Alejandro Berenstein

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.

Management of nontraumatic vascular shunts involving the cavernous sinus

The authors managed 38 consecutive cases of nontraumatic vascular shunts involving the cavernous sinus. Selective angiography demonstrated 12 carotid cavernous fistulas (CCFs) and 26 dural arteriovenous shunts (DAVSs). Visual disability occurred from glaucoma, venous retinopathy, optic neuropathy, or diplopia. Ten patients with slow-flow shunts and minimal dysfunction were treated medically to lower intraocular pressure (IOP) and/or instructed in manual compression of the internal carotid artery, ipsilateral to the lesion, using the contralateral hand. Percutaneous intraarterial embolization using detachable balloons, isobutylcyanoacrylate, or polyvinyl alcohol particles was successful in 16/18 DAVSs and 9/10 CCFs. The neuro-ophthalmic signs resolved in these 25 cases. Complications occurred in five patients. These included a transient hemiparesis, twelfth nerve palsy, unilateral nasal field loss, a pseudoaneurysm causing a third-nerve paresis, and temporary cavernous sinus thrombosis. Conservative therapy in mild cases and embolization in cases with visual disability or progressive signs are warranted.

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.

Presentation, Natural History, and Management of Carotid Cavernous Aneurysms

OBJECTIVE:We present the largest reported cohort of carotid cavernous aneurysms (CCA), comparing the neuro-ophthalmic presentation, complications, and outcome with and without endovascular treatment. METHODS:Retrospective review of 185 patients with 206 CCAs examined between 1980 and 2001 at a tertiary neuro-ophthalmology and neurovascular service. Patients’ symptoms and findings at presentation were recorded and compared with those at outcome. The effect of treatment on outcome and on complication rate was analyzed using the &khgr;2 test, multivariate analysis of covariance, model-selection log-linear analysis, and multinomial logistic regression. RESULTS:Long-term follow-up was available for 189 of 206 CCAs. Seventy-four CCAs underwent treatment (endovascular, 67 [91%]; surgical treatment, 6 [9%]), and 115 were followed for an average of 4 years, two of which required later treatment. Treatment reduced the incidence and severity of pain, even after adjusting for the severity of initial pain (F(1,192 = 9.59, P = 0.002). Treatment did not significantly affect the patient’s final diplopia after adjusting for their initial diplopia (F(1, 182 = 2.01, P = 0.158). Statistical examination revealed that the treated group had a higher proportion of neurological and visual complications than people who were not treated (2(2). = 25.26, P = 0.0003). CONCLUSION:Endovascular treatment of carotid cavernous aneurysms leads to a significantly higher rate of pain resolution compared with untreated patients, even after adjusting for initial pain severity. Diplopia may not resolve after treatment. The results of this study underscore our approach indicating treatment only in cases of debilitating pain, visual loss from compression, or diplopia in primary gaze or in patients with risk factors for major complications such as pre-existing coagulopathy or sphenoid sinus erosion.

Cavernous sinus dural arteriovenous malformations: Patterns of venous drainage are related to clinical signs and symptoms

OBJECTIVE To provide evidence that venous congestion and drainage patterns are responsible for the manifestations of cavernous sinus area dural arteriovenous malformations (CSdAVMs). DESIGN Retrospective observational case series. PARTICIPANTS Records of 85 patients with complete clinical and angiographic evaluations of CSdAVMs were evaluated for the clinical features of the disorder. A neuroradiologist analyzed patterns of venous drainage to and from the cavernous sinus without knowledge of the clinical features. Four venous drainage patterns (reversal of flow from the CSdAVMs into the anterior cavernous sinus, ophthalmic vein thrombosis, drainage into the inferior petrosal sinus or drainage into the superior petrosal sinus) were statistically tested for their predictive value of signs and symptoms using logistic regression. MAIN OUTCOME MEASURES The power of prediction of orbital congestion, elevated IOP, extraocular muscle dysfunction, optic neuropathy, venous-stasis retinopathy, choroidal effusion, anterior chamber shallowing, bruits, cranial nerve paresis, and central nervous system dysfunction from four patterns of venous drainage. RESULTS Reversal of drainage into the anterior cavernous sinus and ophthalmic veins was highly predictive (P = 0) of orbital congestion, which was seen in 77 (91%) patients. In contrast, eight (9%) patients without orbital congestion had shunts that did not drain into the anterior cavernous sinus and ophthalmic veins. Cavernous sinus dural arteriovenous malformation drainage into the anterior cavernous sinus and ophthalmic veins also predicted elevated IOP (P = 0.0023) and optic neuropathy (P = 0.047). Ophthalmic vein thrombosis significantly predicted cases with choroidal effusion (P = 0.002) and anterior chamber shallowing (P = 0.01). Third nerve paresis could be predicted from flow toward the inferior petrosal sinuses (P = 0.017). Central nervous system symptoms or dysfunction, occurring in 7 (8%) patients, was predicted by venous drainage into the superior petrosal sinus (P = 0.0008). CONCLUSIONS The clinical features found in patients with CSdVAMs are related to the abnormal venous drainage and can be predicted by these venous drainage patterns. Venous congestion and hypertension seem to cause the clinical dysfunction in this disorder.

Congenital arteriovenous malformation of the female pelvis: A gynecologic perspective

Nine female patients with the rare congenital arteriovenous malformation of the pelvis were treated at New York University Medical Center in the past 8 years. The patients varied significantly in the anatomic location of the arteriovenous malformation, clinical presentation, and natural course of disease. A gynecologic perspective on the management of this condition is presented, which ranges from a conservative approach with preservation of childbearing potential to extensive pelvic surgery. The important role of modern interventional radiology technology and the multidisciplinary approach are stressed. The unpredictable course of disease after any intervention should be emphasized in planning the management of pelvic arteriovenous malformation.

Occipital arteriovenous malformations : Visual disturbances and presentation

Background: Occipital arteriovenous malformations (AVMs) cause a variety of visual disturbances and headaches. Early diagnosis may lead to treatment that reduces the risk of hemorrhages, visual field loss and other neurologic deficits, and death. Methods: We reviewed the records of the 70 patients with occipital AVMs referred to New York University Medical Center to investigate the mode of presentation and the outcome of treatment. Results: Sixty-eight patients presented with one or more symptoms, including homonymous visual disturbances in 39, headache in 39, seizures in 20, and hemorrhage in twenty-six. Visual field loss was more common (p equals 0.0007) and more severe (p equals 0.0002) in patients who bled than in those with unruptured AVMs (16/44). The frequency of visual field loss was not associated with calcarine artery supply to the AVM. Prior to treatment, the fields improved in five patients with visual loss associated with a hemorrhage. Forty-six patients were treated with embolization, surgery, radiosurgery, or a combination of therapies. The AVM was eliminated in 19 of 20 patients (nine with preoperative partial embolization) treated with surgery versus in 4 of 27 patients treated only with embolization. There were two AVM-associated deaths, two subarachnoid hemorrhages, and four new neurologic deficits after treatment. Visual fields were worse in 15 patients, unchanged in 22, and improved in eight. Conclusions: Whereas some features of headache and visual symptoms are similar for occipital AVMs and migraine, the two disorders are usually distinguishable. Visual field improvement can spontaneously occur in patients who have had loss secondary to an intracerebral bleed. Treatment with embolization or surgery, particularly with surgical excision of the AVM, can result in new or worse visual field loss. NEUROLOGY 1996;46: 953-957.

PHACES Association: A Neuroradiologic Review of 17 Patients

BACKGROUND AND PURPOSE: We present neuroradiologic findings in 17 patients with posterior fossa malformations, hemangiomas, arterial anomalies, cardiac defects, eye abnormalities, and sternal or ventral defects (PHACES) association and identify those at highest risk of central nervous system (CNS) structural, cerebrovascular, and neurodevelopmental abnormalities. Materials and METHODS: Patients with PHACES association were identified in the Vascular Anomalies Program at New York University Medical Center from 1998 to 2007. Many patients were followed in conjunction with other specialists at the Birthmark Institute at Roosevelt Hospital. Clinical records and imaging studies were reviewed retrospectively. Criteria for diagnosis of PHACES were based on previously published indicators. Imaging studies were independently re-reviewed by a neuroradiologist. Segmental mapping of cutaneous hemangioma distribution by photograph review and presence or absence of other PHACES-associated findings were correlated with radiologic findings. RESULTS: Patients with large facial cutaneous (S1-S4) hemangiomas were especially at risk of CNS structural and cerebrovascular anomalies; S1 with ocular anomalies; and S3 with airway, ventral, and cardiac anomalies. All patients with CNS structural malformations had a cerebrovascular abnormality, and this cohort was at risk for developmental and/or other neurologic sequelae. Four patients had supratentorial CNS anomalies, including cortical dysgenesis and migration abnormalities. Some patients with CNS arteriopathy progressed to aneurysms. CONCLUSION: Our data support and expand the work of others, identifying risk factors for segmental hemangiomas. In addition to posterior fossa CNS anomalies, supratentorial anomalies may be present in patients with PHACES, and this may correlate with significant clinical sequelae. The long-term prognosis of these patients remains unknown.

Visual system toxicity following intra‐arterial chemotherapy

We studied the effects of intra-arterial chemotherapy on the visual system of 29 consecutive patients with gliomas. As expected, infra-ophthalmic carotid infusion of cisplatin or carmustine (BCNU) was associated with clinically apparent anterior visual pathway lesions. Electroretinography revealed retinal dysfunction in patients without clinical abnormalities. Supra-ophthalmic carotid infusion of cisplatin or BCNU caused no retinal or optic nerve lesions. Electroretinography was abnormal in only one of these patients. Our results indicated that BCNU and cisplatin cause ischemic damage and are toxic to both retinal and neural tissue in patients with gliomas.