Endovascular treatment of head and neck arteriovenous malformations.

INTRODUCTION: Head and neck arteriovenous malformations (H&N AVM) are associated with considerable clinical and psychosocial burden and present a significant treatment challenge. We evaluated the presentation, response to treatment, and outcome of patients with H&N AVMs treated by endovascular means at our institution. METHODS: Patients with H&N AVMs treated by endovascular means from 1984 to 2012 were evaluated retrospectively. These included AVMs involving the scalp, orbit, maxillofacial, and upper neck localizations. Patient's clinical files, radiological images, catheter angiograms, and surgical reports were reviewed. RESULTS: Eighty-nine patients with H&N AVMs (46 females, 43 males; 48 small, 41 large) received endovascular therapy. The goals of treatment were curative (n = 30), palliative (n = 34), or presurgical (n = 25). The total number of endovascular treatment sessions was 244 (average of 1.5 per patient). The goal of treatment was met in 92.1 % of cases. Eventual cure was achieved in 42 patients accounting for 58.4 % (52/89) of all patients who underwent treatment for any goal. Twenty-eight of these patients were cured by embolization alone (28/89, 31.4 %) of which 18 were single-hole AVFs. Twenty-four were cured by planned surgical excision after presurgical embolization (24/89, 27 %). Seven patients (7/89, 7.2 %) suffered transient and two (2/89, 2.2 %) permanent endovascular treatment complications. CONCLUSION: Endovascular treatment is effective for H&N AVMs and relatively safe. It is particularly effective for symptom palliation and presurgical aid. Embolization is curative mostly in small lesions and single-hole fistulas. In patients with large non-curable H&N AVMs, endovascular therapy is often the only palliative option.

Management and clinical outcome of posterior fossa arteriovenous malformations: report on a single-centre 15-year experience.

OBJECTIVES: Posterior fossa brain arteriovenous malformations (PFbAVMs) are rare lesions. Management is complicated by eloquence of adjacent neurological structures, multimodality treatment is often necessary, and obliteration is not always possible. We describe a 15-year experience in the management of posterior fossa brain AVMs with a focus on clinical outcome. METHODS: From 1989 to 2004, prospectively collected information on 106 patients with diagnosis of a PFbAVMs was obtained. Clinical and angioarchitectural characteristics, management options and complications are described and reviewed to evaluate their impact on final outcome as measured by the Modified Rankin Score (mRS). RESULTS: Ninety-eight patients were followed for an average of 3.3 years (1-14.6). The male-to-female ratio was 1:1. Ninety-five out of 98 patients (96.9%) were symptomatic at presentation, with 61 (62.2%) intracranial haemorrhages. Sixty-two patients were treated (46 cerebellar, 16 brainstem). Ten haemorrhages occurred in follow-up (4.1%/year). The mRS was obtained in 62 patients and was classified as low (good, mRSor=3). Haemorrhage was the only predictor of poor mRS at presentation (p = 0.0229). A poor clinical outcome was correlated with the presence of AA (p = 0.0276), a poor initial mRS (p<0.0001) and the number of treatments needed (p = 0.0434). Patients were significantly more likely to improve than to deteriorate over time (p = 0.0201). CONCLUSION: The final clinical outcome in PFbAVMs relates directly with the presence of associated aneurysms, number of treatments needed to obliterate the AVM and mRS at presentation. Despite the fact that patients tend to improve after brain AVM haemorrhage, the relationship of MRS at presentation and final outcome suggests that an expedited, more definitive treatment is probably a better choice, especially in patients with good grades after the initial bleeding.

Cerebral arteriovenous fistulas induced by dural arteriovenous shunts.

Dural arteriovenous shunts and pial arteriovenous fistulas are uncommonly associated. Their etiology, pathogenesis, and natural history are still unclear and are likely different. We present three cases of high-flow dural arteriovenous shunts associated with pial arteriovenous fistulas and discuss their pathogenesis, anatomic association, and angioarchitecture. We propose that venous steal effect in the dural sinus secondary to the high-flow dural arteriovenous shunt induced the pial arteriovenous fistulas. Treatment of the high-flow dural arteriovenous shunts and the induced pial arteriovenous fistulas are discussed.

Urgent and emergent embolization of lesions of the head and neck in children: indications and results.

Indications for and results and complications of embolization of lesions of the head and neck were analyzed retrospectively. The procedures were performed since 1980 on an emergent or urgent basis in 30 infants and children by an experienced interventional neuroradiologist in Bicetre, France. Indications for embolization included hemorrhage, occular occlusion, respiratory obstruction, CNS complications or potential complications, interference with nutrition, and functional impairment related to the effect of the lesion on the developing facial skeleton and teeth. The specific lesions included seven hemangiomas (palpebral, subglottic, and nasal) and 20 vascular malformations (maxillofacial, auricular, dural, cerebral [including three vein of Galen malformations] and spinomedullary). Embolization was efficacious in 28 of 30 patients. Hemangiomas (potentially involutive tumors) responded dramatically with arrest of the proliferative phase and shrinking of the mass. Combined hemovascular lymphatic malformations (hemolymphangiomas) of the tongue demonstrated a variable decrease in size. High-flow evolutive arteriovenous malformations involving the teeth and dura were controlled but required multiple embolizations. One infant with a vein of Galen arteriovenous malformation died. Three local complications occurred in two patients. No cerebral ischemic or femoral artery complications occurred.

The role of dural anomalies in vein of Galen aneurysms: report of six cases and review of the literature.

It is proposed that the vein of Galen aneurysm represents a venous ectasia secondary to an increased flow (usually caused by a deep-seated arteriovenous shunt draining either directly into the vein of Galen aneurysm or into a tributary of the vein of Galen) associated with obstruction of a dural sinus distal to the aneurysm. The closer the venous obstruction is to the vein of Galen, the better the chances are of developing obstructive (noncommunicating) hydrocephalus and the more likely it is that the venous drainage from the rest of the brain will be unaffected. The farther the venous obstruction is from the vein of Galen aneurysm, the better the chances are of developing a communicating type of hydrocephalus. The development of cardiac failure is related to the magnitude of the arteriovenous shunt. Brain damage, seizures, and hemorrhage may be related to the retrograde venous engorgement, causing impaired drainage of the healthy brain. Careful attention should be paid to the venous drainage characteristics of the lesion because the types of dural venous obstructions and anomalies vary from case to case. The term "vein of Galen aneurysm" should be abandoned in favor of the term "vein of Galen ectasia."

Angiographic and clinical characteristics of patients with cerebral arteriovenous malformations associated with hereditary hemorrhagic telangiectasia.

BACKGROUND AND PURPOSE: Cerebral arteriovenous malformations (AVMs) are occasionally associated with hereditary hemorrhagic telangiectasia (HHT), which is characterized by the presence of multiple mucocutaneous telangiectasia, epistaxis, and familial inheritance. We analyzed the angiographic and clinical characteristics of patients with cerebral AVMs related to HHT. METHODS: Among 638 patients with cerebral AVMs, we identified 14 patients with HHT. The AVMs were classified as those with nidi of 1 cm or less (micro AVMs), those with nidi between 1 and 3 cm (small AVMs), and those of the fistulous type (arteriovenous fistulas [AVFs]). RESULTS: A total of 28 AVMs were found; seven of 14 patients had multiple AVMs. The 28 AVMs were categorized as 12 micro AVMs, eight small AVMs, and eight AVFs. All except one micro AVM were asymptomatic, whereas all small AVMs were symptomatic. Three of eight AVFs were asymptomatic. All 28 AVMs were located on the cortex. All micro AVMs and AVFs had single feeders and single draining veins, whereas the small AVMs had multiple feeders in all lesions and single draining veins in six of eight lesions. CONCLUSION: Multiple, cortical, micro AVMs or AVFs harboring single feeding arteries and single draining veins should raise clinical suspicion of HHT-related AVMs.

Acute subdural hematoma from ruptured posterior communicating artery aneurysm.

Acute spontaneous subdural hematoma is infrequent in association with rupture of intracranial saccular aneurysm. In the majority of cases, aneurysms of the middle cerebral artery along the convexity or of the anterior cerebral artery along the interhemispheric fissure are found to be the culprits. We present two recent cases of internal carotid-posterior communicating artery aneurysms causing acute subdural hematoma with little or no subarachnoid hemorrhage and discuss the possible mechanisms for this occurrence.

Deep cerebral venous system thrombosis: case report.

A 38-year-old woman with thrombosis of the deep cerebral venous system, presumed to be secondary to the use of the oral contraceptive pill, is reported. The use of cerebral angiography and magnetic resonance imaging in establishing the diagnosis and management strategies is discussed. It is concluded that magnetic resonance imaging is an appropriate investigative modality for diagnosis and therapeutic decision making, and that, as with superficial cerebral dural sinus and venous thrombosis, anticoagulation is a safe and effective therapy.

Symptomatic arterial luminal narrowing presenting months after subarachnoid hemorrhage and aneurysm clipping.

The authors describe three cases of clinical cerebral ischemia associated with angiographic evidence of cerebral arterial luminal narrowing presenting 7, 14, and 52 weeks after subarachnoid hemorrhage (SAH) and aneurysm clipping. Delayed vasospasm, in its usual time setting 1 or 2 weeks after hemorrhage, did not occur symptomatically in these patients. No evidence for aneurysm clip migration or rebleed was present. All patients responded favorably to volume expansion and elevation of blood pressure. This unusual occurrence of a very delayed vasospasm may further the understanding of the vasospastic process. The symptomatic onset of arterial luminal narrowing months after SAH may suggest that a proliferative vasculopathy more accurately explains the observed vessel narrowing, rather than conventional active constriction of vascular smooth muscle.

The lateral spinal artery of the upper cervical spinal cord. Anatomy, normal variations, and angiographic aspects.

The lateral spinal artery corresponds to the most rostral extent of the posterolateral arterial axis of the spinal cord. It supplies the posterior and lateral aspects of the spinal cord, and courses anterior to the posterior roots of the upper cervical spinal nerves (C-1 to C-4), and posterior to the dentate ligament. The lateral spinal artery anastomoses rostrally with the branches of the posterior inferior cerebellar artery (PICA) at the restiform body and laterally with the extraspinal arteries at the emergence of each nerve. It may originate either from the vertebral artery or from the PICA lateral to the medulla. Certain variations will cause an unusual but normal enlargement of the vessel in a specific portion of its course; these variations include vertebral artery duplication, a C-1 or C-2 vertebral origin of the PICA, a C-1 or C-2 occipital origin of the PICA, and an intradural course of the vertebral artery at C-2. Knowledge of these variations in the arterial supply to the area allows for an understanding of the different anatomic peculiarities present and their angiographic importance.

Neurological manifestations of intracranial dural arteriovenous malformations.

The authors describe their experience with four cases of dural arteriovenous malformation (AVM) which led them to analyze the clinical aspects of these lesions in an attempt to understand their pathophysiology. An additional 191 previously reported cases of dural AVM's were reviewed with special attention to the mechanism of intradural, central, and peripheral nervous system manifestations. Apart from the peripheral cranial nerve symptoms, which are most likely due to arterial steal, the central nervous system (CNS) symptoms appear to be related to passive venous hypertension and/or congestion. Generalized CNS symptoms can be related to cerebrospinal fluid malabsorption due either to increased pressure in the superior sagittal sinus, to venous sinus thrombosis, or to meningeal reaction resulting from minimal subarachnoid hemorrhages. These phenomena are not related to the anatomical type of venous drainage. On the other hand, focal CNS symptoms are specifically indicative of cortical venous drainage. Seizures, transient ischemic attacks, motor weakness, and brain-stem and cerebellar symptoms can be encountered depending on the territory of the draining vein or veins. Therefore, the localizing value of focal CNS symptomatology relates to the venous territory and not to the nidus or to the arterial supply characteristics of dural AVM's. Furthermore, the venous patterns of various dural AVM's at the base of the skull are expressed by differences in their clinical presentation. Dural AVM's of the floor of the anterior cranial fossa and of the tentorium are almost always drained by the cortical veins and, therefore, have a high risk of intradural bleeding. The remarkable similarities in the manifestations of dural and brain AVM's and the differences in the manifestations of dural and spinal dural AMV's are pointed out. High-quality angiograms and a multidisciplinary approach to the study of dural AVM's will provide the best understanding of their symptoms and, therefore, the most appropriate treatment strategy.

Surgical neuroangiography of intracranial vascular malformations.

In the three year period of 1982 to 1985, 152 patients with intracranial vascular malformations were referred to the Bicetre Hospital in Paris, France and the Toronto Western Hospital in Canada. Sixty-six patients with cerebral vascular malformations and 48 patients with dural vascular malformations underwent endovascular treatment. In 8 patients surgery was performed in combination with the embolization procedure. Detailed analysis of the angio-architecture of the vascular malformation reveals certain characteristics which may be of value in predicting the clinical outcome. Comprehensive data analysis and long term follow-up is necessary to assess the role of embolization in the treatment of intracranial vascular malformations.

Super-selective angiography and embolization of skull base tumours.

Treatment planning for patients with tumours of the skull requires a true multidisciplinary approach. Super-selective angiography, using a protocol approach, is necessary in building a proper strategy plan for treatment of these lesions. Embolization done by a well trained team has proven to be a valuable adjunct to the various treatment methods and it may eliminate the need for radiation of benign lesions of the base of the skull.

Selected interventional procedures for pediatric head and neck vascular lesions.

Although vascular malformations are commonly seen in children, they are lesions managed best by an experienced multidisciplinary team. Recognizing, investigating, and diagnosing the type of vascular malformation is critical to determining treatment modality and pathway. Generic identification-despite Mulligan's excellent classification-or confusing vascular malformations with hemangiomas are both inappropriate because treatment is quite different for these separate groups of diseases. Additionally, an understanding of the recognition and classification of vascular malformations is essential for effective family counseling and management of these childhood lesions.

Cement embolization of a segmental artery after percutaneous vertebroplasty: a potentially catastrophic vascular complication.

Serious complications related to percutaneous vertebral augmentation procedures, vertebroplasty and kyphoplasty, are rare and most often result from local cement leakage or venous embolization. We describe an adult patient who underwent multi-level, thoracic percutaneous vertebral augmentation procedures for painful osteoporotic compression fractures. The patient's percutaneous vertebroplasty performed at the T9 level was complicated by the asymptomatic, direct embolization of the right T9 segmental artery with penetration of cement into the radicular artery beneath the pedicle. We review the literature regarding the unusual occurrence of direct arterial cement embolization during vertebral augmentation procedures, discuss possible pathomechanisms, and alert clinicians to this potentially catastrophic vascular complication.

Transvenous embolization of intracranial dural arteriovenous shunts through occluded venous segments: experience in 51 Patients.

BACKGROUND AND PURPOSE: DAVFs with cortical venous reflux carry a high risk of morbidity and mortality. Endovascular treatment options include transarterial embolization with a liquid embolic agent or transvenous access with occlusion of the involved venous segment, which may prove difficult if the venous access route is thrombosed. The aim of this article is to describe the technique and results of the transvenous approach via thrombosed venous segments for occlusion of DAVFs. MATERIALS AND METHODS: Our study was a retrospective analysis of 51 patients treated with a transvenous approach through an occluded sinus that was reopened by gentle rotational advancement of a 0.035-inch guidewire, which opened a path for a subsequently inserted microcatheter. RESULTS: Of 607 patients with DAVFs, the transvenous reopening technique was attempted in 62 patients in 65 sessions and was successful in 51 patients and 53 sessions. Immediate occlusion was seen in 42 patients; on follow-up, occlusion was seen in 49 patients, whereas 2 patients had reduced flow without cortical venous reflux. No permanent procedure-related morbidity was noted. CONCLUSIONS: The reopening technique to gain access to isolated venous pouches or the cavernous sinus for the treatment of DAVFs is a safe and effective treatment, which should be considered if transarterial approaches fail or are anticipated to result only in an incomplete anatomic cure.