Top of the Basilar Syndrome Revisited
February 1, 1998
Top of the Basilar Syndrome Revisited
ABSTRACT & COMMENTARY
Source: Schwarz S, et al. Basilar artery embolism. Clinical syndrome and neuroradiologic patterns in patients without permanent occlusion of the basilar artery. Neurology 1997; 49:1346- 1352.
The clinical syndrome of embolism to the top of the basilar artery has been described by Caplan (Neurology 1980;30:72-79). Such patients typically present with the sudden onset of rostral brainstem and posterior cerebral artery (PCA) territory symptoms without prior artery TIAs. Although basilar artery embolism is fairly common, its prognosis remains unexplored.
Schwarz and coworkers studied 45 patients hospitalized in Heidelberg, Germany, between 1992 and 1997 with basilar artery embolism to clarify the clinical and radiologic features, risk factors, and prognosis of this condition. Patients with clinical or radiographic evidence of new onset ischemic lesions in the basilar artery territory were evaluated by transcranial Doppler sonography or cerebral angiography to demonstrate patency of the basilar artery.
There were 33 men and 12 women, and the mean age was 59 years (range, 21-87 years). The etiologic factors were cardiac arrhythmia (n = 17), vertebral artery occlusion (n = 12), cervical spine injury (n = 4), embolism during angiography (n = 2), and orthopedic surgery (n = 1). Sites of infarction included the thalamus (n = 36), PCA territory (n = 21), cerebellum (n = 20), midbrain (n = 12), and pons (n = 8).
The Glasgow Coma Scale (CGS) on admission was less than 7 in five patients, 7-12 in 11 patients, and greater than 12 in 29 patients. At 8-12 weeks after stroke, 12 patients had no clinical signs of stroke, 15 had minor neurologic deficits, 10 were severely disabled, and eight had died. Outcome correlated with GCS on admission (P < 0.0001) and with the number of ischemic lesions on CT or MRI (P = 0.0001). Symptoms usually improved rapidly and in some patients resolved completely. Compared with untreated basilar artery occlusion that has a mortality of 80-90%, basilar artery embolism without permanent occlusion had a relatively benign outcome.
COMMENTARY
These patients with basilar artery embolism in this series had initial clinical presentations similar to those of patients with atherosclerotic basilar occlusion. Patients with top of the basilar embolism, however, did not have evidence of basilar artery occlusion on CT scanning and transcranial Doppler sonography. It is not surprising, therefore, that the clinical course of patients with basilar embolism was benign in that their neurological deficits usually improved except in those who were in coma or needed assisted ventilation on admission.
In clinical trials of thrombolytic therapy (see Neuro Alert 1998;16:35), the clinical course of acute basilar occlusion was not affected by IV t-PA, while basilar embolism appeared to have a more favorable response. In view of the good prognosis of untreated basilar embolism noted in the present series, the question inevitably arises as to whether such patients benefit from thrombolytic therapy. The present study provides a benchmark against which the results of future series of treated basilar embolism patients will be compared to establish the efficacy of thrombolytic treatment. jjc
All of the following are poor prognostic signs in patients with acute brainstem ischemia except:
a. presence of coma.
b. need for assisted ventilation.
c. multiple infarcts on CT or MRI.
d. basilar occlusion on transcranial Doppler sonography.
e. presence of a cardiac arrhythmia.
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