J Neurosurg 72:216-223, 1990

Surgical management of epilepsy associated with cerebral arteriovenous malformations HWA-SHAIN YEH, M . D . , SHIRO THOMAS S. BERGER, M . D .

KASHIWAGI, M.D.,

JOHN M . TEW, JR., M.D., AND

Department of Neurosurgery, University of Cincinnati College of Medicine and Mayfield Neurological Institute, Cincinnati, Ohio; and Department of Neurosurgery, Yamaguchi University School of Medicine, Yamaguchi, Japan ~" Between 1982 and 1986, 27 patients with seizure disorders due to cerebral arteriovenous malformation (AVM) were surgically treated by the authors. These patients had no history or clinical manifestation of intracranial hemorrhage. All were treated with anticonvulsant agents by their neurologists but became disabled due to inadequate control of seizures by medication, side effects of the anticonvulsant drugs, or the effects on their professional lives of even infrequent seizures. The age of the patients ranged from 13 to 61 years. There were 13 males and 14 females. The AVM's were smaller than 2 cm in four patients, between 2 and 4 cm in five, and larger than 4 cm in 18. The most frequent location of the AVM's was in the temporal lobe, followed by the frontal, parietal, and occipital lobes. All patients had preoperative electroencephalography (EEG) and intraoperative electrocorticography. Intraoperative recording of the amygdala and the hippocampus by depth electrodes was performed if the AVM's were located in the temporal lobe. Superficial or posterior temporal lobe AVM's often have remote seizure foci that involve the amygdala and hippocampus. All patients underwent craniotomy and total excision of their AVM's. Surgery was carried out under local anesthesia to allow localization by electrical stimulation if the AVM involved the speech area or the sensorimotor cortex. Based on the EEG findings, excision of the epileptogenic lesion in addition to the AVM was performed in 18 patients. In seven patients with AVM's located in the temporal lobe, remote seizure foci were identified and excised. The remote epileptic activity was particularly prominent in AVM's in the temporal lobe and usually involved mesial temporal structures. Microscopic study of excised seizure loci showed gliosis in 26 cases, hemosiderin deposits in 10, and focal hemorrhage in four. There were no operative deaths. Two patients developed a hemiparesis and three suffered temporary dysphasia after surgery. Two patients had visual field deficits. The results of postoperative seizure control during the average follow-up period of 3 years 11 months were excellent in 21 patients, good in three, fair in two, and poor in one. The latter patient, whose epileptic lesion was not completely excised because of its location in the motor cortex, had poor seizure control postoperatively. Another patient required a second operation to remove a remote seizure focus. In this series, proposed mechanisms of seizure associated with cerebral AVM include focal cerebral ischemia secondary to arteriovenous shunting, gliosis of the surrounding brain, and a secondary epileptogenesis in the temporal lobe. Successful seizure control can be obtained with wide excision of the epileptogenic foci surrounding the AVM's. In some circumstances, seizure foci remote from the vascular malformation must be excised. KEY WORDS 9 seizure surgical treatment

H

arteriovenous malformation

EMORRHAGE is the m o s t f r e q u e n t finding o n a d m i s s i o n in patients with a r t e r i o v e n o u s malf o r m a t i o n ( A V M ) o f the brain. T h e results o f direct surgery o f cerebral h e m i s p h e r i c A V M ' s after h e m o r r h a g e are good. 4,5.10,aH4,15,2~ Epilepsy is the second m o s t f r e q u e n t s y m p t o m i n these patients; 26 however, the results of surgical t r e a t m e n t for seizure control are d i s a p p o i n t i n g in some reports. 3'5,6,18,w W e describe 216

~

electrocorticography

9

our experience in treating patients with seizures associated with cerebral A V M ' s w i t h o u t a clinical history of s y m p t o m m a n i f e s t a t i o n o f intracranial hemorrhage. S u m m a r y of Cases Between J a n u a r y , 1982, a n d December, 1986, 27 patients who had seizure disorders a n d cerebral A V M ' s

J. Neurosurg / Volume 72/February, 1990

Surgery for epilepsy associated with AVM's TABLE

1

Clinical summary of 2 7 patients treated surgical@for epilepsy and A VM's* Case No.

Age (yrs), Sex

I

32, M

2 3 4 5

46, 40, 31, 54,

F M M F

6 7 8 9

42, 31, 13, 31,

M M F F

Duration of Symptoms (yrs)

Type of Seizures

_1

1

SP, SG SP

12

CP, SG

5

PG CP, SG

2

12 15

1_ 2

CP, SG PG

1 1

CP, SG SP

Site of AVM

Size of AVM

Cortical Excision

temporal parietal parietal frontal temporal

L L M L M

It temporal It temporal It temporal rt frontotemporal It occipital

Pathology Hemosiderin

Gliosis

+ +

+ + +

+ + + + +

L L L M

+ + +

-

+ + +

M

-

-

+

rt temporal rt frontotemporoparietal rt temporoparietal It occipital rt temporal rt temporal

M L

+ +

-

+ +

L

+

+

+

S L S

+ +

+

+ + +

rt frontal rt frontal rt frontal rt frontal rt frontal rt frontal It temporal

L L L S L L L

+ + + + +

+ + + +

+ + + + + + +

It It It It It

10

36, F

6

SP, SG

11 12

44, M 43, F

12 10

13

29, M

1 89

CP, SG SP, CP, SG PG

14 15 16

14, F 24, F 30, M

3 6 9

17 18 19 20 21 22 23

16, M 39, F 34, F 17, M 37, M 35, F 46, M

89 6 18 19 27

SP, SG PG CP, SG CP, SG SP, SG CP, SG SP, SG

24

28, F

10

CP, SG

It temporal

L

+

-

+

25 26 27

50, M 41, M 61, F

20 18 4

CP, SG CP, SG SP

It temporal It temporal rt parietal

L S L

+ + -

+ -

+ + +

89 22

SP CP SP, CP, SG

Complications + mild dysphasia It mild hemiparesis rt homonymous hemianopsia It hemiparesis It partial hemianopsia temporary dysphasia 1) rt paresthesias 2) transient dysphasia -

Seizure Control

Follow-Up Period

excellent excellent excellent poor fair

6 6 6 5 5

excellent excellent excellent excellent

5 4 4 4

yrs yrs yrs yrs 7 mos yrs 6 mos

good

yrs yrs 10 mos yrs 7 mos yrs 4 rnos , 4 yrs 4 mos

excellent good

4 yrs 3 mos 3 yrs

excellent

3 yrs

fair excellent seizurefree after 2nd op excellent excellent excellent excellent excellent excellent excellent

2 yrs 11 mos 2 yrs 10 mos 3 yrs 2 2 2 2 2 2 2

excellent

2 yrs 2 mos

excellent excellent excellent

2 yrs 2 mos 2 yrs 1 mo 2 yrs ,

yrs yrs yrs yrs yrs yrs yrs

11 mos 11 mos 10 mos 10 mos 8 mos 4 mos 4 mos

* AVM = arteriovenous malformation; SP = simple partial; CP = complex partial; PG = primary generalized; SG = secondary generalized; L = large (> 4 cm); M = medium (2-4 cm); S = small (< 2 cm); + = factor present; - = factor absent. " ~r

with no history of cerebral hemorrhage were treated surgically in our institutions. All of these patients had been treated medically and were considered disabled due to failure or side effects of anticonvulsant therapy or the effect upon their professional lives of even infreq u e n t s e i z u r e s . D u r i n g t h e s a m e i n t e r v a l , 53 p a t i e n t s with cerebral AVM's and intracerebral hemorrhage were treated surgically in our institutions.

Clinical Preparation T h e p a t i e n t s i n c l u d e d 13 m a l e s a n d 14 f e m a l e s w i t h age at presentation for surgical treatment ranging from 13 t o 61 y e a r s ( T a b l e 1). N o n e h a d a n y m a n i f e s t a t i o n or prior history of intracranial hemorrhage. Five pa-

J. Neurosurg. / Volume 7 2 / F e b r u a r y , 1990

tients had generalized seizures without aura or focal s y m p t o m , 10 h a d s i m p l e p a r t i a l s e i z u r e s , 14 h a d c o m p l e x p a r t i a l s e i z u r e s , a n d 17 h a d p a r t i a l s e i z u r e s w i t h s e c o n d a r y g e n e r a l i z a t i o n ( T a b l e 2). S i x t e e n p a t i e n t s h a d two types of seizures and two patients had three types of seizures. The duration of seizure history varied from 6 m o n t h s t o 41 y e a r s , w i t h a n a v e r a g e o f 8 y e a r s 6 m o n t h s ( T a b l e 1). The findings on neurological examination included progressive mental changes in two patients, memory impairment in three, dysphasia in four, and limb ataxia in one. One patient had a right homonymous hemia n o p s i a , a n d a n o t h e r h a d a left h e m i p a r e s i s a f t e r a n embolization procedure at another institution. 21 7

H. S. Yeh, et al. TABLE 2 Types ~f seizures correlated with location of arteriovenous maformation (.4 VM) No. of Partial Generalized Location of AVM Cases Simple Complex Primarily Secondarily frontal 7 2 3 2 5 frontotemporal 1 1 0 0 0 frontotemporo1 0 1 1 0 parietal parietal 3 3 0 0 1 temporal 12 2 10 1 10 temporoparietal 1 0 0 1 0 occipital 2 2 0 0 1 totals 27 10 14 5 17

Location and Size o f A VM's All A V M ' s were supratentorial (Table 1). The most frequent location was in the temporal lobe, followed by the frontal, parietal, and occipital lobes. The size of the A V M ' s is documented in Table 3. An A V M was characterized as small if it measured less than 2 cm in diameter, m e d i u m if it measured between 2 and 4 cm in diameter, and large if it measured m o r e than 4 cm in diameter. There were four small, five medium, and 18 large lesions in this group. Diagnosis Cerebral angiography was performed on all patients. Arteriovenous malformations were demonstrated in 25 patients, while two exhibited a calcified intracerebral mass on computerized t o m o g r a p h y (CT) scanning. Eight patients, including two with negative angiographic studies, underwent magnetic resonance (MR) imaging in addition to angiography and CT. An M R study m a y offer better anatomical information, and it is decidedly more sensitive than C T in detecting cryptic vascular malformations. In Case 26, M R imaging demonstrated extensive hemosiderin deposit and thrombosis in an angiographically occult A V M (Fig. 1). Electroencephalographic S t u d y All patients underwent preoperative electroencephalographic (EEG) evaluation. Sphenoidal electrodes were used in patients presenting with complex partial seizures, especially those with an A V M in the temporal lobe. Prolonged E E G recording with activation procedures such as hyperventilation, drug-induced sleep, or the careful withdrawal of anticonvulsant medication was used to enhance EEG abnormalities. Fourteen patients had focal epileptiform activity, six had nonspecific slow-wave activity, and the other seven had normal E E G recordings. Intraoperative electrocorticography (ECoG) was performed routinely before surgical removal of the AVM's. Epileptiform activity was demonstrated adjacent to or remote from the A V M ' s in 18 patients. 23 8

TABLE 3 Size and location of arteriovenous malJ'ormations (A VM's) Size of AVM large (> 4 cm) medium (2-4 cm) small (< 2 cm) totals

No. of Cases 18 5 4 27

Left Right Hemisphere Hemisphere 9 9 3 2 2 2 14 13

Most of the epileptiform activities were found on the surface of the cortex in proximity to the AVM's. There were seven patients who, in addition, had remote independent epileptiform activity involving mesial temporal structures such as amygdala or hippocampus.

Neuropsychological S t u d y Neuropsychological studies were performed on all patients. The intracarotid Amytal (amobarbital) test for speech and m e m o r y function was carried out in most patients, especially if the A V M was in the dominant hemisphere. This test m a y not be reliable because of profound arteriovenous shunting in a large AVM. Most of the Amytal reaches the high-flow A V M ' s first, and aphasia m a y develop after ipsilateral and contralateral carotid arterial injection. In this circumstance, a smaller dose of Amytal (such as 25 mg) may be used instead of the conventional dose (175 mg). M e m o r y testing was also performed during the intracarotid Amytal study. If there was epileptiform activity in the mesioinferior portion of a temporal lobe (hippocampus), it was removed only when the contralateral temporal lobe was functioning normally. Surgical Techniques Most of these operations were performed under local anesthesia using Marcaine (bupivacaine hydrochloride). With Marcaine, the onset of action is rapid and anesthesia is long-lasting. In the average adult, 40 ml or less of 0.5% Marcaine with epinephrine 1:200,000 is used for injection into the superficial skin, fascia, muscles, and periosteum, as well as the dura m a t e r adjacent to meningeal vessels. Intermittent intravenous fentanyl, droperidol, and a short-acting barbiturate such as Brevital (methohexital sodium) were given in addition to local anesthesia during cranial opening. Long-acting barbiturates, Valium (diazepam), or other medications that might disturb or suppress EEG recording were avoided. A wide craniotomy was performed routinely. After the dura was opened, m o t o r and sensory cortex and speech areas were mapped by electrical stimulation. In some patients, somatosensory evoked potential monitoring was used to identify the m o t o r and sensory areas in patients who could not tolerate local anesthesia. Intraoperative E C o G was carried out using a 16-elecJ. Neurosurg. / Volume 72/February, 1990

Surgery for epilepsy associated with AVM's examination in all cases. Twenty-six o f the 27 patients had significant gliosis o f the brain tissue adjacent to the AVM or between the abnormal vessels. Ten patients had hemosiderin deposits in the brain p a r e n c h y m a surrounding the AVM's. Four patients had other histological evidence o f old focal intracerebral hemorrhage.

FIG. 1. Magnetic resonance images in Case 26. Left: A large area of low attenuation is visible in the middle and posterior portions of the left temporal lobe on this T2-weighted image, indicating a hemosiderin deposit. Right."A small area of low attenuation is an incidental finding in the right anterior frontal region, most likely representing a small arteriovenous malformation.

trode recording set,* arranged in four rows of four electrodes each. The technique provided monopolar and bipolar recordings in both a horizontal and vertical grid for cortex-to-cortex linkages. Two blunt-tipped depth electrodes were inserted into the second temporal convolution, 3 and 5 cm behind the anterior end of the middle fossa, if seizure activity involved the temporal region. The length of these depth electrodes was 3.5 cm. The anterior needle was aimed for the amygdaloid nucleus and the posterior needle for the anterior hippocampal gyrus. After completion of the cortical EEG recording and electrical stimulation procedures, the AVM's were usually removed first, followed by cortical excision if indicated; if the cortical excision was extensive, epileptiform activity was recorded at a distance from the AVM's. The cortical incision was made with the CO2 laser which was directed through a micromanipulator adapted to the Zeiss Contravas operating microscope. Cortical resection was performed at 10 W of focused CO2 laser power in a continuous mode. Bleeding from small vessels was controlled by a defocused laser beam at 2 to 5 W and larger vessels were electrically coagulated as necessary with the bipolar coagulator. A cortical EEG recording was routinely made after the excision. Intraoperative angiography was performed if any residual AVM's were suspected. Eighteen patients underwent additional cortical excision based upon the intraoperative cortical EEG findings, the preoperative EEG studies, and the patient's seizure pattern. Remote areas of epileptiform activity were identified in seven patients whose AVM's were located in the temporal lobe. The diagnosis of AVM was confirmed by histological * Electrocorticography recording set manufactured by the Montreal Neurological Institute, Montreal, Quebec, Canada. J. Neurosurg. / Volume 72 / February, 1990

Operative Results None o f the 27 patients who underwent surgical treatment for epilepsy associated with cerebral AVM's died postoperatively. Two patients developed postoperative hemiparesis, and three patients developed transient dysphasias. All of their AVM's and epileptiform foci were in the motor area or the language-dominant temporal lobe. Subtle deficits in verbal fluency and other aspects o f speech function were found by detailed neuropsychological testing in patients after excision o f AVM's involving the dominant temporal lobe. These findings were not disabling and the patients usually returned to their preoperative condition within 12 months after resection of the lesions. One patient developed paresthesia of the right trunk and limbs because of a small let~ thalamic infarct after resection of a 6-cm AVM from the left temporal lobe. T w o patients suffered visual field defects. The follow-up period o f these patients ranged from 2 to 6 years (average 3 years 11 months). All patients continued receiving anticonvulsant therapy for 1 year after resection of the seizure focus. Anticonvulsant drugs were discontinued as patients became seizurefree. For the purpose o f the follow-up analysis o f seizure control, outcome is classified as excellent if the patient became seizure-free or experienced no more than an occasional aura, good if the patient had a 90% reduction in seizure frequency, fair if the patient had a 50% reduction in seizure frequency, and poor if there was less than a 50% reduction in the frequency o f seizures. The results of seizure control in a limited follow-up period were excellent in 21 patients, good in three, fair in two, and poor in one. One patient became seizurefree after a second operation. T h e patient with a poor result had an epileptiform focus located in the m o t o r cortex. Sixteen of 18 patients who underwent excision of epileptic foci in addition to their AVM's showed excellent results. In another two patients excision o f the epileptic lesion was incomplete because the foci were in the motor cortex and the speech area: one had a good and one a fair result. Four patients with small AVM's, three of them with two angiographically occult AVM's, underwent extensive cortical excision based upon E E G evaluation with an excellent result. Four o f five patients with medium-sized AVM's underwent additional cortical excision with excellent results; the fifth had an occipital AVM and still has occasional seizures after AVM removal only. Sixteen of 18 patients with large 23 9

H. S. Yeh, et al. AVM's had excellent results; nine of these underwent cortical excision in addition to AVM removal. Discussion

Epilepsy is the second most c o m m o n clinical presentation of an AVM. In most patients, AVM's of the brain are diagnosed because of a spontaneous intracranial hemorrhage. The incidence of patients with AVM's presenting with seizures and with no clinical evidence of intracranial hemorrhage varies between 17% and 40% in published series. 2'17"2~ Many patients with a long history of a seizure disorder are unexpectedly found on diagnostic imaging to have AVM's. 22 The natural history of intracranial AVM's and associated seizures has been reported in several series o f more than 50 untreated patients who were followed for more than 5 years. 2"8'24In 1984, Fults and Kelly 8 reviewed their series of 83 nonsurgically managed patients with an average follow-up period of 8 years; 26 patients presented with seizures, seven (26.9%) of whom suffered a hemorrhage. The condition of 18 patients was described as good, but seizure control was not reported. In 1986, a large series of unoperated cerebral AVM's was reported by Crawford, et al. 2 The risk o f developing epilepsy during the 20-year followup period was 18% in their 153 nonoperated patients; the risk of developing epilepsy was greatest if the AVM involved the temporal lobe (37% in 10 years). The authors also concluded that the younger the patient at diagnosis the more likely they were to develop epilepsy during the follow-up period. Patients aged 10 to 19 years had a 44% risk at 20 years of follow-up monitoring as compared to a 6% risk in those patients diagnosed when over the age of 30 years? Reports suggest that larger AVM's with superficial components are more likely to be complicated by epilepsy than by hemorrhage. 3"~6O f the 27 patients in our series, 18 had AVM's

that were 4 cm or greater in size. The larger AVM's tended to have more arteriovenous shunting of blood, a factor that is associated with focal cerebral ischemia. Although none of the patients in this study had a history suggestive of intracranial hemorrhage, specimens in 10 patients contained hemosiderin deposits suggesting the probability of an unrecognized or subclinical intracranial hemorrhage. Leblanc, et al., 13 reported that seven of 27 AVM patients who had no history of hemorrhage exhibited focal hemosiderin deposits; only two of these had other histological evidence of previous hemorrhage. Focal hemosiderin deposits may result from diapedesis of red blood cells through abnormally permeable blood vessels of AVM's and cavernous hemangiomas without massive hemorrhage.12 The seizure pattern seemed related to the location of the AVM's in this series. Most temporal lobe AVM's presented with complex partial seizures and secondary generalization, frontal lobe AVM's were associated with generalized seizures without aura, and parietal or occipital lobe AVM's presented with simple partial seizures. Aminofff reported that seizures due to cerebral AVM's respond effectively to pharmacological measures. Many of these patients initially responded well to anticonvulsant therapy but became recalcitrant after long-term therapy. It is not unusual for ECoG to record epileptiform activity at a distance from the AVM's (Fig. 2). Strikingly independent epileptiform foci were observed in the amygdaloid and anterior hippocampal regions when the AVM was located in the cortex of the posterior temporal region (Fig. 3). One patient (Case 16) was seizure-free after excision of a 2-cm thrombosed AVM in the right posterior temporal lobe, but developed another type of complex partial seizure in 3 months. In this patient, EEG studies (including sphenoidal electrode recordings) showed a very active ictal discharge

F1G. 2. Case 18. Left: Computerized tomography scan showing a large enhancing lesion in the right anterior frontal region. Right: Intraoperative cortical electroencephalographic recordings made from the frontal cortex at the sites marked as A, B, C, E, and H indicate active epileptiform discharges. These areas were at a distance from the arteriovenous malformation itself. 220

J. Neurosurg. / Volume 72/February, 1990

Surgery for epilepsy associated with AVM's from the right sphenoidal electrode. After fight anterior temporal lobectomy, he became seizure-free for more than 2 years. Secondary foci m a y account for failure of the primary resection to eliminate the seizure. Preoperative EEG evaluation (with conventional scalp EEG recording) is valuable in the localization of an epileptiform focus. Implantation of subdural or depth electrodes is not feasible because of the high risk of cerebral hemorrhage, especially in patients with large AVM's of the cerebral hemisphere. Intraoperative cortical E E G recording with depth electrodes provides invaluable information, indicating the necessity for and extent of cortical excision to improve seizure control. Anterior temporal lobectomy is performed for removal of a secondary epileptogenic focus located in the anterior and the mesial portions of the temporal lobe only when normal contralateral temporal lobe function is documented by neuropsychological testing. Eighteen patients in our series underwent extensive cortical excision in the area with active epileptic activities in addition to removal of the A V M ' s and the surrounding gliotic brain tissue. Gliotic brain tissue in

the interstices o f the vascular malformations, which might be associated with epileptiform activities, was removed in all patients. Functional localization o f the cerebral cortex was carried out by m e a n s of electrical stimulation in awake patients to prevent d a m a g e to indispensable areas such as speech and s o m a t o m o t o r cortical areas. O n e patient continued to have seizures when an active epileptiform focus in the central m o t o r region was spared. The results o f seizure control in our series are likely not related to the size of the A V M ' s but are associated with the adequacy o f excision of the epileptic foci in addition to r e m o v a l o f the AVM's, especially in those patients with a small or medium-sized AVM. N o cortical excision was p e r f o r m e d in one patient with a small AVM and in a n o t h e r with a medium-sized A V M ; neither showed i m p r o v e m e n t of seizure control after surgery. Seven patients with large A V M ' s who underwent excision of the m a l f o r m a t i o n s only, without cortical excision, gained excellent seizure control. Cerebral ischemia secondary to arteriovenous shunting m a y have been responsible for their seizures. It is our opinion that

FIG. 3. Case 26. Electrocorticography recordings (right) from 16 surface electrodes and two acute depth electrodes at the sites shown at left. A = the amygdaloid region and H = the anterior hippocampus. The recordings show epileptiform activity in the cortical and subcortical structures of the left temporal region anterior to the thrombosed arteriovenous malformation which is located near Electrode 2.

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221

H. S. Yeh, et al. the principal m e c h a n i s m o f epilepsy in patients with A V M ' s is focal cerebral ischemia as a result of arteriovenous shunting and gliosis o f the surrounding brain tissue with secondary epileptogenesis, especially in the temporal lobe. Epilepsy as an indication for surgical treatment of A V M ' s has been questioned in the literature, since the results of surgery have been disappointing. Parkinson and Bachers ~9 reported surgery o f 100 patients with cerebral AVM's, 28 o f w h o m presented with a seizure disorder. Only one patient b e c a m e seizure-free after surgery. Moreover, 8% o f the patients who had no epilepsy before surgery developed seizures some time later. Forster, et aL, 6 reported 150 patients treated surgically for A V M ' s of the brain, with an average follow-up period o f over 15 years. Only 14% of patients who had previously suffered f r o m epilepsy showed a reduction of seizure frequency or became easier to control after surgery, while 22 % not previously epileptic developed seizures after surgery. Foy and coworkers 7 reported that the incidence o f postoperative epilepsy in patients with A V M ' s was 50% as compared with a 17% incidence of patients in general undergoing supratentorial craniotomy. A significant factor influencing the development of epilepsy in patients with cerebral A V M ' s is surgical treatment, according to a report by Crawford, et aL,'on 75 patients who underwent total AVM excision. Twenty years after surgery there was a 57% risk of developing epilepsy a m o n g surgically treated patients. Patients aged 10 to 19 years at the time o f diagnosis faced an 82% risk of developing seizures 20 years after surgery? Drake s operated on five patients with epilepsy among 166 cases of cerebral A V M ; in three the seizures were eliminated. He concluded that excision of an AVM alone would not relieve seizure disorders unless the epileptogenic focus was r e m o v e d during excision of the AVM's. Rasmussen 2~ reported the surgical results of 18 patients who had cerebral vascular malformations with a median follow-up period o f 11 years; 67% achieved complete or nearly complete elimination o f seizures after cortical excision o f the seizure foci and vascular malformations. Goldring and Gregorie 9 described the result of surgical t r e a t m e n t o f occult AVM's in six patients; one continued to have seizures, one was lost to follow-up review, and three patients were followed for only 2 months to 1 year. There were no details of surgery, and their follow-up period was too short to draw conclusions. In our series of 27 patients, seizure control during the average follow-up period o f 3 years 11 months was excellent in 21 patients (77.8%), good in three (11.1%), fair in two (7.4%), and p o o r in one (3.7%). It is concluded that surgery is indicated in patients with intractable seizures associated with cerebral AVM's. The A V M and the epileptiform focus can be totally excised with an acceptable risk o f mortality or permanent neurological deficit. Critical factors in successful treatment 222

are the surgeon's experience, the condition of the patient, the anatomy of the malformations, and the thoroughness of the EEG study. Acknowledgments The authors thank Dr. Charles D. Aring and Dr. Theodore Rasmussen for their critical review of this manuscript. References 1. Aminoff M J: Treatment of unruptured cerebral arteriovenous malformations. Neurology 37:815-819, 1987 2. Crawford PM, West CR, Chadwick DW, et al: Arteriovenous malformations of the brain: natural history in unoperated patients, J Neurol Neurosurg Psychiatry 49: 1-10, 1986 3. Crawford PM, West CR, Shaw MDM, et al: Cerebral arteriovenous malformations and epilepsy: factors in the development of epilepsy. Epilepsia 27:270-275, 1986 4. Davis C, Symon L: The management of cerebral arteriovenous malformations. Acta Neurochir 74:4-11, 1985 5. Drake CG: Cerebral arteriovenous malformations: considerations for and experience with surgical treatment in 166 cases. Clin Neurosurg 26:145-208, 1979 6. Forster DMC, Steiner L, HAkanson S: Arteriovenous malformations of the brain. A long-term clinical study. J Neurosurg 37:562-570, 1972 7. Foy PM, Copeland GP, Shaw MDM: The incidence of postoperative seizures. Acta Neurochir 55:253-164, 1981 8. Fults D, Kelly DL Jr: Natural history of arteriovenous malformations of the brain: a clinical study. Neurosurgery 15:658-662, 1984 9. Goldring S, Gregorie EM: Experience with lesions that mimic gliomas in patients presenting with a chronic seizure disorder. Clin Neurosnrg 33:43-70, 1986 10. Guidetti B, Delitala A: Intracranial arteriovenous malformations. Conservative and surgical treatment. J Neurosnrg 53:149-152, 1980 11. Heros RC, Tu YK: Is surgical therapy needed for unruptured arteriovenous malformations? NeuroLogy 37: 279-286, 1987 12. Krieger G, Robitaille Y, Carpenter S, et al: Subacute necrotic myelopathy (Foix-Alajouanine): an immunological study. Can J Neurol Sei 9:289, 1982 (Abstract) 13. Leblanc R, Feindel W, Ethier R: Epilepsy from cerebral arteriovenous malformations. Can J Neurol Sci 10: 91-95, 1983 14. Luessenhop AJ, Presper JH: Surgical embolization of cerebral arteriovenous malformations through internal carotid and vertebral arteries. Long-term results. J Neurosurg 42:443-451, 1975 15. Luessenhop A J, Rosa L: Cerebral arteriovenous malformations. Indications for and results of surgery, and the role of intravascular techniques. J Neurosurg 60:14-22, 1984 16. Mingrino S: Supratentorial arteriovenous malformations of the brain. Adv Tech Stand Neurosurg 5:93-123, 1978 17. Moody RA, Poppen JL: Arteriovenous malformations. J Neurosurg 32:503-511, 1970 18. Murphy M J: Long-term follow-up of seizures associated with cerebral arteriovenous malformations. Results of therapy. Arch Neurol 42:477-479, 1985 19. Parkinson D, Bachers G: Arteriovenous malformations. Summary of 100 consecutive supratentorial cases. J Neurosurg 53:285-299, 1980 20. Perret G, Nishioka H: Report of the Cooperative Study J. Neurosurg. / Vohune 72/February, 1990

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of Intracranial Aneurysms and Subarachnoid Hemorrhage. Section VI. Arteriovenous malformations. An analysis of 545 cases of cranio-cerebral arteriovenous malformations and fistulae reported to the Cooperative Study. J Neurosurg 25:467-490, 1966 Rasmussen T: Surgery of epilepsy associated with brain tumors, in Purpura DP, Perry JK, Walter RD (eds): Advances in Neurology, Vol 8. Neurosurgical Management of the Epilepsies. New York: Raven Press, 1975, pp 227-239 Steiger H J, Tew JM Jr: Hemorrhage and epilepsy in cryptic cerebrovascular malformations. Arch Neurol 41: 722-724, 1984 Stein BM, Wolpert SM: Arteriovenous malformations of the brain, II: Current concepts and treatment. Arch Neurol 37:69-75, 1980 Svien H J, McRae JA: Arteriovenous anomalies of the

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brain. Fate of patients not having definitive surgery. J Neurosurg 23:23-28, 1965 25. Wilson CB, U HS, Domingue J: Microsurgical treatment of intracranial vascular malformations. J Neurosurg 51: 446-454, 1979 26. Yeh HS, Tew JM: Management of arteriovenous malformations of the brain. Contemp Neurosnrg 9:1-8, 1988 Manuscript received May 11, 1988. Accepted in final form July 3, 1989. Address for Dr. Kashiwagi: Department of Neurosurgery, Yamaguchi University School of Medicine, Yamaguchi, Japan. Address reprint requests to." Hwa-Shain Yeh, M.D., Department of Neurosurgery, University of Cincinnati College of Medicine, 231 Bethesda Avenue, Cincinnati, Ohio 452670515.

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Surgical management of epilepsy associated with cerebral arteriovenous malformations.

Between 1982 and 1986, 27 patients with seizure disorders due to cerebral arteriovenous malformation (AVM) were surgically treated by the authors. The...
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