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Year : 1992  |  Volume : 38  |  Issue : 2  |  Page : 75-8

Endovascular treatment of cerebral arteriovenous malformations.

Dept of Neurosurgery, Seth G S Medical College & KEM Hospital, Parel, Bombay.

Correspondence Address:
A P Karapurkar
Dept of Neurosurgery, Seth G S Medical College & KEM Hospital, Parel, Bombay.

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Source of Support: None, Conflict of Interest: None

PMID: 0001432834

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Keywords: Human, Intracranial Arteriovenous Malformations, classification,diagnosis,therapy,Vascular Surgical Procedures, instrumentation,methods,trends,

How to cite this article:
Karapurkar A P. Endovascular treatment of cerebral arteriovenous malformations. J Postgrad Med 1992;38:75

How to cite this URL:
Karapurkar A P. Endovascular treatment of cerebral arteriovenous malformations. J Postgrad Med [serial online] 1992 [cited 2023 Sep 29];38:75. Available from:

The management of cerebral arteriovenous malformations (AVM) remains a debatable issue. Given the great advances in modern radiographic technology, newer catheters and embolic material on the one hand and the advances in microsurgical techniques on the other, this debate assumes great relevance. Despite the large number of long term follow up studies of untreated AVM, no clear guidelines regarding the management of unruptured AVM is forthcoming.

Review of the literature shows that the average risk of hemorrhage in patients with cerebral AVM is 1A3 approximately 2% per year[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13]. By 20 years, nearly 40% would have had a bleed. Most authors have found the incidence of hemorrhage to be highest in the small AVM. Graf[5] found a 10% risk of hemorrhage in patients having a small AVM in the first year and a risk of 52% at 5 years. Patients having large AVMs had no chance of a bleed in the first year, 10% would have bled in 5 years, 31 % in 10 years and 34% in 20 years. Brown[1] however found no difference in the risk of haemorrhage between small and large AVM. Waltimo[13] in a long-term study of the change in the size of AVM found that the small AVM enlarged with the passage of time, medium sized AVM remained unchanged and the large ones either remained unchanged or became smaller. The risk of a rebleed in the first five years varied from a high of 17.9%[4] to a low of 2.5%[2]. Recurrent hemorrhage does not increase the risk of mortality[4].

The aim of treatment today is to cure all AVMs since these, regardless of their size, bleed at the rate of about 2% every year and the risk rises to about 6% in a patient who has already had a bleed. The aim is to remove it surgically. If the AVM is large with a high flow through it, embolization is indicated to reduce its size so that it can then be treated by surgery. Large diffuse AVMs in functional areas, or large deep AVMs of the basal ganglia, thalamus and brain stem are inoperable. These are embolised and when less than 3 cm in size can be subjected to radiosurgery.

Many classifications[13],[14],[15] have been proposed to aid in deciding therapy. The earlier classifications, based on size alone, did not aid in decision making as the risk of intervention was not the same for a small AVM located on the superolateral surface as for a deep seated AVM located in the thalamus or basal ganglia. Spetzier[14] added 2 more criteria - eloquence of the adjacent brain and venous drainage (superficial or deep). The risk of intervention was highest in large AVMs, which were located in eloquent areas having a deep venous drainage. The risk was lowest in small superficial AVMs located in non-eloquent areas and had superficial venous drainage. He graded them from one to five according to the risk and added a sixth grade of large diffuse AVM, which he called inoperable. Shi[15] included four criteria in his classification - size, location, arterial supply and venous drainage.

Modern radiographic machines are dedicated to interventional neuroradiology[16],[17]. They are equipped with an isocentric C - arm. Simultaneous biplane filming and fluoroscopy reduce procedure time and the volume of contrast material used. Tomography and stereoscopic viewing help in better visualization of the lesion in three planes[18]. (To obtain stereoscopic views two series of exposures - at an angle of 5 degrees to each other - are made in lateral and ante ro- posterior planes. Seen through special stereoscopic lenses, such films give a very useful three dimensional view.) Magnification is necessary to identify small branches. Rapid sequential filming, sometimes at a rate oi 25 per second is necessary to properly demonstrate the blood supply in a high flow AVM. Previously existing shadows are eliminated in subtraction and there is better visualization of the contrast being injected. Formerly only photographic subtraction was possible. Today real time electronic subtraction allows the procedure to be visualized as it is being done. This is absolutely essential in interventional neuroradiology. Facilities such as road mapping permit superselective catherterization of tiny cerebral vessels. Special radiolucent headholders have been fabricated to allow intraoperative digital subtraction angiography (DSA) studies to assess extent of removal and to perform intraoperative embolization. High resolution tape recorders and floppy discs allow hard copies to be made on multiformat cameras effecting a big saving in cut firm cost. Laser printers reproduce high quality images. DSA also affects big savings on film cost because hard copies of only relevant films can be made.

Catheter materials have undergone a revolution over the last decade. Initially, only thick walled high torque catheters were available. These were replaced by thin walled low torque catheters, which allowed larger embolic materials to be injected. To allow catheterization of tortuous vessels, tapered catheters were designed [20]. These were replaced by silicone catheters, which were remarkably -supple and could be made to enter small arteries. However, as they had no torque control, they were flow guided. They were coiled in special chambers, which had three airtight outlets. Through one outlet, saline was infused to fill up the chamber; through the second, saline was injected to force the coiled catheter to advance through the third outlet into the artery[21],[22],[23]. However, as these were entirely flow guided leak balloons were added to these catheters to allow better navigation and to inject liquid embolic materials[21],[22],[23],[24],[25],[26],[27] Balloon catheters permitted the arrest of blood flow and better visualization of the AVM especially when it was a high flow AVM associated with an arteriovenous fistula. Arrest of flow also allowed better control when embolizing with liquid embolic materials such as isobutyl-2 cyanoacrylate. Picard and Moret[21] had devised a classification based on the flow though the AVM with the balloon inflated and deflated. Based on this classification they decided on the method of embolization.

As some workers had catastrophic ruptures of arteries due to over inflation of the balloon, catheters without balloons were developed[28],[29],[30],[31]. Benati[28] designed a winged catheter. Dion[28] described a progressive suppleness pursil catheter, which had a proximal polyethylene portion and a distal silicone portion. This allowed a certain amount of torque control and also retained the suppleness of a silicone catheter. To enhance the ability to navigate a catheter in tiny cerebral vessels, a Tracker catheter was fabricated which allowed the passage of fine platinum tipped guide wires, which could be navigated in cerebral vessels, such as the thalarn operf orators. Today, every single vessel in the brain from the anterior choroidal to the lenticulostriate vessels can be selectively catheterised. The Tracker catheter also allows the passage of microcoils, which can be placed in tiny cerebral vessels.

Along with catheters, embolic materials also have undergone a dramatic change. Leussenhop[32] had introduced the use of spheres coated with iron and later barium. These spheres were large and caused proximal occlusion of the feeders. Mullan[32] introduced smaller particles of silicone, which were injected through smaller catheters. Wolpert[34] suggested criteria to avoid erratic embolization. However, with the use of silastic spheres there was proximal occlusion with the nidus being untouched. With passage of time, there was recruitment of other feeders. Hence, a more permanent material was sought. Kerber[25] along with the leak balloon and silicone catheter introduced Isobutyl 2- cyanoacrylate, an acrylate which hardened as soon as it came in contact with an ionic solution such as blood or saline. To modify the polymerizing time, various amounts of [35],[36] pantopaque were added. If a fistula was associated with an AVM, pure IBC was injected. However, the drug was withdrawn by the FDA when reports of its carcinogenic properties were received[37]. A similar polymer N-butyl cyanoacrylate (NBCA) is now in clinical use[38]. Though some authors[21],[23],[38],[40] have demonstrated complete obliteration of the AVM, the risk of complications is much higher with the use of IBC and NBCA[38],[41],[42]. There are numerous reports of catheters getting glued to the artery because it could not be withdrawn quickly. There are also reports of hemorrhage due to rupture of arteries and the AVM when the balloon catheter is withdrawn[41],[42]. On long-term follow up, it has been shown that the IBC and NBCA do get reabsorbed[43],[44],[45],[46]. Hence, there is constant search for safer embolic materials. Polyvinyl alcohol sponge (PVA) is a nonabsorbable embolic material but it has been to shown to allow late recanalization[47],[48]. It can be injected through Tracker catheters. Mehta[50], Dion[51], Fox[52] and Horton[53] have introduced cocktails containing combinations of substances such as gelfoam, ethanol, Avitene and PVA. Polylene[54] or Silk[32],[58] suture, a mixture of estrogen - alcohol-polyvinyl acetate[55], ethyl-vinyl alcohol (EVAL), hydrogel spheres made from crosslinked polymethyl methacryate[58], have been tried. Microcoils are the latest acquisitions in the armamentarium of the interventional neuroradiologist. IBCS and NBCA are the only agents, which permit a permanent cure. All the other embolic materials are reabsorbable and hence can be used only as a preoperative measure to facilitate surgery, or to make the lesion small enough for radio surgery to be effective.

Leussenhop[58] first started endovascular therapy for AVM by introducing silastic-steel spheres through an open arteriotomy of the carotid artery. Mullan[33] introduced the spheres and later silastic pieces by the transfemoral route. The procedure could be repeated as often as necessary if the artery recanalised[60]. Staged embolization to eliminate the risk of break-through bleeding in normal brain surrounding the AVM (due to sudden increase in intra-arterial pressure in the hitherto ischemia brain) was also possible since the silicone spheres were floated freely in the main carotid or vertebral artery the rate of complication was high because of emboli straying into normal arteries, or causing too proximal an occlusion. Embolization in the anterior cerebral territory was difficult and perforating vessels could not be embolized with any degree of safety. Hence superselective catheterization and embolization became popular. It is usually difficult to enter perforating arteries. They can be entered via the opposite internal carotid-anterior communicator or via the vertebral and posterior communicator. Sometimes, it is necessary to inflate a balloon to occlude the parent artery beyond the origin of the perforator, so as to change the hemodynamics and allow entry of the catheter. This of course increases the risk of complications. To increase the safety of embolization when embolizing in functional territory the sodium amytal test is done by injecting 30mg in the feeder. If the test is negative then embolization is carried out. There is a 6% chance of a false negative test with ensuing complication if embolization is done. If it is positive, the artery is not embolised[21].

After Spetzier[61] described break through bleeding following one stage excision of high flow large AVM, it was realized[62] that embolization like surgery especially for large high flow AVM should be staged. The end point of a sitting of embolization is a significant change in the hemodynamics of the AVM, when new arteries are visualized, or when the size of the AVM has been reduced. It is difficult, sometimes to decide when to stop. Doing too much is irreversible and it is safer to do too little than to do too much. To determine the end point of asitting of embolization, various methods are followed. Arterial pressure is recorded from the microcatheter before and as embolization proceeds[63],[64]. Tarr[66] has described the assessment of cerebral vasoreactivity with serial xenon cerebral blood flow studies with acetazolamide challenge. Cromwell[67] and Spetzier[68] have combined surgery with embolization. A craniotomy is done, the feeding artery is exposed and a microcatheter is introduced. After angiography, the embolic material is injected.

Complications include rupture of vessels. These may be because of associated aneurysms or dysplastic vessels[68]. Often no treatment is needed. The resultant hole as soon as it is recognized had been closed with pure histoacryl or by placement of coils or balloons across the rent[21],[68].

Endovascular treatment of cerebral AVM has progressed by leaps and bounds. Yet, just 15-20% of AVMs can be cured by endovascular therapy alone. Small accessible AVMs can be cured by surgery. Small inaccessible AVMs should be treated by radiosurgery or linear accelerator. Medium and large AVM should be treated by endovascular therapy and the residual portion either excised or treated by radiosurgery or linear accelerator. Large inoperable AVM are best treated by the endovascular route to reduce the steal and mass effect. They may still not be amenable for surgery or radiosurgery.

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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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