Venous Varix Research Articles

A Complex Pulmonary Vein Varix - Diagnosis with ECG gated MDCT, MRI and Invasive Pulmonary Angiography

A case of an asymptomatic 32-year-old male with a complex congenital pulmonary vein varix is reported herein. Chest X-ray incidentally revealed a tubular opacity passing from the periphery of the left lingula to the mediastinum. ECG gated multidetector computed tomography showed the opacity to be a vessel emptying into the left atrium via the left superior pulmonary vein. In addition, a second vascular structure was noted within the posterior mediastinum that was emptying into the same pulmonary vein. These findings were also confirmed by magnetic resonance imaging, 4D magnetic resonance angiography and invasive arterial angiography. Based on multimodality imaging findings the diagnosis of complex congenital pulmonary venous varix with posterior mediastinal extension was established.

Vascular complications of stereotactic radiosurgery for arteriovenous malformations

ObjectiveAlthough vasculopathy and de novo aneurysm formation are known complications of traditional radiation therapy, their occurrence following AVM SRS is rare and thus infrequently addressed in the literature. We sought to evaluate these phenomena through a review of our institutional experience. MethodsOur review afforded 32 patients treated with LINAC-based SRS over an eight year period. We noted obliteration rates, complication rates and long-term outcomes, with particular attention paid to follow-up angiographic studies. ResultsAfter a mean follow-up of 4.3 years, the overall obliteration rate was 50%, increasing to 87% for AVMs less than 3cm. Eight patients had nine hemorrhages following SRS (25%). One occurred in the context of a de novo arterial pseudoaneurysm and another in the context of a new venous varix. Two patients with post-SRS hemorrhage had intranidal aneurysms that were not as apparent on initial angiography. Two patients that did not suffer from latency period hemorrhage developed dysplastic changes of feeding arteries, and one patient suffered from early venous thrombosis with resultant permanent hemiparesis from infarction. After a mean follow-up of 4.3 years, 8 patients were clinically improved (25%), 19 were the same (59%), and 5 were worse (16%), including 2 that died as a result of latency period hemorrhage. ConclusionWhile radiosurgery of AVMs is safe and successful in the vast majority of cases, vasculopathic complications including de novo aneurysm and varix development, early venous occlusion and stenotic vasculopathy, while infrequent, can occur. Closer long-term angiographic surveillance of these patients may thus be warranted.

Decision-Making in the Scheduling of Endovascular Treatment after Brain Arteriovenous Malformation Haemorrhage: A Retrospective Single Centre Study

The appropriate timing for endovascular intervention after brain arteriovenous malformation (bAVM) rupture is not known. This paper aims to determine factors that lead to early endovascular intervention and to investigate whether early intervention has the same complication rate as late intervention in a single centre. All patients who underwent endovascular treatment for a ruptured bAVM at our institution in the period January 2007 and July 2010 were included in this retrospective observational study. Of 50 patients, 33 had early endovascular intervention, defined as within 30 days of haemorrhage and the remaining 17 patients had endovascular treatment at day 30 or beyond. A greater proportion of patients treated within the first 30 days were in neuro-intensive care preoperatively (51.5% vs. 23.5%, p=0.07). A 'high-risk' angioarchitectural feature was identified in more patients who had acute intervention (78.8% vs. 11.8%, p<0.0001) and targeted embolization was also more frequent in this group (48.5% vs. 5.9%, p=0.004). Nidal aneurysms, venous varices and impaired venous outflow (venous stenosis) were the principal 'high risk' features. Clinically apparent complications occurred in 10.8% of procedures with permanent neurological deficit in 3.6%. There was no directly procedure-related mortality. There was no statistically significant difference in the complication rate of early procedures compared with delayed interventions (12.5% vs. 7.4%, p=0.71). Greater initial injury severity and the presence of high-risk lesion characteristics are the factors that lead to early endovascular intervention. Early intervention is associated with a higher complication rate, but this difference is not statistically significant.

Internal cerebral veins varix due to midline arteriovenous malformation: how much is the risk of bleeding?

We report a case of 40-year-old sportsman admitted to our department for a generalized seizure associated with bladder and bowel incontinence occurred during exercise. The patient quickly regained consciousness without postcritical deficits. Neurological examination appeared completely normal. A head computer tomography (CT) scan showed a midline arteriovenous malformation (AVM) without the evidence of bleeding (Fig. 1a, b). A digital subtraction angiography revealed a dysplastic nidus fed by branches of bilateral internal–external carotid and vertebrobasilar arteries, and draining both in the superficial and deep venous system, which showed varicose dilatation with Galen’s vein stenosis (Fig. 1c–g). Cerebral varix is defined as an ectasia which doubles vein diameter. It can be due to an arteriovenous shunt and appears more common in patients with direct fistulas, than in cerebral AVM with dysplastic nidi [1]. Differently from those associated with Galen’s vein fistulae, huge intracranial varix associated with cerebral AVMs were seldom reported. Headache, bruit, focal mass effect and hydrocephalus are common presentation symptoms [2]. Intracranial haemorrhage has been instead less often reported at clinical onset [3]. In the most of the cases of giant varix, direct arteriovenous communications in the context of nidus were observed, especially between feeding arteries and the varicose veins [4]. This discrete angiographic finding separate these vascular malformations from the classical and more common AVMs in which an abnormal vascular network is identified between the arterial feeders and draining veins [4]. Venous hypertension with retrograde drainage often results in focal neurological deficits and seizures [1]. Although it is commonly assumed that venous ectasia increases the bleeding risk, varix haemorrhagic presentation has been rarely reported [4]. It is may be due to the progressive thickening of the arterialized veins wall, with intimal proliferation of synthetic smoothmuscle cells and disappearance of the internal elastic lamina, that make arterialized veins not greatly prone to rupture [1, 4]. On the other hand, instead, the presence of venous varix on the draining veins has been recognized as a factor increasing the risk of haemorrhage in dural arteriovenous fistulae [5]. In the case reported here, the presence of multiple feeders causing high flow shunt rate, direct drainage in a cisternal venous system, and an impaired venous outlet due to the Galen’s vein stenosis, may have contributed to the varix formation. Prolonged sporting activity, instead, has not been a factor influencing AVM rupture.

Venous anastomotic circle, multiple varices and oculomotor palsy—a rare coincidence

Oculomotor nerve palsy due to a venous varix arising from flow anomalies caused by a dural arteriovenous fistula (AVF) is a rare phenomenon. We report a case of surgical third nerve palsy with a rare underlying AVF as the cause and discuss in detail the patho-anatomy and its significance. A tentorial dural AVF mimicking the arterial circle was found with multiple varix formation causing compressive oculomotor palsy. This was treated successfully with Onyx™ injection with a satisfactory angiographic result and complete resolution of symptoms.

Late onset of cervical dystonia in a 39-year-old patient following cerebellar hemorrhage

Cervical Dystonia (CD) is the most common form of focal dystonia with an incidence of 8.9 per 10,000 people [9]. The majority of cases are idiopathic, and secondary CD is associated with perinatal, vascular, traumatic, infectious and drug-induced processes affecting the central and peripheral nervous system [12]. A few reports have suggested that the cerebellum plays a role in pathogenesis of dystonia, There have been four cases in the literature describing CD that developed following a cerebellar stroke [2, 10, 11, 15]. We hereby present a rare case of CD developing 15 months after a cerebellar hemorrhage secondary to a ruptured AVM of the cerebellar vermis. A 37-year-old right-handed male presented to us with a sudden onset of headache, vomiting and dizziness. Neurological examination revealed right-sided horizontal nystagmus, ataxic gait, right-sided dysmetria and difficulty with finger nose test. His previous medical history and family history were unremarkable. An emergency noncontrast computerized tomography scan revealed a 2.4 9 1.6 cm hemorrhage in the vermis and in the occipital horns of the lateral ventricles. Magnetic Resonance Imaging (MRI) revealed an arteriovenous malformation (AVM) with venous varices in the cerebellar vermis (see Fig. 1). The AVM was embolized using ONYX and surgically excised 3 months later. After treatment, his cerebellar gait ataxia and dysarthria slightly worsened over the next 1 year. Fifteen months after the cerebellar hemorrhage, the patient developed intermittent rotational torticollis towards the left without trauma or exposure to dopamine blocking drugs. Primidone, topiramate, alprazolam, cyclobenzaprine, NSAIDs and physical therapy failed to provide relief. The patient received injections of Botulinum toxin type A (BOTOX ) to cervical muscles with a significant improvement. We believe that our case represents the fifth report of CD following a cerebellar stroke and the first one following a cerebellar hemorrhage. Alarcon et al. [2] performed a study in Ecuador on 56 patients with movement disorder after stroke. One of these patient had suffered a cerebellar ischemic stroke and developed dystonia 2 months later. Zadro et al. [15] described another patient who developed right-sided rotation of the head on the second day after having a left-sided cerebellar ischemic stroke. O’Rourke et al. [10] described a patient who developed paroxysmal CD following bilateral cerebellar infarction. Rumbach et al. [11] described a case of cerebellar infarction following vertebral artery occlusion who developed hemidystonia 2 months later. It is noteworthy that in our case CD developed after a substantially longer latency of 15 months. Other authors have also described CD in patients with space-occupying lesions (see Table 1) [1, 3, 6–8, 13, 14]. N. Usmani C. Sengun A. Pandey C. Singer Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA

Anterior Cranial Fossa Dural Arteriovenous Fistula With Bilateral Cortical Drainers -Case Report-

A 58-year-old man presented with sudden onset of severe headache. Computed tomography demonstrated subarachnoid hemorrhage and right acute subdural hematoma. He had no neurological deficits. Cerebral angiography showed an anterior cranial fossa dural arteriovenous fistula (AVF) supplied by the bilateral ethmoidal arteries. A fistula was suggested on the right side, and the dural AVF drained into the superior sagittal sinus via the bilateral frontal cortical veins. Venous varix was observed at both drainage sites. Bifrontal craniotomy with right-side dural incision was performed and the fistula was interrupted. Postoperative angiography demonstrated a persistent fistula draining into the left cortical vein. Nineteen days later, bifrontal craniotomy with left-side dural incision was performed and the draining vein was completely coagulated with the aid of intraoperative angiography. Postoperatively, there was no detectable residual fistula. He was discharged without neurological deficits 2 weeks after surgery. The present case of anterior cranial fossa dural AVF with bilateral cortical drainers shows that drainer occlusion at two points may be needed for complete obliteration of the drainers because the fistulous connection may not be simple.

Sinus pericranii in children: report of 16 patients and preoperative evaluation of surgical risk

Sinus pericranii (SP) is a rare venous varix in an extracranial location connected to the intracranial venous system. The aim of this retrospective study was to report on 16 pediatric cases of SP with consideration of the preoperative evaluation of surgical risk. The study population consisted of 10 patients who had undergone surgery for SP and 6 patients with concomitant craniosynostosis and SP. The mean age of the patients at presentation was 3.7 years. To identify characteristics of SP with high operative risk, 8 cases in this report and 11 previously reported cases of SP with sufficient information were categorized on the basis of the number and size of SP, the number and size of transcranial channels, the venous drainage type, and the amount of blood loss. Hemorrhage amounts were classified into 3 grades based on the description of intraoperative blood loss. Sinus pericranii not associated with craniosynostosis were resected without any postoperative morbidity. Sinus pericranii associated with craniosynostosis were preserved. After craniofacial reconstruction, 2 cases of SP with craniosynostosis regressed, completely in one patient and partially in another. These 2 patients with SP were confirmed to have compromised intracranial sinus before craniofacial reconstruction. Among a total of 19 patients, multiplicity or size (> 6 cm) of SP (p = 0.036) and multiplicity (> 3) or size (> 3 mm) of transcranial channels (p = 0.004) was associated with more severe hemorrhage grade. Sinus pericranii with peripheral venous drainage (drainer type) was not associated with hemorrhage grade after classification into 3 grades (p = 0.192). However, all 3 cases of SP with massive Grade 3 hemorrhage were the drainer type. Hemorrhage grade was correlated with the number of risk factors for SP (r = 0.793, p < 0.001). Three risk factors of SP and the presence of compromised intracranial sinus are markers for highrisk SP. "Squeezed-out sinus syndrome" is suggested as a concept for SP associated with compromised intracranial sinus, mainly caused by craniosynostosis. Sinus pericranii in squeezed-out sinus syndrome probably serves as a crucial alternative to venous drainage of the brain with intracranial venous compromise. Conservative treatment for such patients with SP is recommended.

Gastrointestinal Hemorrhage with Splenic Injury

Purpose: A 55-year-old man with history of polycystic kidney disease status post renal transplant 1 year ago presented to emergency room with symptomatic anemia and melena for 3 weeks with finding of acute drop in hemoglobin to 6 g/dL. The patient takes aspirin, clopidogrel, and immunosuppressants, including oral corticosteroids. He had endoscopic evaluations 5 weeks prior for chronic anemia, which revealed mild esophagitis, small non-bleeding antral ulcer, diverticulosis, non-bleeding internal hemorrhoids, and small arteriovenous malformations of the ascending colon that were treated with argon plasma coagulation therapy. Physical examination revealed a well-appearing man with stable hemodynamics, benign abdomen with normactive bowel sounds, and melenotic stool in rectum. His laboratory values showed hemoglobin of 6.4 g/dL, INR of 1.2, platelet count of 179/mm3, and ferritin level of 11. His EGD revealed a 5 cm serpiginous vascular-appearing anomaly in the midbody of the stomach with red spots suggestive of recent hemorrhage. This vascular anomaly was noted to bleed spontaneously. There were no visible vessels or mucosal defects. Hemastasis was achieved with epinephrine injection. MRA examination showed venous varix in the posterior gastric wall with vascular supply from splenic vessels. Splenic dysmorphism was noted to be an interval development, with normal spleen seen 5 years ago. The patient later admitted to a fall off the roof of his house resulting in trauma to left thorax and broken left foot three years prior. Splenosis is an acquired condition defined as autotransplantation of viable splenic tissue after traumatic or iatrogenic rupture of the spleen during surgery. It is usually found incidentally in asymptomatic patients and commonly found within the abdominal and pelvic cavities. Splenic tissue show distorted architecture without hilum and poorly formed capsule with blood supply from surrounding vessels. The average time interval between trauma and splenosis formation is 10 years. Splenosis can mimic as malignancies radiographically. Gastrointestinal splenosis has been associated with abdominal pain, mass causing bowel obstruction, and rarely as cause of gastrointestinal or intraperitoneal hemorrhage. Definitive diagnosis of splenosis is made through heat damaged erythrocyte scintigraphy and surgical biopsy. In this case, the etiology of gastrointestinal hemorrhage likely resulted from penetration of splenic implants into the gastric mucosa. Massive hemorrhage from splenosis is rare in reported literature, yet it must be included in the differential diagnosis of patients with gastrointestinal hemorrhage and history of splenectomy or splenic injury.

Illuminations

HomeRadioGraphicsVol. 29, No. 5 PreviousNext IlluminationsFree AccessDanger Lies AheadKai-hung FungKai-hung FungAuthor AffiliationsHong Kong, ChinaKai-hung FungPublished Online:Sep 1 2009https://doi.org/10.1148/radiographics.29.5.10.1148_027153330290051332MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked InEmail With rainbow rendering of computed tomographic data, exploration inside the cranium is simultaneously bedazzling and ominous. In a view toward the vertex, the superior sagittal sinus appears as a large, gentle C-curve. But the center of the surreal “landscape” seems dominated by the venous varix and draining vein of a thalamic arteriovenous malformation, which throb in orange above a mass of luminous tentacles, representing the basilar artery and bilateral internal carotid arteries (lower left).Download as PowerPointOpen in Image Viewer Article HistoryPublished in print: Sept 2009 FiguresReferencesRelatedDetailsRecommended Articles Radiologic Clues to Cerebral Venous ThrombosisRadioGraphics2019Volume: 39Issue: 6pp. 1611-1628Acute Headache in the Emergency SettingRadioGraphics2019Volume: 39Issue: 6pp. 1739-1759Intracranial Arteriovenous Malformation: Cinematic Rendering with Digital Subtraction AngiographyRadiology2019Volume: 294Issue: 3pp. 506Imaging of Neurologic Conditions in Pregnant PatientsRadioGraphics2016Volume: 36Issue: 7pp. 2102-2122Clinical-Radiologic Correlation of Extraocular Eye Movement Disorders: Seeing beneath the SurfaceRadioGraphics2016Volume: 36Issue: 7pp. 2123-2139See More RSNA Education Exhibits Keep an Eye Peeled: Imaging Findings in Vascular Causes of Visual DisturbanceDigital Posters2020Stroke in Pediatric Age Group: How MRI Can Help?Digital Posters2018Cervical and Intracranial Neurovascular Devices: What the Neuroradiologist Needs to KnowDigital Posters2020 RSNA Case Collection Cavernous internal carotid artery pseudoaneurysmRSNA Case Collection2021Carotid paragangliomaRSNA Case Collection2020Superior sagittal sinus thrombosisRSNA Case Collection2022 Vol. 29, No. 5 Metrics Downloaded 827 times Altmetric Score

A Dural Arteriovenous Fistula of the Anterior Cranial Fossa Angiographically Mimicking an Anterior Ethmoidal Artery Aneurysm

Venous aneurysm or varix at the venous side of the fistula commonly exist in dural arteriovenous fistula (DAVF) of the anterior cranial fossa, which may be initially mistaken with aneurysm on computed tomography and magnetic resonance imaging, but always identified by angiography. We report a very unusual case of anterior cranial fossa DAVF angiographically mimicking an anterior ethmoidal artery aneurysm, which was ultimately corrected by surgery. A 41-year-old male presented with right frontal intraparenchymal hematoma with intraventricular extension. Angiography revealed a vascular lesion adjacent to the anterior fossa mimicking an anterior ethmoidal artery aneurysm, which was surgically proven to be a partially thrombosed venous varix of drainaging vein originated from the cribriform plate. A diagnosis of anterior cranial fossa DAVF was made, and venous varix was excised. Follow-up angiography after the operation revealed complete disappearance of the lesion. Our case illustrates a unique occasion that a proximal venous varix without obvious outflow angiographically in DAVF might be mistaken with an aneurysm.

Hydrocephalus caused by a venous varix

Introduction Vascular malformations are uncommon causes of aqueductal obstruction. To our concern, only one case of hydrocephalus caused by a venous varix draining an unruptured arteriovenous malformation has been described in the literature. Case report We report the case of a 70-year-old woman presenting with progressive cognitive impairment, gait disturbance and urinary incontinence. Magnetic resonance imaging and magnetic resonance angiography revealed a large venous varix draining an unruptured arteriovenous malformation causing hydrocephalus. Conclusion Although uncommon, it is necessary to consider the presence of a vascular malformation in adults who presented with signs of aqueductal obstruction.

Endovascular Treatment of Brain Arteriovenous Fistulas

Brain arteriovenous fistulas (BAVFs) are dangerous lesions with significant risks for hemorrhage and re-hemorrhage; thus, the management of BAVFs is an important subject. Flow disconnection can be accomplished by surgical or endovascular techniques. We reviewed the experience in our endovascular treatment of patients with BAVFs. From March 2006 to March 2008, a total of 9 consecutive patients with nontraumatic BAVFs were treated at Beijing Tiantan Hospital. Dural arteriovenous fistulas and Galen aneurysmal malformations were excluded from this study. We retrospectively reviewed the medical records, cerebral angiograms, and endovascular reports for each patient. Radiographic outcome was assessed by posttreatment angiography. Clinical outcome was assessed for every patient. There were 9 patients with a total of 11 BAVFs. The mean age at presentation was 17.8 years. The clinical presentations were intracranial hemorrhage in 4 patients, headaches in 2 patients, and seizure in 1 patient, with 2 patients diagnosed incidentally. All lesions were supratentorial, and a venous varix was found on angiographic examination. Seven patients were treated with coils, 1 with Onyx-34, and 1 with a combination of coils and glue. All 9 lesions were completely obliterated as demonstrated on follow-up angiographic examination. With a mean follow-up of 5.7 months (range, 3-12 months), all patients were neurologically excellent with no symptoms (modified Rankin Scale, 0). BAVFs are more frequent in younger patients and frequently lead to intracranial hemorrhage. Staged endovascular coil embolization of BAVFs may be a good appropriate treatment technique.

A CASE OF VENOUS VARIX OF THE VOLAR DIGIT AND REVIEW OF THE LITERATURE

Venous varix of the volar digit (VVVD) is a rare condition that is usually described as a firm, blue, and painful mass. However, the clinical features of VVVD are still unclear. We treated a patient who had a firm, normal-skin-colored, and painless mass on the volar aspect of a digit. The mass was removed and was diagnosed as VVVD by histological examination. Magnetic resonance imaging was useful for assisting with the pre-operative diagnosis. We also review 11 previously reported cases.

Treatment of dural arteriovenous fistulas

The treatment of a dural arteriovenous fistula (DAVF) depends on the severity of the symptoms, its angiographic characteristics, and the risk it presents for intracranial hemorrhage. In many instances, therapy may involve a combination of more than one modality. Low-risk DAVFs, either incidental or with minimal symptoms, can be treated conservatively (observation, blood pressure control, manual carotid compressions). If the patient does not tolerate the symptoms, definite or palliative treatment can be offered. All high-risk DAVFs (Borden Grade II or III) should receive treatment because they carry a high probability of intracranial hemorrhage or neurologic deterioration. For small, well-circumscribed fistulas, radiosurgery can have excellent results, but thrombosis can occur many months after the treatment. For large DAVFs with severe symptoms (vision deterioration, ophthalmoplegia with diplopia, seizures, or neurologic deficit) or with high risk for hemorrhage (cortical venous drainage or venous varices), the first treatment option should be endovascular embolization. With the combination of modern materials and techniques, this procedure can yield a high rate of cure with minimal complications. In patients not amenable to embolization or after incomplete embolization, surgery should be considered if the DAVF is located in an easily accessible area, because of its immediate and definite results. Surgery can be facilitated by preoperative embolization of the fistula to reduce the arterial supply and minimize intraoperative bleeding. Radiosurgery can also be used adjunctively after embolization or surgery has significantly reduced the size of large DAVFs.

Endovascular treatment of high-risk tentorial dural arteriovenous fistulas: clinical outcomes

An increasing number of intracranial dural arteriovenous fistulas (DAVFs) are amenable to endovascular treatment with Onyx-18. We reviewed our experience with the endovascular management of tentorial dural arteriovenous fistulas (TDAVFs) treated transarterially and transvenously. Clinical records for 19 consecutive patients (three women, 16 men) with TDAVFs treated endovascularly between 2005 and 2008 were reviewed to determine their presenting symptoms, angiographic features, endovascular treatments, and clinical outcomes. Most patients (78.9%) presented with intracranial hemorrhage (ICH). All patients had high-risk angiographic features such as leptomeningeal venous varix. Transarterial embolization was performed in 19 patients. Transvenous embolization was additionally performed in two patients and caused one death. At the time of the last follow-up evaluation, 16 (84.2%) patients had good or excellent outcomes (modified Rankin score, 0 or 1) and one (5.3%) was deceased. Six patients had a residual fistula and were treated with gamma knife radiosurgery. The overall morbidity and mortality rate was 10.5%. High-risk TDAVFs can be successfully managed with good outcomes. When anatomic features can be accessed endovascularly, endovascular treatment is indicated. Patients with residual filling of the DAVF should be considered for adjuvant therapy, including further radiosurgery.

Radiculopathy Caused by Lumbar Epidural Venous Varix -Case Report-

A 33-year-old man presented with a rare case of lumbar epidural venous varix causing radiculopathy manifesting as sciatica exacerbated during bowel movements. The left straight-leg raising test was positive and patellar tendon reflex was lost. Lumbar magnetic resonance imaging showed a mass lesion in the epidural space at the L4 level just anterior to the dural sac on the left, appearing as hypointense on T(1)- and hyperintense on T(2)-weighted images, with ring-like enhancement with gadopentetate dimeglumine. He underwent surgery under a preoperative diagnosis of cystic nerve sheath tumor. After left hemilaminectomy, intraoperative ultrasonography showed a low echoic mass lesion ventral to the L4 nerve root. The mass was dark blue with a smooth wall. Tearing of the wall resulted in continuous bleeding. After removal of the lesion, we confirmed that the dura of the nerve root was intact. Histological examination of the surgical specimen confirmed venous tissue. The postoperative course was excellent. Lumbar epidural varix is difficult to diagnose preoperatively. Lumbar epidural varix should be considered if the lesion is smaller on preoperative than intraoperative imaging, or disappears with bleeding cessation, as this may avoid unnecessary widening of the operative field. The correct preoperative diagnosis remains difficult, so we recommend surgical removal and histological confirmation.

Dural Arteriovenous Fistula in the Anterior Cranial Fossa -Four Case Reports-

Three of 4 cases of dural arteriovenous fistulas (DAVFs) in the anterior cranial fossa were detected incidentally by magnetic resonance (MR) imaging, and one case manifested as intracerebral hemorrhage. Cerebral angiography revealed fistulas located in the anterior cranial fossa. Three patients underwent surgery, and the fistulas were successfully obliterated. One patient with nonruptured DAVF requested conservative medical management. Incidental detection of asymptomatic or nonruptured DAVFs in the anterior cranial fossa has increased with the wider use of MR imaging. Increase in the size of a venous varix is the indicator for aggressive therapeutic intervention in a patient receiving conservative medical management for asymptomatic or nonruptured DAVFs in the anterior cranial fossa.

SURGICAL TREATMENT OF HIGH-RISK INTRACRANIAL DURAL ARTERIOVENOUS FISTULAE

An increasing number of intracranial dural arteriovenous fistulae (DAVFs) are amenable to endovascular treatment. However, a subset of patients with high-risk lesions requires surgical intervention for complete obliteration. We reviewed our experience with the surgical management of high-risk intracranial DAVFs and offer recommendations to minimize complications based on fistula location and type. Hospital records for 53 patients (16 women, 37 men) with high-risk intracranial DAVFs treated surgically between 1995 and 2004 were reviewed to determine their presenting symptoms, location, endovascular and surgical interventions, angiographic outcome, and treatment complications. Most patients (76%) presented with intracranial hemorrhage, progressive neurological deficits, or seizures. All patients had high-risk angiographic features such as cortical venous drainage or venous varix. Preoperative embolization was performed in 27 patients. Surgical approaches were tailored to the lesion location. Fistulae were located in the transverse-sigmoid junction (n = 18), tentorium (n = 17), ethmoid (n = 7), superior sagittal sinus (n = 6), torcula (n = 4), and sphenoparietal sinus (n = 3). At the time of the last follow-up evaluation, 49 patients (92%) had good or excellent outcomes (Glasgow Outcome Scale score, 4 or 5) and three (6%) were deceased. Five patients had a residual fistula. One residual spontaneously thrombosed, one was treated with gamma knife radiosurgery, and two were successfully embolized. The overall morbidity and mortality rate was 13%. Despite fulminant presenting symptoms, high-risk intracranial DAVFs can be successfully managed with good outcomes. When anatomic features prevent endovascular access, or embolization fails to obliterate the lesion, urgent surgical treatment is indicated. Patients with residual filling of the DAVF should be considered for adjuvant therapy, including further embolization or radiosurgery.

Unruptured arteriovenous malformation in a patient presenting with obstructive hydrocephalus

The authors report on a patient harboring an unruptured cortical arteriovenous malformation (AVM), who had presented with obstructive hydrocephalus due to compression of the cerebral aqueduct by a large venous varix. Although patients with ruptured AVMs are known to either present with or later suffer from obstructive hydrocephalus, those with unruptured AVMs who present in this manner are quite rare. Moreover, hydrocephalus caused by a venous varix draining an AVM, to our knowledge, has never been previously reported in the literature. This report serves to illustrate two primary points, namely, that tortuous venous varices draining AVMs can result in obstructive hydrocephalus and that this unusual circumstance can be fostered in the setting of venous outflow obstruction.