Surg Neurol 1992;38:85-94
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Superselective Embolization of Spinal Arteriovenous Malformations Using the Tracker Catheter Hajime Keisuke
Touho,
M.D., Jun Karasawa, M.D., Hideyuki
Yamada,
M.D., and Keiji Shibamoto,
Ohnishi, M.D.,
M.D.
Department of Neurosurgery, Osaka Neurological Institute, Osaka, Japan
Touho H, KarasawaJ, Ohnishi H, Yamada K, Shibamoto K. Superselective embolization of spinal arteriovenous malformations using the Tracker catheter. Surg Neurol 1992;38:85-94. Eighteen patients with spinal arteriovenous malformations had been treated with conventional embolization, surgical removal, feeder ligation, and/or feeder coagulation between February 1985 and March 1990. The lesions included six glomus, four juvenile, three extramedullary, and five dural arteriovenous malformations or fistulas. Embolic therapy was conducted in 14 patients by introducing the tip of a catheter into the segmental arteries and injecting polyvinyl alcohol strips (500-1000/,m) (conventional embolization). Follow-up spinal angiography disclosed recanalization in 10 patients (71.4%) and the appearance of new feeding arteries in five patients (35.7%). We introduced the Tracker vascular access system in April 1990. Eight patients (four glomus, one juvenile, and three dural arteriovenous malformations) were treated with the minicatheter and Ivalon particles (150-350 tzm). Five patients showed neurological improvement immediately after treatment. The other three patients had severe paraparesis before treatment and did not show any improvement. One patient with a glomustype arteriovenous malformation showed transient neurological deterioration just after embolization with the Tracker-lO to occlude a lesion fed by the posterior spinal artery, because the Ivalon particles migrated into the anterior spinal artery via the anterior spinal canal artery. In one patient with a juvenile arteriovenous malformation, the Tracker-18 catheter perforated the radiculomedullary artery originating from the right vertebral artery, and subarachnoid hemorrhage occurred. However, the Tracker-10 could later successfully occlude the arteriovenous malformation. The rates of recanalization and appearance of the new feeding vessels were 4/8 (50.0%) and 2/8 (25%), respectively. KEY WORDS: Spinal arteriovenous malformation; Conventional embolization; Superselective embolization; Ivalon Address reprint requests to." Hajime Touho, M.D., Department of Neurosurgery, Osaka Neurological Institute, 2-6-23 Shonai-Takaramachi, Toyonaka 561, Osaka, Japan. Received December 23, 1991; acceptedJanuary 14, 1992.
c~91992by ElsevierSciencePublishingCo., Inc.
Spinal arteriovenous malformations (AVMs) are a relatively rare clinical entity. T h e r e are two major types o f spinal AVMs, i.e., the dural arteriovenous fistula (AVF) and the intradural AVM or AVF. Recently, Rosenblum et al and Oldfield et al reported the following classification of spinal AVMs: dural AVF, glomus-type intradural AVM, juvenile-type intradural AVM, and intradural AVF. This classification was based on differences in the anatomy and pathophysiology of these spinal lesions [15,16,24,28]. Since the reports of Doppman et al [ 6 - 8 ] , Djindjian et al [4,5], and Rich~ et al [27], the treatment o f spinal AVMs has included artificial embolization and/or surgical excision. The dural AVF, intradural retromedullary AVF, and intradural AVM in the conus region are relatively easy to embolize and/or obliterate surgically. On the other hand, an intramedullary AVM or intradural premedullary AVF may be supplied by the anterior spinal artery and be situated either in the spinal cord parenchyma itself or anterior to the spinal cord. Thus, the complete embolization and/or surgical obliteration of such lesions has been quite difficult. In particular, juvenile and glomus-type AVMs have been considered for embolization rather than surgical extirpation [2,4,19,23,2 5,29]. However, embolization o f such lesions is occasionally unsuccessful, because the embolic material becomes wedged proximal to or at the radiculomedullary artery (proximal embolization), and collaterals subsequently develop via extradural and/or intradural anastomoses [2,3,11]. In this study, we used the Tracker-18 vascular access system [13,26] to avoid proximal embolization and treated spinal AVMs by superselective catheterization plus embolizattion with Ivalon.
Clinical Materials and Methods Between April 1985 and March 1990, 18 patients with spinal AVMs were admitted to Osaka Neurological Institute for surgical and/or interventional therapy. The lesions included six glomus, four juvenile, three extramedullary, and five dural AVMs or AVFs (Table 1). 0090-3019/92/$5.00
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Table 1. Summary of 18 Patients with Spinal AVMs Case No. Age, yr
Sex
Type of AVM
Clinical Course
Neurological Deficits
l+
29
F
Juvenile
Apoplectic progressive
Rt hemiparesis
2~
35
M
Glomus
Progressive
Monoparesis (It leg)
3
54
M
Glomus
Progressive
4
34
F
Conus
Apoplectic progressive
5
44
M
Dural
Progressive
Monoparesis (It leg), paresthesia (T5-T10) Paraparesis, urinary incontinence, sacral anesthesia Monoparesis (rt leg)
6 7
38 28
M M
Juvenile Juvenile
8
28
M
Glomus
Apoplectic Apoplectic progressive Apoplectic
9
8
M
Retromedullary
Progressive
10
54
M
Dural
Progressive
11"
61
M
Dural
Progressive
12
29
M
Conus
Progressive
13
57
F
Juvenile
Progressive
14+
29
M
Glomus
Progressive apoplectic
15~
50
F
Glomus
Progressive apoplectic
16+
86
M
Dural
Apoplectic
17+
86
M
Dural epidural
Apoplectic progressive
Paraparesis, urinary incontinence Paraparesis, urinary incontinence, hypesthesia (L3-) Paraparesis, urinary incontinence Paraparesis, hypesthesia (L4-), urinary incontinence Paraparesis, hypesthesia (L5--) Paraparesis, hypesthesia (L3-) anesthesia (L6-), urinary incontinence Paraparesis, hypesthesia (L10-), urinary incontinence Paraparesis, urinary incontinence Paraparesis, urinary incontinence
18*
38
M
Glomus
Progressive
Feeding Arteries
Past Results (Follow-up Periods, no)
Past Treatments
C7-T2
Emb, It VA feeder lig
Unchanged (60)
T9
Emb
Improved (42)
T7
Emb
Improved (72)
ASA (rt L2)
L1-2
Emb, removal
Improved (71)
RMA (rt T5)
T5-6
Improved (39)
Monoparesis (It leg) Lt hemiparesis
ASA (It T4, rt L1, rt S) Bi VA (ASA, PSA)
L1 C1-3
Emb, removal Emb Feeder lig
Paraparesis
ASA (rt L1), PSA (rt L1) ASA (rt T12)
T12
Paraparesis, muscle atrophy (rt leg), hypesthesia ($1-5), urinary incontinence
Bi VA (ASA, PSA), rt costocervical (PSA), rt T3 (ASA), it T5 (PSA) ASA (rt T10), PSA (It T10) ASA (It T4)
Level of Nidus
Unchanged (72) Unchaged (141) Unchanged (85)
L1
Emb, feeder lig Feeder coagulation
RMA (rt T7)
T7-8
Removal
Unchanged (43)
RMA (rt T7)
T7-8
Emb
Unchanged (29)
ASA (It T9), PSA (rt L2)
L1
Emb, removal
Improved (26)
ASA (it T8), PSA (rt T7) ASA, PSA (T4)
T1-3
Unchanged (22)
T2-3
Emb, removal Emb
ASA (rt L2, It L2)
TI2
Emb
Unchanged (22)
Rt T12, L1
L1
Bi T3-5
T3-5
ASA (It L2), PSA (rt T l l )
T12
Improved (69)
Unchanged (28)
--
Emb, surgical obliteration (dural) Emb
(27)
Unchanged (47)
Worsened (30)
Abbreviations: AVM, arteriovenous malformation; F, female; rt, right; Bi, bilateral; VA, vertebral artery; ASA, anterior spinal artery; PSA, posterior spinal artery; It, left; emb, embolization; lig, ligation; M, male; RMA, radiculomedullary artery. +Patient treated with minicatheter and Ivalon.
Embolization was performed in 14 patients by introducing the angiographic catheter into the origin of the segmental artery and injecting potyvinyl alcohol (PVA) strips (500-1000 ~,m) in a flow-directed manner (conventional embolization). Follow-up spinal angiograms performed from 2 to 12 months after the last embolization disclosed angiograhic recanalization in 10 patients
(71.4%) and the appearance of newly developed feedings arteries in five patients (35.7%). Due to the high rate of recanalization and/or appearance of new feeding systems, we introduced the Tracker vascular access system for treating patients in April 1990. The appearance of new feeding systems was thought to occur because emboli lodged promixal to the nidus and occluded either
Selective Embolization of Spinal AVMs
the segmental artery itself, the dorsal spinal artery, the radicular branch, or the anterior or posterior spinal artery. It was thought to be reasonable that an embolic agent injected near to the nidus by the minicatheter could be navigated into the lesion itself. Seven patients (four glomus, one juvenile, and two dural AVFs), who had been treated with conventional embolization and showed recanalization and/or the appearance of new feeding systems, as well as one elderly patient with dural AVFs who had not been treated previously, underwent superselective embolization using the minicatheter and Ivalon. Superselective embolization was conducted by introducing the Tracker-18 or Tracker-10 near to the lesion through the guiding catheter, the tip of which was placed at the origin of the segmental artery. The Tracker vascular access system is composed of a 150-cm Tracker18 or Tracker-10 catheter, a 175-cm tapered steerable guidewire, a guidewire introducer, and a rotating hemostatic valve (Target Therapeutics, Inc., San Jose, Calif.). The guiding catheter used was an HNB 6F angiographic catheter or a BPS 6.5F spinal angiography catheter (Cook Group, Bloomington, Ind.). We used 180- to 350-/~m Ivalon particles, which were suspended in contrast medium (Ioparmiron®, iopamidol, Schering AG, Berlin, Germany) and were embolized in a flow-directed manner toward the nidus via the microcatheter. The procedure was terminated when flow through the lesion was almost eliminated and/or reflux of the contrast medium began to appear proximal to the catheter tip. Vital signs and neurological function were carefully monitored during and after the procedure.
Results In the eight patients treated with the Tracker catheter system, it could be introduced at least to the dorsal spinal artery, and it could usually enter the radicular, radiculospinal, or radiculomedullary artery. Moreover, the catheter could be navigated into the anterior spinal artery in juvenile-type AVM. We could obliterate the lesion with Ivalon while preserving the anterior or posterior spinal artery in these patients. Recanalization and the appearance of new feeding systems due to proximal occlusion occurred in 4/8 (50.0%) and 2/8 (25.0%) patients, respectively, in 10 to 21 months of follow-up. Five patients showed marked neurological improvement just after treatment, but the other three patients (who already had severe paraparesis or paraplegia before treatment) did not show any improvement after superselective embolization. Case 2 showed marked neurological improvement after the first superselective embolization of the AVM via the right T10 intercostal artery using a Tracker- 18 catheter, and manifested transient neurological deterioration just after the last embolization of the
Surg Neurol 1992;38:85-94
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residual nidus via the left T10 intercostal and posterior spinal arteries using a Tracker-10 catheter. This was because the anterior spinal artery, which originated from the right T10 intercostal artery and had supplied feeding branches to the AVM, was connected via the anterior spinal canal artery with the posterior spinal artery originating from the left T10 intercostal artery. Thus, Ivalon particles migrated to the right side in addition to occluding the lesion via the posterior spinal artery. The transient neurological deficit almost completely improved after 1 week. In one patient with a juvenile AVM at the cervicothoracic level, the Tracker-18 system perforated the radiculomedullary artery at its site of entry into the dura mater during manipulation of the guide wire, and subarachnoid hemorrhage (SAH) occurred. However, the Tracker-10 could later be introduced into the anterior originating from the right vertebral artery, and successful obliteration of the lesion was achieved 2 weeks after SAH. The rate of complications due to superselecrive embolization was 2/8 (25.0%).
I l l u s t r a t i v e Cases Case 1 A 29-year-old woman had a history of SAH on two occasions over the past 2 years. She was admitted to Osaka Neurological Institute on May 12, 1986. Spinal angiograms demonstrated a juvenile AVM in the cervicothoracic region, with feeding vessels branching from the bilateral vertebral arteries, right costocervical trunk, right T3 intercostal artery, and left T5 intercostal artery. Conventional embolization was conducted with 500- to 1000-/xm PVA strips, excepts for the branches from the bilateral vertebral arteries. When the feeding system was occluded by embolization, the segmental branch that originated from the left vertebral artery was ligated surgically. However, she became quadriparetic in November 1987, and this state was exacerbated despite medical treatment. She was admitted with quadriparesis (upper extremities, 3-4/5; lower extremities, 1-2/5) on June 18, 1990. On June 25, 1990, spinal angiography was performed, and it disclosed that the AVM still existed and was fed by the right anterior and posterior spinal arteries and the left anterior spinal artery, as shown in Figure 1 A. The segmental branch of the left vertebral artery, which gave off feeding branches via the anterior spinal artery, was too narrow to catheterize. After placing the guiding catheter at the origin of the right vertebral artery, the Tracker-18 was introduced into the segmental artery. However, the guide wire perforated the arterial wall at the site where the radiculomedullary artery entered the dura, and SAH occurred, which resolved by the next
88
Surg Neurol 1992;38:85-94
,
a
Touho et al
,,
Figure 1. (A) Anteroposterior views of bilateral vertebral angiograms in case I. The intramedullary component of the arteriovenous malformation was fed via the anterior (arrow) and posterior (arrowhead./spinal arteries from the right vertebral artery (left), and it was also fed via the anterior spinal artery (arrow) from the/eft vertebral artery (right). (B) Superselective catheterization to the segmental artery of the right vertebral artery with the Tracker-18 catheter. The miniangiograms show arteriovenous malformation with an arterial aneurysm (arrow). (C) Follow-up angiograms of the right vertebral artery. These showed that the nidus had become even smaller and the aneurysm had disappeared.
day. Selective embolization using the Tracker-18 catheter was attempted again 3 days after SAH, and this time the minicatheter was successfully introduced into the proximal portion of the segmental branch and miniangiograms were obtained through the catheter (Figure 1 B). After confirming that there was no reflux into the right vertebral artery, 180- to 350-~m Ivalon was fed into the catheter. When the contrast medium stopped flowing into the aneurysm, the procedure was terminated. The function of her upper extremities improved just after embolization. Follow-up angiography was performed 17 days later. This disclosed that the AVM had become even smaller, and the associated aneurysm had disappeared (Figure 1 C). She was discharged 19 days after embolization, with her neurological symptoms having shown no further change. She was admitted again on March 12, 1991, for follow-up angiography. Her neurological deficits had not changed. On March 14, spinal angiography was conducted, revealing that the AVM
b
,t
C
J
had partially recanalized and that the right anterior and posterior spinal arteries gave off feeding branches to the AVM (Figure 2 A). The aneurysmal dilation was no longer visualized. We performed the superselective embolization with a Tracker-10 and Ivalon on March 19. The minicatheter was introduced into the anterior spinal artery originating from the right vertebral artery, and the AVM was embolized with 180- to 350-/zm Ivalon, resulting in complete occlusion of the anterior part of the lesion, which was fed by the anterior spinal artery (Figure 2 B and C). Before and during the embolization, blood pressure in the anterior spinal artery was intermittently monitored through the catheter. Before the embolization, systolic blood pressure was about 82 mm Hg (Figure 3 A), gradually increasing during the embolization (Figure 3 B), and at the end of the embolization, it became about 100 mm Hg (Figure 3 C). Blood pressure in the vertebral artery is shown in Figure 3D. On March 26, embolization was again performed to occlude the posterior part of the lesion, which was fed by the posterior spinal artery (Figure 4). The preembolization angiograms showed that the anterior part of the AVM fed by the anterior spinal artery was no longer visualized and the diameter of the artery had become normal, while the posterior part of the AVM was still intact. Then, the Tracker-10 was introduced into the segmental artery, which originated from the right vertebral artery and gave off the posterior spinal artery, and
Selective Ernbolization of Spinal AVMs
Surg Neurol
89
1992;38:85-94
!i~ i~ ~
Figure 2. (A) Anteroposterior ~,ieu of the right vertebral angiogram in case l. The anteriovenous malformation isfed l,ia the anterior (arrow) and posterior spinal arteries (arrowhead). (B) The Tracker-l O catheter was successfully introduced into the anterior spinal artery, and a miniangiogram was obtained. (C) Postembolization angiograms of the right vertebral artery. The compartment of the nidus that was fed via the anterior spinal artery has disappeared. Central arteries as feeding ressels are c/early depicted (arrou ).
t
a
150-180/zm Ivalon was injected through the catheter, after confirming that there was no reflux into the vertebral artery on the miniangiograms (Figure 4 A). Thus, we could occlude the posterior part of the AVM while sparing the posterior spinal artery (Figure 4 B). Just after the first embolization, her fine finger movements were improved, and sensory disturbance in her upper extremities (hypesthesia and paresthesia) improved just after the second embolization. She was discharged on March 30, 1991.
"
b
JI
C
•
Figure 4. (A) Anteroposterior view of the superselective angiography in case 1. The Tracker-l O catheter was introduced into the radiculomedullary branch (arrow). (B) Postembolization angiograms of the right vertebral arter). The nidus has almost disappeared, while both the antertor and posterior spinal arteries have been spared.
Case 2 A 35-year-old man was admitted to Osaka Neurological Institute. He had suffered from slowly progressive too-
Figure 3. Blood pressure in the anterior spinal artery in case 1. (A) before the embolization, (B) during the embolization, and (C) at the end of the embolization. (D) Blood pressure in the right vertebral artery. 120 t~
-r
100
E E 8O rn
a
60
b
'
a
"
b
'
90
Surg Neurol 1992;38:85-94
noparesis in his left lower extremity and low back pain for the last 5 years. On October 30, 1987, spinal angiography disclosed a glomus-type spinal AVM of the thoracic cord that was fed by the anterior and posterior spinal arteries via the right and left T10 intercostal arteries, respectively. He was initially treated with conventional embolization using 500-/zm PVA strips via the right T10 intercostal artery, resulting in near disappearance of the lesion and the transient return of spinal reflexes. He showed a marked improvement in his monoparesis and low back pain just after embolization, but these symptoms returned about 2 weeks later. He was admitted on August 13, 1990, for treatment of the AVM by superselective embolization. Spinal angiography showed complete recanalization of the AVM, which was fed by the anterior and posterior spinal arteries originating from the right and left intercostal arteries, respectively (Figure 5 A ). After performing conventional angiography, the guiding catheter was introduced into the right T 10 intercostal artery and the Tracker- 18 catheter was superselectively introduced into the radiculomedullary artery (Figure 5 B). Then 150- to 180-/zm Ivalon was injected through the catheter, resulting in almost complete occlusion of the AVM while sparing the anterior spinal artery (Figure 5 C). The patient showed a marked improvement in his monoparesis and back pain beginning just after embolization and was discharged 7 days later. On November 12, 1990, he was readmitted for embolization of the other part of the AVM, fed by the posterior spinal artery originating from the left intercostal artery. Spinal angiography showed that the lesion was slightly visualized via the anterior spinal artery from the right intercostal artery, while the part of the AVM fed by the posterior spinal artery had not changed on the angiograms (Figure 6 A and B). A left T10 intercostal angiogram following forceful injection of the contrast medium showed that the anterior spinal artery originating from the right T 10 intercostal artery was visualized via the anterior spinal canal artery (Figure 6 C). We attempted to introduce the Tracker-10 catheter into the posterior spinal artery but failed. However, it could be introduced into the dorsal spinal artery originating from the left T10 intercostal artery (Figure 7 A). We tried to embolize the residual AVM via the posterior spinal artery. Ivalon (150-180 /~m) was injected, and the AVM was completely occluded (Figure 7 B). Postembolization angiograms demonstrated that the residual AVM fed by the anterior spinal artery was also nearly occluded, while the parent artery was spared (Figure 7 C). He had transient worsening of the motor weakness in his left lower extremity (3/5), but it gradually improved after a few weeks (4/5).
Touho et al
The exacerbation of his neurological deficit was thought to be due to Ivalon particles migrating into the anterior spinal artery via the anterior spinal canal artery, resulting in occlusion of both the residual AVM and normal central branches to the spinal cord. He was discharged 2 weeks after the last embolization.
Discussion Elsberg first treated a spinal AVM by surgery in 1916 [10]. Thereafter, the treatment of these lesions has included artificial embolization as reported by Doppman et al [7,8] and Newton and Adams [21], as well as more recently by Djindjian [4], Rich6 et al [27], and Horton et al [14]. Technical limitations on the embolization of spinal AVMs have been described in several reports. Recently, Hall et al reported that embolization is only a temporary measure for many spinal AVMs and that recanalization plays a major role in the poor long-term results [12]. We feel that one cause of this temporary efficacy is that the embolic material lodges proximal to the radicular artery or at the artery itself (proximal embolization), which allows new collaterals to develop via extradural anastomoses, including vertebral body vessels, the anterior spinal canal artery, and various muscular branches, or via intradural anastomoses, including the anterior and posterior spinal arteries [ 3,11]. The primary goal in treating spinal AVMs is to permanently obliterate the lesion without damaging the spinal cord parenchyma. The goal in treating a dural AVF is to eliminate the transmission of venous hypertension to the spinal cord. This can be accomplished by interruption of the AVF by embolization during interventional angiography. Embolization can also arrest the progression of venous congestion of the spinal cord until surgical intervention can be performed. Permanent elimination of the AVF is accomplished surgically by resection of the lesion or by interruption of the vein that drains into the AVF at the entrance to the intrathecal space. Intradural spinal AVMs include glomus and juvenile AVMs. The former type is supplied by a segmental spinal artery and usually has a single feeding artery. When a glomus-type AVM is located in the cervical spine, surgical resection is relatively easy, but when it lies in the thoracic or lumbar spine, surgery carries a much greater risk [6,15,17,18,20,22,23,25,31]. Therfore, it is reasonable for this type of AVM to be treated by embolization rather than surgical intervention. Tadarvarthy et al first introduced PVA as an embolic material in four patients with gastrointestinal bleeding, arteriovenous malformation, hemangioma, and traumatic vessel rupture in 1975 [32]. Experimental animals have been used in the evaluation of the effects of Ivalon [1,32,35]. Three days after embolization, the vessels
Selective Embolization of Spinal AVMs
Surg Neurol 1992;38:85-94
a
91
I
Figure 5. (A) The right TIO intercostal artery angiograms in case 2 shouing that the Adamkiewicz artery originated from the segmental artery, and the glomus-type malformation was fed via the former artery. (B) Superselective catheterization to the radiculomedullary artery originating from the right T10 intercostal artery. (C) Postembolization angiograms of the right T10 intercostal artery in case2. The nidus has almost disappeared, {vith sparing of the descending segment of the anterior spinal artery.
t _ _
b
were completely occluded by Ivalon, and flesh clots plus dense fibrous tissue within and around the Ivalon was found 5 months after embolization. Castaneda-Zuniga et al reported that an organized and partially calcified thrombus containing Ivalon was found 9 months after the embolization [1]. However, White et al found that after experimental embolization of the gastrosplenic and renal arteries in three pigs, Ivalon could be detected histologically in only one animal, and distal migration of the emboli was the explanation given [3,4]. Horton et
II
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J
al[ 14] and Hall et al[ 12] have reported a recanalization rate of 2/3 (66.7%) and 5/6 (83.3%), respectively. The latter authors also reported that embolization provided only temporary relief for many spinal AVMs, and that delayed reassessment with spinal angiography and/or MRI is indicated after embolic occlusion, particularly if symptoms persist or recur. Surgical excision provides the only means of permanently eliminating flow through an AVM in most patients and should be considered the treatment of choice when it is feasible. In the present
92
Surg Neurol 1992;38:85-94
Touho et al
a
'
,,
b
,,
c
,
Figure 6. The spinal angiograms in case 2 on readmission. (A) The right TIO intercostal arter) angiograms show that the nidus is slightly visualized via the anterior spinal artery. (B) The/eft TIO intercostal artery angiograms show that the nidus is fed via the posterior spinal artery. (C) The left TIO intercostal artery angiogram when the contrast agent was forcefully injected into the artery. The anterior spinal artery originating from the right TIO intercostal artery (arrow) is visualized via the anterior spinal canal artery (arrowheads).
study, recanalization occurred in 10/14 patients (71.4%) after conventional embolization. Thus, a spinal AVM is unlikely to be cured completely and permanently by conventional embolization. An important factor in unsuccessful embolization is the development of collaterals via intradural and/or extradural anastomotic channels when the embolus lodges proximal to or at the radiculomedullary artery, as o c -
curred in case 1. The distance between the tip of the catheter and the AVM is occasionally too great for the embolic material to reach the lesion, and it occludes vessels proximal to and/or at the level of the radiculomedullary artery. Newly developed feeding systems were seen in 5/14 (35.7%) patients treated by conventional embolization in our study. Clinical application of the Tracker microcatheter to
Figure 7. (A) Superselectit'e catheterization with the Tracker- l O into the dorsal spinal artery originating from the left T I O intercostal artery (right obh'que views). (B) Postembolization angiograms of the left TI 0 intercostal artery. The nidus has almost disappeared, sparing the posterior spinal artery. (C) The right T10 intercostal artery angiogram after the embolization of the/eft side. The residual nidus fed t,ia the anterior spinal artery has disappeared.
,
a
,,
b
"
c
'
Selective Embolization of Spinal AVMs
the embolization of spinal AVMs was also evaluated to determine if it could occlude the lesion while sparing the vessels supplying the spinal cord. This, new variablestiffness catheter, the Tracker-18 vascular access system, has recently become widely available commercially, allowing greater access to the cerebral circulation for the delivery of particulate emboli [13,26]. With the introduction of this microcatheter, superselective catheterization and embolization with PVA of a smaller diameter can be used in the management of spinal AVMs. The external diameter of the microcatheter is 3. OF, 2.2F, and 2.7F at the proximal shaft, distal shaft, and tip, respectively. The maximum caliber of the internal lumen is 0.018 inches. Moreover, the Tracher-10 has a smaller diameter (2.0F) than the Tracker-18 and gives excellent access to spinal AVMs. Ivalon particles for embolization have a diameter of about 150 to 350/.tm and can easily pass through this catheter. These small particles permit the occlusion of the lesion itself with preservation of the anterior and/or posterior spinal arteries and the normal central spinal arteries. Suh and Alexander have established that the diameter of the normal anterior spinal artery ranges from 340 to 1100/a.m in humans, while the diameter of the normal central spinal artery varies from 60 to 72 /s.m [30]. Thus, the calibrated particles used in this study will pass through the anterior spinal artery and will not enter the normal perforating spinal arteries, although they will enter dilated central arteries that supply intramedullary AVMs. Serial digital subtraction angiography allows for more precise control over the rate of occlusion of an AVM [9,35]. Theron et al described the application of temporary balloon occlusion of the vertebral artery followed by embolization with Ivalon to the management of cervical spinal AVMs. However, the microparticles could possibly still migrate into the distal portion of the vertebral artery after deflation of the balloon [33]. As shown in case 1, embolic therapy can be performed safely when the microcatheter is introduced into the segmental artery arising from the vertebral artery. In case 2, the intramedullary AVM was supplied from the artery of Adamkiewicz, and embolization with Ivalon via the Tracker-18 microcatheter successfully occluded the lesion itself while preserving the artery. Moreover, a descending segment of the artery of Adamkiewicz distal to the feeding arteries of the AVM subsequently became larger and normalized in diameter (Figure 6). After superselective embolization using the Tracker catheter, recanalization and the appearance of newly developed feeding systems was seen in 4/8 (50.0%) and 2/8 (25.0%) patients, respectively, which is a lower failure rate than for conventional embolization. Particularly, the occurrence of new feeding systems was much less
Surg Neurol 1992;38:85-94
93
frequent with the Tracker catheter. Superselective embolization with the Tracker vascular access system has several advantages in the management of spinal AVMs, because intramedullary AVMs cannot be treated surgically at present and because complications such as SAH and migration of embolic material to another site are reduced.
Conclusion Embolization appears to be the treatment of first choice in the management of glomus or juvenile AVMs, as these lesions are not amenable to surgery because myelotomy is required. Use of the Tracker access system and calibrated microparticles of Ivalon allows occlusion of the lesion itself with preservation of the normal spinal arteries. Long-term follow-up after embolization of patients with spinal AVMs is required to fully establish the adequacy of this technique.
References 1. Castaneda-Zuniga WR, Sanchez R, Amplatz K. Experimental observations on short and long-term effects of arterial occlusion with lvalon. Radiology 1978;126:783-5. 2. Cogan P, Stein BM. Spinal cord arteriovenous malformations with significant intramedullary components. J Neurosurg 1983;59: 471-8. 3. Crock HV, Yoshizawa H. The blood supply of the vertebral column and spinal cord in man. New York: Springer-Verlag, 1977. 4. Djindjian R. Embolization of angiomas of the spinal cord. Surg Neurol 1975;4:411-20. 5. Djindjian R, Merland JJ, Djindjian M, Houdart R. Embolization in the treatment of medullary arteriovenous malformations in 38 cases. Neuroradiology 1978;16:428-9. 6. Doppman JL. The nidus concept of spinal cord arteriovenous malformations. A surgical recommendation based upon angiographic observations. Br J Radio 1971 ;44:758-63. 7. Doppman JL, Di Chiro G, Ommaya AK. Obliteration of spinal cord arteriovenous malformations by percutaneous embolization. Lancet 1968;1:477. 8. DoppmanJL, Di Chiro G, Ommaya AK. Percutaneous embolization of spinal cord arteriovenous malformations. J Neurosurg 1971;34:48-55. 9. Doppman JL, Krudy AG, Miller DL, Otdfield E, Di Chiro G. [ntraarterial digital subtraction angiography of spinal arteriovenous malformations. AJNR 1983;4:1081-5. 10. Elsberg CA. Diagnosis and treatment of surgical disease of the spinal cord and its membranes. Philadelphia: WB Saunders, 1916:194-204. 11. Gillilan LA. The arterial blood supply of the human spinal cord. J Comp Neurol 1958;110:75-103. 12. Hall WA, Oldfield EH, Doppman JL. Recanalization of spinal arteriovenous malformations following embolization. J Neurosurg 1989;70:714-20. 13. Hilal SK, Khandji A, Chi TL, Stein BM, Bello JA, Sliver AJ. Synthetic fibercoated platinum coils successfully used for the endovascular treatment of arteriovenous malformations, aneurysms and direct arteriovenous fistulas of the CNS. AJNR 1988;9:1030 (abstract).
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14. Horton JA, Latchaw RE, Gold LH, Pang D. Embolization of intramedultary arteriovenous malformations of the spinal cord. AJNR 1986;7:113-8. 15. KarasawaJ, Kikuchi H, Miyamoto S. Surgical treatment of spinal arteriovenous malformation. Neurosurgeons (Proceedings of the 4th annual meeting of the Japanese Congress of Neurological Surgeons) 1984;4:309-321. 16. Kendall BE, Logue V. Spinal epidural angiomatous malformations d raining into intrathecal veins. Neuroradiology 1977; 13:181-9. l 7. Krayenbiihl H, Yasargil MG, McClintock HG. Treatment of spinal cord vascular malformations by surgical excision. J Neurosurg 1969;30:427-35. 18. Logue V, Aminoff MJ, Kendall BE. Results of surgical treatment for patients with a spinal angioma. J Neurol Neurosurg Psychiatry 1974;37:1074-81. 19. Merland JJ, Richd MC, Chira SJ. Intraspinal extramedullary arteriovenous fistula draining into the medullary veins. J Neuroradiol 1980;7:271-320. 20. Morgan MK, Marsch WR. Management of spinal arteriovenous malformations. J Neurosurg 1989;70:832-6. 21. Newton TH, AdamsJE. Angiographic demonstration and nonsurgical embolization of the spinal cord angioma. Radiology 1968;91:873-6. 22. Oldfield EH, Di Chiro G, Quindlen EA, Rieth KG, Doppman JL. Successful treatment of a group of spinal cord arteriovenous malformations by interruption of dural fistula. J Neurosurg 1983;59:1019-30. 23. Oldfield EH, Criscuolo GR. Spinal arteriovenous malformations. In: Tindall GT, ed. Contemporary neurosurgery, vol. 11. Baltimore: Williams & Wilkins, 1989. 24. Oldfield EH, Doppman JL. Spinal arteriovenous malformations. Clin Neurosurg 1987;34:161-83.
T o u h o et al
25. Ommaya AK, Di Chiro G, DoppmanJL. Ligation of arterial supply in the treatment of spinal cord arteriovenous malformations. J Neurosurg 1969;30:679-92. 26. Purdy PD, Samson D, Batjer HH, Risser RC. Preoperative embolization of cerebral arteriovenous malformations with polyvinyl alcohol particles: experience in 51 adults. AJNR 1990;11:501-10. 27. Rich~ MC, Melki JP, Merland JJ. Embolization of spinal cord vascular malformations via the anterior spinal artery. AJNR 1983;4:378-81. 28. Rosenblum B, Oldfield EH, DoppmanJL, Di Chiro G. Embolization of vascular malformations: a comparison of dural arteriovenous fistulas and intradural AVM's in 81 patients. J Neurosurg 1987;67:795-802. 29. Scialfa G, Scotti G, Biondi A, De Grandi C. Embolization of vascular malformations of the spinal cord. J Neurosurg Sci 1985;29:1-9. 30. Suh TH, Alexander L. Vascular system of the human spinal cord. Arch Neurol Psychol 1939;41:659-77. 31. Symon L, Kuyama H, Kendall B. Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 1984;60:238-47. 32. Tadarvarthy SWM, Moiler JH, Amplatz K. Polyvinyl alcohol (Ivalon)--a new embolic material. A m J Roentgenol 1975;125:60916. 33. Theron J, Cosgrove R, Melanson D, Ethier R. Spinal arteriovenous malformations: advance in therapeutic embolization. Radiology 1986;158:163-9. 34. White RI Jr, Strandberg JV, Gross GS, Barth KH, Therapeutic embolization with long~term occluding agents and their effects on embolized tissues. Radiology 1977;125:677-87. 35. Yeates A, Drayer G, Heinz ER, Osborne D. Intra-arterial digital subtraction angiography of the spinal cord. Radiology 1985;155:387-90.
85
Superselective Embolization of Spinal Arteriovenous Malformations Using the Tracker Catheter Hajime Keisuke
Touho,
M.D., Jun Karasawa, M.D., Hideyuki
Yamada,
M.D., and Keiji Shibamoto,
Ohnishi, M.D.,
M.D.
Department of Neurosurgery, Osaka Neurological Institute, Osaka, Japan
Touho H, KarasawaJ, Ohnishi H, Yamada K, Shibamoto K. Superselective embolization of spinal arteriovenous malformations using the Tracker catheter. Surg Neurol 1992;38:85-94. Eighteen patients with spinal arteriovenous malformations had been treated with conventional embolization, surgical removal, feeder ligation, and/or feeder coagulation between February 1985 and March 1990. The lesions included six glomus, four juvenile, three extramedullary, and five dural arteriovenous malformations or fistulas. Embolic therapy was conducted in 14 patients by introducing the tip of a catheter into the segmental arteries and injecting polyvinyl alcohol strips (500-1000/,m) (conventional embolization). Follow-up spinal angiography disclosed recanalization in 10 patients (71.4%) and the appearance of new feeding arteries in five patients (35.7%). We introduced the Tracker vascular access system in April 1990. Eight patients (four glomus, one juvenile, and three dural arteriovenous malformations) were treated with the minicatheter and Ivalon particles (150-350 tzm). Five patients showed neurological improvement immediately after treatment. The other three patients had severe paraparesis before treatment and did not show any improvement. One patient with a glomustype arteriovenous malformation showed transient neurological deterioration just after embolization with the Tracker-lO to occlude a lesion fed by the posterior spinal artery, because the Ivalon particles migrated into the anterior spinal artery via the anterior spinal canal artery. In one patient with a juvenile arteriovenous malformation, the Tracker-18 catheter perforated the radiculomedullary artery originating from the right vertebral artery, and subarachnoid hemorrhage occurred. However, the Tracker-10 could later successfully occlude the arteriovenous malformation. The rates of recanalization and appearance of the new feeding vessels were 4/8 (50.0%) and 2/8 (25%), respectively. KEY WORDS: Spinal arteriovenous malformation; Conventional embolization; Superselective embolization; Ivalon Address reprint requests to." Hajime Touho, M.D., Department of Neurosurgery, Osaka Neurological Institute, 2-6-23 Shonai-Takaramachi, Toyonaka 561, Osaka, Japan. Received December 23, 1991; acceptedJanuary 14, 1992.
c~91992by ElsevierSciencePublishingCo., Inc.
Spinal arteriovenous malformations (AVMs) are a relatively rare clinical entity. T h e r e are two major types o f spinal AVMs, i.e., the dural arteriovenous fistula (AVF) and the intradural AVM or AVF. Recently, Rosenblum et al and Oldfield et al reported the following classification of spinal AVMs: dural AVF, glomus-type intradural AVM, juvenile-type intradural AVM, and intradural AVF. This classification was based on differences in the anatomy and pathophysiology of these spinal lesions [15,16,24,28]. Since the reports of Doppman et al [ 6 - 8 ] , Djindjian et al [4,5], and Rich~ et al [27], the treatment o f spinal AVMs has included artificial embolization and/or surgical excision. The dural AVF, intradural retromedullary AVF, and intradural AVM in the conus region are relatively easy to embolize and/or obliterate surgically. On the other hand, an intramedullary AVM or intradural premedullary AVF may be supplied by the anterior spinal artery and be situated either in the spinal cord parenchyma itself or anterior to the spinal cord. Thus, the complete embolization and/or surgical obliteration of such lesions has been quite difficult. In particular, juvenile and glomus-type AVMs have been considered for embolization rather than surgical extirpation [2,4,19,23,2 5,29]. However, embolization o f such lesions is occasionally unsuccessful, because the embolic material becomes wedged proximal to or at the radiculomedullary artery (proximal embolization), and collaterals subsequently develop via extradural and/or intradural anastomoses [2,3,11]. In this study, we used the Tracker-18 vascular access system [13,26] to avoid proximal embolization and treated spinal AVMs by superselective catheterization plus embolizattion with Ivalon.
Clinical Materials and Methods Between April 1985 and March 1990, 18 patients with spinal AVMs were admitted to Osaka Neurological Institute for surgical and/or interventional therapy. The lesions included six glomus, four juvenile, three extramedullary, and five dural AVMs or AVFs (Table 1). 0090-3019/92/$5.00
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Touho et al
Table 1. Summary of 18 Patients with Spinal AVMs Case No. Age, yr
Sex
Type of AVM
Clinical Course
Neurological Deficits
l+
29
F
Juvenile
Apoplectic progressive
Rt hemiparesis
2~
35
M
Glomus
Progressive
Monoparesis (It leg)
3
54
M
Glomus
Progressive
4
34
F
Conus
Apoplectic progressive
5
44
M
Dural
Progressive
Monoparesis (It leg), paresthesia (T5-T10) Paraparesis, urinary incontinence, sacral anesthesia Monoparesis (rt leg)
6 7
38 28
M M
Juvenile Juvenile
8
28
M
Glomus
Apoplectic Apoplectic progressive Apoplectic
9
8
M
Retromedullary
Progressive
10
54
M
Dural
Progressive
11"
61
M
Dural
Progressive
12
29
M
Conus
Progressive
13
57
F
Juvenile
Progressive
14+
29
M
Glomus
Progressive apoplectic
15~
50
F
Glomus
Progressive apoplectic
16+
86
M
Dural
Apoplectic
17+
86
M
Dural epidural
Apoplectic progressive
Paraparesis, urinary incontinence Paraparesis, urinary incontinence, hypesthesia (L3-) Paraparesis, urinary incontinence Paraparesis, hypesthesia (L4-), urinary incontinence Paraparesis, hypesthesia (L5--) Paraparesis, hypesthesia (L3-) anesthesia (L6-), urinary incontinence Paraparesis, hypesthesia (L10-), urinary incontinence Paraparesis, urinary incontinence Paraparesis, urinary incontinence
18*
38
M
Glomus
Progressive
Feeding Arteries
Past Results (Follow-up Periods, no)
Past Treatments
C7-T2
Emb, It VA feeder lig
Unchanged (60)
T9
Emb
Improved (42)
T7
Emb
Improved (72)
ASA (rt L2)
L1-2
Emb, removal
Improved (71)
RMA (rt T5)
T5-6
Improved (39)
Monoparesis (It leg) Lt hemiparesis
ASA (It T4, rt L1, rt S) Bi VA (ASA, PSA)
L1 C1-3
Emb, removal Emb Feeder lig
Paraparesis
ASA (rt L1), PSA (rt L1) ASA (rt T12)
T12
Paraparesis, muscle atrophy (rt leg), hypesthesia ($1-5), urinary incontinence
Bi VA (ASA, PSA), rt costocervical (PSA), rt T3 (ASA), it T5 (PSA) ASA (rt T10), PSA (It T10) ASA (It T4)
Level of Nidus
Unchanged (72) Unchaged (141) Unchanged (85)
L1
Emb, feeder lig Feeder coagulation
RMA (rt T7)
T7-8
Removal
Unchanged (43)
RMA (rt T7)
T7-8
Emb
Unchanged (29)
ASA (It T9), PSA (rt L2)
L1
Emb, removal
Improved (26)
ASA (it T8), PSA (rt T7) ASA, PSA (T4)
T1-3
Unchanged (22)
T2-3
Emb, removal Emb
ASA (rt L2, It L2)
TI2
Emb
Unchanged (22)
Rt T12, L1
L1
Bi T3-5
T3-5
ASA (It L2), PSA (rt T l l )
T12
Improved (69)
Unchanged (28)
--
Emb, surgical obliteration (dural) Emb
(27)
Unchanged (47)
Worsened (30)
Abbreviations: AVM, arteriovenous malformation; F, female; rt, right; Bi, bilateral; VA, vertebral artery; ASA, anterior spinal artery; PSA, posterior spinal artery; It, left; emb, embolization; lig, ligation; M, male; RMA, radiculomedullary artery. +Patient treated with minicatheter and Ivalon.
Embolization was performed in 14 patients by introducing the angiographic catheter into the origin of the segmental artery and injecting potyvinyl alcohol (PVA) strips (500-1000 ~,m) in a flow-directed manner (conventional embolization). Follow-up spinal angiograms performed from 2 to 12 months after the last embolization disclosed angiograhic recanalization in 10 patients
(71.4%) and the appearance of newly developed feedings arteries in five patients (35.7%). Due to the high rate of recanalization and/or appearance of new feeding systems, we introduced the Tracker vascular access system for treating patients in April 1990. The appearance of new feeding systems was thought to occur because emboli lodged promixal to the nidus and occluded either
Selective Embolization of Spinal AVMs
the segmental artery itself, the dorsal spinal artery, the radicular branch, or the anterior or posterior spinal artery. It was thought to be reasonable that an embolic agent injected near to the nidus by the minicatheter could be navigated into the lesion itself. Seven patients (four glomus, one juvenile, and two dural AVFs), who had been treated with conventional embolization and showed recanalization and/or the appearance of new feeding systems, as well as one elderly patient with dural AVFs who had not been treated previously, underwent superselective embolization using the minicatheter and Ivalon. Superselective embolization was conducted by introducing the Tracker-18 or Tracker-10 near to the lesion through the guiding catheter, the tip of which was placed at the origin of the segmental artery. The Tracker vascular access system is composed of a 150-cm Tracker18 or Tracker-10 catheter, a 175-cm tapered steerable guidewire, a guidewire introducer, and a rotating hemostatic valve (Target Therapeutics, Inc., San Jose, Calif.). The guiding catheter used was an HNB 6F angiographic catheter or a BPS 6.5F spinal angiography catheter (Cook Group, Bloomington, Ind.). We used 180- to 350-/~m Ivalon particles, which were suspended in contrast medium (Ioparmiron®, iopamidol, Schering AG, Berlin, Germany) and were embolized in a flow-directed manner toward the nidus via the microcatheter. The procedure was terminated when flow through the lesion was almost eliminated and/or reflux of the contrast medium began to appear proximal to the catheter tip. Vital signs and neurological function were carefully monitored during and after the procedure.
Results In the eight patients treated with the Tracker catheter system, it could be introduced at least to the dorsal spinal artery, and it could usually enter the radicular, radiculospinal, or radiculomedullary artery. Moreover, the catheter could be navigated into the anterior spinal artery in juvenile-type AVM. We could obliterate the lesion with Ivalon while preserving the anterior or posterior spinal artery in these patients. Recanalization and the appearance of new feeding systems due to proximal occlusion occurred in 4/8 (50.0%) and 2/8 (25.0%) patients, respectively, in 10 to 21 months of follow-up. Five patients showed marked neurological improvement just after treatment, but the other three patients (who already had severe paraparesis or paraplegia before treatment) did not show any improvement after superselective embolization. Case 2 showed marked neurological improvement after the first superselective embolization of the AVM via the right T10 intercostal artery using a Tracker- 18 catheter, and manifested transient neurological deterioration just after the last embolization of the
Surg Neurol 1992;38:85-94
87
residual nidus via the left T10 intercostal and posterior spinal arteries using a Tracker-10 catheter. This was because the anterior spinal artery, which originated from the right T10 intercostal artery and had supplied feeding branches to the AVM, was connected via the anterior spinal canal artery with the posterior spinal artery originating from the left T10 intercostal artery. Thus, Ivalon particles migrated to the right side in addition to occluding the lesion via the posterior spinal artery. The transient neurological deficit almost completely improved after 1 week. In one patient with a juvenile AVM at the cervicothoracic level, the Tracker-18 system perforated the radiculomedullary artery at its site of entry into the dura mater during manipulation of the guide wire, and subarachnoid hemorrhage (SAH) occurred. However, the Tracker-10 could later be introduced into the anterior originating from the right vertebral artery, and successful obliteration of the lesion was achieved 2 weeks after SAH. The rate of complications due to superselecrive embolization was 2/8 (25.0%).
I l l u s t r a t i v e Cases Case 1 A 29-year-old woman had a history of SAH on two occasions over the past 2 years. She was admitted to Osaka Neurological Institute on May 12, 1986. Spinal angiograms demonstrated a juvenile AVM in the cervicothoracic region, with feeding vessels branching from the bilateral vertebral arteries, right costocervical trunk, right T3 intercostal artery, and left T5 intercostal artery. Conventional embolization was conducted with 500- to 1000-/xm PVA strips, excepts for the branches from the bilateral vertebral arteries. When the feeding system was occluded by embolization, the segmental branch that originated from the left vertebral artery was ligated surgically. However, she became quadriparetic in November 1987, and this state was exacerbated despite medical treatment. She was admitted with quadriparesis (upper extremities, 3-4/5; lower extremities, 1-2/5) on June 18, 1990. On June 25, 1990, spinal angiography was performed, and it disclosed that the AVM still existed and was fed by the right anterior and posterior spinal arteries and the left anterior spinal artery, as shown in Figure 1 A. The segmental branch of the left vertebral artery, which gave off feeding branches via the anterior spinal artery, was too narrow to catheterize. After placing the guiding catheter at the origin of the right vertebral artery, the Tracker-18 was introduced into the segmental artery. However, the guide wire perforated the arterial wall at the site where the radiculomedullary artery entered the dura, and SAH occurred, which resolved by the next
88
Surg Neurol 1992;38:85-94
,
a
Touho et al
,,
Figure 1. (A) Anteroposterior views of bilateral vertebral angiograms in case I. The intramedullary component of the arteriovenous malformation was fed via the anterior (arrow) and posterior (arrowhead./spinal arteries from the right vertebral artery (left), and it was also fed via the anterior spinal artery (arrow) from the/eft vertebral artery (right). (B) Superselective catheterization to the segmental artery of the right vertebral artery with the Tracker-18 catheter. The miniangiograms show arteriovenous malformation with an arterial aneurysm (arrow). (C) Follow-up angiograms of the right vertebral artery. These showed that the nidus had become even smaller and the aneurysm had disappeared.
day. Selective embolization using the Tracker-18 catheter was attempted again 3 days after SAH, and this time the minicatheter was successfully introduced into the proximal portion of the segmental branch and miniangiograms were obtained through the catheter (Figure 1 B). After confirming that there was no reflux into the right vertebral artery, 180- to 350-~m Ivalon was fed into the catheter. When the contrast medium stopped flowing into the aneurysm, the procedure was terminated. The function of her upper extremities improved just after embolization. Follow-up angiography was performed 17 days later. This disclosed that the AVM had become even smaller, and the associated aneurysm had disappeared (Figure 1 C). She was discharged 19 days after embolization, with her neurological symptoms having shown no further change. She was admitted again on March 12, 1991, for follow-up angiography. Her neurological deficits had not changed. On March 14, spinal angiography was conducted, revealing that the AVM
b
,t
C
J
had partially recanalized and that the right anterior and posterior spinal arteries gave off feeding branches to the AVM (Figure 2 A). The aneurysmal dilation was no longer visualized. We performed the superselective embolization with a Tracker-10 and Ivalon on March 19. The minicatheter was introduced into the anterior spinal artery originating from the right vertebral artery, and the AVM was embolized with 180- to 350-/zm Ivalon, resulting in complete occlusion of the anterior part of the lesion, which was fed by the anterior spinal artery (Figure 2 B and C). Before and during the embolization, blood pressure in the anterior spinal artery was intermittently monitored through the catheter. Before the embolization, systolic blood pressure was about 82 mm Hg (Figure 3 A), gradually increasing during the embolization (Figure 3 B), and at the end of the embolization, it became about 100 mm Hg (Figure 3 C). Blood pressure in the vertebral artery is shown in Figure 3D. On March 26, embolization was again performed to occlude the posterior part of the lesion, which was fed by the posterior spinal artery (Figure 4). The preembolization angiograms showed that the anterior part of the AVM fed by the anterior spinal artery was no longer visualized and the diameter of the artery had become normal, while the posterior part of the AVM was still intact. Then, the Tracker-10 was introduced into the segmental artery, which originated from the right vertebral artery and gave off the posterior spinal artery, and
Selective Ernbolization of Spinal AVMs
Surg Neurol
89
1992;38:85-94
!i~ i~ ~
Figure 2. (A) Anteroposterior ~,ieu of the right vertebral angiogram in case l. The anteriovenous malformation isfed l,ia the anterior (arrow) and posterior spinal arteries (arrowhead). (B) The Tracker-l O catheter was successfully introduced into the anterior spinal artery, and a miniangiogram was obtained. (C) Postembolization angiograms of the right vertebral artery. The compartment of the nidus that was fed via the anterior spinal artery has disappeared. Central arteries as feeding ressels are c/early depicted (arrou ).
t
a
150-180/zm Ivalon was injected through the catheter, after confirming that there was no reflux into the vertebral artery on the miniangiograms (Figure 4 A). Thus, we could occlude the posterior part of the AVM while sparing the posterior spinal artery (Figure 4 B). Just after the first embolization, her fine finger movements were improved, and sensory disturbance in her upper extremities (hypesthesia and paresthesia) improved just after the second embolization. She was discharged on March 30, 1991.
"
b
JI
C
•
Figure 4. (A) Anteroposterior view of the superselective angiography in case 1. The Tracker-l O catheter was introduced into the radiculomedullary branch (arrow). (B) Postembolization angiograms of the right vertebral arter). The nidus has almost disappeared, while both the antertor and posterior spinal arteries have been spared.
Case 2 A 35-year-old man was admitted to Osaka Neurological Institute. He had suffered from slowly progressive too-
Figure 3. Blood pressure in the anterior spinal artery in case 1. (A) before the embolization, (B) during the embolization, and (C) at the end of the embolization. (D) Blood pressure in the right vertebral artery. 120 t~
-r
100
E E 8O rn
a
60
b
'
a
"
b
'
90
Surg Neurol 1992;38:85-94
noparesis in his left lower extremity and low back pain for the last 5 years. On October 30, 1987, spinal angiography disclosed a glomus-type spinal AVM of the thoracic cord that was fed by the anterior and posterior spinal arteries via the right and left T10 intercostal arteries, respectively. He was initially treated with conventional embolization using 500-/zm PVA strips via the right T10 intercostal artery, resulting in near disappearance of the lesion and the transient return of spinal reflexes. He showed a marked improvement in his monoparesis and low back pain just after embolization, but these symptoms returned about 2 weeks later. He was admitted on August 13, 1990, for treatment of the AVM by superselective embolization. Spinal angiography showed complete recanalization of the AVM, which was fed by the anterior and posterior spinal arteries originating from the right and left intercostal arteries, respectively (Figure 5 A ). After performing conventional angiography, the guiding catheter was introduced into the right T 10 intercostal artery and the Tracker- 18 catheter was superselectively introduced into the radiculomedullary artery (Figure 5 B). Then 150- to 180-/zm Ivalon was injected through the catheter, resulting in almost complete occlusion of the AVM while sparing the anterior spinal artery (Figure 5 C). The patient showed a marked improvement in his monoparesis and back pain beginning just after embolization and was discharged 7 days later. On November 12, 1990, he was readmitted for embolization of the other part of the AVM, fed by the posterior spinal artery originating from the left intercostal artery. Spinal angiography showed that the lesion was slightly visualized via the anterior spinal artery from the right intercostal artery, while the part of the AVM fed by the posterior spinal artery had not changed on the angiograms (Figure 6 A and B). A left T10 intercostal angiogram following forceful injection of the contrast medium showed that the anterior spinal artery originating from the right T 10 intercostal artery was visualized via the anterior spinal canal artery (Figure 6 C). We attempted to introduce the Tracker-10 catheter into the posterior spinal artery but failed. However, it could be introduced into the dorsal spinal artery originating from the left T10 intercostal artery (Figure 7 A). We tried to embolize the residual AVM via the posterior spinal artery. Ivalon (150-180 /~m) was injected, and the AVM was completely occluded (Figure 7 B). Postembolization angiograms demonstrated that the residual AVM fed by the anterior spinal artery was also nearly occluded, while the parent artery was spared (Figure 7 C). He had transient worsening of the motor weakness in his left lower extremity (3/5), but it gradually improved after a few weeks (4/5).
Touho et al
The exacerbation of his neurological deficit was thought to be due to Ivalon particles migrating into the anterior spinal artery via the anterior spinal canal artery, resulting in occlusion of both the residual AVM and normal central branches to the spinal cord. He was discharged 2 weeks after the last embolization.
Discussion Elsberg first treated a spinal AVM by surgery in 1916 [10]. Thereafter, the treatment of these lesions has included artificial embolization as reported by Doppman et al [7,8] and Newton and Adams [21], as well as more recently by Djindjian [4], Rich6 et al [27], and Horton et al [14]. Technical limitations on the embolization of spinal AVMs have been described in several reports. Recently, Hall et al reported that embolization is only a temporary measure for many spinal AVMs and that recanalization plays a major role in the poor long-term results [12]. We feel that one cause of this temporary efficacy is that the embolic material lodges proximal to the radicular artery or at the artery itself (proximal embolization), which allows new collaterals to develop via extradural anastomoses, including vertebral body vessels, the anterior spinal canal artery, and various muscular branches, or via intradural anastomoses, including the anterior and posterior spinal arteries [ 3,11]. The primary goal in treating spinal AVMs is to permanently obliterate the lesion without damaging the spinal cord parenchyma. The goal in treating a dural AVF is to eliminate the transmission of venous hypertension to the spinal cord. This can be accomplished by interruption of the AVF by embolization during interventional angiography. Embolization can also arrest the progression of venous congestion of the spinal cord until surgical intervention can be performed. Permanent elimination of the AVF is accomplished surgically by resection of the lesion or by interruption of the vein that drains into the AVF at the entrance to the intrathecal space. Intradural spinal AVMs include glomus and juvenile AVMs. The former type is supplied by a segmental spinal artery and usually has a single feeding artery. When a glomus-type AVM is located in the cervical spine, surgical resection is relatively easy, but when it lies in the thoracic or lumbar spine, surgery carries a much greater risk [6,15,17,18,20,22,23,25,31]. Therfore, it is reasonable for this type of AVM to be treated by embolization rather than surgical intervention. Tadarvarthy et al first introduced PVA as an embolic material in four patients with gastrointestinal bleeding, arteriovenous malformation, hemangioma, and traumatic vessel rupture in 1975 [32]. Experimental animals have been used in the evaluation of the effects of Ivalon [1,32,35]. Three days after embolization, the vessels
Selective Embolization of Spinal AVMs
Surg Neurol 1992;38:85-94
a
91
I
Figure 5. (A) The right TIO intercostal artery angiograms in case 2 shouing that the Adamkiewicz artery originated from the segmental artery, and the glomus-type malformation was fed via the former artery. (B) Superselective catheterization to the radiculomedullary artery originating from the right T10 intercostal artery. (C) Postembolization angiograms of the right T10 intercostal artery in case2. The nidus has almost disappeared, {vith sparing of the descending segment of the anterior spinal artery.
t _ _
b
were completely occluded by Ivalon, and flesh clots plus dense fibrous tissue within and around the Ivalon was found 5 months after embolization. Castaneda-Zuniga et al reported that an organized and partially calcified thrombus containing Ivalon was found 9 months after the embolization [1]. However, White et al found that after experimental embolization of the gastrosplenic and renal arteries in three pigs, Ivalon could be detected histologically in only one animal, and distal migration of the emboli was the explanation given [3,4]. Horton et
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al[ 14] and Hall et al[ 12] have reported a recanalization rate of 2/3 (66.7%) and 5/6 (83.3%), respectively. The latter authors also reported that embolization provided only temporary relief for many spinal AVMs, and that delayed reassessment with spinal angiography and/or MRI is indicated after embolic occlusion, particularly if symptoms persist or recur. Surgical excision provides the only means of permanently eliminating flow through an AVM in most patients and should be considered the treatment of choice when it is feasible. In the present
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Touho et al
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Figure 6. The spinal angiograms in case 2 on readmission. (A) The right TIO intercostal arter) angiograms show that the nidus is slightly visualized via the anterior spinal artery. (B) The/eft TIO intercostal artery angiograms show that the nidus is fed via the posterior spinal artery. (C) The left TIO intercostal artery angiogram when the contrast agent was forcefully injected into the artery. The anterior spinal artery originating from the right TIO intercostal artery (arrow) is visualized via the anterior spinal canal artery (arrowheads).
study, recanalization occurred in 10/14 patients (71.4%) after conventional embolization. Thus, a spinal AVM is unlikely to be cured completely and permanently by conventional embolization. An important factor in unsuccessful embolization is the development of collaterals via intradural and/or extradural anastomotic channels when the embolus lodges proximal to or at the radiculomedullary artery, as o c -
curred in case 1. The distance between the tip of the catheter and the AVM is occasionally too great for the embolic material to reach the lesion, and it occludes vessels proximal to and/or at the level of the radiculomedullary artery. Newly developed feeding systems were seen in 5/14 (35.7%) patients treated by conventional embolization in our study. Clinical application of the Tracker microcatheter to
Figure 7. (A) Superselectit'e catheterization with the Tracker- l O into the dorsal spinal artery originating from the left T I O intercostal artery (right obh'que views). (B) Postembolization angiograms of the left TI 0 intercostal artery. The nidus has almost disappeared, sparing the posterior spinal artery. (C) The right T10 intercostal artery angiogram after the embolization of the/eft side. The residual nidus fed t,ia the anterior spinal artery has disappeared.
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Selective Embolization of Spinal AVMs
the embolization of spinal AVMs was also evaluated to determine if it could occlude the lesion while sparing the vessels supplying the spinal cord. This, new variablestiffness catheter, the Tracker-18 vascular access system, has recently become widely available commercially, allowing greater access to the cerebral circulation for the delivery of particulate emboli [13,26]. With the introduction of this microcatheter, superselective catheterization and embolization with PVA of a smaller diameter can be used in the management of spinal AVMs. The external diameter of the microcatheter is 3. OF, 2.2F, and 2.7F at the proximal shaft, distal shaft, and tip, respectively. The maximum caliber of the internal lumen is 0.018 inches. Moreover, the Tracher-10 has a smaller diameter (2.0F) than the Tracker-18 and gives excellent access to spinal AVMs. Ivalon particles for embolization have a diameter of about 150 to 350/.tm and can easily pass through this catheter. These small particles permit the occlusion of the lesion itself with preservation of the anterior and/or posterior spinal arteries and the normal central spinal arteries. Suh and Alexander have established that the diameter of the normal anterior spinal artery ranges from 340 to 1100/a.m in humans, while the diameter of the normal central spinal artery varies from 60 to 72 /s.m [30]. Thus, the calibrated particles used in this study will pass through the anterior spinal artery and will not enter the normal perforating spinal arteries, although they will enter dilated central arteries that supply intramedullary AVMs. Serial digital subtraction angiography allows for more precise control over the rate of occlusion of an AVM [9,35]. Theron et al described the application of temporary balloon occlusion of the vertebral artery followed by embolization with Ivalon to the management of cervical spinal AVMs. However, the microparticles could possibly still migrate into the distal portion of the vertebral artery after deflation of the balloon [33]. As shown in case 1, embolic therapy can be performed safely when the microcatheter is introduced into the segmental artery arising from the vertebral artery. In case 2, the intramedullary AVM was supplied from the artery of Adamkiewicz, and embolization with Ivalon via the Tracker-18 microcatheter successfully occluded the lesion itself while preserving the artery. Moreover, a descending segment of the artery of Adamkiewicz distal to the feeding arteries of the AVM subsequently became larger and normalized in diameter (Figure 6). After superselective embolization using the Tracker catheter, recanalization and the appearance of newly developed feeding systems was seen in 4/8 (50.0%) and 2/8 (25.0%) patients, respectively, which is a lower failure rate than for conventional embolization. Particularly, the occurrence of new feeding systems was much less
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frequent with the Tracker catheter. Superselective embolization with the Tracker vascular access system has several advantages in the management of spinal AVMs, because intramedullary AVMs cannot be treated surgically at present and because complications such as SAH and migration of embolic material to another site are reduced.
Conclusion Embolization appears to be the treatment of first choice in the management of glomus or juvenile AVMs, as these lesions are not amenable to surgery because myelotomy is required. Use of the Tracker access system and calibrated microparticles of Ivalon allows occlusion of the lesion itself with preservation of the normal spinal arteries. Long-term follow-up after embolization of patients with spinal AVMs is required to fully establish the adequacy of this technique.
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