J Honnorat, J-C Froment, P Trouillas, et al. Clinical and imaging predictors of intracerebral haemorrhage in stroke patients treated with intravenous tissue plasminogen activator J. Neurol. Neurosurg. Psychiatry, January 1, 2005; 76(1): 70 - 75. [Abstract] [Full Text] [PDF]
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D. Georgiadis, J. Oehler, S. Schwarz, V. Rousson, M. Hartmann, and S. Schwab Does acute occlusion of the carotid T invariably have a poor outcome? Neurology, July 13, 2004; 63(1): 22 - 26. [Abstract] [Full Text] [PDF]
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M. Castellanos, R. Leira, J. Serena, M. Blanco, S. Pedraza, J. Castillo, and A. Davalos Plasma Cellular-Fibronectin Concentration Predicts Hemorrhagic Transformation After Thrombolytic Therapy in Acute Ischemic Stroke Stroke, July 1, 2004; 35(7): 1671 - 1676. [Abstract] [Full Text] [PDF]
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M.-C. Arnould, C. B. Grandin, A. Peeters, G. Cosnard, and T. P. Duprez Comparison of CT and Three MR Sequences for Detecting and Categorizing Early (48 Hours) Hemorrhagic Transformation inHyperacute Ischemic Stroke AJNR Am. J. Neuroradiol., June 1, 2004; 25(6): 939 - 944. [Abstract] [Full Text] [PDF]
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P. Trouillas, L. Derex, F. Philippeau, N. Nighoghossian, J. Honnorat, M. Hanss, P. Ffrench, P. Adeleine, and M. Dechavanne Early Fibrinogen Degradation Coagulopathy Is Predictive of Parenchymal Hematomas in Cerebral rt-PA Thrombolysis: A Study of 157 Cases Stroke, June 1, 2004; 35(6): 1323 - 1328. [Abstract] [Full Text] [PDF]
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D. M. Kent, J. Hinchey, L. L. Price, S. R. Levine, and H. P. Selker In Acute Ischemic Stroke, Are Asymptomatic Intracranial Hemorrhages Clinically Innocuous? Stroke, May 1, 2004; 35(5): 1141 - 1146. [Abstract] [Full Text] [PDF]
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The IMS Study Investigators Combined Intravenous and Intra-Arterial Recanalization for Acute Ischemic Stroke: The Interventional Management of Stroke Study Stroke, April 1, 2004; 35(4): 904 - 911. [Abstract] [Full Text] [PDF]
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L. Zhang, Z. G. Zhang, R. L. Zhang, M. Lu, M. Krams, and M. Chopp Effects of a Selective CD11b/CD18 Antagonist and Recombinant Human Tissue Plasminogen Activator Treatment Alone and in Combination in a Rat Embolic Model of Stroke Stroke, July 1, 2003; 34(7): 1790 - 1795. [Abstract] [Full Text] [PDF]
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J. Aronowski, R. Strong, A. Shirzadi, and J. C. Grotta Ethanol Plus Caffeine (Caffeinol) for Treatment of Ischemic Stroke: Preclinical Experience Stroke, May 1, 2003; 34(5): 1246 - 1251. [Abstract] [Full Text] [PDF]
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J. Montaner, C. A. Molina, J. Monasterio, S. Abilleira, J. F. Arenillas, M. Ribo, M. Quintana;, and J. Alvarez-Sabin Matrix Metalloproteinase-9 Pretreatment Level Predicts Intracranial Hemorrhagic Complications After Thrombolysis in Human Stroke Circulation, February 4, 2003; 107(4): 598 - 603. [Abstract] [Full Text] [PDF]
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J.B. Fiebach, P.D. Schellinger, O. Jansen, M. Meyer, P. Wilde, J. Bender, P. Schramm, E. Juttler, J. Oehler, M. Hartmann, et al. CT and Diffusion-Weighted MR Imaging in Randomized Order: Diffusion-Weighted Imaging Results in Higher Accuracy and Lower Interrater Variability in the Diagnosis of Hyperacute Ischemic Stroke Stroke, September 1, 2002; 33(9): 2206 - 2210. [Abstract] [Full Text] [PDF]
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A.K. Gilligan, R. Markus, S. Read, V. Srikanth, T. Hirano, G. Fitt, M. Arends, B.R. Chambers, S.M. Davis, and G.A. Donnan Baseline Blood Pressure but Not Early Computed Tomography Changes Predicts Major Hemorrhage After Streptokinase in Acute Ischemic Stroke Stroke, September 1, 2002; 33(9): 2236 - 2242. [Abstract] [Full Text] [PDF]
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R. von Kummer Brain Hemorrhage After Thrombolysis: Good or Bad? Stroke, June 1, 2002; 33(6): 1446 - 1447. [Full Text] [PDF]
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C. A. Molina, J. Alvarez-Sabin, J. Montaner, S. Abilleira, J. F. Arenillas, P. Coscojuela, F. Romero, and A. Codina Thrombolysis-Related Hemorrhagic Infarction: A Marker of Early Reperfusion, Reduced Infarct Size, and Improved Outcome in Patients With Proximal Middle Cerebral Artery Occlusion Stroke, June 1, 2002; 33(6): 1551 - 1556. [Abstract] [Full Text] [PDF]
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C. Neumann-Haefelin, G. Brinker, U. Uhlenkuken, F. Pillekamp, K-A. Hossmann, and M. Hoehn Prediction of Hemorrhagic Transformation After Thrombolytic Therapy of Clot Embolism: An MRI Investigation in Rat Brain Stroke, May 1, 2002; 33(5): 1392 - 1398. [Abstract] [Full Text] [PDF]
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D. Tanne, S. E. Kasner, A. M. Demchuk, N. Koren-Morag, S. Hanson, M. Grond, S. R. Levine, and the Multicenter rt-PA Stroke Survey Group Markers of Increased Risk of Intracerebral Hemorrhage After Intravenous Recombinant Tissue Plasminogen Activator Therapy for Acute Ischemic Stroke in Clinical Practice: The Multicenter rt-PA Acute Stroke Survey Circulation, April 9, 2002; 105(14): 1679 - 1685. [Abstract] [Full Text] [PDF]
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C. S. Kidwell, J. L. Saver, J. Carneado, J. Sayre, S. Starkman, G. Duckwiler, Y.P. Gobin, R. Jahan, P. Vespa, J.P. Villablanca, et al. Predictors of Hemorrhagic Transformation in Patients Receiving Intra-Arterial Thrombolysis * Editorial Comment Stroke, March 1, 2002; 33(3): 717 - 724. [Abstract] [Full Text] [PDF]
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N. Nighoghossian, M. Hermier, P. Adeleine, K. Blanc-Lasserre, L. Derex, J. Honnorat, F. Philippeau, J.F. Dugor, J.C. Froment, and P. Trouillas Old Microbleeds Are a Potential Risk Factor for Cerebral Bleeding After Ischemic Stroke: A Gradient-Echo T2*-Weighted Brain MRI Study Stroke, March 1, 2002; 33(3): 735 - 742. [Abstract] [Full Text] [PDF]
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L. Zhang, Z. G. Zhang, R. L. Zhang, M. Lu, J. Adams, P. J. Elliott, and M. Chopp Postischemic (6-Hour) Treatment With Recombinant Human Tissue Plasminogen Activator and Proteasome Inhibitor PS-519 Reduces Infarction in a Rat Model of Embolic Focal Cerebral Ischemia Stroke, December 1, 2001; 32(12): 2926 - 2931. [Abstract] [Full Text] [PDF]
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