Yasunari Niimi

Endosaccular Treatment of Intracranial Aneurysms Using Matrix Coils: Early Experience and Midterm Follow-Up

Background and Purpose— The authors report their experience using Matrix coils in the treatment of cerebral aneurysms. Methods— The outcomes of 72 consecutive patients (76 aneurysms) who underwent coiling using Matrix coils at our institution were retrospectively analyzed. Results— Seventy-four aneurysms in 70 patients were coiled using Matrix coils (ranging 3% to 100% by coil length; mean 68.8%). Two patients underwent regular platinum coil embolization after failed Matrix coil placement. Thirty-two (42%) ruptured aneurysms were acutely treated. In 46 aneurysms, Matrix composed >50% of coil length. Complete aneurysm occlusion was obtained in 13 aneurysms (17.6%), neck remnant in 30 (40.5%), and dome filling in 31 (41.9%). Procedural morbidity and mortality rates were 1.4% and 1.4%, respectively. Angiographic follow-up was obtained in 63.5% (47 of 74 aneurysms; average 12.2 months; range 0 to 34). In these 47 angiographically followed aneurysms, the overall recanalization rate was 57.4%. In aneurysms with >50% Matrix coils, 76.1% had angiographic follow-up (35 of 46), and in this group, the overall recanalization rate was 54.3% (19 of 35): 25% (1 of 4) for very small (<5 mm); 33% (4 of 12) for small-size (<10 mm)/small-neck (<4 mm); and 63% (5 of 8) for small-size/wide-neck (≥4 mm). A total of 82% (9 of 11) recanalization occurred in large aneurysms (≥10 to 25 mm). Ten aneurysms (21.3%; 10 of 47) underwent retreatment. Clinical follow-up was obtained in 61 (86%) patients (average 15 months; range 1 to 37): 87% of patients were Glasgow Outcome Scale 4 or 5. Conclusion— The use of Matrix coils resulted in worse recanalization rates than that reported for Guglielmi detachable bare platinum coils.

Tumor Necrosis Factor α is a Key Modulator of Inflammation in Cerebral Aneurysms

OBJECTIVE: Although intracranial aneurysms (IAs) are a major public health problem in the United States, few etiological factors are known. Most aneurysms remain asymptomatic until they rupture, producing subarachnoid hemorrhage, one of the most severe forms of stroke. Despite the technical advances in endovascular and microsurgical treatment, these patients still have high mortality and morbidity rates. Hence, the biology of aneurysm formation and growth is of intense interest. The presence of T and B lymphocytes, as well as macrophages, in human IA tissues suggests a role for inflammation in IA pathogenesis. However, the types of cytokines that are involved and regulated during cerebral aneurysm formation and growth are not known. To study the underlying pathogenesis of IA, we analyzed the expression of cytokines that participate in proinflammatory and anti-inflammatory responses. METHODS: Polymerase chain reaction was used to assess relative messenger ribonucleic acid expression levels of cytokines and an apoptotic modulator, Fas-associated death domain protein. Western blot analysis was used to determine protein expression from these genes. RESULTS: We show that the proinflammatory cytokine, tumor necrosis factor α and its proapoptotic downstream target, Fas-associated death domain protein, are increased in human aneurysms. In contrast, interleukin 10, which is secreted predominantly by T helper 2 cells, was absent in aneurysms. Polymerase chain reaction-derived gene expression data were confirmed by Western blotting using specific antibodies. CONCLUSION: Increased tumor necrosis factor α and Fas-associated death domain protein may have deleterious primary and secondary effects on cerebral arteries by promoting inflammation and subsequent apoptosis in vascular and immune cells, thereby weakening vessel walls.

TNF-α-mediated inflammation in cerebral aneurysms: A potential link to growth and rupture

Intracranial aneurysm (IA) rupture is one of the leading causes of stroke in the United States and remains a major health concern today. Most aneurysms are asymptomatic with a minor percentage of rupture annually. Regardless, IA rupture has a devastatingly high mortality rate and does not have specific drugs that stabilize or prevent aneurysm rupture, though other preventive therapeutic options such as clipping and coiling of incidental aneurysms are available to clinicians. The lack of specific drugs to limit aneurysm growth and rupture is, in part, attributed to the limited knowledge on the biology of IA growth and rupture. Though inflammatory macrophages and lymphocytes infiltrate the aneurysm wall, a link between their presence and aneurysm growth with subsequent rupture is not completely understood. Given our published results that demonstrate that the pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), is highly expressed in human ruptured aneurysms, we hypothesize that pro-inflammatory cell types are the prime source of TNF-alpha that initiate damage to endothelium, smooth muscle cells (SMC) and internal elastic lamina (IEL). To gain insights into TNF-alpha expression in the aneurysm wall, we have examined the potential regulators of TNF-alpha and report that higher TNF-alpha expression correlates with increased expression of intracellular calcium release channels that regulate intracellular calcium (Ca2+), and Toll like receptors (TLR) that mediate innate immunity. Moreover, the reduction of tissue inhibitor of metalloproteinase-1 (TIMP-1) expression provides insights on why higher matrix metalloproteinase (MMP) activity is noted in ruptured IA. Because TNF-alpha is known to amplify several signaling pathways leading to inflammation, apoptosis and tissue degradation, we will review the potential role of TNF-alpha in IA formation, growth and rupture. Neutralizing TNF-alpha action in the aneurysm wall may have a beneficial effect in preventing aneurysm growth by reducing inflammation and arterial remodeling.

Vein of Galen malformations in neonates: new management paradigms for improving outcomes.

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.

Embolization of a Spinal Arteriovenous Malformation: Correlation between Motor Evoked Potentials and Angiographic Findings: Technical Case Report

OBJECTIVE AND IMPORTANCE Endovascular procedures for the treatment of spinal arteriovenous malformations place the spinal cord at risk of ischemia. This report illustrates the usefulness of motor evoked potentials (MEPs) in detecting functional changes within the spinal cord motor pathways during embolization of a spinal arteriovenous malformation under general anesthesia. CLINICAL PRESENTATION A 28-year-old man presented with a history of progressive lower extremity numbness and weakness followed by bladder dysfunction. Magnetic resonance imaging and angiography disclosed a T11-T12 spinal arteriovenous malformation. INTERVENTION During the endovascular procedure, before injection of particles, the disappearance of MEPs from the tibialis anterior muscle led to prompt angiographic reevaluation, which disclosed the arrest of spinal blood flow secondary to radiculomedullary artery occlusion by the catheter. Embolization and catheter withdrawal were followed by temporary recovery of spinal blood flow and MEPs. A second arrest of spinal cord blood flow, caused by severe vasospasm of the feeding radiculomedullary artery, was documented by a control angiogram, and its functional relevance was revealed by a second disappearance of MEPs. The therapeutic effect of papaverine infusion and induced moderate hypertension was confirmed angiographically by complete reopacification of the anterior spinal artery and confirmed neurophysiologically by the complete recovery of MEPs. At the end of the procedure, no additional neurological deficits were noted. CONCLUSION During spinal cord embolization, MEPs may play a critical role in early detection of spinal cord dysfunction by aiding in the prevention of damage to the spinal cord as well as by predicting the clinical outcome.

Morphological and clinical risk factors for posterior communicating artery aneurysm rupture

OBJECT Recent studies have shown that posterior circulation aneurysms, specifically posterior communicating artery (PCoA) aneurysms, are more likely to rupture than other aneurysms. To date, few studies have investigated the factors contributing to PCoA aneurysm rupture. The authors aimed to identify morphological and clinical characteristics predisposing to PCoA aneurysm rupture. METHODS The authors retrospectively reviewed 134 consecutive patients with PCoA aneurysms managed at their facility between July 2003 and December 2012. The authors divided patients into groups of those with aneurysmal rupture (n = 39) and without aneurysmal rupture (n = 95) and compared morphological and clinical characteristics. Morphological characteristics were mainly evaluated by 3D CT angiography and included diameter of arteries (anterior cerebral artery, middle cerebral artery, and internal carotid artery), size of the aneurysm, dome-to-neck ratio, neck direction of the aneurysmal dome around the PCoA (medial, lateral, superior, inferior, and posterior), aneurysm bleb formation, whether the PCoA was fetal type, and the existence of other intracranial unruptured aneurysm(s). RESULTS Patients with ruptured PCoA aneurysms were significantly younger (a higher proportion were < 60 years of age) and a significantly higher proportion of patients with ruptured PCoA aneurysms showed a lateral direction of the aneurysmal dome around the PCoA, had bleb formation, and the aneurysm was > 7 mm in diameter and/or the dome-to-neck ratio was > 2.0. Multivariate logistic regression analysis showed age < 60 years (OR 4.3, p = 0.011), history of hypertension (OR 5.1, p = 0.008), lateral direction of the aneurysmal dome around the PCoA (OR 6.7, p = 0.0001), and bleb formation (OR 11, p < 0.0001) to be significantly associated with PCoA aneurysm rupture. CONCLUSIONS The present results demonstrated that lateral projection of a PCoA aneurysm may be related to rupture.

Onyx embolization of an extensive mandibular arteriovenous malformation via a dual lumen balloon catheter: a technical case report

Summary The first known use of Onyx delivered via a dual lumen balloon catheter is reported. A mandibular arteriovenous malformation was successfully embolized with Onyx via an Ascent balloon catheter. Case presentation A teenage girl presented with facial deformity and episodes of oral bleeding. Angiogram showed an extensive left mandibular arteriovenous malformation with ectatic intraosseous venous pouches. A dual lumen Ascent balloon catheter was placed in the inferior alveolar artery. With balloon inflation, Onyx was injected transarterially with excellent penetration into the venous puches. There was closure of over 80% of the lesion with reduction in arteriovenous shunting. Conclusion Onyx embolization via a dual lumen balloon catheter allows for great penetration without the necessity of the long plug creation process for the usual ‘plug and push technique’ or the use of detachable tip microcatheters. The technique is limited by the deliverability of the balloon catheter, and is safest in the external carotid circulation.

Development, clinical presentation and endovascular management of congenital intracranial pial arteriovenous fistulas

Introduction Pial arteriovenous fistulas (AVF) are vascular disorder of the brain consisting of a direct connection between arteries and veins without a nidus located in the subpial space, and are frequently associated with venous varix. Materials and Results This study reviewed a series of 16 children with congenital pial AVF, treated between January 2005 and August 2011. All cases presented before 5 years of age and the mode of presentation varied with age. Fourteen had a single fistula while two had multiple fistulas, one among them had cutaneous features suggestive of RASA1 mutation. MRI is the preferred initial imaging, to demonstrate anatomical location, feeders, venous varix and regional, hemispheric or diffuse cerebralmalacia. Digital subtraction angiography performed during the first therapeutic attempt showed venous varix along with arterial enlargement as the most common angio-architecture. All cases were embolized with N-butyl-cyanoacrylate (NBCA) with or without coiling of the venous sac to attain flow control. Hypotension and a higher concentration of glue were used to aid controlled glue injections. Dural AVF and reactive angiogenesis are not uncommon sequlae found on follow-up angiogram. Outcomes were excellent in 75% and good in 19%. Conclusion Congenital pial AVF are caused by a missed step in vascular development during the early embryonic stage. Transarterial endovascular embolizaiton using NBCA with or without using coils to attain flow control is the treatment of choice, with low morbidity. The efficacy of treatment is high as demonstrated by the high cure rate. Follow-up angiogram is mandatory to look for recanalization, reactive angiogenesis and denovo dural AVF development.

Cortical Blindness, Transient and Otherwise, Associated with Detachable Coil Embolization of Intracranial Aneurysms

BACKGROUND AND PURPOSE: Cortical visual loss is a rare complication of cerebral angiography without a definitive pathophysiology. Given the rapid increase in endovascular procedures used to treat cerebral aneurysms, we explored the prevalence of this complication and whether we could add to the understanding of this disorder. Materials and METHODS: We performed a retrospective review of all procedures performed with the same contrast agent and detachable coils for treatment of posterior circulation aneurysms by 1 endovascular surgery service from 1996 to 2006. All patients were evaluated before and after each procedure by a team that included a neuro-ophthalmologist. RESULTS: Of 137 intra-arterial treatment procedures performed for posterior circulation aneurysms, we identified 4 patients with cerebral vision loss complications. During the same time period, >500 aneurysms of the anterior cerebral circulation were treated without this complication. The visual field loss was unilateral in 2 and bilateral in 2 patients. Recovery was complete in 3 and almost normal in the fourth patient. The amount of contrast used and the duration of the procedure were similar among all patients. The 4 patients had no identified specific risk factors for developing procedure-associated occipital dysfunction, all 4 had undergone prior angiography, and 1 patient had undergone repeat coiling, without complication. CONCLUSION: The 2.9% prevalence of cerebral visual loss with endovascular coil treatment of posterior circulation aneurysms is higher than that for angiography alone. Our patients recovered well with corticosteroid and intravenous hydration treatment. Recognizing the self-limiting nature of this problem might prevent an unneeded intervention.

Spinal Arteriovenous Metameric Syndrome: Clinical Manifestations and Endovascular Management

BACKGROUND AND PURPOSE: SAMS is a rare form of SCAVM. We discuss the clinical presentation, endovascular management, and outcome of this disease in our series. MATERIALS AND METHODS: Retrospective review was performed in patients with SCAVM and SAMS who underwent angiography with intent to treat at our institution from 1980 to 2010. RESULTS: One hundred forty-eight SCAVMs were identified, and 28 (19%) of these were SAMS. Of these 28 patients, 24 had nidus-type AVMs and 4 had fistulas. SAMS were more prevalent in females (71% versus 48%), and also presented earlier than non-SAMS SCAVMs. Intradural hemorrhage (SAH or hematomyelia) was the most common presentation and more common than in non-SAMS lesions. Twenty-six patients underwent embolization of the intradural lesion in 50 sessions. Thirteen patients underwent treatment of intradural aneurysms in 16 sessions. Six patients underwent embolization of extradural lesions in 16 sessions. Twenty-three patients had an average of 94 months of clinical follow-up (3–309 months) after the first treatment, during which 5 patients had hemorrhages. Angiographic follow-up was performed in 20 patients at an average of 85 months (range, 3–309 months), which showed new development or enlargement of an aneurysm in 5 patients. This type of angiographic progression was more common in patients with SAMS. CONCLUSIONS: SAMS most commonly presents with hemorrhage from the SCAVM. Endovascular embolization can be performed safely with good functional outcome, though most patients clinically deteriorate in the long term. Periodic angiographic follow-up with intent to perform preventive target embolization is important to control the disease.