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Arteriovenous malformations of the dura mater
Surg Neurol 1987;28:135-40
135
Arteriovenous Malformations of the Dura Mater M. Sean Grady, M.D., and Louis Pobereskin, M.D. Department of Neurological Surgery, University of Virginia Hospital, Charlottesville, Virginia, and Department of Neurological Surgery, Freedom Fields Hospital, Plymouth, Devonshire, England
Grady MS, Pobereskin L. Arteriovenous malformations of the dura mater. Surg Neurol 1987;28:135-40.
The presentation, angiographic findings, and treatment of eight dural arteriovenous malformations is reviewed. The majority presented as intracranial hemorrhage, one of which was an intracerebral hemorrhage, and an aneurysm was found in conjunction with two of the eight. Preoperative embolization of one of the malformations was used with an excellent result. Five of eight were treated surgically with a good outcome. Patient outcome, whether surgically treated or not, was good in all cases though follow-up is a maximum of 3 years, except for one case of 23 years. KEYWORDS:
Dural AVM; Aneurysm; Intracranial hemorrhage
Dural arteriovenous malformations (AVMs) have been described since 1931 [16], and have been recognized as a special subgroup of AVMs since the 1960s. Approximately 10% of cranial AVMs originate from arteries that supply the dura mater, with drainage either into one of the major sinuses or into variceal veins that stretch over the cortex [12]. Recent surgical experience with two dural AVMs led us to review the cases seen at Freedom Fields Hospital, a subregional neurosurgery unit serving 1.4 million people. Since 1981, 55 cases of AVMs have been evaluated, 7 (13%) of which originated solely from arteries supplying the dura mater. Another dural AVM has been included because of its discovery in 1963 and subsequent 23-year follow-up. The presenting symptoms, radiologic findings, and management of these 8 individuals is reviewed, along with current opinion regarding these lesions.
Clinical Method Table 1 provides a capsule summary of each patient, but each case will be described individually. Address reprint requests to: M. Sean Grady, M.D., Department of Neurological Surgery, P. O. Box 2 ! 2, University of Virginia Hospital, Charlottesville, Virginia 22908.
© 1987 by Elsevier Science Publishing Co., Inc.
Case 1 This 78-year-old man presented in 1963 complaining of left-sided pulsatile tinnitus for several years. An audible bruit was present on examination. A unilateral left common carotid artery angiogram demonstrated a dural AVM centered on the left sigmoid sinus, fed by the left middle meningeal, left posterior auricular, and left occipital arteries. The occipital artery was ligated in 1963 with moderate improvement in symptoms. Recurrence of tinnitus was gradual and became disabling once more in 1980. Angiography showed primary feeding by the left middle meningeal artery and this was ligated in 1980. The tinnitus was markedly reduced and follow-up through 1986 showed that he has no complaint of tinnitus and there is no bruit.
Case 2 A 52-year-old man was evaluated by computed tomography (CT) scan for the onset of epilepsy in 1981. Additionally, he complained of headache for the previous year. There was a region of abnormal vascularity involving the right sphenoid wing. Angiography showed a dural AVM fed by the right middle meningeal and ophthalmic arteries with a long draining vein into the basal vein of Rosenthal. The lesion was totally excised by removal of the dura mater over the sphenoid wing in 1981. Follow-up 3 years later showed that his seizures have stopped on medication and there are no other symptoms.
Case 3 A 56-year-old man was referred to us in 1983 following a subarachnoid hemorrhage (SAH) proven by lumbar puncture. Other than mild meningismus, his examination was normal. CT scan was normal, 3 days after hemorrhage. Angiography showed a dural AVM located in the cribriform plate, fed by the right maxillary artery and branches from the right ophthalmic artery. Drainage was by way of a long varicose vein that entered the superior sagittal sinus. The AVM was totally excised in 1983 and he has remained asymptomatic. 0090-3019/87/$3.50
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Grady and Pobereskin
Table 1. Symptoms, Radiologic Findings, and Management of Patients with Dural A VMs Angiography
Signs and symptoms
Age/sex
Afferent
Efferent
Treatment
Outcome and follow-up
1. 56/M
Bruit
MM, O A , TA, PA
TS, VG
Ligation of feeders
2. 52/M
Grand mal seizure, headaches
MM, O p A
BVR
Excision
3. 56/M
SAH
Max A, O p A
SSS
Excision
4. 58/M
SAH
MM, ~ O A
TS
Clipping of aneurysm
5. 54/M
SAH
OA
TS
None
6. 60/M
Seizures
MM
CS
None
7. 56/M
Intracerebral hemorrhage, h o m o n y m o u s hemianopia, bruit SAH
MM, O A , PA, T A
SSS, TS
Excision and isolation of sinus
Recurrence of bruit after l 7 years, second ligation in 1980, asymptomatic in 1986 Seizures and headache resolved 3 years Recovered well 2 years Recovered well 2 years Recovered well 1 year Recovered well 6 months Recovered well 6 months
AF, M M b
SSS
Clipping of aneurysm and excision
Recovered well 6 months
8. 59/M
Abbreviations: AF, anterior falcine artery; MM, middle meningeal artery; Max A, maxillary artery; OA, occipital artery; OpA, ophthalmic artery; PA, posterior auricular artery; TA, tentorial artery; BVR, basal vein of Rosenthal; CS, cavernous sinus; SSS, superior sagittal sinus; TS, transverse sinus; VG, vein of Galen. ~Posterior communicating artery aneurysm also identified. ~Ophthalmic artery aneurysm also identified.
Case 4 This 58-year-old man was referred in 1984 because of SAH proven by lumbar puncture, and had a 21-year history of epilepsy, well controlled on phenytoin therapy. Physical examination was normal. His CT scan, taken 7 days after hemorrhage, was normal. Angiography showed a right posterior communicating artery aneurysm as well as a left occipital dural AVM fed by the left occipital artery and posterior branch of the middle meningeal artery. The aneurysm was successfully clipped. A small clot and stained arachnoid was found at the site so it was presumed that aneurysm was the cause of the SAH. The AVM was not surgically approached. In follow-up so far, he remains asymptomatic.
Case 5 A 54-year-old man was referred in 1985 because of SAH. There were no physical findings and CT scan, obtained 5 days after hemorrhage, was normal. Angiography (Figure 1) demonstrated a dural AVM located at the foramen magnum, filled by the right occipital artery and draining into the torcula. He refused surgical therapy and remains asymptomatic.
Case 6 A 60-year-old man presented with a new onset of epilepsy in 1985. Physical examination was normal, how-
ever, his CT scan was abnormal, showing vascularity in the floor of the right middle fossa. Angiography showed a dural AVM filling from the right middle meningeal artery as well as intracavernous branches from the right internal carotid artery. Drainage was into the cavernous sinus and the basal vein of Rosenthal. He was placed on antiepileptic drug therapy and remains asymptomatic.
Case 7 This 56-year-old man presented with sudden headache and vomiting followed rapidly by collapse into unconsciousness. He had a long history of migraine headache. A CT scan showed a large right occipital hematoma (Figure 2). He regained consciousness in 3 hours and examination showed a left hemiparesis and a left homonymous hemianopia, as well as a loud right occipital bruit with a palpable thrill. Angiography showed a supratentorial and infratentorial occipital dural AVM, fed by the right middle meningeal, right occipital, right posterior auricular, and right tentorial arteries with direct drainage into the right transverse sinus (Figure 3). One large pial vein drained the AVM into the sagittal sinus. The AVM was mainly dural but extended through the bone to lie in the subgaleal tissue. Seven days after the ictus, this lesion was embolized using metal coils in order to reduce the vascularity. Repeat angiography 3 days later showed much reduced
Dural Arteriovenous Malformations
Figure 1. Lateral external ~arotid artery angiogram of case 5, showing a tangle of ve~se/s at the foramen magnum.
filling (Figure 4). A craniectomy was performed with removal of the AVM and isolation of the sinus from meningeal or tentorial artery supply. Follow-up angiography 6 weeks later failed to show any AVM (Figure 5). His only deficit is a small left temporal field cut.
Figure 2. C T scan of case 7, demonstrating a right occipital intracerebral hematoma.
Surg Neurol 1987;28:1 ~5-40
137
Figure 3. Preoperative right common carotid artery angiogram of case 7, showing feeders derired from both external carotid circulation as well as the artery of the tentorium.
Case 8 A 59-year-old man presented with SAH in 1986. Physical examination was normal, as was his CT scan obtained 2 days posthemorrhage. Angiography showed a left ophthalmic artery aneurysm and a dural AVM located on the falx. This was fed by a large anterior falcine artery, and both right and left middle meningeal arteries (Figure 6). Drainage was directly into the superior sagittal sinus. On the morning of surgery he was noted to be somewhat drowsy but operation was performed with the intent of clipping the aneurysm. A thin clot was found over the
Figure 4. Postembolization angiogram of case 7. now clearl3~demonstrating the artery of the tentorium continuing to fill the A VM but marked reduction in flow derived from the external carotid circulation.
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Surg Neurol 1987;28:135-40
Grady and Pobereskin
Figure 5. Postoperative angiogram showing elimination of the A VM and the margins of resection.
left frontal lobe but no blood was found by the aneurysm. The aneurysm was clipped and the anterior falcine and left middle meningeal arteries to the AVM were ligated, as it was clear that the AVM had been the cause of the SAH. The exposure was suboptimal as the operation planned was aneurysm clipping and a bifrontal exposure was not possible. Recovery was uncomplicated. Repeat angiography 4 weeks later showed that the aneurysm was secured but the AVM was still present, fed by the right middle meningeal artery. A bifrontal craniotomy was performed with resection o f the sagittal sinus where the AVM originated. T h e r e have been no complications and the patient is asymptomatic to date. In summary, five of eight patients presented with intracranial hemorrhage, one o f which was an intracerebral hemorrhage. All the patients were men. Two presented with unusual CT scan findings in the evaluation of new onset epilepsy. O f the five cases surgically approached, four had either total removal or isolation of all feeding vessels. T h e r e was no mortality or surgical morbidity. O u t c o m e to date has been good in all cases, whether surgically treated or not, but except for one follow-up o f 23 years, the maximum follow-up is 3 years. Two o f the malformations were found along with intracranial aneurysms in the evaluation of SAH, complicating the surgical approach.
Discussion The origins o f dural AVMs is controversial. As with parenchymal AVMs some authors believe they are con-
Figure 6. Lateral common carotid artery angiogram of case 8 demonstrating a duralAVM draining into the sagittalsinus, with feeding from the middle meningeal and ophthalmic arteries.
genital [1]. Obrador et al [14] reviewed the world's literature in 1975 and found that 3% of cases presented before the age of 1 year. The youngest individual reported is a 3-month-old child who presented with SAH [4]. Cases occurring at this young age strongly argue in favor of congenital origin for at least some dural AVMs. More recently, evidence has accumulated suggesting that these are acquired lesions resulting from occlusion of one of the major venous sinuses, particularly in the case of those lesions centered around the transverse and sigmoid sinuses. H o u s e r et al [8] reported an 8 0 % incidence of stenosis or occlusion in their cases and documented two cases who presented initially with sinus occlusion and then went on to develop dural AVMs a few years later. Chaudhary et al [2] described four cases in which AVMs developed following head trauma. In two of their four cases documented occlusion of the transverse and sigmoid sinuses occurred before the development of the AVM. N o n e of our cases had a history of head trauma, although mild head injury may well have been overlooked. The location of the AVMs in our series may be categorized into one of two groups, based on a classification scheme devised by Aminoff [1]. If the venous drainage is into a basal sinus such as the cavernous, petrosal, or sphenoparietal sinus, then the AVM is placed in the anterior-inferior group. If, however, venous drainage is into a dural sinus such as the sagittal, transverse, or sigmoid sinus, then the AVM is in the superior-posterior
Dural Arteriovenous Malformations
group. We had three of the anterior-inferior variety and five of the superior-posterior variety. Dural AVMs are more often of the superior-posterior variety rather than anterior-inferior [1,7,8]. T h e varying locations of the AVMs in our study may be ascribed to a less aggressive posture with regard to tinnitus, one of the primary symptoms of dural AVMs in the occipitomastoid (superiorposterior) region [8]. In such instances, conservative treatment by the patient's personal physician may lead to a false lower incidence of these lesions. Furthermore, our group is quite unique in that all the patients are male, rather than the usual slight female predominance. T h e r e is no ready explanation as to the sex bias in our cases. All are middle-aged or older which agrees with other studies [7,14]. The incidence of intracranial hemorrhage from dural AVMs is quite variable. In a review by Malik et al [10], those located within a major sinus only presented as an intracranial hemorrhage in 7.5% o f their cases, whereas 51% of those outside a major sinus presented with an intracranial hemorrhage. SAH is the most frequent type of hemorrhage, but intracerebral hematomas have been reported [5,6,13,14,17 ]. Particularly critical with regard to the risk of hemorrhage was the presence of a variceal draining vein. In our series, two of the five AVMs that presented with intracranial hemorrhage had such veins. As dural AVMs are quite unusual, the incidence of hemorrhage is not well established, but the presence of long draining veins seems to heighten the risk of SAH. In two cases with SAH, an aneurysm as well as the AVM was present, without CT scan indication as to which site had hemorrhaged. Observations at the time of surgery showed that in one instance the AVM had bled. In this instance, the AVM drained directly into the superior sagittal sinus. The association of aneurysm and dural AVM has not been reported, to our knowledge. CT scan has been useful in detecting these lesions though angiography is essential to define them [3,11]. In two of our cases, CT scan suggested a vascular abnormality which led us to perform an angiography as well. Both of these cases were being investigated for epilepsy, showing that cortical irritation may occur with AVMs restricted to the dura mater, though it is more common in AVMs of the brain parenchyma. At present, surgical intervention is the optimal form o f therapy to relieve symptoms or prevent further hemorrhage [9,10,18]. Spontaneous regression of a dural AVM is reported, but, in general, these lesions are progressive l15]. All authors agree that excision of the AVM itself, which may include a major venous sinus, or total isolation of the malformation is the surgical goal [9,10,18]. This was the mode o f therapy in 50% of our cases, and
Surg Neurol 1987;28:135-40
139
resulted in no mortality or morbidity. We have found preoperative embolization to be very helpful. In our case 7, the lesion expanded through the bone and into the soft tissues. Preoperative embolization 4 days before surgical removal greatly reduced the vascularity of the lesion and very little blood was lost during the procedure. One complicating feature is the presence of an aneurysm. If the presenting symptom is SAH and no specific site can be elucidated, one must be prepared to approach both lesions if possible. In conclusion, our eight dural AVMs presented more commonly with SAH rather than tinnitus, bruit, and headache. CT scan suggested a vascular abnormality in two cases, both being evaluated for epilepsy. Two of the five cases of SAH had associated aneurysms. Distal ligation of feeders in one case resulted in recurrence 17 years later. In four cases the AVM was excised or isolated with no complications. T h r e e cases were not surgically explored and as yet have had no complications. Given the information available in the literature as well as our own experience, aggressive surgical management is indicated for these lesions. References l. Aminoff MJ. Vascular anomalies in the intracranial dura mater. Brain 1973;96:601-12. 2. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: an acquired lesion. AJNR 1982;3:13-9. 3. Chesna EJ, Naheedy MH, Azar-Kia B. CT demonstration of a dural arteriovenous malformation, Comput Radio11984;8:49-52. 4. Decker K, Backmond H. P~diatrische Neuroradiologie. Stuttgart: Thieme, 1970:108-9. 5. Enker SH. Progression of a dural arteriovenous malformation resulting in an intracerebral hematoma. Angiology 1979;30: 198-204. 6. Fardoun R, Adam Y, Mercier P, Guy G. Tentorial arteriovenous malformation presenting as an intracerebrat hematoma. J Neurosurg 1981;55:976-8. 7. Houser OW, Baker HL, Rhoton AL, Okazaki H. Intracranial dural arteriovenous malformation. Radiology 1972;105:55-64. 8. Houser OW, Campbell JK, Campbell RJ, Sundt TM. Arteriovenous malformation affecting the transverse dural venous sin u s - a n acquired lesion. Mayo Clin Proc 1979;54:651-61. 9. Kosnik EJ, Hunt WE, Miller CA. Dural arteriovenous malformations. J Neurosurg 1974;40:322-9. 10. Malik GH, Pearce JE, Ausman Jl, Mehta B. Dural arteriovenous malformations and intracranial hemorrhage. Neurosurgery 1984;15: 332-9, 11. Miyasaka K, Takei H, Nomura M, Sugimoto S, Aida T, Abe H, Tsuru M. Computerized tomography findings in dural arteriovenous malformations. J Neurosurg 1980;53:698-702. 12. Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969;93:1071-8. 13. Newton TH, Weidner W, Greitz T. Dural arteriovenous malformation in the posterior fossa. Radiology 1968;90:27-35. 14. Obrador S, Soto M, SilvelaJ. Clinical syndromes ofarteriovenous
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Surg Neurol 1987;28:135-40
malformations of the transverse-sigmoid sinus. J Neurol Neurosurg Psychiatry 1975;38:436-51. 15. Olutola PS, Eliam M, Molot M, Talalla A. Spontaneous regression of a dural arteriovenous malformation. Neurosurgery 1983;12: 687-90. 16. Sachs E. The diagnosis and treatment of brain tumors. London: Kimpton, 1931:168-71.
Grady and Pobereskin
17. Sakaki S, Fujita H, Kohno K, Matsuoka K. Dural arteriovenous malformation in the posterior fossa associated with intracerebellar hematoma. J Neurosurg 1984;60:1067-9. 18. Sundt TM, Piepgrass DG. The surgical approach to arteriovenous malformations of the lateral and sigmoid dural sinuses. J Neurosurg 1983;59:32-9.
135
Arteriovenous Malformations of the Dura Mater M. Sean Grady, M.D., and Louis Pobereskin, M.D. Department of Neurological Surgery, University of Virginia Hospital, Charlottesville, Virginia, and Department of Neurological Surgery, Freedom Fields Hospital, Plymouth, Devonshire, England
Grady MS, Pobereskin L. Arteriovenous malformations of the dura mater. Surg Neurol 1987;28:135-40.
The presentation, angiographic findings, and treatment of eight dural arteriovenous malformations is reviewed. The majority presented as intracranial hemorrhage, one of which was an intracerebral hemorrhage, and an aneurysm was found in conjunction with two of the eight. Preoperative embolization of one of the malformations was used with an excellent result. Five of eight were treated surgically with a good outcome. Patient outcome, whether surgically treated or not, was good in all cases though follow-up is a maximum of 3 years, except for one case of 23 years. KEYWORDS:
Dural AVM; Aneurysm; Intracranial hemorrhage
Dural arteriovenous malformations (AVMs) have been described since 1931 [16], and have been recognized as a special subgroup of AVMs since the 1960s. Approximately 10% of cranial AVMs originate from arteries that supply the dura mater, with drainage either into one of the major sinuses or into variceal veins that stretch over the cortex [12]. Recent surgical experience with two dural AVMs led us to review the cases seen at Freedom Fields Hospital, a subregional neurosurgery unit serving 1.4 million people. Since 1981, 55 cases of AVMs have been evaluated, 7 (13%) of which originated solely from arteries supplying the dura mater. Another dural AVM has been included because of its discovery in 1963 and subsequent 23-year follow-up. The presenting symptoms, radiologic findings, and management of these 8 individuals is reviewed, along with current opinion regarding these lesions.
Clinical Method Table 1 provides a capsule summary of each patient, but each case will be described individually. Address reprint requests to: M. Sean Grady, M.D., Department of Neurological Surgery, P. O. Box 2 ! 2, University of Virginia Hospital, Charlottesville, Virginia 22908.
© 1987 by Elsevier Science Publishing Co., Inc.
Case 1 This 78-year-old man presented in 1963 complaining of left-sided pulsatile tinnitus for several years. An audible bruit was present on examination. A unilateral left common carotid artery angiogram demonstrated a dural AVM centered on the left sigmoid sinus, fed by the left middle meningeal, left posterior auricular, and left occipital arteries. The occipital artery was ligated in 1963 with moderate improvement in symptoms. Recurrence of tinnitus was gradual and became disabling once more in 1980. Angiography showed primary feeding by the left middle meningeal artery and this was ligated in 1980. The tinnitus was markedly reduced and follow-up through 1986 showed that he has no complaint of tinnitus and there is no bruit.
Case 2 A 52-year-old man was evaluated by computed tomography (CT) scan for the onset of epilepsy in 1981. Additionally, he complained of headache for the previous year. There was a region of abnormal vascularity involving the right sphenoid wing. Angiography showed a dural AVM fed by the right middle meningeal and ophthalmic arteries with a long draining vein into the basal vein of Rosenthal. The lesion was totally excised by removal of the dura mater over the sphenoid wing in 1981. Follow-up 3 years later showed that his seizures have stopped on medication and there are no other symptoms.
Case 3 A 56-year-old man was referred to us in 1983 following a subarachnoid hemorrhage (SAH) proven by lumbar puncture. Other than mild meningismus, his examination was normal. CT scan was normal, 3 days after hemorrhage. Angiography showed a dural AVM located in the cribriform plate, fed by the right maxillary artery and branches from the right ophthalmic artery. Drainage was by way of a long varicose vein that entered the superior sagittal sinus. The AVM was totally excised in 1983 and he has remained asymptomatic. 0090-3019/87/$3.50
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Table 1. Symptoms, Radiologic Findings, and Management of Patients with Dural A VMs Angiography
Signs and symptoms
Age/sex
Afferent
Efferent
Treatment
Outcome and follow-up
1. 56/M
Bruit
MM, O A , TA, PA
TS, VG
Ligation of feeders
2. 52/M
Grand mal seizure, headaches
MM, O p A
BVR
Excision
3. 56/M
SAH
Max A, O p A
SSS
Excision
4. 58/M
SAH
MM, ~ O A
TS
Clipping of aneurysm
5. 54/M
SAH
OA
TS
None
6. 60/M
Seizures
MM
CS
None
7. 56/M
Intracerebral hemorrhage, h o m o n y m o u s hemianopia, bruit SAH
MM, O A , PA, T A
SSS, TS
Excision and isolation of sinus
Recurrence of bruit after l 7 years, second ligation in 1980, asymptomatic in 1986 Seizures and headache resolved 3 years Recovered well 2 years Recovered well 2 years Recovered well 1 year Recovered well 6 months Recovered well 6 months
AF, M M b
SSS
Clipping of aneurysm and excision
Recovered well 6 months
8. 59/M
Abbreviations: AF, anterior falcine artery; MM, middle meningeal artery; Max A, maxillary artery; OA, occipital artery; OpA, ophthalmic artery; PA, posterior auricular artery; TA, tentorial artery; BVR, basal vein of Rosenthal; CS, cavernous sinus; SSS, superior sagittal sinus; TS, transverse sinus; VG, vein of Galen. ~Posterior communicating artery aneurysm also identified. ~Ophthalmic artery aneurysm also identified.
Case 4 This 58-year-old man was referred in 1984 because of SAH proven by lumbar puncture, and had a 21-year history of epilepsy, well controlled on phenytoin therapy. Physical examination was normal. His CT scan, taken 7 days after hemorrhage, was normal. Angiography showed a right posterior communicating artery aneurysm as well as a left occipital dural AVM fed by the left occipital artery and posterior branch of the middle meningeal artery. The aneurysm was successfully clipped. A small clot and stained arachnoid was found at the site so it was presumed that aneurysm was the cause of the SAH. The AVM was not surgically approached. In follow-up so far, he remains asymptomatic.
Case 5 A 54-year-old man was referred in 1985 because of SAH. There were no physical findings and CT scan, obtained 5 days after hemorrhage, was normal. Angiography (Figure 1) demonstrated a dural AVM located at the foramen magnum, filled by the right occipital artery and draining into the torcula. He refused surgical therapy and remains asymptomatic.
Case 6 A 60-year-old man presented with a new onset of epilepsy in 1985. Physical examination was normal, how-
ever, his CT scan was abnormal, showing vascularity in the floor of the right middle fossa. Angiography showed a dural AVM filling from the right middle meningeal artery as well as intracavernous branches from the right internal carotid artery. Drainage was into the cavernous sinus and the basal vein of Rosenthal. He was placed on antiepileptic drug therapy and remains asymptomatic.
Case 7 This 56-year-old man presented with sudden headache and vomiting followed rapidly by collapse into unconsciousness. He had a long history of migraine headache. A CT scan showed a large right occipital hematoma (Figure 2). He regained consciousness in 3 hours and examination showed a left hemiparesis and a left homonymous hemianopia, as well as a loud right occipital bruit with a palpable thrill. Angiography showed a supratentorial and infratentorial occipital dural AVM, fed by the right middle meningeal, right occipital, right posterior auricular, and right tentorial arteries with direct drainage into the right transverse sinus (Figure 3). One large pial vein drained the AVM into the sagittal sinus. The AVM was mainly dural but extended through the bone to lie in the subgaleal tissue. Seven days after the ictus, this lesion was embolized using metal coils in order to reduce the vascularity. Repeat angiography 3 days later showed much reduced
Dural Arteriovenous Malformations
Figure 1. Lateral external ~arotid artery angiogram of case 5, showing a tangle of ve~se/s at the foramen magnum.
filling (Figure 4). A craniectomy was performed with removal of the AVM and isolation of the sinus from meningeal or tentorial artery supply. Follow-up angiography 6 weeks later failed to show any AVM (Figure 5). His only deficit is a small left temporal field cut.
Figure 2. C T scan of case 7, demonstrating a right occipital intracerebral hematoma.
Surg Neurol 1987;28:1 ~5-40
137
Figure 3. Preoperative right common carotid artery angiogram of case 7, showing feeders derired from both external carotid circulation as well as the artery of the tentorium.
Case 8 A 59-year-old man presented with SAH in 1986. Physical examination was normal, as was his CT scan obtained 2 days posthemorrhage. Angiography showed a left ophthalmic artery aneurysm and a dural AVM located on the falx. This was fed by a large anterior falcine artery, and both right and left middle meningeal arteries (Figure 6). Drainage was directly into the superior sagittal sinus. On the morning of surgery he was noted to be somewhat drowsy but operation was performed with the intent of clipping the aneurysm. A thin clot was found over the
Figure 4. Postembolization angiogram of case 7. now clearl3~demonstrating the artery of the tentorium continuing to fill the A VM but marked reduction in flow derived from the external carotid circulation.
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Figure 5. Postoperative angiogram showing elimination of the A VM and the margins of resection.
left frontal lobe but no blood was found by the aneurysm. The aneurysm was clipped and the anterior falcine and left middle meningeal arteries to the AVM were ligated, as it was clear that the AVM had been the cause of the SAH. The exposure was suboptimal as the operation planned was aneurysm clipping and a bifrontal exposure was not possible. Recovery was uncomplicated. Repeat angiography 4 weeks later showed that the aneurysm was secured but the AVM was still present, fed by the right middle meningeal artery. A bifrontal craniotomy was performed with resection o f the sagittal sinus where the AVM originated. T h e r e have been no complications and the patient is asymptomatic to date. In summary, five of eight patients presented with intracranial hemorrhage, one o f which was an intracerebral hemorrhage. All the patients were men. Two presented with unusual CT scan findings in the evaluation of new onset epilepsy. O f the five cases surgically approached, four had either total removal or isolation of all feeding vessels. T h e r e was no mortality or surgical morbidity. O u t c o m e to date has been good in all cases, whether surgically treated or not, but except for one follow-up o f 23 years, the maximum follow-up is 3 years. Two o f the malformations were found along with intracranial aneurysms in the evaluation of SAH, complicating the surgical approach.
Discussion The origins o f dural AVMs is controversial. As with parenchymal AVMs some authors believe they are con-
Figure 6. Lateral common carotid artery angiogram of case 8 demonstrating a duralAVM draining into the sagittalsinus, with feeding from the middle meningeal and ophthalmic arteries.
genital [1]. Obrador et al [14] reviewed the world's literature in 1975 and found that 3% of cases presented before the age of 1 year. The youngest individual reported is a 3-month-old child who presented with SAH [4]. Cases occurring at this young age strongly argue in favor of congenital origin for at least some dural AVMs. More recently, evidence has accumulated suggesting that these are acquired lesions resulting from occlusion of one of the major venous sinuses, particularly in the case of those lesions centered around the transverse and sigmoid sinuses. H o u s e r et al [8] reported an 8 0 % incidence of stenosis or occlusion in their cases and documented two cases who presented initially with sinus occlusion and then went on to develop dural AVMs a few years later. Chaudhary et al [2] described four cases in which AVMs developed following head trauma. In two of their four cases documented occlusion of the transverse and sigmoid sinuses occurred before the development of the AVM. N o n e of our cases had a history of head trauma, although mild head injury may well have been overlooked. The location of the AVMs in our series may be categorized into one of two groups, based on a classification scheme devised by Aminoff [1]. If the venous drainage is into a basal sinus such as the cavernous, petrosal, or sphenoparietal sinus, then the AVM is placed in the anterior-inferior group. If, however, venous drainage is into a dural sinus such as the sagittal, transverse, or sigmoid sinus, then the AVM is in the superior-posterior
Dural Arteriovenous Malformations
group. We had three of the anterior-inferior variety and five of the superior-posterior variety. Dural AVMs are more often of the superior-posterior variety rather than anterior-inferior [1,7,8]. T h e varying locations of the AVMs in our study may be ascribed to a less aggressive posture with regard to tinnitus, one of the primary symptoms of dural AVMs in the occipitomastoid (superiorposterior) region [8]. In such instances, conservative treatment by the patient's personal physician may lead to a false lower incidence of these lesions. Furthermore, our group is quite unique in that all the patients are male, rather than the usual slight female predominance. T h e r e is no ready explanation as to the sex bias in our cases. All are middle-aged or older which agrees with other studies [7,14]. The incidence of intracranial hemorrhage from dural AVMs is quite variable. In a review by Malik et al [10], those located within a major sinus only presented as an intracranial hemorrhage in 7.5% o f their cases, whereas 51% of those outside a major sinus presented with an intracranial hemorrhage. SAH is the most frequent type of hemorrhage, but intracerebral hematomas have been reported [5,6,13,14,17 ]. Particularly critical with regard to the risk of hemorrhage was the presence of a variceal draining vein. In our series, two of the five AVMs that presented with intracranial hemorrhage had such veins. As dural AVMs are quite unusual, the incidence of hemorrhage is not well established, but the presence of long draining veins seems to heighten the risk of SAH. In two cases with SAH, an aneurysm as well as the AVM was present, without CT scan indication as to which site had hemorrhaged. Observations at the time of surgery showed that in one instance the AVM had bled. In this instance, the AVM drained directly into the superior sagittal sinus. The association of aneurysm and dural AVM has not been reported, to our knowledge. CT scan has been useful in detecting these lesions though angiography is essential to define them [3,11]. In two of our cases, CT scan suggested a vascular abnormality which led us to perform an angiography as well. Both of these cases were being investigated for epilepsy, showing that cortical irritation may occur with AVMs restricted to the dura mater, though it is more common in AVMs of the brain parenchyma. At present, surgical intervention is the optimal form o f therapy to relieve symptoms or prevent further hemorrhage [9,10,18]. Spontaneous regression of a dural AVM is reported, but, in general, these lesions are progressive l15]. All authors agree that excision of the AVM itself, which may include a major venous sinus, or total isolation of the malformation is the surgical goal [9,10,18]. This was the mode o f therapy in 50% of our cases, and
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resulted in no mortality or morbidity. We have found preoperative embolization to be very helpful. In our case 7, the lesion expanded through the bone and into the soft tissues. Preoperative embolization 4 days before surgical removal greatly reduced the vascularity of the lesion and very little blood was lost during the procedure. One complicating feature is the presence of an aneurysm. If the presenting symptom is SAH and no specific site can be elucidated, one must be prepared to approach both lesions if possible. In conclusion, our eight dural AVMs presented more commonly with SAH rather than tinnitus, bruit, and headache. CT scan suggested a vascular abnormality in two cases, both being evaluated for epilepsy. Two of the five cases of SAH had associated aneurysms. Distal ligation of feeders in one case resulted in recurrence 17 years later. In four cases the AVM was excised or isolated with no complications. T h r e e cases were not surgically explored and as yet have had no complications. Given the information available in the literature as well as our own experience, aggressive surgical management is indicated for these lesions. References l. Aminoff MJ. Vascular anomalies in the intracranial dura mater. Brain 1973;96:601-12. 2. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: an acquired lesion. AJNR 1982;3:13-9. 3. Chesna EJ, Naheedy MH, Azar-Kia B. CT demonstration of a dural arteriovenous malformation, Comput Radio11984;8:49-52. 4. Decker K, Backmond H. P~diatrische Neuroradiologie. Stuttgart: Thieme, 1970:108-9. 5. Enker SH. Progression of a dural arteriovenous malformation resulting in an intracerebral hematoma. Angiology 1979;30: 198-204. 6. Fardoun R, Adam Y, Mercier P, Guy G. Tentorial arteriovenous malformation presenting as an intracerebrat hematoma. J Neurosurg 1981;55:976-8. 7. Houser OW, Baker HL, Rhoton AL, Okazaki H. Intracranial dural arteriovenous malformation. Radiology 1972;105:55-64. 8. Houser OW, Campbell JK, Campbell RJ, Sundt TM. Arteriovenous malformation affecting the transverse dural venous sin u s - a n acquired lesion. Mayo Clin Proc 1979;54:651-61. 9. Kosnik EJ, Hunt WE, Miller CA. Dural arteriovenous malformations. J Neurosurg 1974;40:322-9. 10. Malik GH, Pearce JE, Ausman Jl, Mehta B. Dural arteriovenous malformations and intracranial hemorrhage. Neurosurgery 1984;15: 332-9, 11. Miyasaka K, Takei H, Nomura M, Sugimoto S, Aida T, Abe H, Tsuru M. Computerized tomography findings in dural arteriovenous malformations. J Neurosurg 1980;53:698-702. 12. Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969;93:1071-8. 13. Newton TH, Weidner W, Greitz T. Dural arteriovenous malformation in the posterior fossa. Radiology 1968;90:27-35. 14. Obrador S, Soto M, SilvelaJ. Clinical syndromes ofarteriovenous
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malformations of the transverse-sigmoid sinus. J Neurol Neurosurg Psychiatry 1975;38:436-51. 15. Olutola PS, Eliam M, Molot M, Talalla A. Spontaneous regression of a dural arteriovenous malformation. Neurosurgery 1983;12: 687-90. 16. Sachs E. The diagnosis and treatment of brain tumors. London: Kimpton, 1931:168-71.
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17. Sakaki S, Fujita H, Kohno K, Matsuoka K. Dural arteriovenous malformation in the posterior fossa associated with intracerebellar hematoma. J Neurosurg 1984;60:1067-9. 18. Sundt TM, Piepgrass DG. The surgical approach to arteriovenous malformations of the lateral and sigmoid dural sinuses. J Neurosurg 1983;59:32-9.