J Neurosurg 57:520-526, 1982 Thrombosed arteriovenous malformations of the brain An important entity in the differential diagnosis of intractable focal seizure disorders ROBERT E. WHAREN, JR., M.D., BERND W. SCHEITHAUER, M.D., AND EDWARD R. LAWS, JR., M.D. Departments of Neurologic Surgery and Surgical Pathology, Mayo Medical School, Mayo Clinic, Rochester, Minnesota ~/ Thrombosed arteriovenous malformations (AVM's) in patients with no previous history of hemorrhage are uncommon but benign lesions that present with clinical and radiographic findings which are often indistinguishable from those of other mass lesions, particularly low-grade gliomas. The authors report seven cases of thrombosed AVM's presenting as intractable seizure disorders in which the radiographic studies had suggested a low-grade glioma. All seven patients are now seizure-free 2 to 40 months postoperatively. The importance of surgical exploration in the management of such patients is emphasized. A review of 32 cases reported in the literature is presented. The reasons why angiography may fail to demonstrate an AVM, and the possible etiologies for the spontaneous thrombosis of an AVM are discussed. KEY WORDS thrombosed arteriovenous malformation cerebral angiography 9 vascular malformation 9 S INCE Olivecrona and Riives z8 in 1948 suggested that arteriograms always disclosed the presence of an arteriovenous malformation (AVM), many a u t h o r s 2'4-6'8-12'15'17'18-22'24-27'29'30'32'34'38-43h a v e reported occasional cases of AVM or other vascular malformations which were not demonstrated by angiography. Most of these cases, however, have been reported as the cause of a spontaneous intracerebral hemorrhage. 2,4-6,10,11,15,19,22,24,25,27,29,32,34,38-40,42Complete thrombosis of an AVM with no previous history o f hemorrhage is uncommon, for only 32 cases have been reported in the l i t e r a t u r e . 2,s,9,12,17,2~176 Those AVM's with no clinical history of hemorrhage, that are not demonstrated by angiography, present as seizure disorders, 2,s,9,12,17,21,24,26,3~ focal neurological deficits, ~2,2a,24 or headaches, z,a2,2a and can easily be misinterpreted as low-grade gliomas. This paper reports seven cases of thrombosed AVM's which presented as intractable seizure disorders. In all cases, angiography was either normal or suggested an avascular mass, and failed to demon520 9 seizure disorder 9 strate any characteristic features of an AVM. The appearance on computerized tomography (CT) was that of a mass of increased density, usually showing slight diffuse enhancement with contrast administration. In each case, the clinical presentation and radiographic studies suggested a low-grade glioma, emphasizing the importance of surgical exploration for accurate diagnosis and treatment of localized highattenuation lesions of an uncertain nature. A review of the literature is presented. The reasons why angiography may fail to demonstrate an AVM, and some possible etiologies for the spontaneous thrombosis of an AVM are discussed. Case Reports Case 1 This 25-year-old right-handed man presented with a 2-month history of frequent psychomotor seizures and one grand real seizure precipitated by hyperventilation. The neurological examination was normal. An electroencephalogram (EEG) revealed a Grade 2 J. Neurosurg. / Volume 57/October, 1982 Thrombosed AVM's in focal seizures FIG. 1. Case 1. Computerized tomography scan with contrast administration demonstrating a left-sided enhancing lesion just above the tentorium. dysrhythmia in the left temporal lobe, but no epileptiform discharges. Plain skull films were normal. The CT scan (Fig. 1) demonstrated an irregular lesion of slightly increased density in the medial aspect of the posterior temporo-occipital region, which enhanced slightly with contrast administration. The lesion produced slight displacement of the tentorium on the coronal views but no other mass effect. Angiography demonstrated a 2-cm lesion in the inferomedial portion of the left temporo-occipital lobe; this had a peripheral tumor blush evident only on the anteroposterior vertebral series, and had no mass effect, malignant neovascularity, or arteriovenous shunting. The preoperative diagnosis was a low-grade glioma. Surgical exploration revealed a firm mulberryshaped thrombosed AVM, and total removal was performed. Postoperatively, there were no complications; neurological examination demonstrated a right incomplete homonymous hemianopsia and a mild dyslexia which is improving. The patient has been seizure-free for 7 months, and is maintained on anticonvulsant medication. Case 2 This 15-year-old right-handed boy presented with a 6-year history of focal sensorimotor seizures, involving the right lower extremity, which were refractory to medication. In addition, he had occasional grand mal seizures. The neurological examination was normal. Multiple EEG's demonstrated sleep activation of a left central spike focus on one recording. Plain skull films were normal. The CT scan (Fig. 2) demonstrated a small, partially calcified, left parasagittal mass near the vertex. Angiography showed the mass to be avascular. The preoperative diagnosis was low-grade glioma. At surgery, a 2.5-cm mulberry-shaped thrombosed AVM with a surrounding border of degenerating glial tissue with abundant hemosiderin pigmentation was J. Neurosurg. / Volume 57/October, 1982 FIG. 2. Case 2. Computerized tomography scans, before (left) and after (right) contrast infusion, showing a left parasagittal lesion. resected. Postoperatively there were no complications, and the patient has been seizure-free for 17 months. His neurological examination is normal. Case 3 This 29-year-old right-handed man presented with an 18-month history of daily uncinate seizures, and personality change including episodes of rage and visual hallucinations. Medical therapy had not altered the clinical problem. The neurological examination was normal. The EEG revealed only a mild, diffuse, nonspecific abnormality most prominent in the temporal regions, with no epileptiform discharges. Plain skull films were normal. A C T scan series performed 1 year previously both with and without contrast administration was normal, but repeat CT scanning with the addition of contrast material (Fig. 3) demonstrated a well circumscribed 12-mm area of contrast enhancement in the medial right temporal lobe. Right carotid and vertebral angiograms showed no abnormality. These findings were thought to be most consistent with a glioma. 521 R. E. Wharen, Jr., B. W. Scheithauer and E. R. Laws, Jr. FIG. 3. Case 3. Computerized tomography scan with contrast infusion showing a left medial temporal lobe lesion. At surgery, cortical and depth electrode EEG recordings demonstrated epileptiform activity confined to a midtemporal depth electrode. A 6-cm right temporal lobectomy was performed, revealing a 2-cm mass containing blood clot with surrounding hemosiderin-laden brain in the posteromedial aspect of the lobectomy. This mass was totally removed and proved to be a thrombosed AVM with gliosis of the adjacent cortical tissue. Postoperativly, there were no complications and the neurological examination is normal except for a left superior quadrantic homonymous hemianopsia. Approximately 2 months after surgery, the patient was hospitalized because of frequent visual hallucinations and personality changes, but no gross convulsive seizures. Subsequent CT scanning with contrast injection revealed only postoperative changes, and confirmed complete removal of the previous lesion; an EEG showed no epileptiform activity. At follow-up examination 4 months after surgery, he continues to have daily visual hallucinations. Case 4 This 42-year-old right-handed woman presented with a 5-year history of uncinate seizures and one grand mal seizure. The neurological examination was normal. Plain skull films and EEG recordings were normal. The CT scan demonstrated a 1.5-cm mass containing flecks of calcium at the medial aspect of the right temporal lobe; the mass enhanced slightly with contrast administration. Angiography was normal. A low-grade glioma was suspected. At surgery, an incision was made in the middle temporal gyrus down to an area of hemosiderin-laden brain containing a greenish, tangled, partially calcified mass. A 4-cm temporal lobectomy was performed, with removal of a 1.5-cm thrombosed AVM from the anteromedial aspect of the right temporal lobe. Postoperatively, there were no complications and the patient has been free of seizures for 7 months. 522 Case 5 This 43-year-old right-handed man presented with a 3-year history of complex partial seizures and occasional generalized seizures intractable to medical therapy. The neurological examination was normal. The EEG recordings revealed an epileptiform focus in the left temporal lobe. Skull films were normal. The CT scan demonstrated a lesion of increased density in the left temporal lobe showing some enhancement with contrast material; angiography was normal. The preoperative diagnosis was a glioma. At surgery, the middle temporal gyrus appeared widened and the cortical veins appeared to be increased in size. A 5-cm temporal lobectomy was performed and a thick fibrous mass with evidence of old hemorrhage was removed from the midportion of the temporal lobe. Pathological evaluation revealed a thrombosed AVM with hemorrhage into the surrounding tissue. The postoperative course was uncomplicated, and, except for one seizure on the night of surgery, the patient has remained seizure-free for 4 months. The neurological examination is normal except for a minimal right superior quadrantanopsia. Case 6 This 2 l-year-old right-handed man presented with an 8-year history of temporal lobe seizures. In addition, he had frequent right-sided throbbing headaches. The neurological examination was normal. Skull films and EEG recordings were normal. The CT scan demonstrated a mass with increased density in the posterior portion of the third ventricle anterior to the pineal body, causing some obstruction of the third ventricle. It did not enhance with contrast material. Angiography revealed enlargement and separation of the posterior thalamoperforating arteries, which ended in small irregular channels. These findings were strongly suggestive of a glioma, and radiation therapy without surgical exploration was considered. Surgical exploration was performed, however, and in the posterior third ventricle a mass of thickened yellow brain tissue and nodular, black, partially calcified tissue suggestive of thrombosed vessels was found. Biopsy demonstrated a thrombosed AVM, with the surrounding brain containing moderate amounts of hemosiderin. The patient did well postoperatively until he developed acute increased intracranial pressure 1 month later, requiring a right ventriculoperitoneal shunt. He subsequently has required four shunt revisions and had one episode of Staphylococcus epidermidis meningitis. A C T scan 3 years later demonstrated no change in the appearance of the residual thrombosed AVM, which enhanced slightly with contrast material. There have been no seizures since surgery. Case 7 This 38-year-old right-handed woman presented with a 2-year history of left facial focal motor seizures J. Neurosurg. / Volume57/October, 1982 Thrombosed AVM's in focal seizures which had become intractable to medical therapy. The neurological examination was normal; E E G recordings revealed a right centroparietal epileptiform focus. Plain skull films were normal. The CT scan demonstrated a nonenhancing area of increased attenuation in the right frontal region. Angiography was normal. Although the nature of the lesion was indefinite, the preoperative diagnosis was a low-grade glioma. Right frontal craniotomy revealed a 2-cm nodular mass lesion which appeared blue and was firm and well encapsulated. Pathological evaluation demonstrated a thrombosed AVM, with evidence of hemosiderin deposition in the surrounding tissue. Postoperatively, there were no complications and, except for the occurrence of seizures following attempts to withdraw medication on two occasions, the patient has been free o f seizures for 40 months. Pathological Findings Gross and microscopic examination of all seven specimens was performed. Gross evidence of previous hemorrhage was found in all but one case. Numerous microsections, stained by hematoxylin and eosin and by elastica van Gieson methods, were examined in each case. The abnormal vascular channels consisted of arteries, arterialized veins, and veins (Fig. 4). Nondescript fibrous-walled vessels containing little elastic tissue were identified in all cases; such structures were not identifiable either as arteries or veins. Thrombosis with associated recanalization was commonly seen, as was extravascular hemosiderin deposition. Cerebral tissue was interspersed between vessels, and showed extensive degeneration and ischemic changes. The features of cavernous angioma and telangiectasis were not seen. Discussion These seven cases are examples of an uncommon entity: an AVM that has spontaneously thrombosed without clinical evidence of hemorrhage and subsequently is not demonstrated by serial angiography. A review of the literature reveals only 32 similar cases of thrombosed A V M ' s 2,8,9,12,17,20,21,24,26,30,39,41 (Table 1). In addition, there are three reported cases o f a thrombosed venous angioma, 21,41,44 and four cases of thrombosed cavernous angiomas 18,21,33with similar presentations. The thrombosed AVM's presented as seizures in 72% of the cases, headaches in 16%, hemiparesis in 6%, and ataxia in 3% (Table 2). The most common location is the temporal lobe (47% of cases), followed by the frontal lobe (28%), parietal lobe (19%), ventricles (3%), and cerebellum (3%) (Table 3). There were 15 females and eight males ranging in age from 4 to 60 years; in nine cases these data were not given. Thus, the most common presentation of a thrombosed AVM in this series is as a temporal lobe lesion producing complex partial epilepsy, with females outnumbering males by nearly 2:1. O f the seven cases J. Neurosurg. / Volume 57/October, 1982 Fro. 4. Photomicrograph demonstrating the typical microscopic features of an arteriovenous malformation. The well formed arteries show transition to nondescript fibrouswailed channels. Cerebral parenchyma is evident among the vessels. Elastica van Gieson, • 100. reported here (Table 4), five presented with temporal lobe seizures and two with focal seizures. Four o f the lesions were in the temporal lobe, one in the parietal lobe, one in the frontal lobe, and one in the third ventricle. It is interesting, however, that five of our patients were men. The appearance of calcifications on plain skull films is uncommon. Skull films have been reported in 19 previous cases, of which three (16%) demonstrated calcification (multinodular calcification of a right lateral ventricular lesion, and punctate calcifications of a left temporal lesion and of a right temporal lesion). All seven cases presented here had normal skull x-ray films. The presence of abnormal calcifications on plain films has been reported in 15% to 29.5% of cases in various series o f AVM's. 14,16,35 The calcifications are usually faint and consist of punctate densities in either a curvilinear or a nodular form. 13Calcifications not demonstrated by plain films may be evident on the CT scan due to its greater sensitivity. This occurred in two of our cases (Cases 2 and 4). Angiography failed to demonstrate the character523 R. E. Wharen, Jr., B. W. S c h e i t h a u e r a n d E. R. L a w s , Jr. TABLE 1 Summary of A VM's not demonstrated by angiography in 32 cases with no clinical history of hemorrhage* Age (yrs), Sex Clinical Presentation Skull X-Ray Findings Lesion as Seen on CT Angiography Site of Lesion Jabbari, et aL, 1980 Leblanc, et al., 1979 32, M normal Shuey, et al., 1979 Bell, et al., 1978 59, F 24, F 32, F 38, M 47, F 55, F 36, F 32, F 20, F 29, M 22, F I1, F 37, F TL seizures seizures seizures seizures ataxia TL seizures headaches TL seizures focal seizures TL seizures focal seizures hemiparesis headaches focal seizures seizures focal seizures headaches hemiparesis seizures seizures seizures headaches headaches focal seizures focal seizures enhancing enhancing enhancing enhancing enhancing enhancing enhancing nonenhancing enhancing enhancing enhancing enhancing enhancing normal normal normal mass mass mass normal normal normal mass normal normal normal mass normal mass mass normal normal mass mass mass mass mass mass normal normal normal normal normal normal normal It temporal It frontal It temporal It frontal It cerebellum It temporal rt lateral vent. rt temporal rt parietal rt temporal It frontal rt frontal It frontal rt frontal rt temporal It parietal It parietal rt parietal temporal temporal temporal frontal frontal It parietal It parietal rt temporal rt temporal It temporal rt temporal rt temporal rt temporal It frontal Authors, Year Golden & Kramer, 1978 Kramer & Wing, 1977 Dyck, 1977 Lukin, et aL, 1977 Kendall & Claveria, 1976 Edgar & Baldwin, 1960 Paterson & McKissock, 1956 4, F 60, F 47, F 38, M 31, F 40, M 45, M 46, M 14, M TL seizures TL se,zures TL seizures TL setzures TL seizures focal seizures calcification calcification normal normal normal normal normal normal normal calcification normal normal normal normal normal normal normal normal enhancing enhancing enhancing enhancing enhancing enhancing enhancing enhancing enhancing enhancing nonenhancing * AVM = arteriovenous malformation; CT = computerized tomography; TL seizures = temporal lobe seizures. - - = not reported or not done. istic features of an AVM, but did reveal the presence of an avascular mass in 13 (41%) of the 32 cases reported previously and in three of the seven cases presented here. Although some authors have described the presence of large patent vessels at surgery in cases with negative angiograms, 21,41only in Case 3 did we find any patent abnormal vessels. Several explanations have been proposed for the failure of angiography to demonstrate a vascular mal- TABLE 2 TABLE 3 Presenting symptoms in 32 reported cases of thrombosed arteriovenous malformations Location of thrombosed arteriovenous malformations in 32 reported cases Symptoms seizures focal temporal lobe unspecified headaches hemiparesis ataxia unspecified 524 formation. Crawford and Russell, 6 in 1956, were the first to report two cases of AVM's which appeared as avascular masses on angiography after presenting symptoms of spontaneous intracerebral hemorrhage; they attributed this angiographic appearance to the small size of the angioma. Several authors 21,29,42have since emphasized that some malformations are not visualized because of their small size. Certain technical considerations have been emphasized, 2,6,9 includ- Cases No. 23 7 9 7 5 2 1 1 Percent 72 16 6 3 3 Location frontal lobe parietal lobe temporal lobe right left unspecified ventricle cerebellum Cases No. Percent 9 6 15 8 4 3 1 1 28 19 47 3 3 J. Neurosurg. / Volume 5 7 / O c t o b e r , 1982 Thrombosed AVM's in focal seizures TABLE 4 Summary of seven cases of thrombosed A VM's presenting as intractable focal seizure disorders * Case Age (yrs), Clinical Skull X-Ray Lesion as No. Sex Presentation Findings Seen on CT 1 25, M temporallobe seizures normal enhancing 2 15, M focal seizures normal enhancing, calcifications 3 29, M temporallobe seizures normal enhancingt 4 42, F temporal lobe seizures normal enhancing, calcifications 5 43, M temporallobe seizures normal enhancing 6 21, M temporallobe seizures normal enhancing 7 38, F focal seizures normal nonenhancing * AVM = arteriovenousmalformation;CT = computerizedtomography. -~No precontrastscan was performed at this admission. ing the importance of serial angiography and examination of all potential feeding arteries. Other authors have suggested that malformations such as cavernous angiomas may not be visualized by angiography because they are anatomically separate from the main vascular supply? ,is,19,21,3s,42 m more common explanation is that the vascular malformations may either be compressed by adjacent clot 1,2,s,2L32,3sor destroyed at the time of hemorrhage, e,19,29,32,36,37Other AVM's, however, have presumably undergone partial or complete thrombosis, either spontaneously2,s,9,1e,17,2~176 or secondary to hemorrhage, 1,7,~9,as,4~and thus do not accumulate sufficient contrast material to be seen angiographically. That AVM's can undergo spontaneous thrombosis has been documented on rare occasions? ,22,25 and in all three reported cases intracranial hemorrhage had occurred. A number of hypotheses have been offered to explain why some AVM's spontaneously thrombose. Pool and Potts 31 have suggested that arteriosclerosis might contribute to spontaneous thrombosis of malformations. Kushner and Alexander 23 postulated that an embolus could initiate thrombosis. Terao, et al., 42 stated that stagnant or slow flow in an angioma can lead to varying degrees of thrombosis in the lesion. Dyck s proposed that intravascular turbulence due to increased elongation and tortuosity of the lesion contributed to the spontaneous thrombosis of an AVM in his case of a 4-year-old girl, and that subsequent propagation of the thrombus resulted in the spontaneous occlusion of the entire AVM. Shuey, et a/., 41 noting the predominance of hormonally active females in their series of 14 cases of cryptic cerebrovascular malformations, conjectured that spontaneous thrombosis may be initiated by a hypercoagulable state. In six of our seven cases, there was histopathological evidence that the malformation had subclinically bled in the past and apparently had proceeded to undergo various degrees of thrombosis, fibrosis, and calcification. Only in Case 1, a 25-year-old man, was there no evidence o f previous hemorrhage, and in this case hemodynamic factors as suggested by Dyck 8 and Terao, et al., 42 may have been responsible for the spontaneous thrombosis of the AVM. J. Neurosurg. / Volume 5 7 / O c t o b e r , 1982 Angiography mass mass normal normal normal mass normal Site of Lesion It temporal It parietal rt temporal rt temporal It temporal 3rd ventricle rt frontal The characteristic appearance of a thrombosed AVM on CT scanning has been described previously by different authors, 12,2~ and consists of a mass of increased density which enhances slightly with contrast administration. Of the 24 reported cases of thrombosed AVM's demonstrated by CT scans (Table 1), all but two had this characteristic appearance. 2,2~ Each of our cases had this typical CT appearance except for Cases 6 and 7, in which the preoperative scans did not enhance. Golden and Kramer 12 suggested that enhancement of these lesions with contrast material results from both extravasation due to the altered blood-brain barrier, and opacification of vascular channels which, although not apparent angiographically, are demonstrated by CT scanning due to the greater contrast resolution of the technique. If thrombosis of the AVM were extensive enough, it is conceivable that vascular channels would not opacify and hence no enhancement would be observed? ,2~ The difficulty of recognizing this type of lesion is shown by the fact that the preoperative diagnosis in our cases was uniformly incorrect: the clinical presentation and radiographic studies in each case strongly suggested a low-grade glioma. The possibility of a thrombosed AVM must be considered when one is confronted with the clinical history and radiographic findings presented here, in order to avoid subjecting patients to unnecessary radiation in the false assumption that a neoplasm is present. Surgical exploration is the only way to discover this uncommon but benign lesion. References 1. Beck DJK: Operable intracranial hemorrhage. Proc R Soc Med 47:700-701, 1954 2. Bell BA, Kendall BE, Symon L: Angiographically occult arteriovenous malformations of the brain. J Nenrul Neurosurg Psychiatry 41:1057-1064, 1978 3. Bogren H, Svalander G, Wickbom I: Angiography in intracranial cavernous hemangiomas. Acts Radiol (Diagn) 10:81-89, 1970 4. Castaigne P, Buge A, Pertuiset B, et al: Angiome thrumbus6, radiologiquement exclu. Bull Sue Med Hop Paris 77:923-930, 1961 5. Conforti P: Spontaneous disappearance of cerebral 525 R. E. Wharen, Jr., B. W. Scheithauer and E. R. Laws, Jr. arteriovenous angioma. Case report. J Neurosurg 34: 432-434, 1971 6. Crawford JV, Russell DS: Cryptic arteriovenous and venous hamartomas of the brain. J Neurol Neurosurg Psychiatry 19:1-11, 1956 7. Davidoff LM: Intracerebral hemorrhage associated with hypertension and arteriosclerosis. 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H66k O, Johanson C: Intracranial arteriovenous aneurysms. A follow-up study with particular attention to their growth. Arch Neurol Psychiatry 80:39-54, 1958 16. Houdart R, LeBesnerais Y: Les Aneurysmes Art6rioveineux des H~misph~res C~r~braux. Paris: Masson, 1963 17. Jabbari B, Huott H, Di Chiro G, et al: Surgically correctable lesions solely detected by CT scan in adultonset chronic epilepsy. Ann Neurol 7:344-347, 1980 18. Jain KK: Intraventricular cavernous hemangioma of the lateral ventricle. Case report. J Neurosurg 24: 762-764, 1966 19. Kamrin RB, Buchsbaum HW: Large vascular malformations of the brain not visualized by serial angiography. Arch Neuroi 13:413-420, 1965 20. Kendall BE, Claveria LE: The use of computed axial tomography (CAT) for the diagnosis and management of intracranial angiomas. Neuroradiology 12:141-160, 1976 21. Kramer RA, Wing SD: Computed tomography of angiographically occult cerebral vascular malformations. Radiology 123:649-652, 1977 22. Krayenbiihl H, Siebenmann R: Small vascular malformations as a cause of primary intracerebral hemorrhage. J Neurosurg 22:7-20, 1965 23. Kushner J, Alexander E Jr: Partial spontaneous regressive arteriovenous malformation. Case report with angiographic evidence. J Neurosurg 32:360-366, 1970 24. Leblanc R, Ethier R, Little JR: Computed tomography findings in arteriovenous malformations of the brain. J Neurosurg 51:765-772, 1979 25. Levine J, Misko JC, Seres JL, et al: Spontaneous angiographic disappearance of a cerebral arteriovenous malformation. Third reported case. Arch Neurol 28: 195-196, 1973 26. Lukin RR, Chambers AA, Tomsick TA: Cerebral vas526 cular lesions: infarction, hemorrhage, aneurysm, and arteriovenous malformation. Semin Roentgenol 12: 77-89, 1977 27. Margolis G, Odom GL, Woodhall B, et al: The role of small angiomatous malformations in the production of intracerebral hematomas. J Neurosurg 8:564-575, 1951 28. OlivecronaH, Riives J: Arteriovenousaneurysmsofthe brain. Their diagnosis and treatment. Arch Neurol Psychiatry 59:567-602, 1948 29. Papatheodorou CA, Gross SW, Hollin S: Small arteriovenous malformations of the brain. Arch Neuroi 5: 666-672, 1961 30. Paterson JH, McKissock W: A clinical survey of intracranial angiomas with special reference to their mode of progression and surgical treatment: a report of 110 cases. Brain 79:233-266, 1956 31. Pool JL, Potts DG: Aneurysms and Arteriovenous Anomalies of the Brain. Diagnosis and Treatment. New York/Evanston/London: Hoeber Medical/Harper and Row, 1965, p 348 32. Porter AJ, Bull J: Some aspects of the natural history of cerebral arteriovenous malformation. Br J Radiol 42: 667-675, 1969 33. Pozzati E, Gaist G, Poppi M, et al: Microsurgical removal of paraventricular cavernous angiomas. Report of two cases. J Neurosurg 55:308-311, 1981 34. Roberson GH, Kase CS, Wolpow ER: Telangiectases and cavernous angiomas of the brainstem: "cryptic" vascular malformations. Report of a case. Neuroradiology 8:83-89, 1974 35. Rumbaugh CL, Potts DG: Skull changes with intracranial arteriovenous malformations. AJR 98:525-534, 1966 36. Russell DS: The pathology of spontaneous intracranial hemorrhage. Proc R Soc Med 47:689-693, 1954 37. Russell DS, Rubinstein LJ: Pathology of Turnouts of the Nervous System, ed 2. Baltimore: Williams and Wilkins, 1963, p 87 38. Salibi BS: Cerebral angiomatous malformations with misleading manifestations. A report of three cases with surgical care. Wis Med J 68:127-133, 1969 39. Schneider RC, Liss L: Cavernous hemangiomas of the cerebral hemispheres. J Neurosurg 15:392-399, 1958 40. Scott BB, Seegar JF, Schneider RC: Successful evacuation of a pontine hematoma secondary to rupture of a pathologically diagnosed "cryptic" vascular malformation. Case report. J Neurosurg 39:104-108, 1973 41. Shuey HM Jr, Day AL, Quisling RG, et al: Angiographically cryptic cerebrovascular malformations. Neurosurgery 5:476-479, 1979 42. Terao H, Hori T, Matsutani M, et al: Detection of cryptic vascular malformations by computerized tomography. Report of two cases. J Neurosurg 51:546-551, 1979 43. Terbrugge K, Scotti G, Ethier R, et al: Computed tomography in intracranial arteriovenous malformations. Radiology 122:703-705, 1977 44. VentureyraECG, Ivan LP: Venous malformationofthe pineal region. Surg Neurol 11:225-228, 1979 Manuscript received January 4, 1982. Accepted in final form June 3, 1982. Address reprint requests to: Edward R. Laws, Jr., M.D., Department of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota 55905. J. Neurosurg. / Volume 57/October, 1982