The Neuroradiology Journal 19: 537-549, 2006
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Endovascular Therapy for Intracranial Dural Arteriovenous Fistulas W.K.W. CHONG*, M. HOLT** * Interventional Neuroradiology Unit, Diagnostic Imaging, Monash Medical Centre; Clayton, Victoria, Australia ** Diagnostic Imaging, Monash Medical Centre; Clayton, Vic, Australia
Key words: dural arteriovenous fistulas, embolisation, endovascular therapy, N-butyl cyanoacrylate, DAVF
SUMMARY – A retrospective study was conducted on 17 consecutive patients with DAVF admitted to Monash Medical Centre over 12 years. 15 patients, 82.4%, were treated by endovascular means with the intention to obliterate the fistula. Three of these patients also had surgery following embolisation. Angiographic cure was achieved when we have successfully embolised both the arterial and the venous side whether by penetration of liquid adhesive or packing with coils. Our cure rate of 60% (95% CI: 37-83%) compare favourably with published results of 50 to 70%. Our clinical complication rate is 1/15, 6%; and technical complication is1 from 32 embolisation sessions, 3.1%. Endovascular therapy is effective in achieving a durable angiographic and clinical cure in the treatment of intracranial DAVF. Both arterial and venous side need to be occluded.
Introduction The aim of this study is to determine the efficacy of endovascular treatment of intracranial dural arteriovenous fistulas (DAVF) in a single Australian centre. Intracranial dural arteriovenous fistulas are arteriovenous shunting which have developed within the walls of the dural sinus. The essential abnormality found was a connection between the dural arteries and the dural veins within the venous sinus wall, through small vessels (“crack-like vessels”) averaging approximately 30 micron in diameter. DAVF are accepted to be acquired lesions, which develop in middle to late adulthood 1. However, the pathogenesis is still debated. Some DAVF are associated with thrombosis or occlusion of a dural venous sinus, with the implication of a causal link. The natural history is varied. The so called nonaggressive or benign DAVF tend to remain clinically stable over long period of time and 18 to 50 % of this lesion may resolve spontaneously. However, some of these patients may suddenly exhibit paradoxical aggressive clinical behaviour. A significant proportion of DAVF have aggressive behaviour leading to
haemorrhage and ischaemic stroke, seizures, central nervous system depression, intractable headache, hydrocephalus, myelopathy, visual impairment and dementia among others. Therefore there is no question to treat the aggressive ones 1,2. These lesions may be treated with embolisation, operative surgery, stereotactic radiosurgery or with various combinations of the above 3,4,5,6,7,8,9,10,11,12 . Radiosurgery with or without prior embolisation, has a role. O’leary reported angiographic cure in 10 out of 13 patients with one deterioration 9. However, they also reported that 3 patients developed cerebral infarcts months after radiosurgery. Embolisation by itself has an angiographic cure rate of between 50% to 70% 4,6,14,15,16. Permanent complication rates varied from 5% to 12% 14. With the advent of safer and more effective endovascular technique, the threshold to perform both palliative and curative procedures by endovascular means has been substantially lowered. Embolisation with particulate material such as polyvinyl alcohol (PVA) and proximal coil embolisation of feeder arteries do not provide permanent cure. Durable cure may be achieved by transarterial, transvenous or 537
Endovascular Therapy for Intracranial Dural Arteriovenous Fistulas
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A
B
C
D
by a combined approach using liquid adhesives such as N-butyl cyanoacrylate (NBCA) or Onyx in the transarterial route or with coil occlusion of the involved venous sinus 2,12,14. The nidus itself and the venous side of the fistula need to be occluded for cure. More recently, recanalisation and stenting of an occluded transverse/sigmoid sinus resulted in a cure 9.
Methods
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A retrospective study was conducted on 17 consecutive patients admitted to Monash Medical Centre with the diagnosis of intracranial dural arteriovenous fistulas (DAVF) between October 1991 and May 2004 (12 ½ years). The inclusion criteria were all patients who had DAVF involving intracranial dural sinuses
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The Neuroradiology Journal 19: 537-549, 2006
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F
Figure 1 Patient 6. Fifty-one year old female with right sigmoid and transverse sinus DAVF. Note that the sinuses are patent but there is a severe stenosis in the sigmoid sinus. Main arterial pedicles from meningeal branch of right vertebral (A), middle meningeal (B) and occipital (C) arteries. 2 carotid wall stents were deployed within the sigmoid sinus (D). 12 months after the 4th embolisation session there was only a small amount of fistulation from the MMA (E) and occipital arteries (F) with still some cortical reflux. All symptoms resolved.
Table 1 Cognard Classification of DAVF
Type
Venous Drainage
Type I
Sinus Only - Antegrade Flow
Type IIa
Into Sinus - Reflux Into Sinuses
IIb
Into Sinus - Reflux Into Cortical Veins
Type III
Directly Into Cortical Veins
Type IV
Directly Into Cortical Veins - Venous Ectasia
Type V
Into Spinal Perimedullary Veins
with or without intracranial venous reflux. These included 1 case of indirect carotid cavernous fistula (CCF). Patients with fistula draining directly into spinal perimedullary veins without concomitant cortical reflux, purely spinal DAVF, and direct (type 1) CCF were excluded. Therefore the patients corresponded to Cognard 13 Type I to V (table 1 & table 2).
15 of the 17 patients, 82.4%, were treated by endovascular means. Three of these patients also had surgery following embolisation. 2 patients had surgery only (table 3 & table 4). Both of these patients had anterior cranial fossa DAVF, one spontaneous and one following a motor vehicle accident 16 years prior. In both patients, the neurosurgeons decide to operate without first attempting embolisation. 539
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Table 2 Location and Cognard Classification of Treated DAVF Patient
Age (years)/sex
Type
1
59/female
I
2
76/female
3
Fistula Location
Presentation
Arterial pedicles
Venous drainage
Rt Sigmoid Sinus
Pulsatile tinnitus
Rt Occip, AscPh, MMA, MHT
Rt Sigmoid Sinus. Rt transverse sinus occluded No cortical venous reflux
II b
Rt superior petrosal sinus
Subarachnoid haemorrhage
Rt MMA, Occip, MHT, PICA
Cortical venous reflux into transverse/sigmoid sinus Superior petorsal sinus occluded Spheno-bregmatic venous aneurysm
58/female
II b
Superior sagittal sinus
Intraventricular haemorrhage
Bil Occip, MMA. Bil Meng Br of Vertebral
Superior sagittal Sinus All sinuses patent Extensive Rt occipital cortical venous reflux
4
51/male
II b
Lt transverse sinus
Lt occipital & temporal lobe haemorrhage
Bil Occip. Lt MMA, Meng Br of Vertebral
Lt transverse sinus Lt sigmoid sinus occluded. Stenosis in Lt transverse sinus Extensive cortical venous reflux in occipital region
5
79/female
II b
Superior sagittal sinus
Confusion, dysphasia
Bil MMA
Superior sagittal sinus Occluded posterior superior sagittal & Lt transverse sinus Extensive cortical venous reflux in Lt parietal, temporal & occipital region
6
51/female
II b
Rt sigmoid & transverse sinus
Tinnitus & headache
Bil Meng Br of Vertebral RT MMA, Occip, AscPh, MHT
Rt sigmoid & transverse sinus All sinuses patent, Stenosis of sigmoid sinus Extensive cortical venous reflux in Rt temporal & occipital region
7
28/male
II b
Superior sagittal sinus
Headaches
Bil Occip, MMA Lt Meng Br of Vertebral
Superior sagittal sinus All sinuses patent. Extensive cortical venous reflux Venous varix adjacent to superior sagittal sinus
8
33/male
II b
Rt sigmoid sinus
Headache and tinnitus after recent head injury
Rt Occip
Posterior fossa veins into patent transverse sinus Distal sigmoid sinus occluded Posterior fossa cortical venous reflux
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The Neuroradiology Journal 19: 537-549, 2006
Table 2 (cont’d) Location and Cognard Classification of Treated DAVF Fistula Location
Presentation
Arterial pedicles
Venous drainage
II b
Superior sagittal sinus
Cosmetic, prominent vein on forehead
Rt MMA, Occip, STA, Meng Br of Vertebral, Ethm Br of Opth
Superior sagittal sinus Anterior superior sagittal sinus occluded Extensive Cortical venous reflux
53/male
III
Lt parietal cortical vein
Lt Occipital haemorrhage
Lt MMA, AscPh
Cortical venous reflux drained into superior sagittal sinus All sinuses patent
11
46/male
IV
Lt occipital cortical vein
Subarachnoid haemorrhage preceded by tinnitus
Lt MMA, Occip.
Single pial vein containing 6 mm venous aneurysm drained into superior sagittal sinus All sinuses patent Cortical venous reflux
12
55/male
IV
Lt frontal cortical vein
Severe headache
Lt Occip, MMA, STA
Cortical venous reflux drained into superio sagittal sinus All sinus patent
13
69/male
IV
Lt superior petrosal sinus
Headache, Lt ear deafness & ataxia
LT MMA, Occip, Int Max
Drained into giant venous varix at occluded superior petrosal sinus Varix drained into straight sinus Lt transverse sinus occluded Posterior fossa cortical venous reflux
14
20/male
V
Marginal/ occipital sinus
Sudden dizziness, vomiting and headache
Rt Occip, Meng Br of Vertebral
Drained directly into spinal perimedullary veins Near occlusion of transverse sinus
15
66/male
Indirect Rt CCF
Rt cavernous Sinus
Rt trochlear nerve palsy, ptosis, tinnitus
Bil ICA Rt Int Max, MMA, Ethm Br of Opth
Superior & Inferior opthalmic veins into angular vein of face Occluded superior & inferior petrosal sinus No cortical venous reflux
Patient
Age (years)/sex
Type
9
36/male
10
List of Abbreviations Used in Tables 2 and 3 – MMA middle meningeal artery; PICA posterior inferior cerebellar artery; MHT meningo hypophyseal trunk; Meng Br of Vertebral meningeal branch of vertebral artery; Occip occipital artery; Asc Phg ascending pharyngeal artery; Rt right; Lt left; Bil bilateral; Int Max Internal maxillary artery; STA superficial temporal artery; PVA polyvinyl alcohol particles; CCF carotid cavernous fistula; ICA internal carotid arteries; Ethm Br of Opth Ethmoidal branch of ophthalmic artery; NBCA N-butylcyanoacrylate; Angio angiogram
Embolization Methods These are discussed in detail in table 3. All embolization were performed as inpatient procedures. Diagnostic angiograms were first per-
formed and the cases were discussed with the neurosurgical team before the interventional procedures were performed. Except for 2 patients (cases 2 and 5), the majority of the procedures were performed under general anaes541
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W.K.W. Chong
Table 3 Treatment details and follow up
Transarterial/ Transvenous
Embolic agent
Immediate Outcome after last embolisation session
Follow up: Angiographic/ Clinical after last embolisation session
Patient
Number of Embolization sessions
1
2
Rt Occip, MMA.
20-25% NBCA
Fistula persists
None
6 weeks: No tinnitus No clinical symptoms No angio follow up
2
3
Rt MMA, Occip, MHT.
150-500 micron PVA
Fistula persists
Transient left arm weakness Recovered after several days
12 months: Fistula persists Decreased cortical reflux Patient well
3
2
Rt & Lt MMA
20% NBCA
Fistula persists
None
Surgery 2 days post embolisation 1 year: Fistula occluded Patient well
4
2
Lt Occip
50% NBCA
None
Lt MMA, Occip
Onyx 18
Fistula persists, but decreased
1 month: Fistula occluded No further haemorrhage
1
Sigmoid sinus
Non retrievable microcoils, Detachable Platinum coils (total 46)
5
2
Rt & Lt MMA
50% NBCA
Fistula occluded
None
No follow up
6
4
Bil Meng Br of Vertebral RT MMA, Occip, AscPh,
150-500 micron PVA, 20% NBCA,
Wire perforation of MMA. Treated with NBCA
Sigmoid sinus
2xCarotid Wallsetents, Detachable Platinum coils (total 20), Onyx 18 & 34.
Fistula persists, but nearly occluded Supplied by Lt Meng Br of Vertebral Stent and sigmoid sinus Thrombosed
7 months after 3rd embolisation Small persistent fistulation from Lt Meng Br of Vertebral Tinnitus and headache resolved No symptoms from perforation
LT Occip
150-500 micron PVA & 50% NBCA
None
Lt MMA
60% NBCA & 6% Embolyx
Surgery 3 days post embolisation 19 months: Fistula occluded Patient well
Rt MMA
40% NBCA & 6% Embolyx
Fistula persists, 90% embolised Residual pedicle from Lt Meng Br of Vertebral.
RT Occip
30-40% NBCA
Fistula occluded
None
Immediate: Tinnitus & bruit resolved No long term follow up
7
8
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3
2
Clinical Complication
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The Neuroradiology Journal 19: 537-549, 2006
Table 3 (cont’d) Treatment details and follow up Immediate Outcome after last embolisation session
Follow up: Angiographic/ Clinical after last embolisation session
Patient
Number of Embolisation sessions
9
3
& Lt MMA, STA
Embolyx 6%
Fistula persists
None
Surgery 2 days post embolisation 21 months: Fistula occluded Patient well
10
1
Lt MMA
60% NBCA
Fistula occluded
None
6 months: Fistula occluded Patient well
11
1
Lt MMA
40% NBCA
Fistula occluded
None
60 months: Fistula occluded Patient well, but intermittent tinnitus
12
1
Lt MMA
Onyx 34
None
Rt MMA
40% NBCA
Fistula occluded
6 months: Clinical only-symptom free
LT MMA, Occip
20% NBCA
None
Lt Int Max
150-250 micron PVA
Fistula occluded
Lt MHT
20% NBCA
12 months: Fistula occluded Symptoms almost completely resolved Patient well
Venous Varix
Detachable Platinum coils (total 8) & 1 ml absolute alcohol
13
2
Transarterial/ Transvenous
Embolic agent
Clinical Complication
14
1
Rt occip
20% NBCA
Fistula occluded
None
2 months: readmitted with headache but normal CT. No angiogram
15
2
Rt MMA
20% NBCA
None
Rt Cavernous sinus
Detachable Platinum coils (total 21) 80 % cavernoussinus packed
Fistula persists, but decreased
3 months: Fistula occluded Patient well, no symptoms
thetics which greatly facilitated the procedures due to lack of patient movement and patient discomfort. The number of embolization sessions varied from 1 to 4 per patient. There was no provocative testing used for any of the embolisation. Full heparinisation was used in all patients with an initial bolus dose of 5000 units and additional doses were use to keep the Activated Clotting Time (ACT) to about 200. The
heparin was allowed to wear off after the procedure. There was no post procedural anticoagulation or routine use of anti-platelet agents. Antibiotics were used if the arterial punctures were closed with percutaneous closure devices (Perclose - Abbot Vascular, Redwood City, CA, USA and Angioseal - St. Jude Medical, Minnetonka, Mn, USA). Five or six french guide catheters, Envoy MPC (Cordis Corporation, Miami 543
Endovascular Therapy for Intracranial Dural Arteriovenous Fistulas
W.K.W. Chong
A
B
C
D
Table 4 Treatment methods and results - 16 patients
Embolization only
Number cured with embolization only
Embolization & Surgery
Number cured with embolization & surgery
Surgery only
Number cured with surgery only
12
9
3
3
2
2
Florida, USA) and Fasguide (Boston Scientific, Fermont, California, USA) were used to access the carotid and vertebral arteries and the internal jugular veins in the neck. Via the guide 544
catheters, various combinations of microcatheters and microguidewires were used to cannulate the feeding arterial pedicles with the aim of reaching the fistula itself or as close to it as
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The Neuroradiology Journal 19: 537-549, 2006
E
F
G
H
Figure 2 Patient 13. Sixty-nine year old male. This patient has a Type III DAVF with the fistula draining directly into a giant varix located at the left superior petrosal sinus. Lateral arterial (A) and venous (B) phases. A renegade microcatheter has been navigated into the giant Varix via the transverse, sigmoid and straight sinuses and a tortuous peri-mesencephalic vein (C). The fistula was embolized with 8 coils and 1 ml of absolute alcohol was injected into the fistula via the varix. Note the residual fistulation from the meningo hypophyseal trunk of the internal carotid (D). The residual feeder from the meningo hypophyseal trunk was embolized with 20% NBCA resulting in occlusion of fistula (E). Follow-up angiogram at 12 months demonstrated complete closure of the fistula (F). Initial MRI (G) demonstrating giant varix in the posterior fossa. 12 months (H) follow-up MRI demonstrated that the varix has virtually disappeared.
possible. The microcatheters included Tracker 10, Tracker 18 and Renegade (Boston Scientific, Fermont, California, USA), and Ultraflow HPC (Microtherapeutics, Irvine, California, USA).
The microguidewires included Fasdasher-14 (Boston Scientific, Fermont, California, USA) and SilverSpeed-10 (Microtherapeutics, Irvine, California, USA). Embolic agents included 545
Endovascular Therapy for Intracranial Dural Arteriovenous Fistulas
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A
B
C
D
Table 5 Characteristics of DAVF presenting with Haemorrhage
Patient Number
Venous Aneurysm/Varix
Cortical venous reflux
Sinus Occlusion
Type
Location
2
+
+
+
IIb
Superior Petrosal sinus
3
–
+
–
IIb
Superiro rsagittal sinus
4
–
+
+
IIb
Transverse sinus
10
–
+
–
III
Lt parietal cortical vein
11
+
+
–
IV
Lt occipital cortical vein
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Figure 3 Patient 15. Sixty-six year old male. Note indirect right cavernous sinus fistula draining into the superior and inferior ophthalmic vein (A) and refluxing into the angular vein of the face (B). This was cannulated via ultrasound control to navigate a micro-catheter into the cavernous sinus. There was a major arterial pedicle from the middle meningeal artery (C) which was embolised with 20% NBCA (D). Dense packing was achieved with 21 coils (E). Six months follow-up demonstrated complete occlusion of the fistula (F).
150-250 and 355-500 microns polyvinyl alcohol particles (Contour, Boston Scientific, Fermont, California, USA), N-butylcyanoacrylate ( Histoacryl, B Braun Surgical, Germany) diluted to 20 to 60 % with iodised oil (Lipiodol Ultra Fluid, Guerbet, Aulnay-sous-Bois, France) and Onyx18 and Onyx-34(previously known as Embolyx 6% and 8%) Liquid Embolic System (Microtherapeutics, Irvine, California, USA). The venous side was embolised with non-retrievable Straight or Complex Helical Fibred Platinum Coils (Boston Scientific, Fermont, California, USA) retrievable detachable platinum coils (GDC, Boston Scientific, Fermont, California, USA) and Detachable Coil System, William Cook Europe, Bjaeverskov, Denmark). Review of clinical notes of the authors and review of patient medical histories and correspondence from referring doctors were used to determine the clinical status of the patients. There were three notable cases. In patient six (figure 1), two self expanding Carotid Wallstent Monorail (Boston Scientific, Fermont, California, USA) were initially inserted into the sigmoid sinus after pre dilatation with a 5 mm balloon in an attempt to open up the stenosis at the junction of the sig-
moid sinus and jugular bulb. The stents subsequently thrombosed along with the sigmoid sinus. GDC and Cook detachable coils were deposited in the sinus within the stent and in the vein of Labbe to stop the significant cortical reflux, subsequently Onyx 18 and Onyx 34 were deposited into the stent and the sigmoid sinus. Extensive embolisation was performed in the external carotid system and into the meningeal branches of the left vertebral artery. In case 13 (figure 2), a 69 year old male presented with headache, deafness in the left ear and ataxia. Trans arterial and venous embolisations were performed using NBCA, PVA particles, coils and absolute alcohol resulting in stable complete occlusion and resolution of symptoms at 12 months follow up. In case 15 (figure 3), ultrasound guided puncture of the angular vein on the face was used to gain retrograde access to the cavernous sinus. Results These are discussed in detail in table 3 and 4. Of the initial 17 patients, there were 6 females and 11 males. The patients’ ages ranged 547
Endovascular Therapy for Intracranial Dural Arteriovenous Fistulas
from 20 to 79 years. Cognard Type IIb was the most common (8/17, 47.1%) and all of these involved either the superior sagittal or the transverse/sigmoid sinus. Both anterior cranial fossa DAVF patients who went directly to surgery had Type III lesions. Superior sagittal and transverse/sigmoid lesions were the most common (4 each). There were 6 lesions draining directly into cortical veins, without or with venous aneurysm or varix, Type III and IV. All patients presenting with haemorrhages had venous cortical reflux, but the converse was not true as some patients with extensive reflux only had minor symptoms such as tinnitus and mild headaches. The 2 patients with venous aneurysm presented with subarachnoid haemorrhage (patient 2 and patient 11). The remainder of the results relate to the group of 15 patients where embolisation was first attempted with the intention to obliterate the fistula (table 3, table 4). 9 patients (60%) had obliteration of the fistula by embolisation alone. Of note, obliteration of the fistula was observed in 7 of these patients immediately after the last session of embolisation. 3 patients had angiogram follow up at 6, 12 and 60 months which confirmed the durability of the occlusion. None of these patients had recurrence of haemorrhage and all symptoms either markedly or completely resolved. The other 4 of these patients had no angiogram follow up, but 1 of these patients (number 12) waiting for a 12 month follow up angiogram remain symptom free 6 months later. The patient with the Type V lesion presented 2 months later with headaches but was neurologically normal and had a normal CT scan. He was discharged without a follow up angiogram. The other 2 were lost to follow up. 2 of the original 9 patients (patient 4, 15), had their fistulae nearly occluded at the time of the last embolisation session went on to complete occlusion at the 3 and 1 months angiogram follow up. 3 patients (Patients 3, 7, 9) went on to surgery 2-3 days after the last session of embolisation and all had angiographic cure at 12, 19 and 21 month follow up. 2 patients (number 1 and 2) had no further treatment despite persistent of fistula. However, 1 patient (number 1) had complete resolution of symptoms after 6 weeks. The other patient (number 2) aged 76 was 548
W.K.W. Chong
considered unfit for extensive cranial surgery, but had no recurrence of haemorrhage at 12 months. Complications There were only 2 complications. The first DAVF patient (number 2) that we treated in 1991 had a transient left arm weakness which recovered after a few days. This was the only clinical complication. The other complication was a wire perforation of the right middle meningeal artery during cannulation, the perforation was occluded with NBCA and the patient did not suffer any clinical sequelae. Discussion It would appear that cortical venous reflux is related to parenchymal haemorrhage and that venous aneurysm to subarachnoid haemorrhage. However, location of the lesion and the type is not crucial (table 5). It can take multiple sessions to successfully treat DAVF. All of the patients that we have achieved angiographic cure were those patients that we have successfully treated both the fistula and the venous side whether by penetration of liquid adhesive or packing with coils. Those DAVF that we failed to achieve this persisted and did not close. We used PVA particle only as a supplementary embolic agent, particularly if we were unable to get close to the nidus with the microcatheter. Our cure rate of 60% compare favourably with published results of 50 to 70 % 4,6,14,15,16 Whilst 7 of the 9 patients had immediate occlusion following the last session of embolisation, the other 2 (number 4 & 15) went on to occlude 1 to 3 months afterwards. This suggests that waiting a short period of time after the lesion is substantially treated would an appropriate strategy. Symptoms either resolved or improved and there were no recurrence of haemorrhage after the fistulae was occluded confirming that the treatment is effective. For 1 of the 3 patients (number 7) who went on to surgery after embolisation, the neurosurgeons were able to perform a smaller operation around the residual fistula site than they would have to do otherwise. Combination of embolisation and surgery is effective for large complex lesions. Partial but significant occlu-
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sion can relieve symptoms especially tinnitus and headaches (number 1 & 6 ). Our complication rate is excellent compared to reports of 5% to 12 % permanent deficit 14. On percentage terms, we had 1/15 (6.0%) for temporary clinical deficit and 1 technical complication out of a total of 32 embolisation sessions, that is, 3.1%.
The Neuroradiology Journal 19: 537-549, 2006
Conclusion Endovascular therapy is effective in achieving a durable angiographic and clinical cure in the treatment of intracranial DAVF. However, multiple sessions may be needed. Both the fistula and the venous side need to be embolised. Complication rate is low.
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13 Cognard C, Gobin YP, Pierot L et Al: Cerebral dural arteriovenous fistulas: clinical and angiographic correlation with a revised classification of venous drainage. Radiology 194: 671-80, 1995. 14 Halback VV, Higashida RT, Hieshima GB: Endovascular Therapy of Dural Fistulas. In: Vinuela F, Halback VV, Dion JE: Interventional Neuroradiology:Endovascular Therapy of the Central Nervous System, Raven Press, New York 1992: 29-50. 15 Berenstetin A: Dural arteriovenous malformations. Seventh annual Stowin medial conference abstracts. Am J Neuroradiol 11: 221-222. 16 Picard L, Bracard S, MalletJ et Al: Spontaneous dural arteriovenous fistulas. Seminar Intervent Radiol 4: 219-240, 1987.
Chong W, MD Interventional Neuroradiology Unit Diagnostic Imaging Monash Medical Centre Locked Bag No. 29 Clayton - Victoria 3168 Australia E-mail:
[email protected] Tel.: + 613 9594 2200 Fax.: + 613 9594 6029
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