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Meila D.,Klinikum Duisburg Sana Kliniken | Meila D.,Hannover Medical School | Tysiac M.,Klinikum Duisburg Sana Kliniken | Petersen M.,Klinikum Duisburg Sana Kliniken | And 7 more authors.
Clinical Neuroradiology | Year: 2012

Purpose: The aim of this study was to show the different origins and courses of the extracranial VA on CTA with special emphasis on embryological considerations. The duplicated VA is an anomaly that has been assumed to predispose for dissection and to be associated with aneurysms. We report its frequency and clinical significance. Methods: We retrospectively reviewed CTA of 539 patients by using a contrast-enhanced CTA protocol of the VA on CT. Results: Ninety-four-point-two percent of left VA originated from left subclavian artery and entered the transverse foramen at C6 in nearly all cases. Six-point-three-percent of left VA (m = 4 %, f = 10 %) originated from the aortic arch and entered the transverse foramen either at C4, C5 or C7 but never at C6. One case of an aberrant retroesophageal right VA originated from the aortic arch distal to the left subclavian artery and entered at C7 (0.19 %). All other right VA originated from the right subclavian artery (99.8 %) and entered between C4 and C6. We diagnosed four cases of duplicated VA (0.74 %) with a female predominance (1.9 %) without any signs of dissection on CTA. Two cases with VA duplication had intracranial arterial aneurysms. Conclusions: The VA is a longitudinal anastomosis of segmental metameric arteries. The level of entrance into the transverse foramen indicates which metameric artery or arteries persist. Duplication corresponds to persistence of two segmental arteries and is a rare phenomenon. VA duplication might be associated with vascular lesions. © 2012 Springer-Verlag.

Fifi J.T.,Hyman Newman Institute for Neurology and Neurosurgery | Brockington C.,St Lukes Roosevelt Hospital Center | Narang J.,St Lukes Roosevelt Hospital Center | Leesch W.,Hyman Newman Institute for Neurology and Neurosurgery | And 4 more authors.
American Journal of Neuroradiology | Year: 2013

BACKGROUND AND PURPOSE: Antiplatelet drug resistance has been associated with thromboembolic complications in patients after coronary stent placement. It has not been well-studied in patients who have neurovascular stent-placement procedures. This study aimed to analyze the relationship between antiplatelet drug resistance and neurovascular stent-placement complications. MATERIALS AND METHODS: A prospective data base of all patients treated at our institution was used to identify patients with neurovascular stent-placement procedures. During a 4.5-year period, all patients undergoing neurovascular stent placement were evaluated for aspirin and clopidogrel resistance by using the VerifyNow assay. During an observational phase, all patients received 75 mg of clopidogrel and aspirin (group A). During the intervention phase (group B), patients were given additional clopidogrel on the basis of the clopidogrel resistance assay.Weassessed the development of thromboembolic complications within 30 days of the procedure in patients who were resistant-versus-nonresistant to clopidogrel. RESULTS: Of 96 patients who had neurovascular stent placement, 5.2% were resistant to aspirin and 36.5% were resistant to clopidogrel. Periprocedural thromboembolic complications were seen in 7 patients (7.3%). In a multivariate logistic regression model, clopidogrel resistance, higher diastolic blood pressure, and lack of statin use were significantly associated with periprocedural thromboembolic complication. There was a nonsignificant decrease in thromboembolic complications in patients whose clopidogrel dosage was tailored to the assay. CONCLUSIONS: In our series, clopidogrel resistance was associated with increased periprocedural thromboembolic complications from neurovascular stent-placement procedures. Targeting the clopidogrel dose to platelet inhibition assays may improve clinical outcomes and requires further study.

Paramasivam S.,Hyman Newman Institute for Neurology and Neurosurgery | Niimi Y.,Hyman Newman Institute for Neurology and Neurosurgery | Meila D.,Klinikum Duisburg Sana Kliniken | Berenstein A.,Hyman Newman Institute for Neurology and Neurosurgery
Interventional Neuroradiology | Year: 2014

Dural arteriovenous fistulas (DAVF) associated with our series of patients with vein of Galen malformations (VOGM) are analyzed and discussed. We retrospectively analyzed 87 consecutive cases of VOGM treated between May 2002 and December 2011 and identified 26 patients with DAVF. We gathered information from the clinical case records, angiographic images, MRI on presentation and during follow-up. The findings were analyzed to aid discussion. Among 87 patients treated by multi-stage endovascular embolization, age range from newborn to 19 years, 26(30%) had DAVF. In seven patients (8%), DAVF were found on initial angiogram and were all into the VOGM. Nineteen (21%) DAVF found on follow-up angiograms were all into the VOGM and distant locations. Sprouting and non-sprouting angiogenesis resulted in the formation of a network of vessels around partially thrombosed VOGM, recruiting blood from the surrounding dura mater resulting in a secondary network on the dura mater supplied by the blood vessels of dura mater in the region or from its natural collaterals. Embolization targeting DAVFs was done in 13 (52%) with complete cure in eight (32%) and recurrence in five (20%). Among 12 non-embolized patients (48%), eight (32%) had spontaneous regression with continued treatment of VOGM. In others, the DAVF either remained stable or progressed. DAVF associated with VOGM represent the dural response to angiogenic stimuli. They are observed to regress spontaneously or mature while continuing to treat the primary feeders of VOGM. It is important to include the external carotid system during angiograms. Persistent DAVF with residual VOGM that do not have access though the pial vessels are used as a conduit to treat the dural shunt and to achieve obliteration of residual VOGM at later stages of treatment.

Berenstein A.,Hyman Newman Institute for Neurology and Neurosurgery | Fifi J.T.,Hyman Newman Institute for Neurology and Neurosurgery | Niimi Y.,Hyman Newman Institute for Neurology and Neurosurgery | Presti S.,St Lukes Roosevelt Hospital Center | And 5 more authors.
Neurosurgery | Year: 2012

BACKGROUND: Untreated patients with symptomatic neonatal presentation of vein of Galen aneurismal malformations (VGAMs) carry almost 100% morbidity and mortality. Medical management and endovascular techniques for neonatal treatment have significantly evolved. OBJECTIVE: To evaluate the clinical and angiographic outcomes of modern management of neonates with refractory heart failure from VGAMs. METHODS: From 2005 to 2010, 16 neonatal patients with VGAM presented to our institution. Medical care from the prenatal to perinatal stages was undertaken according to specified institutional guidelines. Nine patients with refractory heart failure required neonatal endovascular intervention. All patients were treated by transarterial deposition of n-butyl cyanoacrylate into fistula sites. Short-and long-term angiographic studies and clinical outcomes were reviewed. RESULTS: Control of heart failure was achieved in 8 patients. One premature baby died shortly after treatment. Long-term angiographic follow-up shows total or near-total angiographic obliteration in all 8 patients. One patient has a mild hemiparesis from treatment. Another has a mild developmental delay. One patient developed a severe seizure disorder and developmental delay. Overall, 66.7% patients have normal neurological development with near-total or total obliteration of the malformation. CONCLUSION: Treatment of refractory heart failure in neonatal VGAM with modern prenatal, neurointensive, neuroanesthetic, and pediatric neuroendovascular care results in significantly improved outcomes with presumed cure and normal neurological development in most. Copyright © 2011 by the Congress of Neurological Surgeons.

Novak K.,Medical University of Vienna | Novak K.,Hyman Newman Institute for Neurology and Neurosurgery | Widhalm G.,Medical University of Vienna | De Camargo A.B.,Hyman Newman Institute for Neurology and Neurosurgery | And 5 more authors.
Journal of Neurosurgery: Spine | Year: 2012

Object. Thoracic idiopathic spinal cord herniation (TISCH) is a rare neurological disorder characterized by an incarceration of the spinal cord at the site of a ventral dural defect. The disorder is associated with clinical signs of progressive thoracic myelopathy. Surgery can withhold the natural clinical course, but surgical repair of the dural defect bears a significant risk of additional postoperative motor deficits, including permanent paraplegia. Intraoperative online information about the functional integrity of the spinal cord and warning signs about acute functional impairment of motor pathways could contribute to a lower risk of permanent postoperative motor deficit. Motor evoked potential (MEP) monitoring can instantly and reliably detect dysfunction of motor pathways in the spinal cord. The authors have applied MEPs during intraoperative neurophysiological monitoring (IOM) for surgical repair of TISCH and have correlated the results of IOM with its influence on the surgical procedure and with the functional postoperative outcome. Methods. The authors retrospectively reviewed the intraoperative neurophysiological data and clinical records of 4 patients who underwent surgical treatment for TISCH in 3 institutions where IOM, including somatosensory evoked potentials and MEPs, is routinely used for spinal cord surgery. In all 4 patients the spinal cord was reduced from a posterior approach and the dural defect was repaired using a dural graft. Results. Motor evoked potential monitoring was feasible in all patients. Significant intraoperative changes of MEPs were observed in 2 patients. The changes were detected within seconds after manipulation of the spinal cord. Monitoring of MEPs led to immediate revision of the placement of the dural graft in one case and to temporary cessation of the release of the incarcerated spinal cord in the other. Changes occurred selectively in MEPs and were reversible. In both patients, transient changes in intraoperative MEPs correlated with a reversible postoperative motor deficit. Patients without significant changes in somatosensory evoked potentials and MEPs demonstrated no additional neurological deficit postoperatively and showed improvement of motor function during follow-up. Conclusions. Surgical repair of the dural defect is effected by release and reduction of the spinal cord and insertion of dural substitute over the dural defect. Careful monitoring of the functional integrity of spinal cord long tracts during surgical manipulation of the cord can detect surgically induced impairment. The authors' documentation of acute loss of MEPs that correlated with reversible postoperative motor deficit substantiates the necessity of IOM including continuous monitoring of MEPs for the surgical treatment of TISCH.

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