J Neurosurg 75:655-660, 199 !
Embolization of arteriovenous malformations with peripheral aneurysms using ethylene vinyl alcohol copolymer Report of three cases TOMOAKI TERADA, M.D., YOSHINARI NAKAMURA, M.D., KUNIO NAKAI, M.D., MITSUHARU TSUURA~ M.D., TAKASHI NISHIGUCttI, M.D., SEIJI HAYASHI, M.D., TAKUHE[ Kmo, M.D., WAaO TAKI, M.D., HIaOO IWATA, PH.D., AND NoamtKo KOMAI, M.D.
Departments of Neurological Surgery, Wakayama Medical College, and Wakayama Rosai Hospital, Wakayama City; Department of Neurosurgery, Kyoto University Medical School, Kyoto; and Department of Surgical Research, National Cardiovascular Center, Osaka, Japan ~" The authors report three cases of arteriovenous malformations (AVM's) with aneurysms arising from the feeding artery; all were successfully treated with a new nonadhesive liquid embolic material, ethylene vinyl alcohol copolymer (EVAL). In two patients the AVM's were totally removed without difficulty, and in one the AVM was managed conservatively after embolization. No new neurological deficits appeared during or after embolization. After road-mapping techniques, EVAL was injected slowly until the feeding artery and aneurysm were completely obliterated. This embolic agent is easy to handle and is considered safe compared with other adhesive liquid embolic agents, such as isobutyl-2-cyanoacrylate or n-butyl cyanoacrylate. It is concluded that EVAL is an excellent agent for embolizing an AVM with a peripheral aneurysm on the feeding artery. KEY WORDS 9 arteriovenous malformation ethylene vinyl alcohol copolymer
T is well known that arteriovenous malformations (AVM's) may be associated with aneurysms on their feeding arteries. It is possible to treat the AVM causing the aneurysm to regress. However, rupture of an aneurysm may occur when these arteries are embolized, either from mechanical trauma due to the catheter or guidewire or from increased pressure from injection or closure of direct shunting. There is still controversy as to how these arteries should be embolized. An adhesive liquid embolic agent, such as isobutyl-2-cyanoacrylate (IBCA) or n-butyl cyanoacrylate (NBCA), can cause incomplete or too rigorous embolization because it is difficult to determine the appropriate dosage and to determine accurately the required polymerization time. Lt: Embolization using polyvinyl alcohol (PVA) can increase the risk of rupture of an aneurysm because it may occlude the nidus of the AVM and increase
I
J. Neurosurg./ Volume 75/October, 1991
9 aneurysm
9 embolization
9
intraluminal pressure of the feeding artery6 until retrograde thrombosis is complete. We treated three cases of AVM's with peripheral aneurysms arising from their feeding arteries by means of a new nonadhesive liquid embolic agent. ~ This agent, ethylene vinyl alcohol copolymer (EVAL), is useful for this type of embolization because it permits a serial injection to obliterate completely first the AVM then the aneurysm. Case Reports
Case 1 This 29-year-old man was admitted to his local hospital with a sudden severe headache on February 14, 1990. He suffered a second severe headache and became comatose several hours after admission. Computerized tomography (CT) showed cerebellar hemorrhage and 655
T. Terada, et al.
FIG. 1. Angiograms in Case 1. A: Left vertebral angiogram, lateral view, showing the arteriovenous malformation fed from the left anterior inferior cerebellar artery, (AICA) and the posterior inferior cerebellar artery. The aneuD, sm was seen arising from the A1CA (arrowhead). B: Left vertebral angiogram, anteroposterior view, demonstrating a distal AICA aneurysm (arrowhead). C: Superselective angiogram, lateral view, demonstrating the left AICA. D: Left vertebral angiogram, anteroposterior view, following embolization to the AICA. E and F: Postoperative left vertebral angiograms, lateral view (E) and anteroposterior view (F), showing preservation of the left AICA (arrows).
FIG. 2. Magnetic resonance spin-echo images (TR 500 msec, TE 30 msec) in Case I. A: Axial view, showing signal-void area in the base of the right cerebellar hemisphere. B: Axial view, showing the hematoma in the left cerebellar vermis as a high-intensity mass. C and D: Sagittal views showing that the hematoma was separate from the nidus of the arteriovenous malformation.
subarachnoid hemorrhage (SAH) in the posterior fossa with marked ventricular enlargement. Emergency arteriography revealed an AVM, fed by the left posterior inferior cerebellar artery and the left anterior inferior cerebellar artery (AICA) (Fig. 1A to C). Peripheral aneurysms were discovered on the distal segment of the left AICA. 656
Ventricular drainage was instituted, but the patient remained in a semicomatose state with severe tetraparesis. On February 27, 1990, he was transferred to our hospital for treatment. Magnetic resonance imaging confirmed that the ruptured AICA aneurysm was the cause of bleeding, as the hematoma cavity had no connection with the AVM (Fig. 2). Separate procedures J. Neurosurg~ / Volume 75/October, 1991
AVM embolization using ethylene vinyl alcohol copolymer
Ft(~. 3. Compulerized lomography scans in Casc 2. A and B: Admission scans showing cerebellar hemorrhage, subarachnoid hemorrhage,and hydrocephalus. C and D: Postembolizationscans demonstrating a low-densityarea on the uppcr surface of the cerebellum.
FtG. 4. Leftvertebralangiograms in Case 2 demonstrating a peripheral superior cerebellarartery aneurysm. A: Lateral view,arterial phase. B: Anteroposterior view, arterial phase. C: Lateral view,capillary phase. D: Anteroposterior view, capillary phase.
for embolization of the left AICA and of the aneurysm were planned because a simultaneous operation on both would have been difficult, given their different locations. Prior to embolization, the patient's condition improved and he became conscious. He had a left peripheral facial palsy, left lateral gaze palsy, moderate tetraparesis (grade 3/5), and bilateral severe cerebellar ataxia. A microcatheter* was navigated into the left AICA to a point just proximal to the aneurysm (Fig. IC). The patient's neurological condition and auditory brainstem responses were monitored during a selective sodium Amytal (amobarbital) test (40-rag dose) and remained unchanged. The feeding artery and aneurysm were then embolized by injection of 0.6 ml EVAL through the catheter (Fig. 1D). Following embolization, the patient's condition, including his auditory function, did not change. At surgery on May 11, 1990, the AVM was totally removed with minimal bleeding and without * Microcatheter manufactured by Target Therapeutics, Inc., San Jose, California. J. Neurosurg. / l/olume 75/October. 1991
neurological complication. Postoperative arteriography revealed that the aneurysm and AVM had completely disappeared while the AICA was preserved to the origin of the aneurysm (Fig. IE and F). Case 2
This 53-year-old man was admitted to our hospital because of disturbance in his level of consciousness following a severe headache on September 14, 1989. A CT scan demonstrated cerebellar hemorrhage, SAH, and marked hydrocephalus (Fig. 3A and B). Cerebral arteriography revealed an AVM fed from the AICA as well as duplicated superior cerebellar arteries (SCA's) with a peripheral aneurysm (Fig. 4). This ruptured peripheral aneurysm was suspected of having caused the bleeding found on CT. Ventricular drainage was performed on the day of admission, and the patient recovered consciousness the next day. However, a mild right hemiparesis, bilateral ataxia, and bilateral abducens palsy were noted. It was believed that total removal of the AVM by direct surgery would be difficult because of the size and 657
T. Terada, a al.
FIG. 5. Angiograms in Case 2. A and B: Superselectiveleft superior cerebellar artery (SCA) angiograms. In A the aneurysm is clearly opacified (arroa'head). and in B the aneurysm is completely obliterated with ethylene vinyl alcohol copolymer (arrowhead). The hemisphericand lower branches of the SCA are opacified. C and D: Left vertebral angiograms, laleral (C) and anteroposterior (D) views, followingembolization from the SCA. The arteriovenous malformation is decreased in size and fed mainly from the left anterior inferior eerebellararteD'.
location of the lesion, so embolization was planned for the duplicated SCA's, including the aneurysm. Normal arterial supply to the cerebellum was demonstrated distal to the peripheral SCA aneurysm. However, we concluded that no new neurological deficit would result from embolizing the SCA proximal to the aneurysm, because the left cerebellar peduncle was already injured by a massive cerebellar hemorrhage. On October 11, 1989, embolization was performed after a decrease in mass effect of the hematoma. A microcatheter was introduced into the upper SCA following negative results of Amytal testing. The catheter was advanced to a point just proximal to the origin of the peripheral aneurysm, and 0.6 ml of EVAL was injected through it to occlude the aneurysm completely (Fig. 5A and B). The inferior SCA was embolized by PVA particles (150 to 250 t~ in size) because, when appropriate, we routinely use preoperative PVA embolization for arteries feeding AVM's. After embolization, arteriography revealed that 80% of the AVM was occluded and no new neurological deficits were noted. On follow-up arteriography performed 189 months later, the feeding arteries and aneurysms had not recanatized (Fig. 5C and D), although retrograde thrombosis caused occlusion of both left SCA's, resulting in a small cerebellar infarct (Fig. 3C and D). The AVM was totally removed by the suboccipital approach without difficulty or additional neurological deficit. Case 3 This 46-year-old man was admitted to our hospital on February 2, 1990, because of SAH from a left thalamic AVM. He was in a semicomatose state with a fight hemiparesis. He had a history of SAH 12 years previously. A C T scan revealed a left thalamic hemorrhage and acute hydrocephalus. On bilateral ventricular drainage, his level of consciousness improved, but the
6fi8
severe right hemiparesis and aphasia persisted. Cerebral angiography revealed that the left thalamic AVM was fed mainly from the left medial posterior choroidai arteries. A peripheral aneurysm was found on the distal medial posterior choroidal artery (Fig. 6A to D). Embolization was planned for these feeding arteries because of the anticipated difficulty with a direct surgical resection. A microcatheter was introduced into the proximal portion of the aneurysm's feeding artery and 0.5 ml of EVAL was injected gradually until it completely filled the aneurysm (Fig. 6). Another feeding artery was embolized by the same procedure using 0.6 ml of EVAL. Almost 95% of the nidus was obliterated and blood flow to the AVM was significantly decreased. No new neurological deficits appeared after embolization. This patient was followed conservatively without surgery. Angiography 2 months after embolization showed no recanalization of the feeding artery and aneurysm (Fig. 6E and F).
Discussion It is well known that AVM's may be associated with a flow-related aneurysm of their feeding artery) '8 However, a procedure for embolizing the feeding artery with an aneurysm has not been established. The best way to treat this problem is to obliterate the artery that is feeding the AVM and aneurysm while preserving the normal arterial branches. To perform this type of procedure, it is sometimes necessary to introduce the microcatheter beyond the aneurysm to embolize the feeding arteries. Furthermore, small embolic materials, such as a microballoons or minicoil,6 may be necessary to obliterate the aneurysm. In two of our patients (Cases 1 and 2) the cause of bleeding was thought to be a ruptured aneurysm, and we believe that introducing the catheter beyond the aneurysm would increase the risk of rebleeding. Therefore, we tried to embolize the feedJ. Neurosurg. / Volume 75/October. 1991
AVM embolization using ethylene vinyl alcohol copolymer
FK;. 6. Angiograms in Case 3. A and B: Left vertebral angiograms, lateral views (arterial phase (A) and late arterial phase (B)) demonstrating a peripheral aneurysm on the left medial posterior choroidal artery. C: Vertebral angiogram, anteroposteriot view. D: Superselectiveangiogram of the distal branch of the medial posterior choroidal artery demonstrating the peripheral aneurysm ('arrowhead). E and F: Two-month followup left vertebral angiograms, lateral (E) and anteroposterior (F) views.
ing artery and aneurysm simultaneously using a liquid embolic agent. Two problems must be considered in occluding the feeding artery with the peripheral aneurysm. The first concerns treatment of the normal arterial branch distal to the aneurysm. In Case 2, a small arterial branch to the cerebellum was demonstrated on angiography. We believed that a new neurological deficit would not result if this vessel was occluded, because the patient had a massive hematoma at the left cerebellar peduncle. This was confirmed by Amytal testing via the upper branch of the SCA. In fact, his neurological condition did not change at all after embolization. However, this treatment will not be used for cases in which new neurological deficits may arise due to embolization. The second problem concerns selection of the embolic material. Various types of embolic agents have been reported to embolize brain AVM's including: PVA, coil, Avitene, silk suture, balloon, and liquids? '2'4'5'7"9-'2When PVA or Avitene is used to embolize the feeding artery, intraluminal pressure to the feeding artery increases and the aneurysm may rupture before retrograde thrombosis is complete.6 Silk suture can be delivered proximal J. Neurosurg. / Volume 75/October, 1991
to the aneurysm; however, the fluid pressure needed to inject it may cause rupture. With use of the coil, care must be taken when positioning the device to avoid penetration of the aneurysm. The use of a detachable balloon can be difficult for this kind of peripheral aneurysm, 5 The embolic agent EVAL is a copolymer of polyethylene and PVA. The embolized liquid is a mixture of 5 gm of EVAL and 35 gm of powder metrizamide dissolved in 60 gm of dimethyl sulfoxide (DMSO). This new liquid embolization material solidifies when it comes into contact with blood. There is little known about side effects and tissue reaction, but the initial results are promising? 3 The material has been developed by Taki, et al., j3 and is available through this group for investigational use only. This substance is not approved by the Food and Drug Administration - - as are most other embolization materials. The liquid contains solvent (DMSO) for polyvinyl chloride and polyurethane and thus carries the risk of dissolving certain catheter materials or stopcocks used in association with the embolization material. This substance may pass through AVM's with a large arteriovenous shunt be659
T. Terada, et al. cause of its nonadhesive character. When compared to adhesive polymerizing embolization materials such as IBCA and NBCA (the most widely used glue in the United States), EVAL seems to have the advantage of not sticking to catheter materials and vessel walls and results in less inflammatory reaction. These materials claim to provide more permanent vessel occlusion than embolization with particles. We chose EVAL as an embolic agent for treatment of these patients. It is easy and safe to handle because of its nonadhesive character and the possibility of repeated injection. This agent can be injected slowly until the aneurysm is completely obliterated using road-mapping techniques. We conclude that EVAL is an alternative embolic agent for cases of AVM in which the feeding artery has a ruptured peripheral aneurysm and needs presurgical embolization, providing that none of the vessels involved will cause new neurological deficits when embolized. References
1. Brothers MF, Kaufmann JCE, Fox AJ, et al: N-butyl 2cyanoacrylate - - a substitute for IBCA in interventional neuroradiology. Histopathologic and polymerization studies. AJNR 10:575-577, 1989 2. Dion JE, Vifiuela F, Lylyk P, et al: Ivalon-33% ethanolAvitene embolic mixture: clinical experience with neuroradiological endovascular therapy in 40 arteriovenous malformations. AJNR 9:1029, 1988 (Abstract) 3. Drake CG, Friedman AH, Peerless SJ: Posterior fossa arteriovenous malformations. J Neurosurg 64:1-10, 1986 4. Eskridge JM, Hartling RP: Preoperative embolization of brain AVM's using surgical silk and polyvinyl alcohol. AJNR 10:882, 1989 (Abstract) 5. Hayashi S, Arimoto T, ltakura T, el al: The association
660
6.
7.
8.
9.
10. I I.
12. 13.
of intracranial aneurysms and arteriovenous malformation of the brain. Case report. J Neurosurg 55:971-975, 1981 Higashida RT, Halbach VV, Dormandy B, et al: Endovascular treatment of intracranial aneurysms with a new silicone microballoon and indications for therapy. Radiology 174:687-691, 1990 Hilal SK, Khandji A, Chi TL, et al: Synthetic fiber-coated platinum coils successfully used for the endovascular treatment of arteriovenous malformations, aneurysms and direct arteriovenous fistulas of CNS. AJNR 9:1030, 1988 (Abstract) Jungreis CA, Horton JA, Hecht JA, et al: Blood pressure changes in feeders to cerebral arteriovenous malformations during therapeutic embolization. AJNR 10: 575-577, 1989 Monaco RG, Alvarez H, Goulao A, et al: Posterior arteriovenous malformations. Angioarchitecture in relation to their hemorrhagic episode. Neuroradiology 31: 471-475, 1990 Pelz DM, Fox AJ, Vifiuela F, et al: Preoperative embolization of brain AVMs with isobutyl-2 cyanoacrylate. AJNR 9:757-764, 1988 Purdy PD, Samson D, Batjer HH, et al: Preoperative embolization of cerebral arteriovenous malformations with polyvinyl alcohol particles: experience in 5l adults. AJNR 11:501-510, 1990 Tadavarthy SM, Moller JH, Amplatz K: Polyvinyl alcohol (Ivalon) - - a new embolic material. AJR 125:609-616, 1975 Taki W, Yonekawa Y, lwata H, et al: A new liquid material for embolization of arteriovenous malformations. AJNR 11:163-168, 1990
Manuscript received September 10, 1990. Accepted in final form February 25, 1991. Address reprint requests to: Tomoaki Terada, M.D., Department of Neurological Surgery, Wakayama Medical College, 7-27, Wakayama City 640, Japan.
J. Neurosurg. / Volume 75/October, 1991
Embolization of arteriovenous malformations with peripheral aneurysms using ethylene vinyl alcohol copolymer Report of three cases TOMOAKI TERADA, M.D., YOSHINARI NAKAMURA, M.D., KUNIO NAKAI, M.D., MITSUHARU TSUURA~ M.D., TAKASHI NISHIGUCttI, M.D., SEIJI HAYASHI, M.D., TAKUHE[ Kmo, M.D., WAaO TAKI, M.D., HIaOO IWATA, PH.D., AND NoamtKo KOMAI, M.D.
Departments of Neurological Surgery, Wakayama Medical College, and Wakayama Rosai Hospital, Wakayama City; Department of Neurosurgery, Kyoto University Medical School, Kyoto; and Department of Surgical Research, National Cardiovascular Center, Osaka, Japan ~" The authors report three cases of arteriovenous malformations (AVM's) with aneurysms arising from the feeding artery; all were successfully treated with a new nonadhesive liquid embolic material, ethylene vinyl alcohol copolymer (EVAL). In two patients the AVM's were totally removed without difficulty, and in one the AVM was managed conservatively after embolization. No new neurological deficits appeared during or after embolization. After road-mapping techniques, EVAL was injected slowly until the feeding artery and aneurysm were completely obliterated. This embolic agent is easy to handle and is considered safe compared with other adhesive liquid embolic agents, such as isobutyl-2-cyanoacrylate or n-butyl cyanoacrylate. It is concluded that EVAL is an excellent agent for embolizing an AVM with a peripheral aneurysm on the feeding artery. KEY WORDS 9 arteriovenous malformation ethylene vinyl alcohol copolymer
T is well known that arteriovenous malformations (AVM's) may be associated with aneurysms on their feeding arteries. It is possible to treat the AVM causing the aneurysm to regress. However, rupture of an aneurysm may occur when these arteries are embolized, either from mechanical trauma due to the catheter or guidewire or from increased pressure from injection or closure of direct shunting. There is still controversy as to how these arteries should be embolized. An adhesive liquid embolic agent, such as isobutyl-2-cyanoacrylate (IBCA) or n-butyl cyanoacrylate (NBCA), can cause incomplete or too rigorous embolization because it is difficult to determine the appropriate dosage and to determine accurately the required polymerization time. Lt: Embolization using polyvinyl alcohol (PVA) can increase the risk of rupture of an aneurysm because it may occlude the nidus of the AVM and increase
I
J. Neurosurg./ Volume 75/October, 1991
9 aneurysm
9 embolization
9
intraluminal pressure of the feeding artery6 until retrograde thrombosis is complete. We treated three cases of AVM's with peripheral aneurysms arising from their feeding arteries by means of a new nonadhesive liquid embolic agent. ~ This agent, ethylene vinyl alcohol copolymer (EVAL), is useful for this type of embolization because it permits a serial injection to obliterate completely first the AVM then the aneurysm. Case Reports
Case 1 This 29-year-old man was admitted to his local hospital with a sudden severe headache on February 14, 1990. He suffered a second severe headache and became comatose several hours after admission. Computerized tomography (CT) showed cerebellar hemorrhage and 655
T. Terada, et al.
FIG. 1. Angiograms in Case 1. A: Left vertebral angiogram, lateral view, showing the arteriovenous malformation fed from the left anterior inferior cerebellar artery, (AICA) and the posterior inferior cerebellar artery. The aneuD, sm was seen arising from the A1CA (arrowhead). B: Left vertebral angiogram, anteroposterior view, demonstrating a distal AICA aneurysm (arrowhead). C: Superselective angiogram, lateral view, demonstrating the left AICA. D: Left vertebral angiogram, anteroposterior view, following embolization to the AICA. E and F: Postoperative left vertebral angiograms, lateral view (E) and anteroposterior view (F), showing preservation of the left AICA (arrows).
FIG. 2. Magnetic resonance spin-echo images (TR 500 msec, TE 30 msec) in Case I. A: Axial view, showing signal-void area in the base of the right cerebellar hemisphere. B: Axial view, showing the hematoma in the left cerebellar vermis as a high-intensity mass. C and D: Sagittal views showing that the hematoma was separate from the nidus of the arteriovenous malformation.
subarachnoid hemorrhage (SAH) in the posterior fossa with marked ventricular enlargement. Emergency arteriography revealed an AVM, fed by the left posterior inferior cerebellar artery and the left anterior inferior cerebellar artery (AICA) (Fig. 1A to C). Peripheral aneurysms were discovered on the distal segment of the left AICA. 656
Ventricular drainage was instituted, but the patient remained in a semicomatose state with severe tetraparesis. On February 27, 1990, he was transferred to our hospital for treatment. Magnetic resonance imaging confirmed that the ruptured AICA aneurysm was the cause of bleeding, as the hematoma cavity had no connection with the AVM (Fig. 2). Separate procedures J. Neurosurg~ / Volume 75/October, 1991
AVM embolization using ethylene vinyl alcohol copolymer
Ft(~. 3. Compulerized lomography scans in Casc 2. A and B: Admission scans showing cerebellar hemorrhage, subarachnoid hemorrhage,and hydrocephalus. C and D: Postembolizationscans demonstrating a low-densityarea on the uppcr surface of the cerebellum.
FtG. 4. Leftvertebralangiograms in Case 2 demonstrating a peripheral superior cerebellarartery aneurysm. A: Lateral view,arterial phase. B: Anteroposterior view, arterial phase. C: Lateral view,capillary phase. D: Anteroposterior view, capillary phase.
for embolization of the left AICA and of the aneurysm were planned because a simultaneous operation on both would have been difficult, given their different locations. Prior to embolization, the patient's condition improved and he became conscious. He had a left peripheral facial palsy, left lateral gaze palsy, moderate tetraparesis (grade 3/5), and bilateral severe cerebellar ataxia. A microcatheter* was navigated into the left AICA to a point just proximal to the aneurysm (Fig. IC). The patient's neurological condition and auditory brainstem responses were monitored during a selective sodium Amytal (amobarbital) test (40-rag dose) and remained unchanged. The feeding artery and aneurysm were then embolized by injection of 0.6 ml EVAL through the catheter (Fig. 1D). Following embolization, the patient's condition, including his auditory function, did not change. At surgery on May 11, 1990, the AVM was totally removed with minimal bleeding and without * Microcatheter manufactured by Target Therapeutics, Inc., San Jose, California. J. Neurosurg. / l/olume 75/October. 1991
neurological complication. Postoperative arteriography revealed that the aneurysm and AVM had completely disappeared while the AICA was preserved to the origin of the aneurysm (Fig. IE and F). Case 2
This 53-year-old man was admitted to our hospital because of disturbance in his level of consciousness following a severe headache on September 14, 1989. A CT scan demonstrated cerebellar hemorrhage, SAH, and marked hydrocephalus (Fig. 3A and B). Cerebral arteriography revealed an AVM fed from the AICA as well as duplicated superior cerebellar arteries (SCA's) with a peripheral aneurysm (Fig. 4). This ruptured peripheral aneurysm was suspected of having caused the bleeding found on CT. Ventricular drainage was performed on the day of admission, and the patient recovered consciousness the next day. However, a mild right hemiparesis, bilateral ataxia, and bilateral abducens palsy were noted. It was believed that total removal of the AVM by direct surgery would be difficult because of the size and 657
T. Terada, a al.
FIG. 5. Angiograms in Case 2. A and B: Superselectiveleft superior cerebellar artery (SCA) angiograms. In A the aneurysm is clearly opacified (arroa'head). and in B the aneurysm is completely obliterated with ethylene vinyl alcohol copolymer (arrowhead). The hemisphericand lower branches of the SCA are opacified. C and D: Left vertebral angiograms, laleral (C) and anteroposterior (D) views, followingembolization from the SCA. The arteriovenous malformation is decreased in size and fed mainly from the left anterior inferior eerebellararteD'.
location of the lesion, so embolization was planned for the duplicated SCA's, including the aneurysm. Normal arterial supply to the cerebellum was demonstrated distal to the peripheral SCA aneurysm. However, we concluded that no new neurological deficit would result from embolizing the SCA proximal to the aneurysm, because the left cerebellar peduncle was already injured by a massive cerebellar hemorrhage. On October 11, 1989, embolization was performed after a decrease in mass effect of the hematoma. A microcatheter was introduced into the upper SCA following negative results of Amytal testing. The catheter was advanced to a point just proximal to the origin of the peripheral aneurysm, and 0.6 ml of EVAL was injected through it to occlude the aneurysm completely (Fig. 5A and B). The inferior SCA was embolized by PVA particles (150 to 250 t~ in size) because, when appropriate, we routinely use preoperative PVA embolization for arteries feeding AVM's. After embolization, arteriography revealed that 80% of the AVM was occluded and no new neurological deficits were noted. On follow-up arteriography performed 189 months later, the feeding arteries and aneurysms had not recanatized (Fig. 5C and D), although retrograde thrombosis caused occlusion of both left SCA's, resulting in a small cerebellar infarct (Fig. 3C and D). The AVM was totally removed by the suboccipital approach without difficulty or additional neurological deficit. Case 3 This 46-year-old man was admitted to our hospital on February 2, 1990, because of SAH from a left thalamic AVM. He was in a semicomatose state with a fight hemiparesis. He had a history of SAH 12 years previously. A C T scan revealed a left thalamic hemorrhage and acute hydrocephalus. On bilateral ventricular drainage, his level of consciousness improved, but the
6fi8
severe right hemiparesis and aphasia persisted. Cerebral angiography revealed that the left thalamic AVM was fed mainly from the left medial posterior choroidai arteries. A peripheral aneurysm was found on the distal medial posterior choroidal artery (Fig. 6A to D). Embolization was planned for these feeding arteries because of the anticipated difficulty with a direct surgical resection. A microcatheter was introduced into the proximal portion of the aneurysm's feeding artery and 0.5 ml of EVAL was injected gradually until it completely filled the aneurysm (Fig. 6). Another feeding artery was embolized by the same procedure using 0.6 ml of EVAL. Almost 95% of the nidus was obliterated and blood flow to the AVM was significantly decreased. No new neurological deficits appeared after embolization. This patient was followed conservatively without surgery. Angiography 2 months after embolization showed no recanalization of the feeding artery and aneurysm (Fig. 6E and F).
Discussion It is well known that AVM's may be associated with a flow-related aneurysm of their feeding artery) '8 However, a procedure for embolizing the feeding artery with an aneurysm has not been established. The best way to treat this problem is to obliterate the artery that is feeding the AVM and aneurysm while preserving the normal arterial branches. To perform this type of procedure, it is sometimes necessary to introduce the microcatheter beyond the aneurysm to embolize the feeding arteries. Furthermore, small embolic materials, such as a microballoons or minicoil,6 may be necessary to obliterate the aneurysm. In two of our patients (Cases 1 and 2) the cause of bleeding was thought to be a ruptured aneurysm, and we believe that introducing the catheter beyond the aneurysm would increase the risk of rebleeding. Therefore, we tried to embolize the feedJ. Neurosurg. / Volume 75/October. 1991
AVM embolization using ethylene vinyl alcohol copolymer
FK;. 6. Angiograms in Case 3. A and B: Left vertebral angiograms, lateral views (arterial phase (A) and late arterial phase (B)) demonstrating a peripheral aneurysm on the left medial posterior choroidal artery. C: Vertebral angiogram, anteroposteriot view. D: Superselectiveangiogram of the distal branch of the medial posterior choroidal artery demonstrating the peripheral aneurysm ('arrowhead). E and F: Two-month followup left vertebral angiograms, lateral (E) and anteroposterior (F) views.
ing artery and aneurysm simultaneously using a liquid embolic agent. Two problems must be considered in occluding the feeding artery with the peripheral aneurysm. The first concerns treatment of the normal arterial branch distal to the aneurysm. In Case 2, a small arterial branch to the cerebellum was demonstrated on angiography. We believed that a new neurological deficit would not result if this vessel was occluded, because the patient had a massive hematoma at the left cerebellar peduncle. This was confirmed by Amytal testing via the upper branch of the SCA. In fact, his neurological condition did not change at all after embolization. However, this treatment will not be used for cases in which new neurological deficits may arise due to embolization. The second problem concerns selection of the embolic material. Various types of embolic agents have been reported to embolize brain AVM's including: PVA, coil, Avitene, silk suture, balloon, and liquids? '2'4'5'7"9-'2When PVA or Avitene is used to embolize the feeding artery, intraluminal pressure to the feeding artery increases and the aneurysm may rupture before retrograde thrombosis is complete.6 Silk suture can be delivered proximal J. Neurosurg. / Volume 75/October, 1991
to the aneurysm; however, the fluid pressure needed to inject it may cause rupture. With use of the coil, care must be taken when positioning the device to avoid penetration of the aneurysm. The use of a detachable balloon can be difficult for this kind of peripheral aneurysm, 5 The embolic agent EVAL is a copolymer of polyethylene and PVA. The embolized liquid is a mixture of 5 gm of EVAL and 35 gm of powder metrizamide dissolved in 60 gm of dimethyl sulfoxide (DMSO). This new liquid embolization material solidifies when it comes into contact with blood. There is little known about side effects and tissue reaction, but the initial results are promising? 3 The material has been developed by Taki, et al., j3 and is available through this group for investigational use only. This substance is not approved by the Food and Drug Administration - - as are most other embolization materials. The liquid contains solvent (DMSO) for polyvinyl chloride and polyurethane and thus carries the risk of dissolving certain catheter materials or stopcocks used in association with the embolization material. This substance may pass through AVM's with a large arteriovenous shunt be659
T. Terada, et al. cause of its nonadhesive character. When compared to adhesive polymerizing embolization materials such as IBCA and NBCA (the most widely used glue in the United States), EVAL seems to have the advantage of not sticking to catheter materials and vessel walls and results in less inflammatory reaction. These materials claim to provide more permanent vessel occlusion than embolization with particles. We chose EVAL as an embolic agent for treatment of these patients. It is easy and safe to handle because of its nonadhesive character and the possibility of repeated injection. This agent can be injected slowly until the aneurysm is completely obliterated using road-mapping techniques. We conclude that EVAL is an alternative embolic agent for cases of AVM in which the feeding artery has a ruptured peripheral aneurysm and needs presurgical embolization, providing that none of the vessels involved will cause new neurological deficits when embolized. References
1. Brothers MF, Kaufmann JCE, Fox AJ, et al: N-butyl 2cyanoacrylate - - a substitute for IBCA in interventional neuroradiology. Histopathologic and polymerization studies. AJNR 10:575-577, 1989 2. Dion JE, Vifiuela F, Lylyk P, et al: Ivalon-33% ethanolAvitene embolic mixture: clinical experience with neuroradiological endovascular therapy in 40 arteriovenous malformations. AJNR 9:1029, 1988 (Abstract) 3. Drake CG, Friedman AH, Peerless SJ: Posterior fossa arteriovenous malformations. J Neurosurg 64:1-10, 1986 4. Eskridge JM, Hartling RP: Preoperative embolization of brain AVM's using surgical silk and polyvinyl alcohol. AJNR 10:882, 1989 (Abstract) 5. Hayashi S, Arimoto T, ltakura T, el al: The association
660
6.
7.
8.
9.
10. I I.
12. 13.
of intracranial aneurysms and arteriovenous malformation of the brain. Case report. J Neurosurg 55:971-975, 1981 Higashida RT, Halbach VV, Dormandy B, et al: Endovascular treatment of intracranial aneurysms with a new silicone microballoon and indications for therapy. Radiology 174:687-691, 1990 Hilal SK, Khandji A, Chi TL, et al: Synthetic fiber-coated platinum coils successfully used for the endovascular treatment of arteriovenous malformations, aneurysms and direct arteriovenous fistulas of CNS. AJNR 9:1030, 1988 (Abstract) Jungreis CA, Horton JA, Hecht JA, et al: Blood pressure changes in feeders to cerebral arteriovenous malformations during therapeutic embolization. AJNR 10: 575-577, 1989 Monaco RG, Alvarez H, Goulao A, et al: Posterior arteriovenous malformations. Angioarchitecture in relation to their hemorrhagic episode. Neuroradiology 31: 471-475, 1990 Pelz DM, Fox AJ, Vifiuela F, et al: Preoperative embolization of brain AVMs with isobutyl-2 cyanoacrylate. AJNR 9:757-764, 1988 Purdy PD, Samson D, Batjer HH, et al: Preoperative embolization of cerebral arteriovenous malformations with polyvinyl alcohol particles: experience in 5l adults. AJNR 11:501-510, 1990 Tadavarthy SM, Moller JH, Amplatz K: Polyvinyl alcohol (Ivalon) - - a new embolic material. AJR 125:609-616, 1975 Taki W, Yonekawa Y, lwata H, et al: A new liquid material for embolization of arteriovenous malformations. AJNR 11:163-168, 1990
Manuscript received September 10, 1990. Accepted in final form February 25, 1991. Address reprint requests to: Tomoaki Terada, M.D., Department of Neurological Surgery, Wakayama Medical College, 7-27, Wakayama City 640, Japan.
J. Neurosurg. / Volume 75/October, 1991
