04.11.2019 • 63 yo • SHA • VII cn paresis , • Orbital pain • Dizziness Natural history and Salvatore Mangiafico Interventional Nurovascular unit classification of dAVF Careggi University Hospital Florence 12 34 second case: SHA 56 04.11.2019 Third Case: seizure 78 a problem is always made of several questions and its solution is always to anwser to each one of them • Is it a A‐V malformation ? • May this A‐V shunt explain the clincal presentation? the problem is how to treat it ? • Wich is its possible evolution ? • Where the A‐V shunt is it • Wich way to follow to occlude it ? 910 Dural Arterior Venous Fistulas (DAVF) are acquaided vascular «malformations» DAVF account for approximately 10–15% of all intracranial with un unknown aetiology or secondary vascular malformations due to trhombophilic state, phlogistitic or traumatic process in wich multiple 0.16 per 100 000 per year approximately 12.5%of all arteriovenous shunts develop inside dural intracranial AVMs vascular stuctures without the interposition of a malformative nidus. the mean age of presentation is between 50 and 60 years. DAVF are almost exclusively supplied by meningeal arteries arising from esternal , in Japan 0,29 a 100.000 su 1815 casi Acta Neuroch Suppl 2016 internal carotid and vertebral arteries and rarely from intracranial pial branches Venous drainage can be formed between dural sinus, cortical veins or both 11 12 04.11.2019 Etiopathogenesis : Neo vascularization and venous 3 theories Menigeal arteries have no connection dilatation are induced by an with the sinus and cortical veins (BV) inflammatory process 1)venous sinus occlusion precedes and is 2)DAVFs arise from naturally occurring dormant directly responsible for development of the channels between dural arteries and sinuses, which fistula. Venous sinus thrombosis results in the open when the sinus is occluded and venous pressure is release of angiogenic factors from increased(Pitonet al., 1984; Mullan, 1994). theorganizing thrombus, which subsequently leads to the invasion of small dural arteries and formation of small dural arterio venous 3) Venous hypertension may lead to tissue hypoxia shunts(Houseretal.,1979). and increased production of angiogenic factors, which promote endothelial proliferation and neoangiogenesis (Lawton et al., 1997; Tirakotai et al., 2004; Kojima et al., 2007). 13 14 sinus‐type DAV Fistulas no‐sinus type DAV Fistulas the inflammatory processes and the inflammatory processes throbososis effect a long segment of a and throbosis effect the dural dural sinus It starts from the wall segment of a bridging vein inside the sinus Opening of Dural AV Thrombosis of the EV shunt and increases the AV flow Sinus occlusion and penetration of dural Inside the Sinus and EV, reflux in BV arteries inside the Recruitment of other Recruitment of trans sinus Dural feeders osseus feeders 15 16 Hystology • Histologic studies suggests that microscopic thrombosis is always present and plays an important role in the release of growth factors and theformation o fDAVFs (Uranishi et al., 1999). Site od origin of the DAVF • In immuno‐histochemical studies, expression of basic fibroblast growth factor and vascular endothelial growth factor has been identified in the wall of the dural sinuses in patients withD AVFs (Teradaetal., 1996; Uranishi et al., 1999). 17 18 04.11.2019 • The exact site of the original lesion ( EV , DS , BV) may dictate the arterial CDAVF feeders of the lesions, their venous drainage pattern, and as a consequence, their tendency for a certain clinical behavior. • CDAVFs may develop in three distinct levels of the cranial venous system 3 • the bridging veins, BV ,(1) • the dural sinuses, DS ( 2) , • and the emissary veins, EV (3 ). 2 1 19 20 dural entrances of the BVs are 1) DAVF of the EV overlapped by a layer of ( osteodural sinus type DAVF) numerous small meningeal Emissary veins pass with cranial nerves through apertures in the cranial wall and veins and venous lacunae establish communication between the sinuses inside the skull and the veins external to it (arrowhead) • mastoid emissary vein • veins in the hypoglossal canal • The parietal emissary • Cavernous sinus • The occipital emissary vein • emissary veins of the middle fossa • posterior condylar vein through the foramen ovale, rotundum, lacerum, • temporal emissary • inferior petrosal sinus has also the • superficial petrosal vein position and function of an emissary • meningo‐orbital vein vein connecting the cavernous sinus with the jugular vein 21 22 2 ) DAVF of the SINUS wlall CDAVFs of an Emissary Vein (EV) pure sinus type DAVF • drain mostly to the sinus and not directly the cortical venous Periostal – dural sinus DAVF system Dural –dural sinus DAVF Sinus at the convexity • • Falcine sinus recruits additionally osseous • Superior sagittal sinus arterial feeders • Sinis rectus Base and posterior fossa sinus • adds“purely meningeal” • Tentorial sinus • Transverse sinus branches as the middle • Sigmoid sinus meningeal artery, posterior • Occipital sinus meningeal, or meningeal • branches of the ICA. Torcular 23 24 04.11.2019 3) DAVF of the BV( non‐sinus DAVF) (veno‐sinusal Junction) • The distal segment of a BV embryologically, anatomically, and histologically seems to be part of the dural system. • The BVs are closely attached to the inner dural surface and have a shorter or longer intradural course before they enter the sinus [75]. Therefore,from the embryological point of view, the distal BV segment, veno‐sinusal junction, appears to belong to the dural system. Tentorial sinus DAVF 25 26 Hui Han Neurosurgery 67; 2010 BV DAV shunt ( two subtypes) Comunicating vein • arteriovenous dural shunt can be primarily located on a bridging vein , the veno‐sinus junction is patent ; the A‐V fow is directed towards the sinus and mainly toward the pial vein • thrombosis of the venous –sinus Junction, the shunt venous drainage is exclusively cortical. a BV (arrow) from the occipital lobe (O) drains the BVs (arrows) directly entering the dural Disconneted bridging into the meningeal vein (arrowhead) in the sinuses (asterisks) in the middle cranial fossa. vein cerebral falx (F) before entering the SSS Arrowheads indicate the dural entrance sites (asterisk). vein) 27 28 Comunicanting BV Is the Sinus filling is syncronous with the BV’s 29 30 04.11.2019 Disconnected Bridging vein The Dural AV sunt is on the BV at the conjunction point with Sinus and it does not communicate with the sinus unique drainage trhotugh a pial vein that runs along the falx cerebri Sinus opacifization is delayed 31 32 The natural history of cranial dural arteriovenous malformations (AVM's) is highly variable Natural history • In adults the natural history of DAVFs is influenced by 1. the pattern of venous drainage 2. the presenting symptoms 3. localization 33 34 The natural history of cranial dural arteriovenous malformations (AVM's) is highly variable • In adults the natural history of DAVFs is influenced by 1. the pattern of venous drainage DAVFs without CVD 2. the presenting symptoms Sinus type DAVF 3. localization 35 36 04.11.2019 DAVF without CVD DAVF with CVD ( cerebral vein drainage) • a benign clinic course was observed in 98.5% of the patients • annual rate of conversion to a higher • Syntomatology : bruit grade DAVF of 1%‐1.5% angiographic progression to a more aggressive fistula • Managed conservatively • if treatment is contemplated it should not be too aggressive • Follow up of DAVF without VCD (Borden type I) fistulas is generally recommended Bridging vein type DAVF sinus type DAVF with CVD 37 38 • DAVFs that acquire cortical venin dreinage (CVD) can present with aggressive clinical features, including either ICH or nonhemorrhagic neurologic deficits (NHNDs) • The annual ICH, NHND, and related to focal or regional venous hypertension mortality rate was 7.6%, 11%, and • Or progressive clinical features 3.8% (Strom and colleagues (2009 in a dementia,seizures,parkinsonism,or ataxia due series of 28 patients with DAVFs with CVD) to cerebral edema or ischemia related to diffuse and extensive venous hypertension • annual ICH rate o f 8.1%,NHND rate (Barrow et al., 1985; Lasjaunias et al., 1986;Awad etal.,1990). of 6.9%, and a combined annual event rate of 15% • DAVFs draining into perimedullary spinal veins may cause myelopathy and progressive (Toronto Brain Vascular Malformation tetraplegia Group : 20 DAVFs with CVD that were followed over a 4‐year period ) (Hurst et al., 1999; Lv et al., 2011). 39 40 The natural history of cranial dural arteriovenous physiopathology malformations (AVM's) is highly variable Parenchimal Hem Parenchimal ischemia • In adults the natural history of DAVFs is influenced by ICH is believed to occur from rupture parenchymal ischemia is thought to occur from venous congestion and hypertension, of fragile parenchymal veins as a result 1. the pattern of venous drainage of exposure to increased pressure from Crhronic venous congestion prevents 2. the presenting symptoms retrograde venous reflux.. adequate arterial delivery of oxygen and removal of metabolic byproducts within the 3. localization surrounding parenchyma 41 42 04.11.2019 Difference in natural Hystory according to the clinical presentation • asymptmaic patients : Clinical features of CDVF presenting annual ICH, NHND, and mortality rate was 1.4%, 0%, and 0% with hemorrhage • symptomatic patients : • The vast majority of patients the annual ICH, NHND, and mortality rate was 7.6%, 11%, and 3.8% were male (86%), and the most respectively in common presenting symptom