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Dural Arteriovenous Malformation of the Anterior Cranial Fossa Occurring after Bifrontal Craniotomy
Vascular
Dural Arteriovenous Malformation of the Anterior Cranial Fossa Occurring after Bifrontal Craniotomy Hiroyuki Hashimoto, M.D., Jun-ichi Iida, M.D., Katsuya Masui, M.D., Noriyuki Nishi, M.D., Taiji Yonezawa, M.D., and Toshisuke Sakaki, M.D. Department of Neurosurgery, Okanami General Hospital, Ueno, and Department of Neurosurgery, Nara Medical University, Kashihara, Japan
Hashimoto H, Iida J, Masui K, Nishi N, Yonezawa T, Sakaki T. Dural arteriovenous malformation of the anterior cranial fossa occurring after bifrontal craniotomy. Surg Neurol 1998;49:47–50.
A case of dural arteriovenous malformation of the anterior cranial fossa developing after bifrontal craniotomy is reported. The nidus was fed mainly by the left anterior ethmoidal artery. It was drained into the right sylvian vein and superior ophthalmic vein with patency of the superior sagittal sinus. A left frontal hemorrhage resulted from the nidus itself. This is the first reported case of an acquired dural arteriovenous malformation of the anterior cranial fossa verified by angiography. This rare lesion is discussed with regard to its etiology. © 1998 by Elsevier Science Inc.
exceptional lesion illuminates the pathogenesis of dural AVMs.
Case Report
T
This 49-year-old man was referred to our hospital after an apoplectic episode of unconsciousness following severe headache. Four years previously he had undergone clipping of a ruptured anterior communicating artery (ACOM) aneurysm in another clinic. Since then he had been followed up for postoperative refractory epilepsy and mental disorders. A bifrontal craniotomy was used for the clipping and a ventricular peritoneal shunt was placed following the aneurysm surgery to control secondary hydrocephalus. At that time cerebral angiography indicated no vascular abnormality except for the aneurysm. There was no history of trauma.
Address reprint requests to: Hiroyuki Hashimoto, M.D., Department of Neurosurgery, Okanami General Hospital, 1734 Kuwamachi, Ueno, Mie 518, Japan. Received August 27, 1996; accepted November 7, 1996.
EXAMINATION On admission he was comatose without any response to stimuli and was intubated. He had bilateral fixed pupils of 3 mm that did not respond to light stimulation. A computed tomography (CT) scan on admission revealed a left frontal hemorrhage with intraventricular involvement (Figure 1). Cerebral angiography demonstrated a dural AVM of the anterior fossa and an ACOM aneurysm for which clipping was no longer complete. The dural AVM was fed mainly by the left anterior ethmoidal artery, and partly by the right one. The venous channel of this AVM drained into the right sylvian vein via a cortical vein and the right superior ophthalmic vein (Figure 2). Patency of the su-
KEY WORDS
Dural arteriovenous malformation, anterior cranial fossa, intracranial operation, cerebral hemorrhage.
he incidence of dural arteriovenous malformations (AVMs) is 10%–15% of that of all intracranial AVMs with most being located in the posterior fossa [1,7,14]. Dural AVMs of the anterior fossa are particularly uncommon and are frequently associated with intracranial hemorrhage [9,10,21,23]. Although the etiology of dural AVMs is still controversial, they have been generally classified into congenital [4,6,14,17,20] or acquired [5,15,18,22]. Those developing after surgery are rare and are found predominantly in the posterior fossa [13,18,24]. We here present this case of acquired dural AVM of the anterior fossa with a massive intracranial hemorrhage 4 years after bifrontal craniotomy. This
© 1998 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
0090-3019/98/$19.00 PII S0090-3019(97)00030-X
48
Surg Neurol 1998;49:47–50
Hashimoto et al
Computerized tomography (CT) on admission showing a left frontal hemorrhage with a severe mass effect.
1
perior sagittal sinus (SSS) was also evident in an angiogram of the venous phase. It was difficult preoperatively to evaluate whether the dural AVM or the aneurysm was responsible for the bleeding. Despite the patient’s poor condition his family eagerly desired that he undergoes a surgical exploration. OPERATION The previous skin incision and bifrontal craniotomy, noted above, were reutilized for the present procedure. The falx and the SSS near the frontal base were found to have already been excised. Evacuation of the left frontal hemorrhage was first achieved via the medial aspect of the frontal lobe, producing brain relaxation. The complex of the ACOM aneurysm and clips was disclosed through an anterior interhemispheric approach; there was no evidence of any bleeding from the aneurysm, which was considered to have developed due to the previous incomplete clipping. After removal of the former clips, complete reclipping of the aneurysm was accomplished. The bilateral frontal lobes were firmly attached to each other because of adhesion of the anterior inferior aspects of the frontal lobes. During the search for the dural AVM, a rigid clot was encountered in the anteroinferior portion of the left frontal lobe. On the surface adhesive to the dura mater a small nidus of anomalous vessels was found. These findings strongly suggested that this nidus (fistulous portion) of the dural AVM was the bleeding point. The nidus was completely removed following cauterization of bilateral anterior ethmoidal arteries.
POSTOPERATIVE COURSE The patient’s neurologic status remained the same as observed preoperatively, and after he remained severely disabled for 3 months he was transferred to another clinic. HISTOPATHOLOGIC FINDINGS Histopathologic examination of the surgical specimen showed an usual AVM appearance with corresponding pathologically altered vessels. The intranidus parenchyma was gliotic with deposits of hemosiderin, which indicated the previous hemorrhage from a ruptured aneurysm.
Discussion Intracranial AVMs can be classified into pure dural, mixed dural–pial, and pure pial types according to their blood supply [14]. Dural AVMs comprise 10%– 15% of all intracranial AVMs [1,7,14]. Most are located in the dural wall of the cavenous sinus or the transverse and sigmoid sinuses, and those involving the anterior cranial fossa are rare. Dural AVMs of the anterior cranial fossa can be assigned into a distinct subgroup with an unusually high incidence of hemorrhage and aneurysmal dilatation of the draining vein [9,10]. Although the etiology of dural AVMs remains uncertain, recent reports support the proposal that adult lesions, particularly involving the transverse and sigmoid sinuses, are acquired in nature [2,3,5,8,11,12,15,18,19]. Dural sinus thrombosis or venous thrombosis are definitely the key to the pathogenesis of dural
Dural Arteriovenous Malformation
Surg Neurol 1998;49:47–50
49
Preoperative left carotid angiograms show a dural arteriovenous malformation (AVM) of the anterior cranial fossa and an anterior communicating artery aneurysm with an incomplete clipping. The dural AVM that is fed by the left anterior ethmoidal artery, drains into the right sylvian vein via a cortical vein and the right superior ophthalmic vein. (A) anteroposterior view of early arterial phase; (B) anteroposterior view of late arterial phase; (C) lateral view of early arterial phase; and (D) lateral view of late arterial phase).
2
AVMs. Sundt and Piepgras [19] insisted that recanalization of an occluded dural sinus following organization of a clot is necessary for the development of a dural AVM. There have in fact been many reports [3,8,16,18,19] noting a causal relation between dural AVMs and dural sinus occlusion. However, such cases were mostly located in the posterior fossa and the etiologic roles of dural sinus thrombosis or sinus occlusion in dural AVMs involving the anterior fossa have not been explored in detail. Martin et al. [10] believed that such malformations in the anterior fossa as well as in the spine were congenital since no other predisposing causes could be identified. Therefore, it has not been clear whether dural AVMs in the anterior fossa can develop by the same process as those in the posterior fossa.
However, Nabors et al. [13] described two cases of postoperatively acquired dural AVMs that developed in the posterior fossa at the previous site of surgery without any dural sinus thrombosis or sacrifice. Sakaki et al. [18] reported five cases of dural AVMs in the posterior fossa that were angiographically proved to be acquired and strongly suggested that surgical occlusion of the sigmoid sinus had played an important causative role. In our case it was determined by angiograms that there was no vascular abnormality except for the ACOM aneurysm at the initial stroke. Bifrontal craniotomy and excision of the falx at the anterior edge were therefore performed to give access via the anterior interhemispheric approach. The location of the present dural AVM was rather remote from the previous operative site and cerebral angiography showed SSS patency although without drainage
50
Surg Neurol 1998;49:47–50
from the dural AVM. These findings do not support a causal role for the sinus thrombosis of the SSS. The importance of increased intrasinus pressure or venous hypertension for the development of acquired dural AVMs has been stressed [18,22]. It is probable in the present case that a superficial cortical vein draining into the SSS was damaged during the previous surgery, and increased pressure of the cortical vein triggered the development of the dural AVM in the anterior fossa. However, one cannot rule out the possibility that the dural AVM may have developed without any causal relationship to the previous surgery. The massive hemorrhage was found in the left frontal lobe, whereas the venous channel of the dural AVM drained into a pial vein of the right frontal lobe and the right superior ophthalmic vein. The nidus (fistulous portion) of the dural AVM, which was situated on the surface of the left anterior frontal lobe, was therefore concluded to be the bleeding point. The postoperative adhesion of the bilateral frontal lobes could explain why drainage of the dural AVM was primarily into veins on the opposite side of the hemorrhage. In conclusion, this is the first case to our knowledge, of an acquired dural AVM in the anterior fossa verified by angiography. The intriguing suggestion that dural AVMs in both the anterior and posterior fossae may have similar etiologic backgrounds deserves further attention.
Hashimoto et al
9. 10.
11. 12. 13.
14. 15.
16.
17. 18.
REFERENCES 1. Aminoff MJ. Vascular anomalies in the intracranial dura mater. Brain 1973;96:601–12. 2. Barnwell SL, Higashida RT, Halbach VV, Dowd CF, Hieshima GB. Direct endovascular thrombolytic therapy for dural sinus thrombosis. Neurosurgery 1991; 28:135– 42. 3. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I Jr, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: an acquired lesion. AJNR 1982;3:13–19. 4. Fadhli HA. Congenital arteriovenous fistula involving the occipital artery and lateral venous sinus. Case report. J Neurosurg 1969;30:299 –300. 5. Graeb DA, Dolman CL. Radiological and pathological aspects of dural arteriovenous fistulas. Case report. J Neurosurg 1986;64:962–7. 6. Gordon IJ, Shah BL, Hardman DR, Chameides L. Giant dural supratentorial arteriovenous malformation. AJR 1977;129:734 – 6. 7. Houser OW, Baker HL Jr, Rhoton AL Jr, Okazaki H. Intracranial dural arteriovenous malformations. Radiology 1972;105:55– 64. 8. Houser OW, Campbell JK, Campbell RJ, Sundt TM Jr.
19. 20.
21.
22.
23. 24.
Arteriovenous malformation affecting the transverse dural venous sinus—an acquired lesion. Mayo Clin Proc 1979;54:651– 61. Kobayashi H, Hayashi M, Noguchi Y, Tsuji T, Handa Y, Caner HH. Dural arteriovenous malformations in the anterior cranial fossa. Surg Neurol 1988;30:396 – 401. Martin NA, King WA, Wilson CB, Nutik S, Carter P, Spetzler RF. Management of dural arteriovenous malformations of the anterior cranial fossa. J Neurosurg 1990;72:692–7. Mayberg MR, Zimmerman C. Vein of Galen aneurysm associated with dural AVM and straight sinus thrombosis. Case report. J Neurosurg 1988;68:288 –91. Mullan S. Reflections upon the nature and management of intracranial and intraspinal vascular malformations and fistulae. J Neurosurg 1994;80:606 –16. Nabors MW, Azzam CJ, Albanna FJ, Gulya AJ, Davis DO, Kobrine AI. Delayed postoperative dural arteriovenous malformations. Report of two cases. J Neurosurg 1987;66:768 –72. Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969;93:1071– 8. Nishijima M, Takaku A, Endo S, Kuwayama N, Koizumi F, Sato H, Owada K. Etiological evaluation of dural arteriovenous malformations of the lateral and sigmoid sinuses based on histopathological examinations. J Neurosurg 1992;76:600 – 6. Obrador S, Soto M, Silvela J. Clinical syndromes of arteriovenous malformations of the transversesigmoid sinus. J Neurol Neurosurg Psychiatry 1975; 38:436 –51. Robinson JL, Sedzimir CB. External carotidtransverse sinus fistula. Case report. J Neurosurg 1970;33:718 –20. Sakaki T, Morimoto T, Nakase H, Kakizaki T, Ngata K. Dural arteriovenous fistula of the posterior fossa developing after surgical occlusion of the sigmoid sinus. Report of five cases. J Neurosurg 1996;84:113– 8. Sundt TM Jr, Piepgras DG. The surgical approach to arteriovenous malformations of the lateral and sigmoid dural sinuses. J Neurosurg 1983;59:32–39. Takekawa SD, Holman CB. Roentgenologic diagnosis of anomalous communications between the external carotid artery and intracranial veins. AJR 1965;95: 822–5. Terada T, Kikuchi H, Karasawa J, Nagata I. Intracerebral arteriovenous malformation fed by the anterior ethmoidal artery: case report. Neurosurgery 1984;14: 578 – 82. Terada T, Higashida RT, Halbach VV, Dowd CF, Tsuura M, Komai N, Wilson CB, Hieshima GB. Development of acquired arteriovenous fistulas in rats due to venous hypertension. J Neurosurg 1994;80:884 –9. Tiyaworabun S, Vonofakos D, Lorenz R. Intracerebral arteriovenous malformation fed by both ethmoidal arteries. Surg Neurol 1986;26:375– 82. Watanabe A, Takahara Y, Ibuchi Y, Mizukami K. Two cases of dural arteriovenous malformation occurring after intracranial surgery. Neuroradiology 1984;26: 375– 80.
Dural Arteriovenous Malformation of the Anterior Cranial Fossa Occurring after Bifrontal Craniotomy Hiroyuki Hashimoto, M.D., Jun-ichi Iida, M.D., Katsuya Masui, M.D., Noriyuki Nishi, M.D., Taiji Yonezawa, M.D., and Toshisuke Sakaki, M.D. Department of Neurosurgery, Okanami General Hospital, Ueno, and Department of Neurosurgery, Nara Medical University, Kashihara, Japan
Hashimoto H, Iida J, Masui K, Nishi N, Yonezawa T, Sakaki T. Dural arteriovenous malformation of the anterior cranial fossa occurring after bifrontal craniotomy. Surg Neurol 1998;49:47–50.
A case of dural arteriovenous malformation of the anterior cranial fossa developing after bifrontal craniotomy is reported. The nidus was fed mainly by the left anterior ethmoidal artery. It was drained into the right sylvian vein and superior ophthalmic vein with patency of the superior sagittal sinus. A left frontal hemorrhage resulted from the nidus itself. This is the first reported case of an acquired dural arteriovenous malformation of the anterior cranial fossa verified by angiography. This rare lesion is discussed with regard to its etiology. © 1998 by Elsevier Science Inc.
exceptional lesion illuminates the pathogenesis of dural AVMs.
Case Report
T
This 49-year-old man was referred to our hospital after an apoplectic episode of unconsciousness following severe headache. Four years previously he had undergone clipping of a ruptured anterior communicating artery (ACOM) aneurysm in another clinic. Since then he had been followed up for postoperative refractory epilepsy and mental disorders. A bifrontal craniotomy was used for the clipping and a ventricular peritoneal shunt was placed following the aneurysm surgery to control secondary hydrocephalus. At that time cerebral angiography indicated no vascular abnormality except for the aneurysm. There was no history of trauma.
Address reprint requests to: Hiroyuki Hashimoto, M.D., Department of Neurosurgery, Okanami General Hospital, 1734 Kuwamachi, Ueno, Mie 518, Japan. Received August 27, 1996; accepted November 7, 1996.
EXAMINATION On admission he was comatose without any response to stimuli and was intubated. He had bilateral fixed pupils of 3 mm that did not respond to light stimulation. A computed tomography (CT) scan on admission revealed a left frontal hemorrhage with intraventricular involvement (Figure 1). Cerebral angiography demonstrated a dural AVM of the anterior fossa and an ACOM aneurysm for which clipping was no longer complete. The dural AVM was fed mainly by the left anterior ethmoidal artery, and partly by the right one. The venous channel of this AVM drained into the right sylvian vein via a cortical vein and the right superior ophthalmic vein (Figure 2). Patency of the su-
KEY WORDS
Dural arteriovenous malformation, anterior cranial fossa, intracranial operation, cerebral hemorrhage.
he incidence of dural arteriovenous malformations (AVMs) is 10%–15% of that of all intracranial AVMs with most being located in the posterior fossa [1,7,14]. Dural AVMs of the anterior fossa are particularly uncommon and are frequently associated with intracranial hemorrhage [9,10,21,23]. Although the etiology of dural AVMs is still controversial, they have been generally classified into congenital [4,6,14,17,20] or acquired [5,15,18,22]. Those developing after surgery are rare and are found predominantly in the posterior fossa [13,18,24]. We here present this case of acquired dural AVM of the anterior fossa with a massive intracranial hemorrhage 4 years after bifrontal craniotomy. This
© 1998 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
0090-3019/98/$19.00 PII S0090-3019(97)00030-X
48
Surg Neurol 1998;49:47–50
Hashimoto et al
Computerized tomography (CT) on admission showing a left frontal hemorrhage with a severe mass effect.
1
perior sagittal sinus (SSS) was also evident in an angiogram of the venous phase. It was difficult preoperatively to evaluate whether the dural AVM or the aneurysm was responsible for the bleeding. Despite the patient’s poor condition his family eagerly desired that he undergoes a surgical exploration. OPERATION The previous skin incision and bifrontal craniotomy, noted above, were reutilized for the present procedure. The falx and the SSS near the frontal base were found to have already been excised. Evacuation of the left frontal hemorrhage was first achieved via the medial aspect of the frontal lobe, producing brain relaxation. The complex of the ACOM aneurysm and clips was disclosed through an anterior interhemispheric approach; there was no evidence of any bleeding from the aneurysm, which was considered to have developed due to the previous incomplete clipping. After removal of the former clips, complete reclipping of the aneurysm was accomplished. The bilateral frontal lobes were firmly attached to each other because of adhesion of the anterior inferior aspects of the frontal lobes. During the search for the dural AVM, a rigid clot was encountered in the anteroinferior portion of the left frontal lobe. On the surface adhesive to the dura mater a small nidus of anomalous vessels was found. These findings strongly suggested that this nidus (fistulous portion) of the dural AVM was the bleeding point. The nidus was completely removed following cauterization of bilateral anterior ethmoidal arteries.
POSTOPERATIVE COURSE The patient’s neurologic status remained the same as observed preoperatively, and after he remained severely disabled for 3 months he was transferred to another clinic. HISTOPATHOLOGIC FINDINGS Histopathologic examination of the surgical specimen showed an usual AVM appearance with corresponding pathologically altered vessels. The intranidus parenchyma was gliotic with deposits of hemosiderin, which indicated the previous hemorrhage from a ruptured aneurysm.
Discussion Intracranial AVMs can be classified into pure dural, mixed dural–pial, and pure pial types according to their blood supply [14]. Dural AVMs comprise 10%– 15% of all intracranial AVMs [1,7,14]. Most are located in the dural wall of the cavenous sinus or the transverse and sigmoid sinuses, and those involving the anterior cranial fossa are rare. Dural AVMs of the anterior cranial fossa can be assigned into a distinct subgroup with an unusually high incidence of hemorrhage and aneurysmal dilatation of the draining vein [9,10]. Although the etiology of dural AVMs remains uncertain, recent reports support the proposal that adult lesions, particularly involving the transverse and sigmoid sinuses, are acquired in nature [2,3,5,8,11,12,15,18,19]. Dural sinus thrombosis or venous thrombosis are definitely the key to the pathogenesis of dural
Dural Arteriovenous Malformation
Surg Neurol 1998;49:47–50
49
Preoperative left carotid angiograms show a dural arteriovenous malformation (AVM) of the anterior cranial fossa and an anterior communicating artery aneurysm with an incomplete clipping. The dural AVM that is fed by the left anterior ethmoidal artery, drains into the right sylvian vein via a cortical vein and the right superior ophthalmic vein. (A) anteroposterior view of early arterial phase; (B) anteroposterior view of late arterial phase; (C) lateral view of early arterial phase; and (D) lateral view of late arterial phase).
2
AVMs. Sundt and Piepgras [19] insisted that recanalization of an occluded dural sinus following organization of a clot is necessary for the development of a dural AVM. There have in fact been many reports [3,8,16,18,19] noting a causal relation between dural AVMs and dural sinus occlusion. However, such cases were mostly located in the posterior fossa and the etiologic roles of dural sinus thrombosis or sinus occlusion in dural AVMs involving the anterior fossa have not been explored in detail. Martin et al. [10] believed that such malformations in the anterior fossa as well as in the spine were congenital since no other predisposing causes could be identified. Therefore, it has not been clear whether dural AVMs in the anterior fossa can develop by the same process as those in the posterior fossa.
However, Nabors et al. [13] described two cases of postoperatively acquired dural AVMs that developed in the posterior fossa at the previous site of surgery without any dural sinus thrombosis or sacrifice. Sakaki et al. [18] reported five cases of dural AVMs in the posterior fossa that were angiographically proved to be acquired and strongly suggested that surgical occlusion of the sigmoid sinus had played an important causative role. In our case it was determined by angiograms that there was no vascular abnormality except for the ACOM aneurysm at the initial stroke. Bifrontal craniotomy and excision of the falx at the anterior edge were therefore performed to give access via the anterior interhemispheric approach. The location of the present dural AVM was rather remote from the previous operative site and cerebral angiography showed SSS patency although without drainage
50
Surg Neurol 1998;49:47–50
from the dural AVM. These findings do not support a causal role for the sinus thrombosis of the SSS. The importance of increased intrasinus pressure or venous hypertension for the development of acquired dural AVMs has been stressed [18,22]. It is probable in the present case that a superficial cortical vein draining into the SSS was damaged during the previous surgery, and increased pressure of the cortical vein triggered the development of the dural AVM in the anterior fossa. However, one cannot rule out the possibility that the dural AVM may have developed without any causal relationship to the previous surgery. The massive hemorrhage was found in the left frontal lobe, whereas the venous channel of the dural AVM drained into a pial vein of the right frontal lobe and the right superior ophthalmic vein. The nidus (fistulous portion) of the dural AVM, which was situated on the surface of the left anterior frontal lobe, was therefore concluded to be the bleeding point. The postoperative adhesion of the bilateral frontal lobes could explain why drainage of the dural AVM was primarily into veins on the opposite side of the hemorrhage. In conclusion, this is the first case to our knowledge, of an acquired dural AVM in the anterior fossa verified by angiography. The intriguing suggestion that dural AVMs in both the anterior and posterior fossae may have similar etiologic backgrounds deserves further attention.
Hashimoto et al
9. 10.
11. 12. 13.
14. 15.
16.
17. 18.
REFERENCES 1. Aminoff MJ. Vascular anomalies in the intracranial dura mater. Brain 1973;96:601–12. 2. Barnwell SL, Higashida RT, Halbach VV, Dowd CF, Hieshima GB. Direct endovascular thrombolytic therapy for dural sinus thrombosis. Neurosurgery 1991; 28:135– 42. 3. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I Jr, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: an acquired lesion. AJNR 1982;3:13–19. 4. Fadhli HA. Congenital arteriovenous fistula involving the occipital artery and lateral venous sinus. Case report. J Neurosurg 1969;30:299 –300. 5. Graeb DA, Dolman CL. Radiological and pathological aspects of dural arteriovenous fistulas. Case report. J Neurosurg 1986;64:962–7. 6. Gordon IJ, Shah BL, Hardman DR, Chameides L. Giant dural supratentorial arteriovenous malformation. AJR 1977;129:734 – 6. 7. Houser OW, Baker HL Jr, Rhoton AL Jr, Okazaki H. Intracranial dural arteriovenous malformations. Radiology 1972;105:55– 64. 8. Houser OW, Campbell JK, Campbell RJ, Sundt TM Jr.
19. 20.
21.
22.
23. 24.
Arteriovenous malformation affecting the transverse dural venous sinus—an acquired lesion. Mayo Clin Proc 1979;54:651– 61. Kobayashi H, Hayashi M, Noguchi Y, Tsuji T, Handa Y, Caner HH. Dural arteriovenous malformations in the anterior cranial fossa. Surg Neurol 1988;30:396 – 401. Martin NA, King WA, Wilson CB, Nutik S, Carter P, Spetzler RF. Management of dural arteriovenous malformations of the anterior cranial fossa. J Neurosurg 1990;72:692–7. Mayberg MR, Zimmerman C. Vein of Galen aneurysm associated with dural AVM and straight sinus thrombosis. Case report. J Neurosurg 1988;68:288 –91. Mullan S. Reflections upon the nature and management of intracranial and intraspinal vascular malformations and fistulae. J Neurosurg 1994;80:606 –16. Nabors MW, Azzam CJ, Albanna FJ, Gulya AJ, Davis DO, Kobrine AI. Delayed postoperative dural arteriovenous malformations. Report of two cases. J Neurosurg 1987;66:768 –72. Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969;93:1071– 8. Nishijima M, Takaku A, Endo S, Kuwayama N, Koizumi F, Sato H, Owada K. Etiological evaluation of dural arteriovenous malformations of the lateral and sigmoid sinuses based on histopathological examinations. J Neurosurg 1992;76:600 – 6. Obrador S, Soto M, Silvela J. Clinical syndromes of arteriovenous malformations of the transversesigmoid sinus. J Neurol Neurosurg Psychiatry 1975; 38:436 –51. Robinson JL, Sedzimir CB. External carotidtransverse sinus fistula. Case report. J Neurosurg 1970;33:718 –20. Sakaki T, Morimoto T, Nakase H, Kakizaki T, Ngata K. Dural arteriovenous fistula of the posterior fossa developing after surgical occlusion of the sigmoid sinus. Report of five cases. J Neurosurg 1996;84:113– 8. Sundt TM Jr, Piepgras DG. The surgical approach to arteriovenous malformations of the lateral and sigmoid dural sinuses. J Neurosurg 1983;59:32–39. Takekawa SD, Holman CB. Roentgenologic diagnosis of anomalous communications between the external carotid artery and intracranial veins. AJR 1965;95: 822–5. Terada T, Kikuchi H, Karasawa J, Nagata I. Intracerebral arteriovenous malformation fed by the anterior ethmoidal artery: case report. Neurosurgery 1984;14: 578 – 82. Terada T, Higashida RT, Halbach VV, Dowd CF, Tsuura M, Komai N, Wilson CB, Hieshima GB. Development of acquired arteriovenous fistulas in rats due to venous hypertension. J Neurosurg 1994;80:884 –9. Tiyaworabun S, Vonofakos D, Lorenz R. Intracerebral arteriovenous malformation fed by both ethmoidal arteries. Surg Neurol 1986;26:375– 82. Watanabe A, Takahara Y, Ibuchi Y, Mizukami K. Two cases of dural arteriovenous malformation occurring after intracranial surgery. Neuroradiology 1984;26: 375– 80.