Acute basilar artery thrombosis

Acute basilar artery thrombosis (ABT) has been largely considered a neurological catastrophe. With conventional treatment, only around 20% of patients achieve functional independence. An early presumptive diagnosis is essential to avoid treatment delay. Either multiparametric magnetic resonance imaging or computed tomography angiography source images may represent valid non-invasive tools to confirm ABT and evaluate ischemic tissue viability. The main determinant of ABT outcome is early recanalization but the most effective therapeutic option remains to be clarified. The BASICS prospective registry showed no superiority of intra-arterial over intravenous thrombolysis. Therefore, in the absence of contraindications, intravenous thrombolysis should be started as soon as possible and can be used as the main therapy when interventional procedures are not available. However, recent case series have reported high rates of functional independence (50%) after staged escalation therapy (ultra-early intravenous thrombolysis followed by on-demand endovascular mechanical thrombectomy). These results represent a hope for patients and neurologists and reinforce the need for innovation and research in this field.     

Triphasic perfusion computed tomography in acute middle cerebral artery stroke: a correlation with angiographic findings

OBJECTIVE: To evaluate the usefulness of triphasic perfusion computed tomography (TPCT) in diagnosing middle cerebral artery (MCA) occlusion and in assessing the perfusion deficit and collateral circulation in patients with acute ischemic stroke. BACKGROUND: Conventional angiography is the criterion standard for the diagnosis of MCA occlusion and for the assessment of perfusion deficit and collateral blood supply. The risk of hemorrhagic transformation after recanalization of occluded arteries by thrombolytic therapy is considered high when pretherapeutic residual flow is markedly reduced. PATIENTS AND METHODS: In 8 patients within 3 hours of onset of acute MCA stroke, precontrast computed tomographic scans were taken, and then TPCT was performed after power-injector controlled intravenous administration of contrast media. Sequential images of early, middle, and late phases were obtained. The whole procedure took 5 minutes. Perfusion deficit on TPCT was graded as "severe" or "moderate," depending on the state of collateral flow. Digital subtraction angiography (DSA) was performed in all patients within 6 hours of acute stroke. Direct intra-arterial urokinase infusion was begun immediately after the angiographic superselection of the MCA occlusion site in 6 of the 8 patients within 7 hours of onset (range, 4.3-6.2 hours). RESULTS: The DSA findings showed occlusion of the MCA stem (n = 1) and at the bifurcation (n = 4). The sites of proximal MCA occlusion could be identified on the early and middle images of TPCT in all 5 patients. On DSA findings, all 8 patients had a zone of perfusion deficit with markedly slow leptomeningeal collaterals and a zone of perfusion deficit with no collaterals. The zone of severe perfusion deficit on TPCT corresponded to the zone of perfusion deficit with no or few collaterals on angiography, and the zone of moderate perfusion deficit on TPCT corresponded to that of perfusion deficit with markedly slow leptomeningeal collaterals. Early parenchymal hypoattenuation on precontrast computed tomography was confined to the zone of severe perfusion deficit on TPCT. The initial National Institutes of Health Stroke Scale score correlated better with the total extent of severe perfusion deficit and moderate perfusion deficit on TPCT than that of severe perfusion deficit alone. After direct intra-arterial thrombolysis within 7 hours of onset, symptomatic hemorrhagic transformation did not develop in 4 patients with small severe perfusion deficit (33% or less of the presumed MCA territory). However, the remaining 2 patients with large severe perfusion deficit (more than 50% of the presumed MCA territory) deteriorated to death with hemorrhagic transformation. CONCLUSIONS: Triphasic perfusion computed tomography is useful for diagnosing proximal MCA occlusion and assessing perfusion deficit and collateral circulation as reliably as DSA. The zone of severe perfusion deficit on TPCT may be presumed to be the ischemic core, and that of moderate perfusion deficit, the penumbra zone. Triphasic perfusion computed tomography may be used as a rapid and noninvasive tool to make thrombolysis safer.     

Segmental duplication of the basilar artery with thrombosis

Duplication or fenestration of the basilar artery, a result of an embryologic malformation, has an incidence of up to 5.3% in the general population. The most common complication of this anomaly is the formation of aneurysms. Thrombosis of a partially duplicated basilar artery developed in a 43-year-old man who complained of visual disturbances followed by seizures and coma, and who eventually died. Autopsy showed a partially organized thrombus occluding both halves of a duplicated portion of the basilar artery, old infarcts in the calcarine cortices, and a recent large infarct in the basis pontis. There was only minimal atherosclerosis of other intracranial arteries, including the vertebral arteries. Hemodynamic disturbances and turbulent blood flow at the site of fenestration may be the cause of the thrombosis that occurred in this artery.     

Renal artery lesions in patients with moyamoya disease: angiographic findings

BACKGROUND AND PURPOSE: Renal artery lesions in moyamoya disease have been described sporadically in several case reports. The purpose of this study is to evaluate the angiographic findings of renal artery lesions in moyamoya disease and to determine the prevalence of renal artery lesions in patients with moyamoya disease. METHODS: Eighty-six consecutive patients with idiopathic moyamoya disease were prospectively examined with both cerebral angiography and abdominal aortography. The findings of abdominal aortography were reviewed for the presence and appearance of renal artery lesions and compared with the clinical data and cerebral angiographic findings. RESULTS: Of 86 patients with idiopathic moyamoya disease, 7 patients (8%) were found to have renal artery lesions. Six patients (7%) had stenosis in the renal artery, and 1 patient (1%) had a small saccular aneurysm in the renal artery. Two patients (2%) with a marked renal artery stenosis presented with renovascular hypertension, which resulted in an intraventricular hemorrhage in 1 patient. Furthermore, the renal artery stenosis in the 2 patients with renovascular hypertension was successfully treated with percutaneous transluminal angioplasty. There was no significant correlation between the presence of renal artery lesions and cerebral angiographic findings. CONCLUSIONS: Seven (8%) of 86 patients with moyamoya disease showed renal artery lesions, including 6 stenoses (7%) and 1 aneurysm (1%). Renal artery lesions are a clinically relevant systemic manifestation in patients with moyamoya disease.     

Hypoglycemia presenting as basilar artery thrombosis.

BACKGROUND AND PURPOSE: Following our treatment of a patient with hypoglycemia-induced brain stem symptoms, we examined the possible mechanisms for hypoglycemia presenting as basilar artery disease. CASE DESCRIPTION: We describe a patient who had progressive brain stem symptoms due to a diet-induced hypoglycemia initially diagnosed as basilar artery thrombosis. Symptoms ceased immediately after intravenous glucose. CONCLUSIONS: Before invasive diagnostic and thrombolytic strategies are considered, hypoglycemia as a rare but important cause of acute brain stem dysfunction must be considered in patients suspected to suffer from basilar artery thrombosis.     

Transient global amnesia heralding basilar artery thrombosis

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.     

Transient global amnesia heralding basilar artery thrombosis

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.