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  • Author or Editor: Alan S. Boulos x
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Alan S. Boulos, Eric M. Deshaies, Jiang Qian and A. John Popp

✓ In this report, the authors discuss a novel use of intradural vertebral artery (VA) stent placement to protect a tumor-encased vessel from injury during lesion resection. The tumor was a rare foramen magnum region xanthogranuloma and a component of Erdheim—Chester disease (ECD). This 64-year-old man presented with large masses encasing and compressing the intracranial segments of each VA. Preoperatively, a left VA stent was placed to protect the arterial wall during resection of the tumor. Histopathological study results on the subtotally resected mass were consistent with xanthogranuloma, a rare benign histiocytic tumor frequently occurring in patients with ECD. Further radiographic evaluation in the patient revealed an osteolytic lesion of the eleventh thoracic vertebra supporting the diagnosis of ECD disease. Based on this case study, the authors recommend the following: 1) tumor-encased vessels can be protected preoperatively by stent placement to assist with tumor debulking; and 2) patients diagnosed with a xanthogranuloma should be evaluated for multisystem involvement consistent with ECD.

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Celso Agner, Eric M. Deshaies, Gary L. Bernardini, A. John Popp and Alan S. Boulos

✓ In most cases of deep venous sinus thrombosis, systemic anticoagulation represents the initial treatment of choice for preventing propagation of a clot in the dural sinuses. In patients with deep or extensive venous sinus thrombosis, a combination of treatment modalities may be required including systemic anticoagulation, selective venous thrombolysis, and mechanical thrombectomy. In the current study the authors report on a patient who presented with the acute onset of headache, vomiting, a depressed level of consciousness, and a left hemiparesis and in whom a right middle cerebral artery (MCA) territory ischemic stroke with hemorrhagic conversion was initially diagnosed. Results of diagnostic cerebral angiography demonstrated a patent right MCA and a deep venous sinus thrombosis involving most of the dural sinuses. Despite adequate systemic heparinization, the patient's neurological condition deteriorated and direct administration of alteplase into the transverse sinus in conjunction with mechanical clot disruption using a coronary AngioJet was required. Venous flow was successfully reestablished in the deep and superficial venous sinuses by using a 0.014-in exchange wire routed from the right common femoral vein through the sinuses and out the left common femoral vein. Excellent angiographic results were obtained, and the patient had recovered completely by the 7-month follow up.

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Alan S. Boulos, Eric M. Deshaies, John C. Dalfino, Paul J. Feustel, A. John Popp and Doniel Drazin


Tamoxifen has been shown to be a potent neuroprotectant against stroke in rodents. Because other neuroprotectant medications have failed in human trials, a study of tamoxifen in a large-animal model was necessary to further assess the drug's effectiveness. For this study, the authors developed an endovascular model of anterior circulation infarction in canines to mimic the human clinical condition. They assessed the following hypotheses: 1) that they will be able to consistently produce an internal carotid artery (ICA) terminus infarction and 2) that tamoxifen is an effective neuroprotectant against stroke in canines.


In 24 male beagles (weight 9–11 kg), bilateral femoral artery cutdowns were performed, and the vertebral artery and left ICA were each selectively catheterized. Under fluoroscopic guidance, a microcatheter was introduced via the vertebral artery, guiding the catheter into the basilar artery, posterior communicating artery, and ICA terminus. A 1-ml clot was injected in the terminus, occluding the middle cerebral artery (MCA) and anterior cerebral artery (ACA) origin. In the first 12 canines, the occlusions were confirmed by angiography. A Canine Stroke Score (CSS) was assigned (score range 0–18 [0 = intact on examination, 18 = comatose]). The animals were then killed and their brains stained with 2,3,5-triphenyltetrazolium chloride (TTC). The subsequent 12 canines underwent a blinded randomized study in which the authors compared the results of tamoxifen (5 mg/kg) infused intravenously 1 hour after clot injection with an equal volume of vehicle (dimethylsulfoxide). After 3 hours, the animals underwent MR imaging, were extubated, and clinical examinations were performed. The canines were killed at 8 hours after clot injection, and TTC staining was used.


In the first group, infarct volume and CSSs were consistent with the extent of the occlusion of the angiographic vessels. An occlusion of the ACA, MCA, and posterior cerebral artery resulted in larger infarcts and higher stroke scores than occlusion of the ACA and MCA. In the second group, tamoxifen significantly reduced infarct size and improved clinical outcomes. In tamoxifen-treated animals, the mean infarct volume reduction was 40% (p < 0.05) and the mean CSS was significantly less than vehicle-treated animals (p < 0.001). There were significant correlations among MR imaging-determined volume, TTC-determined volume, and neurological clinical outcome (p < 0.05).


Using this endovascular model of stroke, the authors were able to consistently produce an infarction in the canines that was similar in scope to a carotid terminus occlusion in humans. Also, angiography could predict subsequent clinical course and infarct size. Tamoxifen was effective at significantly improving the canine neurological deficits and reducing the size of the stroke. This study took the first step in demonstrating the effectiveness of a promising human neuroprotectant in a large animal.