13

Dural Arteriovenous Malformation of the Major Venous Sinuses: An Acquired Lesion

Mohammad Y. Chaudhary,1.2 Arteriovenous malformations of the dura are thought to be congenital. However, Ved P. Sachdev3 arteriographic investigations of four patients who, after a head injury, developed dural Soo H. Ch01 arteriovenous fistulae with features of congenital malformations suggest that these Imre Weitzner, Jr.1 abnormal communications may also be acquired. Thrombosis or thrombophlebitis in Smiljan Puljic2 the dural sinus or vein may be the primary event in their formation. The pathogenesis Yun Peng Huang 1 is probably " growth" of the dural arteries normally present in the walls of the sinuses during the organization of an intraluminal thrombus. This may result in a direct communication between artery and vein or sinus, establishing an abnormal shunt. Ultimate fibrosis of the sinus wall and intraluminal thrombus may be the factors responsible for the spontaneous disappearance of such malformations.

Most dural arteriovenous malformations (AVMs) that involve th e major venous sinuses present either spontaneously or as incidental findings during arteriog­ raphy performed for other reasons. They occur predominantly in women over age 40 years [1]. The angiomatous network, multiple feeding arteries, numerous arteriovenous (A V) shunts, and occasional association with cerebral angiomas [2], as well as a few cases reported in children [3], suggest that these AVM s are congenital. Thrombosis of the draining sinus or vein is thought to be responsible for the occasional spontaneous disappearance of these lesions [4, 5]. Our experience with four patients who, after a head injury, developed dural AV fistulae with features of congenital malformations prompted a review of th e literature and this report. In two of our four cases, transverse and sigmoid sinus abnormalities were demonstrated angiographically before the AV fistulae devel­ oped. In case 3, angiography 2 years earlier for unrelated reasons was normal; no AV shunt was seen. Although in case 4, there was no angiographic evidence of a dural fistula before head injury, the posttrauma onset of symptoms and th e angiographic findings strongly suggested that this lesion had been acquired. Cases 1 and 3 were studied by serial angiography with selective internal, Received May 7, 1981 ; accepted after revision external, and common carotid injections, while stereo magnification serial an­ September 9, 1981. giography with selective and superselective catheterization of the feeding arteries Presented at the ann ual meeting of the Ameri­ was performed in cases 2 and 4. The first three patients were followed by can Society of Neuroradiology, Chicago, April periodic angiography for up to 4 years, and the AV shunts were seen to close 1981. spontaneously. ' Department of Radiology, Mount Sinai Hospi­ tal, New York, NY 10029. ' Department of Radiology, New York Medical Case Reports College, Westchester County Medical Center, Val­ halla, NY 10595. Address reprint requests to M. Case 1 Y. Chaudhary (present address). 3Department of Neurosurgery, Mount Sian i A 56-year-old woman was examined for head aches and dizzy spell s. Cerebral angiog­ Hospital , New York, NY 10029. raphy to rule out transient ischemic attacks was norm al (figs 1 A and 1 B). Control of her mild diabetes caused her headaches and dizzy spell s to disappear. AJNR 3:13-19, January / February 1982 0195-6108/ 82/ 0301-0013 $00.00 She was brought to the emergency room after a head injury 2 months later. She had a © American Roentgen Ray Society bruise over the right occipitomastoid area, was confused and disori ented, but she had no 14 CHAUDHARY ET AL. AJ NR:3, January / February 1982

neurologic defi cit. Wh en, after 1 week, her condition had not area and was bleeding from th e left ear. Skull films revealed a left improved, cerebral angiog raph y was perform ed, which showed a temporal fracture traversing th e mastoid air cells; a CT scan showed norm al arteri al phase. In th e ve nous phase, however, th e wall of th e bifrontal intracerebral hematomas. He improved graduall y with con­ ri ght sigmoid sinus was irregular and th e intern al jugul ar ve in (fig. servative treatm ent, but after 3 weeks he had a grand mal seizure. 1 C) was not opacified , in dicating th rombosis or thrombophl ebitis. Cerebral angiograph y confirmed th e bifrontal intracerebral avas­ She recovered completely, but 6 months later returned to th e cular masses and, in addition, showed a dural AV fi stula in th e wall hospital complaining of tinnitus and a bu zz in g noise in her ri ght ear. of th e right lateral sinu s (figs. 3B-30) draining into a cortical ve in . Au scultation revealed an audible bruit over th e right mastoid region. Review of the right common carotid arteri ogram obtained during Cerebral angiograph y showed multiple dural AV fi stulae supplied a workup for headaches 2 years earli er was norm al (fig. 3 A) . In th at by th e occipital and middle meningeal branches of th e right extern al study no AV shunt was seen. Becau se th e pati ent was in poor carotid artery (figs. 10-1 E) . condition, he was treated conservati ve ly and improved graduall y. A At surgery, the menin geal branches of th e occipital artery and repeat CT scan 8 weeks later revealed th at th e hematomas had th e mastoid emissary ve in were li gated extracranially. Postopera­ been replaced by areas of decreased attenuation. An giog raphy 2 ti ve ly, her complaints of tinnitus and buzz in g noise behind her ri ght years after th e patient was discharg ed showed th e fi stula had ear disappeared, but, on auscultati on, bruit was still audible. A closed spontaneously (fig . 3E) . repeat angiog ram showed th at AV shunts were still present but fl ow through th em had decreased (fig. 1 F) . Follow-up arteri og raph y a Case 4 year later (n ot illustrated) showed th at th e right middle meningeal art ery was no longer supplyin g th e fi stulous communications. In­ A 66-year-old man with a left acoustic neurinoma had a complete stead, th e arteri al supply from the transosseous and oth er menin­ hearing loss on th e left and slight facial asymmetry, with minimal geal branches of the occipital and th e ascending pharyngeal arter­ left facial droop. He also had slight weakness of hi s ri ght arm th at ies appeared to have increased. Th e major ve nous flow at this time he attributed to a head injury 3 years earli er, at whic h time he was was noted to be via th e condyloid and oth er emissary ve in s into th e unconscious for 3 days. CT and cerebral angiograph y confirmed a paravertebral ve nous plexus. The intern al jugular ve in opacificati on mass lesion in the left cerebell opontine angle. was delayed, suggesting stenosis or occlu sion in th e reg ion of th e Left extern al carotid arteriography also revealed a dural AV fi stul a jugular bulb. in th e wall of th e superior sagittal sinu s in th e falx (figs. 4A-4F) . At She returned to th e hospital again 3 years after her first ad mi ssion surgery, all of the meningeal feeders were ligated and th e dura complaining of ri ght occipital headaches. Ri ght common, extern al, excised. Surprisingly, after surgery, strength in his right arm in­ and intern al carotid arteri ography showed th at the fi stulous com­ creased. He was readmitted to the hospital 3 months later and th e munications had disappeared spontaneously (fig. 1 G) . Th e ri ght mass lesion in th e left cerebellopontine angle, which proved to be sigmoid sinus was abnorm al; its lumen was narrowed and its wall an acousti c neurinoma, was successfully removed. An angiog ram irregular, particularl y at the site of th e previous fi stulous communi­ at this time showed the dural AV shunt had not recurred. cation (fig. 1 H). The patient was treated conservati ve ly, and her headaches improved with medication. Discussion

Case 2 Normal Arterial Supply of th e Dural Walls of th e Venous Sinuses A 50-year-old male constru cti on worker was ad mitted to th e hospital after a head injury th at caused him to lose consciousness In considering the pathogenesis of these malformations, for 15 min . He was confused but neurolog ically intact on admission. a brief review of the normal arterial supply of the dura walls Skull films showed diastasis of th e ri ght lambdoid al suture, but a of the great venous sinuses may be useful. The dura mater computed tomography (CT) scan was norm al. After 3 weeks, he is highly vascular, especially in the region of the great had not improved and was increasin gly disori ented. CT was re­ venous sinuses. The middle meningeal artery normally ends peated, and compression and blunting of th e frontal horn of the left in the anterior and posterior paramedian meningeal lateral ve ntricle were evident. branches, which run along the insertion of the dural wall of Th ese findings prompted bilateral common carotid arteri og raph y, the superior sagittal sinus at the convexity, as far as the whic h revealed a left frontopari etal subdural hematoma and an AV fi stula in th e scalp on th e ri ght side (figs. 2A and 2B). The subdural cribiform plate anteriorly, and to the foramen magnum pos­ hematoma was evacuated, and it was decided to evaluate th e scalp teriorly. These paramedian vessels also receive collateral s fi stula at a later date. He was readmitted 6 months later. An giog­ from the anterior and posterior meningeal arteries, each of raphy did not show th e previous scalp lesion. In stead , multiple dural which, before termination , gives off branches to the dura of AV fi stulae were seen, draining into the ri ght lateral sinus (figs. 2C- the roof and lateral wall of the superior sagittal sinus [2]. A 2F). The patient refu sed treatmen t but returned a month later for similar rich dural arterial network is created in th e wall s of emboli zation. the lateral and sigmoid sinuses by the abundant collateral A preembolization angiogram showed th at th e fi stulae had dis­ and anastomotic channels between the middle meningeal appeared spontaneously; th e lateral sinus was not opacified but th e artery and the meningeal branches of the occipital, ascend­ angiomatous network was still evident (fig. 2G). Irregularity of th e ing pharyngeal , and intern al carotid arteries. Physiologic AV right lateral sinus wall and th e defect in its lumen noted previously were absent, perh aps in dicating organi zation and fibrosis of th e shunts between these meningeal arteri al networks and dural in traluminal thrombus (fig. 2H) . Foll ow-up on this patient continued. venous sinuses have been described [6-8].

Case 3 Previous Reports

A 38-year-old man was brought to the emergency room in a coma During the past decade, over 70 cases of dural AV mal­ after a head injury. He had a bruise over the left temporooccipital formations have been reported [9]. Although found in both AJNR:3, January/ February 1982 DURAL AVMs 15 genders and at all ages, their incidence is highest in women in two of their patients. They postulated that " the indigenous over 40 years old [1]. Recent reports have described the dysplastic dural vessels present within the sinus wall de­ angiographic anatomy of the feeding arteries [10-12]. A velop further, establishing a direct artery-to-sinus commu­ very high incidence of abnormalities of recipient venous nication during the organization of an intravenous throm­ channels has also been reported [13]. These abnormalities bus. " No experimental work supporting either of the above are described as irregularity and rigidity of the wall, stenosis hypotheses is available. However, patient histories, angio­ and septation with filling defects in the lumen, and retro­ graphic findings of prior venous abnormalities, the pro­ grade flow with partial or complete occlusion of the draining longed interval before fistulae develop, and the dysplastic venous sinus or vein. Such changes are believed to be due vessels in surgical specimens and in angiograms (fig. 2G) to venous thrombosis, which is thought to be responsible tend to support the hypothesis of Houser et al. [1]. for the occasional spontaneous disappearance of these The cases reported in chi ldren may be explained by lesions [4, 5]. compression and injury of the dural sinuses from calvarial While these malformations are generally considered con­ molding during birth [19], resulting in sinus thrombosis and genital [14], a few authors maintain that they are acquired fistulous communications during the organization and re­ [1, 2, 15]. Aminoff [15] suggested that since dural arteries canalization of the intraluminal thrombus. No matter what and veins (unlike brain parenchymal vessels) are closely the mechanism, once the shunts are establi shed, the rapid associated anatomically, trauma, especially a fracture flow of blood through them causes the preexistent rich crossing these vessels, can cause their simultaneous rup­ meningeal arterial network in the sinus wall and surrounding ture, resulting in a fistulous communication . However, this dura mater to dilate and hypertrophy. Abundant collateral concept holds true only for major branches of the middle and anastomotic channels between various meningeal ar­ meningeal arteries and their accompanying veins. It does teries result in multiple feeders. not apply to dural AV malformations located in the walls of major venous sinuses, as venous blood from the dural walls of these sinuses appears to drain directly into the sinuses. Our Experience Furthermore, middle meningeal and other posttrauma AV In our first two cases, the shunts were located in the walls fistulae are usually seen in an immediate postictus period of the lateral and sigmoid sinuses and drained into the lumen and have a classic angiographic appearance [16], with a of the respective sinus. In contrast, in cases 3 and 4, even single AV shunt between the ruptured artery and vein . though the abnormal shunts were located in the walls of the We found at least three case reports of dural A V malfor­ lateral and the superior sagittal sinus, they drained into the mations located in the walls of the venous sinus in which cortical veins in a retrograde manner. Th e fistulae were the onset of symptoms was preceded by head injury [4, 17, located at a point where the recipient cortical veins normally 18]. In each of these, as well as in our cases, the lesion entered the sinus. The retrograde flow in these veins sug­ consisted of multiple AV shunts, and the interval between gested that thrombosis and occlusion had occurred at their trauma and the time at which symptoms appeared varied junction with the respective sinus. Close examination of the from a few weeks to 6 months. Because most reported early films of the arterial phase in each case revealed that, cases did not have a history of trauma, we feel that a like congenital malformations, the abnormal shunts were mechanism other than direct trauma itself is responsible for multiple and confined to an abnormal segment of the dural the development of these fistulae. wall of the respective sinus. The spontaneous disappearance of these abnormal dural fistulae have been reported previously [4, 5] and it is thought Pathogenesis to be due to thrombosis of the recipient sinus or vein. Thrombosis or thrombophlebitis of the draining ve in or However, preexisting venous abnormalities in two of our sinus appears to be a common feature of these lesions and cases, as well as in those reported by Houser et al. [1], may be related to their origin. indicate that thrombosis itself is not responsible for the In a discussion of these fistulae, Djindjian and Merland [2] spontaneous closure of these shunts. Ultimate fibrosis of described in detail the venous abnormalities indicating sinus the intraluminal thrombus and the inflamed sinus wall prob­ thrombosis and suggested that such venous abnormalities ably resulted in occlusion of the fistulous communications. resulted from previous medical problems. They noted that Partial or complete obliteration of the dural sinus [4] may in almost all of their patients, complaints of bruit and other also resu lt. If the sinus remains patent, narrowing and ste­ symptoms had been preceded by a variety of medical ill­ nosis of its lumen and irregularity (cases 1 and 2) of its wall, nesses, surgical and obstetric procedures, and head particularly at the site of the shunts, may be seen. The long trauma. They postulated that thrombosis or thrombophlebitis interval before the shunts closed spontaneously may be resulting from such prior events precedes the development related to the slow organizing and fibrosing process [20]. of fistulous communications. According to this hypothesis, That the angiomatous network persisted after the shunts the abnormal communications are merely a pathologic had closed (case 2) is possibly related to alterations in the "opening-up" of physiologic AV shunts in the dural walls of normal lamination of elastic muscle fibers in the walls of the venous sinuses in response to phlebitis. dural arteries as a result of hemodynamic changes. This hypothesis was partly confirmed by Houser et al. The four dural AV malformations reported here appear to [1], who angiographically demonstrated that venous abnor­ be acquired and this may be the mechanism in many others . malities preceded the formation of fistulous communications Thrombosis or thrombophlebitis of the recipient venous E F

G H Fig. 1.-Case 1. Normal arterial (A) and venous (B) phases of righl (M ev), and jugular vein (JV) are opacified early in arterial phase. JB = jugular common carotid arteriogram 2 months before trauma. Occipital (OA) and bulb; A = anterior and P = posterior branches of middle meningeal artery . mi ddle meningeal (MM) arteri es of normal size and course. Sigmoid sinus F, 1 week after surgery and 7 months after trauma. Meningeal branches of (arrows) and jugular vein (JV) are normally opacified. C, 1 week after injury. occipital artery ligated extracranially. However, fistulae (F, curved arrows) Irregular wall and lumen (arrows) of sigmoid sinus. Jugular vein not opacified. persist and are supplied by posterior branch of middle meningeal artery Arteri al phase was normal. 0 and E, 6 months later. Hypertrophied middle ( arrowheads ) and by a few transosseous meningeal branches of occipital meningeal (arrowheads) and occipital artery branches (OC) terminate directly artery (straight arrows). G, External carotid arteriogram 2'12 years after into meningeal vascular network (straight arrows ) in wall of lateral and traum a. Occipital and middle meningeal arteries of normal size. No AV shunt sigmoid sinuses. This supplies multiple fi stulous communications (F, curved H, Irregular sinus wall (straight arrows) and apparently stenotic lumen of arrows ) in wall of sigmoid sinus (SS). Sigmoid sinus, mastoid emissary vein sigmoid sinus ( curved arrow) at site of previously demonstrated shunt A B c

o E F

G H Fig. 2.-Case 2. A, 3 weeks after trauma. Posterior auricular artery (PA) heads ). Vascular network also supplies fistulous communications (curved suppli es fistulous communi cation in scalp. Earl y appeari ng ve in (open arrows) arrows). Multiple meningeal arteries terminate directly into lumen of right drains into paravertebral venous plexus. Normal occipital artery and menin­ tateral sinus. PV = paravertebral vein . G, Superselective rig ht occipital geal branches (solid arrows). 8 , An teroposteri or view of venous phase. Right arteriogram 1 month later (7 months after trauma). Fistulous communications lateral sinus (RLS) is norm al up to its bend. Filling defect in lumen (arrows) have closed spontaneously. Occipital artery, its mastoid meningea l branches where sin us is crossed by diastatic lambdoidal suture. Sigmoid sinus mark­ ( curved arrows), and transosseous meningeal branches (straight arrows ), edly narrowed and stenotic. C and 0 , 6 mon ths after injury. Selective although still hypertrophied, are relatively small In caliber. Meningeal vascular arteriogram of ri ght occipital artery. Hypertrophied occipital artery. Mastoid network still present, and there Is retrograde opacification of posterior (P) meningeal branches (long curved arrows) and transosseous meningeal temporal convexity branch of the middle meningea l artery and meningeal branches (straight arrows) also enlarged and supply rich dural vascular branch of ascending pharyngeal (Aph) artery, Indicating free communication network (arrowheads). Fistulae (F, short curved arrows) between meningeal between various meningeal arteries. There Is also a network of dural arteries vascular network and right lateral si nus. Lesion mimics malformation and ( crossed arrows), perhaps representing newly formed vessels In wall of consists of multiple AV shunts, indicated by numerous meningeal arteries abnormal segment of lateral sinus. No opacification of the venous system . H, terminating directly into lumen of right lateral si nus. Shunts at previously seen Right internal carotid injection with compression of left jugular vein. Small intraluminal defect (8). Sigmoid sinus (SS), mastoid emissary vein (Mev), and right lateral sinus (RLS) but previous Irreg ularity of wall, septation, and defec t jugular vein (JV ) opacified early in arterial phase. Wall Is irregular (crossed in lumen (arrow) (8-0) are absent. Sigmoid sinus Is still narrowed and arrows) with septation and narrowing of lumen of right lateral sinus. Sigmoid stenotic. Despite compression of left jugular vein , major venous flow Is Into sinus also narrowed in transve rse diameter. E and F, Right Internal maxillary left lateral sinus (LLS), indicating compromise of lumen of right lateral and artery In jection. Posterior (Fij temporal convexity branch of middle meningeal sigmoid sinuses. artery (MM) is hypertrophied and supplies dural vascular network (arrow- 18 CHAUDHARY ET AL. AJNR:3, January / February 1982

A B c

o E Fig . 3.-Case 3. A, 2 years before traum a. Normal occipital (OA) and cortical vein normally enters sinus. Posterior branch of middle meningeal middle meningeal (MM) arteries and no AV shunt. B, 3 weeks after trauma. artery (P, arrowheads). C and D, Late arterial and capillary phases. Superfi­ Hypertrophied occipital and middle meningeal arteri es. Meningeal branches cial cortical vei n (Scv,) drain s into another cortical vein (SCV2) through of ascending pharyngeal artery (Aph), meningeal branches of occipital artery collateral veins. Cortical vein SCV2 drains upward into superior sagittal sinus (uncrossed arrows) and of middle meningeal artery (MM) supply vascular (SSS). Vascular network (crossed arrows ). E, 2 years after trauma. Occipital network (crossed arrows ) in dural wall of lateral sinus. Multiple small men­ artery and posterior temporal convexity branch ( arrowheads) of middle ingea l arteries from this network terminate into superficial cortical vein (Scv,), menin geal artery (MM) are normal and there is no AV shunt. Selective which is opacified retrogradely th rough these shunts. Fistula (F) is where occipital artery injection was also normal.

channel seems to precede the development of abnormal A V 2. Djindjian R, Merland JJ. Superse/ective arteriography of the communications. One may speculate that sim ilar thrombosis external carotid artery. New York: Springer, 1978: 34-35, of developing venous channels during the embryologic pe­ 405-412 3. Epstein B, Pl att N. Visualization of an intracranial arteriovenous riod may be similarly responsible for brain parenchymal AV fistula during angiocardiography in an infan t with congestive malformations. Selective, and, if possible, superselective, heart failure. Radiology 1962;79: 625-627 catheterization of the feeding arteries with mag nification 4. Bitoh S, Sakaki S. Spontaneous cure of dural arteriovenous filming is the most appropriate way to study these lesions. malformation in the posterior fossa. Surg Neurol 1979; 12: Close scrutiny and a detailed review of the draining venous 111-114 channels hold the key to understanding their topography 5 . Magidson MA, Weinberg PE . Spontaneous closure of a dural and pathophysiology. arteriovenous malformation. Surg Neuro/1976;6 : 1 07 - 110 6. Browder J, Kaplan AH. Cerebral dural sinuses and their tribu­ taries. Springfield, IL: Thomas, 1976: 19- 20 REFERENCES 7. Kerber CW, Newton TH. Macro and micro vasculature of the dura mater. Neuroradiology 1973;6: 175-179 1. Houser OW, Campbell JK, Campbell RJ , Sundt TM . Arterio­ 8. Rowbotham CF, Litlie E. Circulation of the cerebral hemi­ venous malformation affecting the transverse dural sinus-an spheres. Br J Surg 1965;52: 8-20 acquired lesion. Mayo Clin Proc 1979;54: 651-661 9. Kuhner A, Krastel A, Stoll W. Arteriovenous malformations of AJNR:3. January / February 1982 DURAL AV Ms 19

A B c

D E F Fig. 4.- Case 4. A and B. Left external carotid arteriog rams. Hypertro­ Ant erior ( double arrowheads) and posteri or ( single arrowheads) convexity phied mastoid meningeal ( curved arrows ) branches of occipital artery (OA). branches of right middle meningeal artery also supply fistu lous communica­ anterior (A. double arrowheads ). and posteri or (P. single arrowheads ) con­ tions (F) th rough paramedian meningeal artery (PM A). Again . ve nous drai nage ve xity branches of middle meningeal (MM) artery constitute paramedian is into superfi cial cortical veins of left cerebral hemi sph ere. which are opa­ meningeal arte ry (PMA). which suppli es fistu lous commu nications (F) in wall cified retrogradely. F. Venous ph ase of left intern al carotid injecti on. Lack of of superior sagittal sin us. Venous drainage into numerous superficial cortical superfi cial cortical veins apparent in left pa ri etooccipital region and blood (Scv. straight arrows ) veins of left cerebral hemisph ere. C. Same injecti on. appears to drain from thi s area through coll ateral venous channels (arrows ) Superfi cial cortical veins (arrows ) of left cerebral hemisphere drain retro­ into superior sag ittal sinus (SSS). a clearl y acquired feature. gradely into left lateral sinus. 0 and E. Ri ght external carotid arte ri ograms.

th e transverse dural sinu s. J Neurosurg 1976;45 : 1 2-19 Brain 1973;96: 60 1-612 10 . Newton TH . Weidner W. Greitz T. Dural arteri ovenous malfor­ 16. Schecter MM, Zingesser LH, Rayport M. Torn meni ngeal ves­ mati ons in the posteri or fossa. Radiology 1968;90: 27 - 3 5 sels: an evaluati on of a clinical spectrum through th e use of 11 . Houser OW. Baker HL. Rh oton AL, Okazaki H. In tracranial angiograph y. Radiology 1965;86: 686-695 dural arteri ovenous malform ati ons. Radiology 1972; 105: 55- 17. Handa J, Yo neda S, Handa H. Venous sinu s occlu sion with a 64 dural arteri ovenous malform ati on of th e posteri or fossa. Surg 12. Urdanibia JF, Silve la J, Soto M. Occipital dural arteriovenous Neurol 1975;4 : 433-437 malformati ons. Neuroradiology 1974;7 : 57- 64 18. Feldman AR , Hieshima G, Gi anotta LS, Gade FG. Trauma ti c 13. Di chgans VJ , Gottschaldt M, Voigt K. Arteriovenose Du ra-An­ dural arteriovenous fi stu la supplied by scalp; meningeal, and giome am Sinus transversus. Klin ische Symptome, charakter­ cortical arteri es. Neurosurgery 1980;6: 6 70-673 istische arteri ell e Versorgung und haufige venose Abflustorun­ 19. Newton TH , Goodin g CA. Compression of superi or sagittal gen. Zentralb Neurochir 1972;33: 1-1 8 sinus by neonatal calva ri al moldin g. Radiology 1975; 115: 14. Takekawa SD, Holman Be . Roentgenolog ic diagnosis of anom­ 635-640 alous communicati ons between extern al carotid artery and 20 . Kalbag MR , Woolf LA . Cerebral ve nous thrombosis with special intracranial veins. AJR 1965;95 : 822- 825 reference to primary aseptic th rombosis. London: Oxford, 15. Aminoff MJ. Vascular anomalies in the intracranial du ra mater. 1967: 246- 247