Diagnosis and thrombolytic therapy of acute basilar artery occlusion: a review.
Acute basilar artery (BA) occlusion is associated with an extremely high mortality. The pathogenesis in younger patients is usually embolism form cardiac sources or less frequently from vertebral artery dissection. Local atherothrombosis is more common in elderly patients. Differently to the carotid territory, for the vertebrobasilar territory there are no placebo controlled studies proving efficacy of thrombolytic treatment. Furthermore, neither the best route of administration nor the best fibrinolytic agent have been evaluated. Several uncontrolled series, however, indicate that intraarterial thrombolysis reduces mortality of patients with BA occlusion. Recanalization rates average 60% and are associated with occlusions of embolic etiology. Mortality with an average rate of 40-60% is significantly lower in the recanalization group in most series. Other independent variables affecting mortality are identified as length of obstruction, proximal BA occlusion, collateralization, high age, and initial poor clinical state. Time from onset of symptoms to start of intraarterial thrombolysis, however, is not associated with recanalization or mortality rate. This indicates that differently from thrombolytic treatment in the anterior circulation there is no fixed time window in BA thrombosis. Rate ofparenchymal hemorrhage seems to be lower with an average of 6% compared with systemic thrombolytic therapy in hemispheric stroke. Recanalization of the BA is clinically beneficial under certain circumstances only: (1) BA occlusion should affect only one segment; (2) an effective collateral supply is essential; and (3) the patient should not already be tetraplegic or comatose for a longer period of time. Clinical outcome and assessment of quality of life on follow-up of survivors with successful recanalization encourage thrombolysis in acute BA occlusions of embolic origin.
Brandt
Tobias
T
Department of Neurology, University of Heidelberg School of Medicine, Heidelberg, Germany. tobias_brandt@med.uni-heidelberg.de
D000208:Acute Disease; D006801:Humans; D010960:Plasminogen Activators / Q000627:therapeutic use; D011379:Prognosis; D015912:Thrombolytic Therapy; D016896:Treatment Outcome; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use; D014715:Vertebrobasilar Insufficiency / Q000175:diagnosis* / Q000188:drug therapy* / Q000209:etiology
D010960:Plasminogen Activators; D014568:Urokinase-Type Plasminogen Activator