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(Stroke. 1996;27:875-881.)
© 1996 American Heart Association, Inc.

Articles

Thrombolytic Therapy of Acute Basilar Artery Occlusion

Variables Affecting Recanalization and Outcome

Tobias Brandt, MD; Rüdiger von Kummer, MD; Markus Müller-Küppers, MD Werner Hacke, MD

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.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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.

View larger version (119K): [in this window] [in a new window]   Figure 1. Distal basilar occlusion of intra-arterial embolic origin from a right vertebral artery dissection with good anterograde intercerebellar collateral channels (vertebral angiograms) before (A and B) and after (C) thrombolysis, with a small lateral pontine and cerebellar infarcts (right posterior and left anterior inferior cerebellar artery territories) on T2-weighted MRI (D), in a 32-year-old patient with good functional outcome (Rankin Scale score of 1).

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).

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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.

View larger version (371K): [in this window] [in a new window]   Figure 2. Midbasilar occlusion of atherothrombotic etiology (vertebral angiogram) (A) in a 67-year-old nonsurviving patient with midbasilar stenosis (B) and immediate local reocclusion (C) on the site of the stenosis.

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.

View this table: [in this window] [in a new window]   Table 1. Characteristics of Patients With and Without Recanalization at 24 Hours After Onset of Symptoms

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).

View this table: [in this window] [in a new window]   Table 2. Clinical and Radiological Variables Associated With Survival

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.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Case reports^{26 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 safe^{10 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.

	Selected Abbreviations and Acronyms

 

BA = basilar artery MCA = middle cerebral artery rTPA = recombinant tissue plasminogen activator SAE = subcortical arteriosclerotic encephalopathy

	Acknowledgments

 
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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Top Abstract Introduction Subjects and Methods Results Discussion References

 

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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]

				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]

				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]

				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]

				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]

				L. I. Kubersky, A. Kramer, and B. B. Worrall Coma reversal after basilar artery thrombolysis Neurology, March 13, 2007; 68(11): E11 - E12. [Full Text] [PDF]

				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]

				W. S. Smith Intra-Arterial Thrombolytic Therapy for Acute Basilar Occlusion: Pro Stroke, February 1, 2007; 38(2): 701 - 703. [Abstract] [Full Text] [PDF]

				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]

				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]

				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]

				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]

				M Arnold, K Nedeltchev, L Remonda, U Fischer, C Brekenfeld, B Keserue, G Schroth, and H P Mattle Recanalisation of middle cerebral artery occlusion after intra-arterial thrombolysis: different recanalisation grading systems and clinical functional outcome J. Neurol. Neurosurg. Psychiatry, October 1, 2005; 76(10): 1373 - 1376. [Abstract] [Full Text] [PDF]

				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]

				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]

				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]

				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]

				S. I. Savitz and L. R. Caplan Vertebrobasilar Disease N. Engl. J. Med., June 23, 2005; 352(25): 2618 - 2626. [Full Text] [PDF]

				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]

				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]

				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]

				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]

				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]

				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]

				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]

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 Patien