(Stroke. 1996;27:875-881.)
© 1996 American Heart Association, Inc.
Articles |
Thrombolytic Therapy of Acute Basilar Artery Occlusion
Variables Affecting Recanalization and Outcome
From the Departments of Neurology (T.B., M.M.-K., W.H.) and Neuroradiology (R. von K.), University of Heidelberg School of Medicine (Germany).
Correspondence to Tobias Brandt, MD, Neurologische Universitätsklinik, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose Thrombolysis may reduce mortality after acute basilar artery (BA) occlusion. We intended to find variables affecting recanalization and clinical outcome in patients with BA occlusion undergoing thrombolytic therapy.
Methods We analyzed in retrospect the clinical and angiographic data of a consecutive series of 51 patients treated with intra-arterial urokinase (n=44; 0.3 to 1.5 mIU) or intravenous or intra-arterial recombinant tissue plasminogen activator (n=7; 22 to 100 mg). We identified effective variables by multiple logistic regression analyses and univariate tests.
Results Sites of occlusion were the caudal (n=23), middle (n=18), and distal (n=10) segments of the BA. The pathogenesis was embolism in 35 and local atherothrombosis in 16 patients. Collateral circulation was good in 32 patients and poor or absent in 19 patients. Recanalization was achieved in 26 of 51 (51%) patients and was associated with occlusions of embolic etiology (P=.0025). Mortality was 46% (12/26) in the recanalization group and 92% (23/25) in the nonrecanalization group (P=.0004). Other independent variables affecting mortality were length of BA obstruction (P=.0011), age (P=.0008), and collateral state (P=.0454). After follow-up (median, 32 months), 10 of the 16 survivors were only minimally impaired, with a Barthel Index score of 95 or greater; 5 patients were moderately and 1 severely disabled.
Conclusions Recanalization of acute BA occlusion reduces mortality significantly. Length of BA obstruction and state of the collaterals are additional independent variables affecting survival. Young patients with monosegmental embolic occlusion of the BA seem to have the best chance to considerably profit from thrombolysis.
Key Words: basilar artery • occlusion • outcome • thrombolytic therapy
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Since the milestone autopsy series of Kubik and Adams1 in 1946, acute BA occlusions have been known to cause mostly fatal brain stem infarctions. In older studies, BA occlusion was regarded as rare.2 Angiography enabled intravital diagnosis, and BA occlusion was detected much more frequently.3 4 5 6 7 8 9 Clinical outcome in series of patients with angiographically demonstrated BA occlusions is associated with a mortality of 80% to 90%.1 8 10 11 A benign outcome without interventional thrombolysis has been reported occasionally in a few small series of short-segment BA occlusions of mostly atherothrombotic origin and with good collateral supply.6 12 13 14
With the introduction of local intra-arterial administration of fibrinolytic agents in the early 1980s, a change in the prognosis of acute BA occlusion was expected. Even with successful recanalization of the BA, however, there is still an approximately 50% mortality rate.10 15 16 17 18 19 A placebo-controlled study of thrombolytic treatment of BA occlusions has not been conducted, and no other large-scale observation has been published since Hacke and coworkers10 described 43 patients undergoing thrombolytic therapy in 1988. There still is a lack of data about other factors besides recanalization and site of BA occlusion that may affect clinical outcome, such as collateral blood supply and length of thrombus. The etiology of occlusions, completeness of recanalization, and CT scan findings on admission have rarely been assessed. Moreover, detailed data regarding functional outcome and long-term follow-up of surviving patients with BA occlusions treated with thrombolysis are scarce.
We report here on a series of 51 consecutive patients with BA occlusions undergoing thrombolytic therapy, with special emphasis on the variables probably affecting arterial recanalization and clinical outcome. Long-term course and functional outcome were assessed to address the question of the quality of life of survivors.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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From December 1987 to September 1994, 51 consecutive patients (19 women, 32 men; age range, 16 to 75 years; mean±SD age, 55±14 years) with acute progressing brain stem stroke and angiographically demonstrated BA occlusion were treated with thrombolytic therapy. All patients were admitted to our hospital within 48 hours after the onset of symptoms. A standardized protocol was applied with defined inclusion criteria, evaluation and follow-up of clinical status by complete neurological examination, assessment of functional outcome, preparation for thrombolysis (a central intravenous line in the basilic vein, urinary catheter, electrocardiographic and blood pressure monitoring, and in all uncooperative patients intubation and mechanical ventilation before angiography), and CT and angiographic diagnostic procedures. Follow-up of the 16 survivors was accomplished personally by one of the authors (T.B. or M.M.-K.) in 10 patients, including complete neurological assessment, and in the remaining 6 by telephone interviews. Functional outcome was assessed after 4 weeks and 5 to 63 months (median, 32 months) after the stroke with the use of the modified Rankin Scale, in which a score of 6 indicated death,20 21 and the Barthel Index.22
Inclusion criteria for this registry were as follows: (1) a precisely defined and witnessed onset of severe progressive brain stem or cerebellar symptoms within the previous 48 hours before thrombolytic treatment; (2) a technically satisfactory CT scan before thrombolytic treatment without evidence of cerebral hemorrhage or an already demarcated hypodense area of a new infarct; (3) BA occlusion shown by intra-arterial digital subtraction angiography; and (4) informed consent from the patient or the patient's relatives. Patients were excluded from the study if brain stem reflexes were completely lacking or coma had lasted longer than 4 hours before thrombolytic therapy.
CT scans were unenhanced, with a slice thickness of 4 mm throughout the brain stem. We used the baseline scans to assess the presence of SAE, defined by subcortical infarctions and ischemic white matter alterations. Follow-up CT or MRI scans were obtained in all patients to depict the site and areas of infarction. The presence of hemorrhage was defined as hemorrhagic infarction or parenchymal hematoma according to criteria described by Pessin et al.23
The site of occlusion was entered by superselective catheterization, with the use of a 2F microcatheter flushed with a heparinized solution before intra-arterial infusion of urokinase (n=44; 0.3 to 1.5 mIU, 1 mIU/h in 100 mL NaCl) or infusion of rTPA (n=1; 22 mg). Six patients were treated intravenously with rTPA (70 to 100 mg). Five of these 6 patients were described in an earlier report.24 Infusion was continued either until the vessel was recanalized or until the maximal dose of the fibrinolytic agent (urokinase, 1.5 MIU; rTPA, 100 mg) was administered. Duration of treatment was generally 90 minutes, unless recanalization occurred earlier. Treatment was continued in all patients with intravenous infusion of 1000 to 1500 IU heparin per hour, increasing activated partial thromboplastin time at 1.5 to 2 times the initial values, and the patients were transferred to the intensive care unit for at least 24 hours.
Site of occlusion, collateral blood flow, and recanalization were determined on the basis of angiograms performed within 4 hours after admission and immediately after thrombolytic treatment. In addition to unilateral or bilateral vertebral artery injections of contrast agent, all but 9 patients received, at least on one side, a carotid artery injection with visualization of the anterior circulation. The angiograms of all 51 patients were analyzed in retrospect, with the investigator blinded to the clinical data of the patient.
Sites of occlusion were classified according to Archer and Horenstein25 following the three anatomic segments of the BA: caudal, from the confluence of the vertebral arteries to the origin of the anterior inferior cerebellar artery; midbasilar, from the origin of the anterior inferior cerebellar artery to the origin of the superior cerebellar arteries; and oral, the top of the BA. Length of occlusion was classified as "short" if only one segment of the basilar artery was occluded and "long" if two or more segments were occluded, corresponding to the category of "extended" or multilevel occlusion described by Brückmann et al9 and Hacke et al.10
The criteria for classifying occlusions as either atherothrombotic or embolic were based on the results of angiographic study and on clinical features. The atherothrombotic category included occlusion of the BA at one of the pathoanatomically known sites of predilection for atheromas, such as the vertebrobasilar junction or the midbasilar artery, local high-grade stenosis after thrombolysis, signs of generalized atherosclerotic disease on angiography, and absence of a cardiac source of embolism.1 3 7 The embolic category included absence of angiographic signs of generalized atherosclerotic disease and no or only minor local wall irregularities (no stenosis) after thrombolysis.1 7 8
The initial collateral state was scored as described
previously.14 The collateralization score included the
following categories: 0, no collaterals; 1 (minimal),
anterograde or retrograde collaterals with partial or faint
filling; 2 (moderate), anterograde or retrograde collaterals
with filling of the superior cerebellar arteries; and 3 (maximal),
collateralization with anterograde and retrograde channels or
maximal bilateral filling of the superior cerebellar arteries.
"Poor" collateral supply was defined in our analysis by
grades 0 and 1 and "good" collateral supply (Fig 1
) by grades 2 and 3.
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Recanalization was assessed by repeated angiography after treatment without delay and scored as "complete," "incomplete" (remaining wall irregularities, filling deficit with remaining thrombus, or branch occlusion), or "absent" (no recanalization or reocclusion). Late recanalization (at 24 hours) was assessed by transcranial Doppler sonography.
The statistical association of clinical and neuroradiological baseline
characteristics with recanalization and clinical
outcome was tested by the 
2 test or Fisher's
exact test and the Mann-Whitney test for unpaired groups. A Bonferroni
correction was performed to adjust the probability values corresponding
to the number of variables (
=15) analyzed. By a
two-tailed analysis, a level of 
=.003 was considered
statistically significant. To account for the intercorrelation of the
variables, a stepwise multiple logistic regression analysis
was performed (SAS Logistic Procedure).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Sites of occlusion were the caudal (n=23), middle (n=18), and distal (n=10) parts of the BA. Recanalization frequency was 51% (26/51) at 8 hours after symptom onset and also 51% (26/51) at 24 hours, including reocclusion in 2 and delayed recanalization in 2 patients, respectively. In 6 patients with midbasilar stenosis, the BA reoccluded directly after urokinase infusion was discontinued (Fig 2
). We
included these 6 patients in the
nonrecanalization group. We achieved
recanalization in 23 of 44 patients (52%) with
urokinase and in 3 of 7 (43%) with rTPA.
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Table 1 compares the characteristics of patients with
and without recanalization.
Recanalization was not affected by sex, site or
length of occlusion, state of collaterals, or time period between onset
of symptoms and start of therapy. Recanalization
was less often observed in patients with atherothrombotic BA occlusion,
patients with CT signs of SAE, and as a trend in older patients. These
observations suggested that urokinase and rTPA are less effective in
terms of arterial recanalization in
patients with basilar occlusion caused by
arteriosclerosis. The multivariate
analysis identified the etiology of occlusion and SAE as
independent variables affecting
recanalization.
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Table 2 shows the clinical and angiographic
variables potentially affecting mortality. Survival after BA
occlusion was associated with younger age, short occlusion, and
recanalization. The survival rate increased with
recanalization from 8% to 54%. Mortality tended
to be higher in patients with tetraplegia on admission, with
atherothrombotic occlusion, with caudal basilar occlusion, and with
poor collaterals. Although recanalization was
achieved in 10 patients with poor collaterals, 17 of 19 patients (89%)
died; the remaining 2 patients showed moderate disability.
Multivariate analysis showed that
recanalization, collateralization, and length of
occlusion were independent variables affecting mortality. In the
subgroup of patients with technically successful
recanalization, the site of BA occlusion and the
completeness of recanalization were associated with
survival, with higher mortality in patients with caudal occlusion
(P=.0027) and incomplete recanalization
(P=.044).
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Hemorrhagic complications after thrombolysis were seen in 7 of 51 patients (14%), but these complications did not result in additional clinical deterioration. Three patients had hemorrhagic infarction, 3 had parenchymal hematoma, and 1 experienced gastric bleeding.
All survivors had brain stem (pons, n=9; midbrain, n=2),
cerebellar (n=9), or thalamic (n=7) infarctions demonstrated by
CT scan or MRI (Fig 1D
). After follow-up, 1 young patient
without recanalization was severely disabled
(Rankin Scale score of 5). Five patients (1 without
recanalization) were moderately disabled, with a
Rankin Scale score of 3 and Barthel Index scores of 45, 55, 65, 70, and
75. Predominating neurological deficits in this group were ataxia and
moderate hemiparesis. Ten patients had no or slight deficits, with
Barthel Index scores of 95 in 2 patients and 100 in 8 patients. In
these patients mostly oculomotor deficits and slight sensorimotor
hemisyndromes or no deficits were seen. No recurrent ischemic
events occurred in the surviving patients. Prophylactic
treatment consisted of anticoagulation with warfarin in 8,
acetylsalicylic acid in 4, ticlopidine in 1, and
none in 3 patients. One patient died of cardiac causes during the
follow-up period.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Case reports26 27 28 of patients with acute vertebrobasilar occlusion who received thrombolytic treatment were followed by somewhat larger series, only 5 with 10 or more patients.10 15 16 19 27 Recanalization frequency was between 40% and 100%, and survival rates varied from 25% to 70% according to the different modes of patient selection and treatment.10 15 16 17 19 29 30 The numbers of patients were too small to draw any valid conclusions. Only little attention has been paid to potentially prognostic factors other than recanalization and initial clinical condition.10 17 18 19 31 Notably, the high mortality despite successful recanalization is unexplained thus far.10 17 19 29
With this post hoc analysis of a relatively large registry of
patients, we intended to identify independent factors affecting
recanalization and clinical outcome to better
define patients who may benefit from thrombolysis. This
analysis does not address the effects of different
thrombolytic agents. The subgroup of patients treated
with rTPA is too small to draw any valid conclusion. We did not exclude
these patients because we wanted to study clinical and
neuroradiological preconditions associated with
recanalization as an end point (Table 1) and
factors potentially affecting outcome, including
recanalization (Table 2), independent from
treatment. We concentrated on variables that could be assessed
reliably in all patients. Therefore, we cannot exclude potential
effects on recanalization and outcome by other
conditions.
As in other series,15 17 recanalization frequency was low in patients with atherothrombotic occlusive disease compared with occlusions of embolic origin. Moreover, signs of SAE on the admission CT correlated with nonrecanalization in our series. Age seems to be a covariable associated with atherothrombotic occlusion. The eldest surviving patient in whom recanalization was successful was 63 years old. This observation is not surprising because thrombolysis is not suitable to reduce arterial stenosis caused by atherosclerotic plaques. Others have suggested combining thrombolysis with angioplasty in patients with atherothrombotic BA occlusions.32 Experience with this approach, however, is very limited thus far.
In contrast to occlusions of the MCA,33 34 35 36 37 the frequency of recanalization was not associated with the state of collaterals. This could be explained by the route of administration of the thrombolytic agent: After intravenous infusion, as performed in the cited studies,33 36 37 larger amounts of the agent could reach the thrombus from both sides in the presence of collateral flow, whereas the effect of local intra-arterial injection adjacent to the proximal end of the thrombus may be independent from the collateral state.
In agreement with previous studies,10 19 we found that recanalization is associated with a significant increase in survival rate. Consequently, variables affecting recanalization also affect mortality. Remarkably, recanalization was only one variable among others affecting clinical outcome. While initial clinical condition, length of the BA occlusion, and collateral supply did not affect the frequency of recanalization, all these factors were associated with clinical outcome. Multivariate analysis identified the length of BA obstruction and the state of collaterals as assessed by angiography as independent variables affecting mortality in addition to recanalization. In agreement with the findings of others in the carotid and BA territories,7 14 35 36 37 our data suggest that the clinical course after BA occlusion is primarily determined by the length of the clot and the collateral supply, which correlate with the number of obstructed perforating arteries and thus with the degree and volume of brain stem ischemia. Long-segment BA obstructions invariably cause irreversible brain stem destruction, vegetative dysfunction, and subsequent death even when recanalization is achieved.1 2 24 In contrast, after recanalization of a short-segment occlusion and reperfusion, small volumes of infarcted brain stem tissue will not considerably impair vegetative functions, which may explain the good functional outcome in our series and those of others.10 16 38 39 Short-segment BA occlusion and good collaterals may restrict the hypoperfused tissue volume in the brain stem and enable survival.14
For the carotid territory, a similar study of factors that potentially affect outcome identified parenchymal hypodensity exceeding 50% of the MCA territory as shown by early CT, scarce collaterals, and the site of arterial occlusion, but not recanalization, as the most significant variables affecting mortality.37 Both studies show in parallel that variables indicating the primary extent of severe perfusion deficit may be used as outcome predictors. If the volume of hypoperfused brain tissue is large, reperfusion cannot prevent poor outcome. In the MCA territory, extended ischemic brain edema causes an increase in intracranial pressure, progressive decrease in perfusion pressure, and finally midbrain incarceration. In the BA territory, it is not the space-occupying effect but primarily the disturbance of brain stem function that threatens life. Thus, relatively smaller volumes of ischemic brain stem tissue can cause death and are responsible for the higher mortality of BA occlusion compared with MCA occlusion. In contrast to the MCA territory, CT is not suited to show early ischemic edema in the brain stem because of its technical limitations. We believe that the extent of ischemic tissue volume can be determined from the length of BA obstruction and the collateral state. The clinical condition on admission did not reliably predict the clinical course. Twenty of 26 patients who were comatose on admission died. This number was, however, too small to identify coma as a statistically significant variable affecting outcome, in contrast to the findings in the previous series of Hacke and coworkers.10 Presumably, the time period of the comatose state is of more importance than coma per se. However, we could not assess the exact beginning of coma with certainty in all patients of our series. Therefore, the interval between onset of coma and initiation of thrombolysis was not analyzed. Only 1 of 16 tetraplegic patients survived, which suggests that this neurological deficit on admission may indicate severe irreversible and extended brain stem damage.
Owing to the small number of patients treated with rTPA, neither the route of administration nor the fibrinolytic agent used in this series had a statistically significant effect on recanalization or outcome. Presently there are no data available showing which agent is more effective and safer or which route of administration is superior in the vertebrobasilar circulation.
The rate of hemorrhagic complications in our series was low (14%), with three parenchymal hemorrhages not associated with clinical deterioration; this is in agreement with the previous results of Hacke and coworkers,10 in which 4 of 43 patients (9%) had hemorrhagic complications (2 parenchymal hemorrhages), and with those of Zeumer and coworkers,19 in which 2 of 28 patients (7%) had parenchymal hemorrhages. Compared with the carotid artery territory, hemorrhagic transformations or parenchymal hemorrhages occurred less frequently.33 38 39
In conclusion, patients with short embolic obstruction of the BA and good collaterals seem to be the ideal candidates for thrombolytic therapy. Recanalization in these patients will prevent death and enable a beneficial clinical outcome. Thrombolysis may be less promising in patients with long BA obstruction, poor collaterals, and atherothrombotic obstruction. Digital subtraction angiography of the BA may help to adequately select patients for thrombolysis and to assess individual prognosis. Knowledge of the high mortality rate of this disease and the fact that intra-arterial thrombolysis of the BA is relatively safe10 19 may justify the use of thrombolytic recanalization in patients with recent embolic BA occlusion, particularly in younger patients, in whom brain stem destruction is not obvious.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The authors gratefully acknowledge the statistical advice and assistance of R. Holle, PhD, and K. Meyer, MSc, Department of Medical Biometry, University of Heidelberg. We thank our colleagues in the Departments of Neurology and Neuroradiology who cared for our acute stroke patients, making this study possible.
Received August 3, 1995; revision received February 6, 1996; accepted February 8, 1996.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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P. W. Schaefer, A. J. Yoo, D. Bell, E. R. Barak, J. M. Romero, R. G. Nogueira, M. H. Lev, L. H. Schwamm, R. G. Gonzalez, and J. A. Hirsch CT Angiography-Source Image Hypoattenuation Predicts Clinical Outcome in Posterior Circulation Strokes Treated With Intra-Arterial Therapy Stroke, November 1, 2008; 39(11): 3107 - 3109. [Abstract] [Full Text] [PDF]
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V. Puetz, P.N. Sylaja, S. B. Coutts, M. D. Hill, I. Dzialowski, P. Mueller, U. Becker, G. Urban, C. O'Reilly, P. A. Barber, et al. Extent of Hypoattenuation on CT Angiography Source Images Predicts Functional Outcome in Patients With Basilar Artery Occlusion Stroke, September 1, 2008; 39(9): 2485 - 2490. [Abstract] [Full Text] [PDF]
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A. Bose, H. Henkes, K. Alfke, W. Reith, T.E. Mayer, A. Berlis, V. Branca, S. P. Sit, and for the Penumbra Phase 1 Stroke Trial Investigator The Penumbra System: A Mechanical Device for the Treatment of Acute Stroke due to Thromboembolism AJNR Am. J. Neuroradiol., August 1, 2008; 29(7): 1409 - 1413. [Abstract] [Full Text] [PDF]
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T. Pfefferkorn, T. E. Mayer, C. Opherk, N. Peters, A. Straube, H.-W. Pfister, M. Holtmannspotter, S. Muller-Schunk, M. Wiesmann, and M. Dichgans Staged Escalation Therapy in Acute Basilar Artery Occlusion: Intravenous Thrombolysis and On-Demand Consecutive Endovascular Mechanical Thrombectomy: Preliminary Experience in 16 Patients Stroke, May 1, 2008; 39(5): 1496 - 1500. [Abstract] [Full Text] [PDF]
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G. Tsivgoulis, V. K. Sharma, S. L. Hoover, A. Y. Lao, A. A. Ardelt, M. D. Malkoff, and A. V. Alexandrov Applications and Advantages of Power Motion-Mode Doppler in Acute Posterior Circulation Cerebral Ischemia Stroke, April 1, 2008; 39(4): 1197 - 1204. [Abstract] [Full Text] [PDF]
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R. Muller, T. Pfefferkorn, B. Vatankhah, T. E. Mayer, J. Schenkel, M. Dichgans, D. Sander, and H. J. Audebert Admission Facility Is Associated With Outcome of Basilar Artery Occlusion Stroke, April 1, 2007; 38(4): 1380 - 1383. [Abstract] [Full Text] [PDF]
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W. Yu, V. Kostanian, and M. Fisher Endovascular Recanalization of Basilar Artery Occlusion 80 Days After Symptom Onset Stroke, April 1, 2007; 38(4): 1387 - 1389. [Abstract] [Full Text] [PDF]
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G. Schulte-Altedorneburg, H. Bruckmann, G.F. Hamann, M. Mull, M. Liebetrau, W. Weber, D. Kuhne, and T.E. Mayer Ischemic and Hemorrhagic Complications after Intra-Arterial Fibrinolysis in Vertebrobasilar Occlusion AJNR Am. J. Neuroradiol., February 1, 2007; 28(2): 378 - 381. [Abstract] [Full Text] [PDF]
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W. S. Smith Intra-Arterial Thrombolytic Therapy for Acute Basilar Occlusion: Pro Stroke, February 1, 2007; 38(2): 701 - 703. [Abstract] [Full Text] [PDF]
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G. Schulte-Altedorneburg, G.F. Hamann, M. Mull, D. Kuhne, M. Liebetrau, W. Weber, H. Bruckmann, and T.E. Mayer Outcome of Acute Vertebrobasilar Occlusions Treated with Intra-Arterial Fibrinolysis in 180 Patients AJNR Am. J. Neuroradiol., November 1, 2006; 27(10): 2042 - 2047. [Abstract] [Full Text] [PDF]
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G. A. Donnan, S. M. Davis, P. D. Schellinger, and W. Hacke Intra-Arterial Thrombolysis Is the Treatment of Choice for Basilar Thrombosis: Pro Stroke, September 1, 2006; 37(9): 2436 - 2437. [Full Text] [PDF]
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P. J. Lindsberg and H. P. Mattle Therapy of Basilar Artery Occlusion: A Systematic Analysis Comparing Intra-Arterial and Intravenous Thrombolysis Stroke, March 1, 2006; 37(3): 922 - 928. [Abstract] [Full Text] [PDF]
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G. Saposnik, S. Di Legge, F. Webster, and V. Hachinski Predictors of major neurologic improvement after thrombolysis in acute stroke Neurology, October 25, 2005; 65(8): 1169 - 1174. [Abstract] [Full Text] [PDF]
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P Favrole, J P Saint-Maurice, M G Bousser, and E Houdart Use of mechanical extraction devices in basilar artery occlusion J. Neurol. Neurosurg. Psychiatry, October 1, 2005; 76(10): 1462 - 1464. [Abstract] [Full Text] [PDF]
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W J Schonewille, A Algra, J Serena, C A Molina, and L J Kappelle Outcome in patients with basilar artery occlusion treated conventionally J. Neurol. Neurosurg. Psychiatry, September 1, 2005; 76(9): 1238 - 1241. [Abstract] [Full Text] [PDF]
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 J. W. Tsao, J. C. Hemphill III, S. C. Johnston, W. S. Smith, and D. C. Bonovich Initial Glasgow Coma Scale Score Predicts Outcome Following Thrombolysis for Posterior Circulation Stroke Arch Neurol, July 1, 2005; 62(7): 1126 - 1129. [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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T. E. Mayer, G. F. Hamann, G. Schulte-Altedorneburg, and H. Bruckmann Treatment of Vertebrobasilar Occlusion by Using a Coronary Waterjet Thrombectomy Device: A Pilot Study AJNR Am. J. Neuroradiol., June 1, 2005; 26(6): 1389 - 1394. [Abstract] [Full Text] [PDF]
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P. J. Lindsberg, L. Soinne, R. O. Roine, and T. Tatlisumak Options for Recanalization Therapy in Basilar Artery Occlusion Stroke, February 1, 2005; 36(2): 203 - 204. [Full Text] [PDF]
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 P. J. Lindsberg, L. Soinne, T. Tatlisumak, R. O. Roine, M. Kallela, O. Happola, and M. Kaste Long-term Outcome After Intravenous Thrombolysis of Basilar Artery Occlusion JAMA, October 20, 2004; 292(15): 1862 - 1866. [Abstract] [Full Text] [PDF]
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 G. W. Albers, P. Amarenco, J. D. Easton, R. L. Sacco, and P. Teal Antithrombotic and Thrombolytic Therapy for Ischemic Stroke: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 483S - 512S. [Abstract] [Full Text] [PDF]
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M Arnold, K Nedeltchev, G Schroth, R W Baumgartner, L Remonda, T J Loher, F Stepper, M Sturzenegger, B Schuknecht, and H P Mattle Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis J. Neurol. Neurosurg. Psychiatry, June 1, 2004; 75(6): 857 - 862. [Abstract] [Full Text] [PDF]
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A. Montavont, N. Nighoghossian, L. Derex, M. Hermier, J. Honnorat, F. Philippeau, M. Belo, F. Turjman, P. Adeleine, J. C. Froment, et al. Intravenous r-TPA in vertebrobasilar acute infarcts Neurology, May 25, 2004; 62(10): 1854 - 1856. [Abstract] [Full Text] [PDF]
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A. Berlis, H. Lutsep, S. Barnwell, A. Norbash, L. Wechsler, C. A. Jungreis, A. Woolfenden, G. Redekop, M. Hartmann, and M. Schumacher Mechanical Thrombolysis in Acute Ischemic Stroke With Endovascular Photoacoustic Recanalization Stroke, May 1, 2004; 35(5): 1112 - 1116. [Abstract] [Full Text] [PDF]
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J. L. Ostrem, J. L. Saver, J. R. Alger, S. Starkman, M. C. Leary, G. Duckwiler, R. Jahan, P. Vespa, J. P. Villablanca, Y. P. Gobin, et al. Acute Basilar Artery Occlusion: Diffusion-Perfusion MRI Characterization of Tissue Salvage in Patients Receiving Intra-Arterial Stroke Therapies Stroke, February 1, 2004; 35 (2): e30 - e34. [Abstract] [Full Text] [PDF]
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M. Ribo, Z. Garami, K. Uchino, J. Song, C. A. Molina, and A. V. Alexandrov Detection of Reversed Basilar Flow With Power-Motion Doppler After Acute Occlusion Predicts Favorable Outcome Stroke, January 1, 2004; 35(1): 79 - 82. [Abstract] [Full Text] [PDF]
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D. L. Brown, K. C. Johnston, D. P. Wagner, and E. C. Haley Jr Predicting Major Neurological Improvement With Intravenous Recombinant Tissue Plasminogen Activator Treatment of Stroke Stroke, January 1, 2004; 35(1): 147 - 150. [Abstract] [Full Text] [PDF]
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W. Yu, D. Binder, A. Foster-Barber, R. Malek, W. S. Smith, and R. T. Higashida Endovascular embolectomy of acute basilar artery occlusion Neurology, November 25, 2003; 61(10): 1421 - 1423. [Abstract] [Full Text] [PDF]
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 J. M. Provenzale, R. Jahan, T. P. Naidich, and A. J. Fox Assessment of the Patient with Hyperacute Stroke: Imaging and Therapy Radiology, November 1, 2003; 229(2): 347 - 359. [Abstract] [Full Text] [PDF]
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L. Restrepo, G. Pradilla, R. Llinas, and N. J. Beauchamp Perfusion- and Diffusion-Weighted MR Imaging-Guided Therapy of Vertebral Artery Dissection: Intraarterial Thrombolysis through an Occipital Vertebral Anastomosis AJNR Am. J. Neuroradiol., October 1, 2003; 24(9): 1823 - 1826. [Abstract] [Full Text] [PDF]
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D. D. M. Lin, P. Gailloud, N. J. Beauchamp, E. M. Aldrich, R. J. Wityk, and K. J. Murphy Combined Stent Placement and Thrombolysis in Acute Vertebrobasilar Ischemic Stroke AJNR Am. J. Neuroradiol., October 1, 2003; 24(9): 1827 - 1833. [Abstract] [Full Text] [PDF]
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J.-N. Vallee, S. Crozier, R. Guillevin, M. Obadia, D. Lo, H. M. Barragan-Campos, Y. Samson, and J. Chiras Acute basilar artery occlusion treated by thromboaspiration in a cocaine and ecstasy abuser Neurology, September 23, 2003; 61(6): 839 - 841. [Abstract] [Full Text] [PDF]
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D. S. Liebeskind Collateral Circulation Stroke, September 1, 2003; 34(9): 2279 - 2284. [Abstract] [Full Text] [PDF]
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S. Hahnel, P. D. Schellinger, A. Gutschalk, K. Geletneky, M. Hartmann, M. Knauth, and K. Sartor Local Intra-arterial Fibrinolysis of Thromboemboli Occurring During Neuroendovascular Procedures With Recombinant Tissue Plasminogen Activator Stroke, July 1, 2003; 34(7): 1723 - 1728. [Abstract] [Full Text] [PDF]
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L. R. Wechsler, R. Roberts, A. J. Furlan, R. T. Higashida, W. Dillon, H. Roberts, H. A. Rowley, L. C. Pettigrew, A. S. Callahan III, A. Bruno, et al. Factors Influencing Outcome and Treatment Effect in PROACT II Stroke, May 1, 2003; 34(5): 1224 - 1229. [Abstract] [Full Text] [PDF]
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H. P. Adams Jr, R. J. Adams, T. Brott, G. J. del Zoppo, A. Furlan, L. B. Goldstein, R. L. Grubb, R. Higashida, C. Kidwell, T. G. Kwiatkowski, et al. Guidelines for the Early Management of Patients With Ischemic Stroke: A Scientific Statement From the Stroke Council of the American Stroke Association Stroke, April 1, 2003; 34(4): 1056 - 1083. [Full Text] [PDF]
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B. R. Mahon, G. M. Nesbit, S. L. Barnwell, W. Clark, T. R. Marotta, A. Weill, P. A. Teal, and A. I. Qureshi North American Clinical Experience with the EKOS MicroLysUS Infusion Catheter for the Treatment of Embolic Stroke AJNR Am. J. Neuroradiol., March 1, 2003; 24(3): 534 - 538. [Abstract] [Full Text] [PDF]
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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]
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H. Kassem-Moussa and C. Graffagnino Nonocclusion and Spontaneous Recanalization Rates in Acute Ischemic Stroke: A Review of Cerebral Angiography Studies Arch Neurol, December 1, 2002; 59(12): 1870 - 1873. [Abstract] [Full Text] [PDF]
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T. E. Mayer, G. F. Hamann, and H. Brueckmann Mechanical Extraction of a Basilar-Artery Embolus with the Use of Flow Reversal and a Microbasket N. Engl. J. Med., September 5, 2002; 347(10): 769 - 770. [Full Text] [PDF]
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T. E. Mayer, G. F. Hamann, and H. J. Brueckmann Treatment of Basilar Artery Embolism With a Mechanical Extraction Device: Necessity of Flow Reversal Stroke, September 1, 2002; 33(9): 2232 - 2235. [Abstract] [Full Text] [PDF]
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B. Eckert, C. Koch, G. Thomalla, J. Roether, and H. Zeumer Acute Basilar Artery Occlusion Treated With Combined Intravenous Abciximab and Intra-arterial Tissue Plasminogen Activator: Report of 3 Cases Stroke, May 1, 2002; 33(5): 1424 - 1427. [Abstract] [Full Text] [PDF]
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R. du Mesnil de Rochemont, T. Neumann-Haefelin, J. Berkefeld, M. Sitzer, and H. Lanfermann Magnetic Resonance Imaging in Basilar Artery Occlusion Arch Neurol, March 1, 2002; 59(3): 398 - 402. [Abstract] [Full Text] [PDF]
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R. Chapot, E. Houdart, A. Rogopoulos, C. Mounayer, J.-P. Saint-Maurice, and J.-J. Merland Thromboaspiration in the Basilar Artery: Report of Two Cases AJNR Am. J. Neuroradiol., February 1, 2002; 23(2): 282 - 284. [Abstract] [Full Text] [PDF]
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M. D. Hill, P. A. Barber, A. M. Demchuk, N. J. Newcommon, A. Cole-Haskayne, K. Ryckborst, L. Sopher, A. Button, W. Hu, M. E. Hudon, et al. Acute Intravenous-Intra-Arterial Revascularization Therapy for Severe Ischemic Stroke Stroke, January 1, 2002; 33(1): 279 - 282. [Abstract] [Full Text] [PDF]
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Intra-arterial Thrombolysis AJNR Am. J. Neuroradiol., September 1, 2001; 22(2007): 18S - 21S. [Full Text] [PDF]
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T. Brandt, E. Orberk, R. Weber, I. Werner, O. Busse, B. T. Muller, F. Wigger, A. Grau, C. Grond-Ginsbach, and I. Hausser Pathogenesis of cervical artery dissections: Association with connective tissue abnormalities Neurology, July 10, 2001; 57(1): 24 - 30. [Abstract] [Full Text] [PDF]
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J. A. Chalela, I. Katzan, D. S. Liebeskind, P. Rasmussen, O. Zaidat, J. I. Suarez, D. Chiu, R. P. Klucznick, E. Jauch, B. L. Cucchiara, et al. Safety of Intra-Arterial Thrombolysis in the Postoperative Period Editorial Comment : Safety of Intra-Arterial Thrombolysis in the Postoperative Period Stroke, June 1, 2001; 32(6): 1365 - 1369. [Abstract] [Full Text] [PDF]
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D. T. Cross III, C. P. Derdeyn, and C. J. Moran Bleeding Complications after Basilar Artery Fibrinolysis with Tissue Plasminogen Activator AJNR Am. J. Neuroradiol., March 1, 2001; 22(3): 521 - 525. [Abstract] [Full Text]
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C. C. Phatouros, J. E. Lefler, R. T. Higashida, P. M. Meyers, A. M. Malek, C. F. Dowd, and V. V. Halbach Primary Stenting for High-grade Basilar Artery Stenosis AJNR Am. J. Neuroradiol., October 1, 2000; 21(9): 1744 - 1749. [Abstract] [Full Text]
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T. Brott and J. Bogousslavsky Treatment of Acute Ischemic Stroke N. Engl. J. Med., September 7, 2000; 343(10): 710 - 722. [Full Text] [PDF]
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T. Brandt, M. Knauth, S. Wildermuth, R. Winter, R. von Kummer, K. Sartor, and W. Hacke CT Angiography and Doppler Sonography for Emergency Assessment in Acute Basilar Artery Ischemia Stroke, March 1, 1999; 30(3): 606 - 612. [Abstract] [Full Text] [PDF]
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L. R. Caplan and M. Hennerici Impaired Clearance of Emboli (Washout) Is an Important Link Between Hypoperfusion, Embolism, and Ischemic Stroke Arch Neurol, November 1, 1998; 55(11): 1475 - 1482. [Abstract] [Full Text] [PDF]
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F. Gonner, L. Remonda, H. Mattle, M. Sturzenegger, C. Ozdoba, K.-O. Lovblad, R. Baumgartner, C. Bassetti, and G. Schroth Local Intra-Arterial Thrombolysis in Acute Ischemic Stroke Stroke, September 1, 1998; 29(9): 1894 - 1900. [Abstract] [Full Text] [PDF]
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M. Fisher and J. Bogousslavsky Further Evolution Toward Effective Therapy for Acute Ischemic Stroke JAMA, April 22, 1998; 279(16): 1298 - 1303. [Abstract] [Full Text] [PDF]
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M. Grond, J. Rudolf, S. Schmulling, C. Stenzel, M. Neveling, and W.-D. Heiss Early Intravenous Thrombolysis With Recombinant Tissue-type Plasminogen Activator in Vertebrobasilar Ischemic Stroke Arch Neurol, April 1, 1998; 55(4): 466 - 469. [Abstract] [Full Text] [PDF]
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U. Junghans, R. J. Seitz, H. J. Wittsack, A. Aulich, and M. Siebler Treatment of Acute Basilar Artery Thrombosis with a Combination of Systemic Alteplase and Tirofiban, a Nonpeptide Platelet Glycoprotein IIb/IIIa Inhibitor: Report of Four Cases Radiology, December 1, 2001; 221(3): 795 - 801. [Abstract] [Full Text] [PDF]
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