|Year : 2020 | Volume
| Issue : 1 | Page : 10-18
Arteriovenous fistulae of the neuraxis: An institutional experience
Sibhi Ganapathy1, Swaroop Gopal2, Paritosh Pandey1
1 Manipal Hospitals, Whitefield, Bengaluru, Karnataka, India
2 Institute of Neurosciences, Sakra World Hospital, Bengaluru, Karnataka, India
|Date of Submission||26-Jul-2020|
|Date of Decision||28-Jul-2020|
|Date of Acceptance||01-Sep-2020|
|Date of Web Publication||1-Oct-2020|
Dr. Sibhi Ganapathy
Manipal Hospitals, Whitefield, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
Introduction: Arteriovenous fistulae (AVF) are rare lesions. Patients typically present with slowly progressive myelopathy that is often mistaken for degenerative cervical or lumbar stenosis. Cranial presentations are even more innocuous ranging from seizures to tinnitus. The purpose of this study is to present a series of cases to aid in the assessment, diagnosis and treatment of this unusual pathology.
Case Series: We present 11 cases of AVFs treated at our centre over an 4-year period. Seventy percent of patients were male. The mean age of presentation was 62.6 years. The most common lesion was a dural AVF emanating from the craniovertebral junction with single feeder. All patients underwent either microsurgical correction or endovascular embolization as the primary procedure. Eight patients showed improvement following treatment as graded by the Nurick system. Two patients failed to improve. None of the patients worsened. One patient had a cortical venous thrombosis after embolization that resolved well with anticoagulants.
Conclusion: The successful treatment of AVF requires a detailed understanding of clinical presentation and imaging findings to allow for precise treatment. Owing to the rarity of the condition, clinicians must continue to share their experiences to advance our knowledge.
Keywords: Arteriovenous fistulae AVF, embolization, digital subtraction angiography DSA
|How to cite this article:|
Ganapathy S, Gopal S, Pandey P. Arteriovenous fistulae of the neuraxis: An institutional experience. J Cerebrovasc Sci 2020;8:10-8
|How to cite this URL:|
Ganapathy S, Gopal S, Pandey P. Arteriovenous fistulae of the neuraxis: An institutional experience. J Cerebrovasc Sci [serial online] 2020 [cited 2021 Feb 28];8:10-8. Available from: http://www.jcvs.com/text.asp?2020/8/1/10/296933
| Introduction|| |
Arteriovenous fistulas (AVF) are the most common vascular shunts of the central nervous system. They occur predominantly in men (80%), commonly involve the thoracolumbar spine, and usually cause progressive myelopathy because of venous congestion of the spinal cord., Patients with AVF often present with non-specific clinical features that are related to progressive myelopathy, seizures or isolated neurological deficits. Frequently, they are misdiagnosed as having other more common pathologies, which can lead to a significant delay in diagnosis, treatment and poorer prognosis. The average patient will present, with 1–3 years before the diagnosis is made. Hence, understanding the radiological features found on magnetic resonance imaging (MRI) and angiography, and treating it earlier saves the patient significant morbidity.,
The aim of this study was to compare the angiographic and clinical characteristics of spinal dural AVFs (SDAVFs) of the neural axis based on the patients treated at a quaternary care centre in south India over 4 years.
| Methods|| |
All patients with dural and epidural AVF within 4 years were considered for the study. Details regarding demography as well as angiography were tabulated. Intervention and/or surgery were studied and documented. The data were analysed, consolidated and presented.
| Results|| |
Results are presented in two formats. General data regarding the trends in patient demographics and presentations along with modality used to treat the disease have been clubbed together. We also present individual data of each case, where radiological features and follow-up details are explained in brief.
Section 1: General data
Eleven patients presented with differing clinical features during the above-mentioned period in 2 tertiary care centres in Bengaluru, India for definitive care. The age and sex distribution are described in [Figure 1]. As shown in [Figure 1] and [Table 1], the maximum individuals were from 30 to 60 years of age group which coincides with the reports from literature, with a gross preponderance of males. These patients presented with varying symptomatology. These included features of compressive myelopathy to seizures. The symptomatology has been depicted in [Figure 2].
|Table 1: Demographic data, disease characteristics and treatment methodology|
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Paraesthesia and compressive symptoms of the spine such as myelopathy, spasticity, limb weakness and bladder disturbances were the most common symptom.
One patient had a sudden severe intracranial bleed needing emergency decompressive craniectomy and subsequent surgery for his DAVF. All other patients had long standing complaints. The distribution of these lesions is also varied from, intracranial to spine to lesions straddling the craniovertebral junction (CVJ) extending into both spaces, as shown in [Figure 3]. Here, the majority of lesions are in the spine with only 3 out of the 11 lesions (27%) occurring intracranially. Of these lesions, 2 were from the posterior fossa around the transverse-sigmoid junction extending to the foramen magnum. The lone temporal DAVF presented with spontaneous intracranial bleed resulting in prostration requiring an emergency decompressive craniectomy.
|Figure 3: Distribution of lesions by location both intracranial and spinal are demonstrated in a layered pie chart|
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[Figure 4] shows the primary treatment modality employed in these lesions. There are occasions where endovascular embolisation of the lesion was employed before surgery, but this depiction is only for the main or primary modality involved. Intricacies of individual treatment strategies will be dealt with on a case to case basis later in the paper. Somewhat surprisingly, endovascular therapies are a minority in our data, with a preference for microsurgical resection, especially in those lesions presenting in the dorsal and lumbar spines. Cranial and cervical lesions were mostly treated endovascularly due to the sensitive nature of the location coupled with difficulties associated with approach and feeder detection.
|Figure 4: Treatment modality used to treat the different arteriovenous fistulae|
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The overall prognosis [Figure 5] was excellent with only 1 patient out of 11 (0.18%) had long-term deficits, which required nursing care, and this was due to the intracranial bleed which had occurred, for which only slow rehabilitation could be done. The patient however made a complete recovery 1 year later. The depiction below shows deficit at discharge. Another two patients were discharged with bladder incontinence (which was the presenting complaint) the condition sadly did not improve later on, even after 1 year. The precarious nature of bladder fibres in the conus however cannot be blamed on the intervention, but nevertheless, we present the data as it is. All others were discharged with mild weakness of limbs which improved on physiotherapy to normal functional status within 6 months of the procedure.
Section 2: Case Reports
A 52-year-old female presented with paraesthesia and spasticity. MRI showed severe cord changes from D6 to D10. The angiogram showed feeders from the radicular arteries of D6 to D10 with prominent veins seen up to D6. Surgery was done and the vein clipped. The patient recovered well and was discharged deficit free [Figure 6].
|Figure 6: Magnetic resonance imaging of the dorsal spine showing flow voids compressing the cord|
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A 60-year-old male patient presented with trigeminal neuralgia like pain across the left side of the face. An MRI showed flow voids extending from the left transverse sigmoid junction up to the cervical spine. The angiogram showed feeders from the middle cerebral artery and posterior cerebral artery (PCA) emptying into the left transverse sinus. Endovascular embolisation was done successfully [Figure 7].
|Figure 7: Computed tomography angiogram with three-dimensional reconstruction showing the arteriovenous fistulae venous sac compressing the craniovertebral junction|
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A 50-year-old male presented with new onset seizures. An MRI suggested enlargement of the torcula with extension into the cerebellar tonsils. An angiogram revealed a large DAVF fed from feeders from the left occipital artery and draining into the superior sagittal sinus with varicosities extending up to the foramen magnum. Endovascular embolisation was done successfully using the venous route to approach the lesion. Post-procedure there was a minor venous thrombosis in the sigmoid sinus, but since this side was non-dominant, there were no major symptoms. The patient was discharged on anti-epileptics and anticoagulants which he continues to take. He remains seizure-free till date [Figure 8].
A 26-year-old female presented with seizures and episodic ataxia. An MRI of her brain revealed a mass lesion with significant flow voids in the right basal ganglia. An angiogram showed a large venous varyx fed from feeders from the right PCA and draining into the right maxillary vein. Endovascular embolisation was successfully done. The patient improved well after the procedure [Figure 9].
|Figure 9: Partial obliteration of the arteriovenous fistulae showing stasis in the draining vein|
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A 36-year-old male presented with long standing incontinence and loss of sensation over the legs. He had been diagnosed to have a DAVF 2 years ago and had been operated for it unsuccessfully. An Angiogram revealed a ventral Conus DAVF fed from the L1 left radical branch. He was taken up for a redo surgery and improved well post-operative.
A 39-year-old male presented with spasticity and paraesthesia in both lower limbs. His MRI showed conus enhancement with flow voids in the subarachnoid space. An angiogram showed radicular branches from the D9 level feeding a large left-sided DAVF compressing the cord. A large venous channel was seen. Hence, surgery was attempted, and the vein clipped. Post-operative recovery was good.
A 58-year-old male presented with significant Ashworth grade 3 spasticity in both lower limbs coupled with radicular pain and paraesthesia. He had been treated with embolisation for the same problem 4 years ago. An MRI of the spine suggested a residual DAVF at the conus level. The angiogram of the spine confirmed this with feeders from the L1 and D12 radicular branches. Surgery was done and the venous channel blocked completely. He made a complete recovery. No recurrence has been noted since for the last 1 year.
A 54-year-old female presented with progressive urgency and incontinence. She also had longstanding paraesthesia of the lower limbs and mild weakness. An MRI of the lumbar spine showed a space occupying mass posterior to the conus and cauda equina compressing the structures in the spinal canal. An angiogram revealed a DAVF fed from the L2 radical artery on the right side. The vessel was embolised and the patient made a good recovery as far as her pain and weakness were concerned. Her bladder symptoms marginally improved but remain after 1 year of follow-up.
A 26-year-old male patient presented with pulsatile tinnitus and paraesthesia of the right upper and lower limb. MRI done was suggestive of a space occupying lesion around the transverse sigmoid region extending onto the CVJ. An angiogram showed a small DAVF fed from branches of the PCA draining directly into the transverse sinus. As the DAVF was superficial, a small temporo-occipital craniotomy was done and the venous connection clipped, with excision of the nidus. The patient made a complete recovery and went home deficit free.
A 75-year-old male patient presented with weakness of the right upper and lower limb for 2 weeks. He had had these symptoms 1 year before, but the symptoms gradually improved, and no medical attention was sought then. This time, the weakness was progressive with spasticity, paraesthesia and pain. An angiogram showed a large epidural fistula with feeders from the vertebral arteries and the deep cervical arteries feeding a large venous lake in the epidural space compressing the cervical cord from C1 to C6. Endovascular glue injection was done immediately and successfully. The patient walked home after 2 days in hospital with no further discomfort. His spasticity and weakness gradually improved over the next 2 months to completely recover [Figure 10]a and [Figure 10]b.
|Figure 10: (a) Magnetic resonance imaging sagittal and axial views depicting the large venous sac compressing the craniovertebral junction leading to myelopathy. (b) Embolisation of the fistula through the vertebral artery|
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A 22-year-old male patient was brought in an air ambulance from a nearby city. The patient had had a sudden onset of loss of consciousness and prostration. He was taken to the local hospital, where a computed tomography (CT) scan had shown a large right temporal lobe intra-cerebral haemorrhage with significant mass effect and impending uncal herniation. Due to the severity of the disease and the urgency of the situation, he was taken up for a decompressive craniectomy and hematoma evacuation. During the surgery, engorged venous channels were seen in the dura. The neurosurgeon at this juncture, decided against hematoma evacuation and stopped after opening the dura decreasing the oedema and preventing further herniation. Post-surgery, the patient was airlifted to our centre.
A CT angiogram of the brain suggested a large DAVF extending from the temporal base to the transverse sigmoid junction. The venous drainage was primarily through a large vein in the temporal base into the maxillary vein. A large number of small dural and pial feeders fed a large nidus occupying the centre of the hematoma. The patient was operated and the hematoma with the nidus and feeders were removed. The vein was clipped and cut thereby disconnecting the system. Post-operative, the patient spent 17 days in the intensive care unit and gradually improved. He was sent home conscious and obeying commands, needing nursing care and physiotherapy. He rapidly improved and made a full recovery as seen during regular follow-up. At the 1 year follow-up, he was seen walking with no weakness and cognitive deficits.
| Discussion|| |
DAVFs are predominantly idiopathic, though a small percentage of patients have a history of previous craniotomy, trauma or dural sinus thrombosis.,,, Two etiologic hypotheses based around sinus thrombosis have been put forward.
The first is that physiologic arteriovenous shunts between meningeal arteries and dural venous sinuses enlarge in response to elevated local venous pressure, resulting in a pathologic shunt.,, The second is that venous hypertension due to outflow obstruction causes decreased cerebral perfusion and promotes neoangiogenesis.,,,,, Heritable risk factors for venous thrombosis, such as anti-thrombin, protein C, and protein S deficiencies, have furthermore been associated with DAVF occurrence., These findings implicate the role of an underlying hypercoagulability in the development of DAVFs. The aetiology of paediatric DAVFs is thought to be congenital or a result of birth trauma, infection, in utero venous thrombosis or maternal hormones.
The Borden classification system stratifies lesions on the basis of the site of venous drainage and the presence or absence of venous drainage. Borden Type I lesions have the direct communication of meningeal arteries with a meningeal vein or dural venous sinus and exhibit normal antegrade flow. Type II lesions have shunts between the meningeal arteries and dural sinus, with retrograde flow into the subarachnoid veins, causing venous hypertension. Type III lesions have direct drainage of meningeal arteries into subarachnoid veins or an 'isolated' sinus segment. The latter phenomenon is the result of thrombosis on either side of the arterialised sinus segment, which directs retrograde flow into the subarachnoid venous system. The Borden classification scheme further sub-classifies lesions as single-hole (a) or multiple-hole (b) fistulas [Table 2].
|Table 2: Borden's classification of intracranial dural arteriovenous fistulae|
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The Cognard classification is based on the direction of dural sinus drainage, the presence or absence of CVD, and venous outflow architecture (non-ectatic cortical veins, ectasia cortical veins or spinal perimedullary veins). Type I lesions drain into the dural sinus, have an antegrade flow direction, and lack CVD. Type II lesions are subdivided into two subcategories: type IIa lesions drain retrogradely into a dural sinus without CVD, type IIb lesions drain antegradely into a dural sinus with CVD, and type IIa + b lesions drain retrogradely into a dural sinus with CVD. Types III, IV and V lesions all have CVD, absent dural venous drainage, and varying cortical venous outflow architecture [Table 3].
|Table 3: Cognard's classification of cranial dural Arteriovenous Fistulae|
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SDAVFs are classified by various methods and systems. The latest Takai Classification stands tall for merging both DAVFs and epidural fistulae as well [Table 4].
|Table 4: Takai classification of dural and epidural arteriovenous fistulae of the spine (2016)|
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A majority of patients with DAVFs present in the fifth and sixth decades with symptoms related to lesion location and pattern of venous drainage.,,,, Pulsatile tinnitus is a common symptom that results from increased blood flow through the dural venous sinuses, particularly in relation to transverse and sigmoid sinus lesions.,,,,,,,,,, Cavernous sinus DAVFs can present with ophthalmoplegia, proptosis, chemosis, retroorbital pain or decreased visual acuity.,,,,,,,,,, Severe presentations include intracranial haemorrhage and non-haemorrhagic neurologic deficits such as seizures, Parkinsonism More Details, cerebellar symptoms, apathy, failure to thrive and cranial nerve abnormalities, including rare cases of trigeminal neuralgia.,,,,,,,,,, Some symptoms, including dementia and cognitive decline, may improve after treatment. Haemorrhagic presentations are more frequent in high-grade (Borden types II and III, Cognard types IIb to IV) DAVFs. Unexplained subarachnoid or lobar haemorrhages should prompt consideration of a DAVF in the differential diagnosis. SDAVFs present with compressive myelopathy like symptoms with paraesthesia and pain. Lower compressions may result in a cauda equina like picture with bowel and bladder involvement as well.,,
Any suspicious flow void cluster around the dural venous sinus should prompt additional evaluation with dynamic CT angiography (CTA), MR angiography (MRA) or digital subtraction angiography. CTA is particularly useful in treatment planning by precisely defining the arteriovenous shunt relative to surrounding brain and skull anatomy. Recent publications on 4D CTA using 320-section multidetector row CTA have highlighted its potential to correctly diagnose, classify and assist treatment planning for DAVFs.,,,, Studies have reported, however, that CTA has reduced sensitivity versus MRA for the detection of DAVFs (15.4% vs. 50%).,, Time-resolved MRA techniques are also promising and may be reliable for DAVF screening and surveillance in the future.,, Due to the current limitations of low resolution and saturation artefacts, the negative predictive value of MRA is inadequate to exclude DAVFs.
Conventional angiography remains the most accurate method for detection and classification of DAVFs.,,,,, The adjunct of FDCT to angiography is yielding previously unachievable high-resolution anatomic detail. Groups have demonstrated the utility of FPCT to precisely delineate the fistula site and provide superior visualisation of arterial feeders and venous outflow.,
Endovascular approaches have become the mainstay of DAVF therapy, but the optimal approach for each case should involve discussions among a multidisciplinary team of interventional neuroradiologists, neurosurgeons, neurologists and radiation oncologists. Careful assessment of a patient's clinical presentation, current status (age, medical condition and comorbidities), and type of lesion (location, classification and angiographic features) should be conducted before embarking on any treatment.,,
Due to the efficacy of endovascular treatment, surgery is currently indicated in cases in which endovascular approaches have failed or are not feasible. A variety of options is available, including direct intraoperative embolisation of meningeal arteries or veins, resection of abnormal dura, packing of the diseased sinus, disconnection of the retrograde leptomeningeal venous drainage and skeletonisation of the dural sinus with disconnection of the dural arterial supply. Certain anatomic locations of DAVFs are more amenable for surgery. These include the floor of the anterior cranial fossa and the superior sagittal sinus, where arterial access is difficult and/or sacrifice of the sinus is often undesirable. DAVFs that involve eloquent feeders are also better addressed by using a surgical or combined approach to ensure vessel preservation.,,
Studies of SRS for DAVFs remain preliminary and have primarily involved low-risk lesions or those that are not amenable to endovascular or surgical approaches., Lesions are irradiated with 20–30 Gy, which causes vessel thrombosis and fistula closure during a latency period ranging from several months to a year. Until completion of vessel thrombosis, the haemorrhage risk remains elevated, so SRS is inappropriate as the primary treatment in DAVFs with CVD.,,,, Early results have been encouraging, with obliteration rates as high as 93% for combined endovascular embolisation and SRS but have also demonstrated rates as low as 50% when only SRS is used. There have also been significant disparities in efficacy depending on the location of the fistula reflecting challenges for shunt targeting in complex lesions.,,,,
Limitations of the study
As performed in different centres by different surgeons with differing degrees of competence in surgery and endovascular techniques, the procedures were not performed according to any protocol but to surgeon preference and convenience to ensure the best result for the patients. Another problem is that we operate in a third world country where financial constraints often dictate treatment protocols and hospital stay duration. We were also subject to the same forces. Since open surgery is cheaper significantly to endovascular procedures, we were obliged to opt for such a strategy despite evidence to the contrary.
| Conclusion|| |
DAVF either cranial or spinal present a complex problem to today's patients. The advance of endovascular and surgical techniques along with advanced imaging modalities enable for early detection and prompt effective treatment which is so crucial in the prevention and minimising of neurological morbidity.
All patients have given written consents for their details to be used in this manuscript.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kwon BJ, Han MH, Kang HS, Chang KH. MR imaging findings of intracranial dural arteriovenous fistulas: Relations with venous drainage patterns. AJNR Am J Neuroradiol 2005;26:2500-7.
Kirsch M, Liebig T, Kühne D, Henkes H. Endovascular management of dural arteriovenous fistulas of the transverse and sigmoid sinus in 150 patients. Neuroradiology 2009;51:477-83.
Morita A, Meyer FB, Nichols DA, Patterson MC. Childhood dural arteriovenous fistulae of the posterior dural sinuses: Three case reports and literature review. Neurosurgery 1995;37:1193-9.
Chung SJ, Kim JS, Kim JC, Lee SK, Kwon SU, Lee MC, et al
. Intracranial dural arteriovenous fistulas: Analysis of 60 patients. Cerebrovasc Dis 2002;13:79-88.
Nabors MW, Azzam CJ, Albanna FJ, Gulya AJ, Davis DO, Kobrine AI. Delayed postoperative dural arteriovenous malformations: report of two cases. J Neurosurg 1987;66:768-72.
Awad IA, Little JR, Akarawi WP, Ahl J. Intracranial dural arteriovenous malformations: Factors predisposing to an aggressive neurological course. J Neurosurg 1990;72:839-50.
Izumi T, Miyachi S, Hattori K, Iizuka H, Nakane Y, Yoshida J. Thrombophilic abnormalities among patients with cranial dural arteriovenous fistulas. Neurosurgery 2007;61:262-8.
Kerber CW, Newton TH. The macro and microvasculature of the dura mater. Neuroradiology 1973;6:175-9.
Kojima T, Miyachi S, Sahara Y, Nakai K, Okamoto T, Hattori K, et al
. The relationship between venous hypertension and expression of vascular endothelial growth factor: Hemodynamic and immunohistochemical examinations in a rat venous hypertension model. Surg Neurol 2007;68:277-84.
Fujita A, Kuwamura K, Saitoh M, Sakagami Y, Takaishi Y, Suzuki S, et al
. Cerebral sinus thrombosis in a patient with protein S deficiency: A case report. No Shinkei Geka 1997;25:467-72.
Gerlach R, Yahya H, Rohde S, Böhm M, Berkefeld J, Scharrer I, et al
. Increased incidence of thrombophilic abnormalities in patients with cranial dural arteriovenous fistulae. Neurol Res 2003;25:745-8.
Borden JA, Wu JK, Shucart WA. A proposed classification for spinal and cranial dural arteriovenous fistulous malformations and implications for treatment. J Neurosurg 1995;82:166-79.
Cognard C, Gobin YP, Pierot L, Bailly AL, Houdart E, Casasco A, et al
. Cerebral dural arteriovenous fistulas: Clinical and angiographic correlation with a revised classification of venous drainage. Radiology 1995;194:671-80.
Brown RD Jr., Flemming KD, Meyer FB, Cloft HJ, Pollock BE, Link ML. Natural history, evaluation, and management of intracranial vascular malformations. Mayo Clin Proc 2005;80:269-81.
Davies MA, Ter Brugge K, Willinsky R, Wallace MC. The natural history and management of intracranial dural arteriovenous fistulae. Part 2: Aggressive lesions. Interv Neuroradiol 1997;3:303-11.
Davies MA, TerBrugge K, Willinsky R, Coyne T, Saleh J, Wallace MC. The validity of classification for the clinical presentation of intracranial dural arteriovenous fistulas. J Neurosurg 1996;85:830-7.
Zipfel GJ, Shah MN, Refai D, Dacey RG Jr., Derdeyn CP. Cranial dural arteriovenous fistulas: Modification of angiographic classification scales based on new natural history data. Neurosurg Focus 2009;26:E14.
Satomi J, van Dijk JM, Terbrugge KG, Willinsky RA, Wallace MC. Benign cranial dural arteriovenous fistulas: Outcome of conservative management based on the natural history of the lesion. J Neurosurg 2002;97:767-70.
Cognard C, Houdart E, Casasco A, Gabrillargues J, Chiras J, Merland JJ. Long-term changes in intracranial dural arteriovenous fistulae leading to worsening in the type of venous drainage. Neuroradiology 1997;39:59-66.
Saito A, Furuno Y, Nishimura S, Kamiyama H, Nishijima M. Spontaneous closure of transverse sinus dural arteriovenous fistula: Case report. Neurol Med Chir (Tokyo) 2008;48:564-8.
Endo S, Koshu K, Suzuki J. Spontaneous regression of posterior fossa dural arteriovenous malformation. J Neurosurg 1979;51:715-7.
Hansen JH, Sogaard I. Spontaneous regression of an extra-and intracranial arteriovenous malformation. Case report. J Neurosurg 1976;45:338-41.
Landman JA, Braun IF. Spontaneous closure of a dural arteriovenous fistula associated with acute hearing loss. AJNR Am J Neuroradiol 1985;6:448-9.
Luciani A, Houdart E, Mounayer C, Saint Maurice JP, Merland JJ. Spontaneous closure of dural arteriovenous fistulas: Report of three cases and review of the literature. AJNR Am J Neuroradiol 2001;22:992-6.
Moriya M, Itokawa H, Fujimoto M, Noda M, Nagashima G, Asai J, et al
. Spontaneous closure of dural arteriovenous fistula after performing diagnostic angiography. No Shinkei Geka 2007;35:65-70.
Olutola PS, Eliam M, Molot M, Talalla A. Spontaneous regression of a dural arteriovenous malformation. Neurosurgery 1983;12:687-90.
Hurst RW, Bagley LJ, Galetta S, Glosser G, Lieberman AP, Trojanowski J, et al
. Dementia resulting from dural arteriovenous fistulas: the pathologic findings of venous hypertensive encephalopathy. AJNR Am J Neuroradiol 1998;19:1267-73.
Lucas Cde P, Zabramski JM. Dural arteriovenous fistula of the transverse-sigmoid sinus causing trigeminal neuralgia. Acta Neurochir (Wien) 2007;149:1249-53.
Hasumi T, Fukushima T, Haisa T, Yonemitsu T, Waragai M. Focal dural arteriovenous fistula (DAVF) presenting with progressive cognitive impairment including amnesia and alexia. Intern Med 2007;46:1317-20.
Hirono N, Yamadori A, Komiyama M. Dural arteriovenous fistula: A cause of hypoperfusion-induced intellectual impairment. Eur Neurol 1993;33:5-8.
Lasjaunias P, Chiu M, Ter Brugge K, Tolia A, Hurth M, Bernstein M. Neurological manifestations of intracranial dural arteriovenous malformations. J Neurosurg 1986 64:724-30.
Lee PH, Lee JS, Shin DH, Kim BM, Huh K. Parkinsonism as an initial manifestation of dural arteriovenous fistula. Eur J Neurol 2005;12:403-6.
Zeidman SM, Monsein LH, Arosarena O, Aletich V, Biafore JA, Dawson RC, et al
. Reversibility of white matter changes and dementia after treatment of dural fistulas. AJNR Am J Neuroradiol 1995;16:1080-3.
Brouwer PA, Bosman T, van Walderveen MA, Krings T, Leroux AA, Willems PW. Dynamic 320-section CT angiography in cranial arteriovenous shunting lesions. AJNR Am J Neuroradiol 2010;31:767-70.
Siebert E, Bohner G, Dewey M, Masuhr F, Hoffmann KT, Mews J, Engelken F, Bauknecht HC, Diekmann S, Klingebiel R. 320-slice CT neuroimaging: initial clinical experience and image quality evaluation. Br J Radiol 2009;82:561-70.
Cohen SD, Goins JL, Butler SG, Morris PP, Browne JD. Dural arteriovenous fistula: Diagnosis, treatment, and outcomes. Laryngoscope 2009;119:293-7.
Nishimura S, Hirai T, Sasao A, Kitajima M, Morioka M, Kai Y, et al
. Evaluation of dural arteriovenous fistulas with 4D contrast-enhanced MR angiography at 3T. AJNR Am J Neuroradiol 2010;31:80-5.
Farb RI, Agid R, Willinsky RA, Johnstone DM, Terbrugge KG. Cranial dural arteriovenous fistula: Diagnosis and classification with time-resolved MR angiography at 3T. AJNR Am J Neuroradiol 2009;30:1546-51.
Koenigsberg RA. Spontaneous pulsatile tinnitus secondary to a dural malformation not visualized by magnetic resonance angiography. Clin Imaging 1996;20:95-8.
Nogueira RG, Dabus G, Rabinov JD, Eskey CJ, Ogilvy CS, Hirsch JA, et al
. Preliminary experience with onyx embolization for the treatment of intracranial dural arteriovenous fistulas. AJNR Am J Neuroradiol 2008;29:91-7.
Kawaguchi S, Sakaki T, Morimoto T, Hoshida T, Nakase H. Surgery for dural arteriovenous fistula in superior sagittal sinus and transverse sigmoid sinus. J Clin Neurosci 2000;7 Suppl 1:47-9.
Hoh BL, Choudhri TF, Connolly ES Jr., Solomon RA. Surgical management of high-grade intracranial dural arteriovenous fistulas: Leptomeningeal venous disruption without nidus excision. Neurosurgery 1998;42:796-804.
Mironov A. Selective transvenous embolization of dural fistulas without occlusion of the dural sinus. AJNR Am J Neuroradiol 1998;19:389-91.
Cognard C, Januel AC, Silva NA Jr., Tall P. Endovascular treatment of intracranial dural arteriovenous fistulas with cortical venous drainage: New management using Onyx. AJNR Am J Neuroradiol 2008;29:235-41.
Toulgoat F, Mounayer C, Tulio Salles Rezende M, et al.
Transarterial embolization of intracranial dural arteriovenous malformations with ethylene vinyl alcohol copolymer (Onyx18) [in French]. J Neuroradiol 2006;33:105-14.
Kiyosue H, Hori Y, Okahara M, Tanoue S, Sagara Y, Matsumoto S, et al
. Treatment of intracranial dural arteriovenous fistulas: current strategies based on location and hemodynamics, and alternative techniques of transcatheter embolization. Radiographics. 2004;24:1637-53.
Tomak PR, Cloft HJ, Kaga A, Cawley CM, Dion J, Barrow DL. Evolution of the management of tentorial dural arteriovenous malformations. Neurosurgery 2003;52:750-60.
Guedin P, Gaillard S, Boulin A, Condette-Auliac S, Bourdain F, Guieu S, et al
. Therapeutic management of intracranial dural arteriovenous shunts with leptomeningeal venous drainage: Report of 53 consecutive patients with emphasis on transarterial embolization with acrylic glue. J Neurosurg 2010;112:603-10.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]
[Table 1], [Table 2], [Table 3], [Table 4]