Eighteen patients with spinal arteriovenous malformations had been treated with conventional embolization, surgical removal, feeder ligation, and/or feeder coagulation between February 1985 and March 1990. The lesions included six glomus, four juvenile, three extramedullary, and five dural arteriovenous malformations or fistulas. Embolic therapy was conducted in 14 patients by introducing the tip of a catheter into the segmental arteries and injecting polyvinyl alcohol strips (500-1000 microns) (conventional embolization). Follow-up spinal angiography disclosed recanalization in 10 patients (71.4%) and the appearance of new feeding arteries in five patients (35.7%). We introduced the Tracker vascular access system in April 1990. Eight patients (four glomus, one juvenile, and three dural arteriovenous malformations) were treated with the minicatheter and Ivalon particles (150-350 microns). Five patients showed neurological improvement immediately after treatment. The other three patients had severe paraparesis before treatment and did not show any improvement. One patient with a glomus-type arteriovenous malformation showed transient neurological deterioration just after embolization with the Tracker-10 to occlude a lesion fed by the posterior spinal artery, because the Ivalon particles migrated into the anterior spinal artery via the anterior spinal canal artery. In one patient with a juvenile arteriovenous malformation, the Tracker-18 catheter perforated the radiculomedullary artery originating from the right vertebral artery, and subarachnoid hemorrhage occurred. However, the Tracker-10 could later successfully occlude the arteriovenous malformation. The rates of recanalization and appearance of the new feeding vessels were 4/8 (50.0%) and 2/8 (25%), respectively.
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http://dx.doi.org/10.1016/0090-3019(92)90083-y | DOI Listing |
Sci Rep
January 2025
Edward B. Singleton Department of Radiology, Texas Children's Hospital, Baylor College of Medicine, Houston, TX, USA.
Cerebral proliferative angiopathy (CPA) is a rare subtype of cerebral arteriovenous malformation, characterized by unique angiographic features and clinical presentations. Although the clinical and angiographic characteristics of CPA have been well described, their impact on the surrounding tissues remains underexplored. Herein, we investigated the presence of calvarial thickening in patients with CPA, and discuss its potential pathogenesis.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
The Third Hospital of Mianyang, Sichuan Mental Health Center, Mianyang, Sichuan, China.
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View Article and Find Full Text PDFRev Esp Enferm Dig
January 2025
Gastroenterology and Hepatology, Hospital Universitario Virgen de las Nieves, España.
Hereditary haemorrhagic telangiectasia (HHT) is a rare genetic disease characterised by mucocutaneous telangiectasias and arteriovenous malformations that can affect multiple organs. Although rare, ischaemic cholangiopathy can occur, a serious complication that can even lead to death. We present the case of a patient with HHT disease with previous mucocutaneous and gastrointestinal manifestations in whom 8 weeks after cholecystectomy a saccular dilatation of the intrahepatic bile duct was observed.
View Article and Find Full Text PDFJ Cardiol Cases
October 2024
Pediatric Cardiology Unit, University of Campania "Luigi Vanvitelli", AORN "Ospedali dei Colli", Monaldi Hospital, Naples, Italy.
Unlabelled: Right-to-left shunt may be a cause of paradoxical embolization (and cryptogenic cerebral ischemic events). Patent foramen ovale and pulmonary arterio-venous malformations are the most common cause of paradoxical embolization; however, some rare cardiovascular lesions may cause a right-to-left shunt with consequent paradoxical embolization. We describe a case of a young child with superior sinus venosus atrial septal defect who underwent surgical closure and developed a cryptogenic cerebral ischemic attack due to a rare cause of paradoxical embolization, during a long-term follow-up.
View Article and Find Full Text PDFHereditary hemorrhagic telangiectasia is an autosomal dominant disorder caused by mutations in the bone morphogenetic protein signaling pathway, leading to arteriovenous malformations. While previously thought to share molecular and cellular dysregulation, this study reveals highly distinct mechanisms depending on whether mutations occur in Alk1 or SMAD4. Loss of SMAD4 enhances endothelial cell responses to flow, including flow-regulated transcription and cell migration against blood flow, causing excessive pruning of capillaries and the formation of single large shunts.
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