Surg Neurol 1985;23:431-9 431 Angiographically Occult Arteriovenous Malformations A. Sattar M. Hashim, M.B., B.S., Tetsuhiko Asakura, M.D., Uetsuhara Koichi, M.D., Koki Kadota, M.D., Hiroshi Awa, M.D., Kazuhiro Kusumoto, M.D., and Kenji Yamashita, M.D. Department of Neurosurgery, Kagoshima University School of Medicine, Kagoshima, Japan Hashim ASM, Asakura T, Koichi U, Kadota K, Awa H, Kusumoto K, Yamashita K. Angiographically occult arteriovenous malformations. Surg Neurol 1985;23:431-9. Angiographically occult arteriovenous malformations not associated with clinically recognizable intracranial hemorrhage appear to be rare. We are reporting three cases of histologically proven arteriovenous malformations of the brain that were angiographically occult. These cases presented with seizures or attacks of dizziness, and were detected by computed tomography scan, radionuclide scan, o r both. The preoperative diagnosis was granuloma in the first case and meningioma in the other two. After surgical exploration, biopsy revealed an arteriovenous malformation in each case. A review of 47 cases in the literature is tabulated and etiologies of the angiographically occult arteriovenous malformations are discussed. The routine use of computed tomography scan and timely, appropriate surgical intervention with the operating microscope for the removal of these deeply situated lesions is necessary for the diagnosis and therapy. KEY WORDS: O c c u l t a r t e r i o v e n o u s m a l f o r m a t i o n ; C e r e b r a l angiography; C o m p u t e d t o m o g r a p h y ; R a d i o n u c l i d e scan According to Dandy [9] the initial discovery of an arteriovenous malformation is always credited to William Hunter, who in 1757 described an extracranial arteriovenous malformation associated with a thrill that could be eliminated by compression o f the nutrient artery. Steinheil in 1895 and Isenschmidt in 1912 were the first to make clinical diagnosis o f a cerebral arteriovenous malformation [39]. Dandy [9] in 1928 reported a significant series of large intracranial arteriovenous malformations that were clinically diagnosed. Since then, cases of typical arteriovenous malformations have been reported frequently in the literature. Bagley [1] in 1932, Address reprint requests to: A. Sattar M. Hashim, M.B., B.S., Department of Neurosurgery, Kagoshima University School of Medicine, 1208-1 Usuki-cho, Kagoshima 890, Japan. © 1985 by Elsevier Science Publishing Co., Inc. for the first time, described a small vascular anomaly that could be visualized microscopically. Kidd and Cumings [21] in 1947 reported an autopsy of a case with intracerebral hemorrhage, in which microscopic sections of the brain demonstrated a small vascular malformation. However, these small vascular malformations became widely recognized after the report of Margolis et al [30] in 1951, in which they called attention to small vascular malformations found on autopsy of six patients, with four of these associated with fatal hemorrhage. The authors pointed out that these four small lesions would probably not have been demonstrable by angiography. Olivecrona and Riives [36] stated that arteriograms, of course, always disclose the presence of an arteriovenous malformation, and also Pool [39] stated that arteriography is, of course, the key test for the diagnosis of an arteriovenous malformation. No abnormal vasculature was seen on angiography in two of the four patients with arteriovenous malformation that were reported by Crawford and Russell [8] in 1956. These authors found that the small vascular malformations were responsible for 20 of 461 cases of intracerebral hemorrhage, and to describe these small vascular malformations, they introduced the term "cryptic" due to their latent character clinically and pathologically. Many authors [2,4-8,12,13,15,17,19,21,23,25,26, 29,31,33,34,37,40,44,46,47] have reported, on the one hand, the cases of arteriovenous malformations or other vascular malformations that were angiographically occult, and were responsible for spontaneous intracerebral hemorrhage. These occult arteriovenous malformations seldom give rise to symptoms or signs unless they bleed, which often results in massive intracerebral hematoma [ 16,39]. On the other hand, there are rare cases of occult arteriovenous malformations presenting as different neurological conditions, but not associated with clinically recognizable intracranial hemorrhage. Only 47 cases of histologically proven arteriovenous malformations not associated with clinically recognizable intracranial hemorrhage have been reported in the literature [3,4,6,10,11, 14,18-20,22,25,27,29,38,47,54], and presented as sei0090-2,019/85/$3.30 432 Surg Neurol 1985;23:431-9 z u r e s [3,4,6,10,11,14,22,25,27,29,38,47,54], motor deficits [4,14,22,25,47], or headaches [3,4,14,19,22]. In all cases, angiography failed to demonstrate the features of an arteriovenous malformation. The lesions have been detected either preoperatively by computed tomography scan as a mass of increased attenuation, or at operation. O t h e r vascular malformations have also been reported: venous angioma [3,22,29,31,33,47] and cavernous angioma [3,6,23,29,33,41,44] with similar presentations. We report the clinical and radiographic features o f three cases of symptomatic, angiographically occult arteriovenous malformations, none of which showed the clinical evidence of an intracerebral hemorrhage. The preoperative diagnosis in all three cases was misleading. Hashim et al A Case Reports Case 1 A 25-year-old man who complained of seizures was admitted to the University Hospital on January 16, 1980. H e had been in good health until age 11 years, when he initially developed generalized seizures with hyperconvulsive activity on the left side. The seizures occurred once a month, and over the years they increased in frequency despite increasing dosage of various anticonvulsants. In October 1979 he was admitted to the epilepsy center, where he responded to antiepileptic therapy. His generalized seizures were improved, but he developed focal seizures characterized by tonic convulsions o f the left upper limb and blinking of the left eyelid. Clinical examination on admission revealed no neurological deficit. X-ray films o f the skull were normal, and an electroencephalogram disclosed bifrontoparietal epileptic discharges, more active on the right side. Radionuclide brain scan was normal. Computed tomography scan revealed a spherical mass of increased attenuation in the left frontoparietal region, which showed slight enhancement after infusion o f a contrast medium (Figure 1). Serial internal carotid angiography showed no abnormalities. Preoperative diagnosis was a granuloma. On January 30, 1980, a small right frontoparietal craniotomy was performed. After dural reflection, a cortical incision was made, and at the depth of 1.5 cm, a small mass about 2 cm in size was found. A frozen section showed a vascular malformation. The mass was resected piecemeal without arterial or venous bleeding. Microscopically, the excised specimen showed dilated and thrombosed veins with organization. There was fibrinoid degeneration o f the venous wall, media o f small arteries, and perivascular old hemorrhage with many hemosiderin-laden cells (Figure 2). Between the abnormal vascular channels the brain parenchyma was gliotic. These features confirmed the diagnosis of a thrombosed Figure 1. Case 1. Computed tomography scan (A) axial and (B) coronal ~'iews without contrastmedium enhancement, shou ing a spherical lesion of high attenuation in the/eft frontoparietal region. (C) After intravenous injection of contrast medium, there is slight enhancement of the lesion. arteriovenous malformation. Postoperative course was uneventful, and there was no neurological deficit. Patient has been seizure-free for 4 years, and is maintained on anticonvulsants. Case 2 A 25-year-old woman was admitted to the University Hospital on April 18, 1983 with the complaint of dizziness. She had been feeling well until age 15 years, when she noted intermittent attacks of postural dizziness. The symptoms became severe over the years and in the 2 years prior to admission, she experienced attacks of postural dizziness followed by nausea and vomiting approximately once a week. T h e r e was no history of headache or stiffness o f her neck. Neurological examination revealed mental retardation. Optic fundi and other clinical findings were normal. X-ray films of the skull showed hyperosteosis of the sphenoid ridge and calcification in the parasellar region. An electroencephalogram revealed slow-wave activity in the left frontal region. A radionuclide brain scan demonstrated the increased isotope accumulation in the left parasellar region. The uninfused computed tomography scan dem- Occult Arteriovenous Malformations Surg Neurol 1985;23:431-9 433 Figure 2. Case 1. Section of excised mass showing dilated abnormal veins and arteries with thick walls (hematoxylin and eosin; × 100). onstrated a patchy rounded mass lesion of high attenuation, immediately anterolateral to the left anterior clinoid process. After the infusion of contrast medium, there was fair enhancement (Figure 3). Bilateral serial carotid angiography revealed no tumor circulation, but displacement of vessels suggested a space-occupying mass lesion in the left parasellar region. This mass was diagnosed as a meningioma of the sphenoid wing, or floor of the anterior cranial fossa. On May 13, 1983, a left frontotemporal craniotomy was performed. After dural reflection the frontal lobe was elevated slightly, and using microsurgical technique a soft mass about 2.5 cm in Figure 3. Case 2. (A) Computed tomography scan without contrastmedium enhancement, showing a patchy, rounded lesion of high attenuation immediately anterolateral to the left anterior clinoid process. (B) After intravenous injection of contrast medium, there is fair enhancement of the lesion. size was found. Frozen section showed a vascular malformation. Adhesions of the mass to the olfactory nerve, optic nerve, and internal carotid artery were released, and the mass was removed in a block. Microscopically, the excised specimen showed many closely clustered vascular spaces and vascular walls of various thickness, from thin to irregularly fibrous and hyalinized thickness (Figure 4). In the lesion there was bone formation with osteoclastic giant cells. Hemosiderin deposition was also noted in surrounding gliotic parenchyma. Calcification of the small vessel walls in the gliotic cortex was also observed. Diagnosis was a thrombosed arteriovenous malformation. Postoperative course was uneventful; there was no neurological deficit, and the patient has been symptom-free for 1 year. Case 3 A B A 31-year-old man was admitted to the University Hospital on N o v e m b e r 8, 1983. H e presented with a 2-year history of episodic left occipitalgia, visual field disturbance, scintillating scotoma, and a 1-month history of one generalized seizure. Neurological examination revealed a right homonymous hemianopsia. X-ray films of the skull and the electroencephalograph showed no abnormalities. A radionuclide brain scan demonstrated increased isotope accumulation in the left temporooccipital region. Computed tomography scan demonstrated an irregular lesion of slightly increased attenuation in the left posterior temporooccipital region, which enhanced well after contrast infusion (Figure 5). There was very slight displacement of the tentorium on coronal Figure 4. Case 2. Section of the excised mass showing closelyclusteredvascular spaces: vascular walls are of various thickness, from thin to irregularly fibrous and hyalinized thickness (hematoxylin and eosin: × I00). C Figure 5. Case 3. Computed tomography scan (A) axial and (B) coronal views without contrast-medium enhancement, showing an irregular lesion of increased attenuation in the posterior temporooccipital region. (C) After injection of contrast medium, there is fair enhancement of the lesion. Occult Arteriovenous Malformations views but no other mass effect. Selective serial vertebral angiography demonstrated an abnormal blush in the arterial phase only, and no mass effect, malignant neovascularity, or arteriovenous shunting. The preoperative diagnosis was a tentorial meningioma, and also an angioma was considered. On D e c e m b e r 12, 1983, a left parietooccipital craniotomy was performed. After dural reflection, using microneurosurgical technique a cortical incision was made, and at the depth of 2 cm, a mass about 3 cm in size was found, consisting of vascular clusters. The mass was resected piecemeal without attending bleeding. Microscopically, specimen showed the proliferation of blood vessels with thickened fibrous wall and narrow lumina with partial thrombosis (Figure 6). T h e r e was gliosis of the surrounding parenchyma. Deposition of hemosiderin was also observed in the perivascular cerebral tissue. Diagnosis was a partially thrombosed arteriovenous malformation. Postoperative course was uneventful; visual field defect improved slowly, and patient has been symptom-free for 6 months. His neu~ rological examination is normal. Discussion Intracranial vascular malformations are generally considered as congenital anomalies. These have been classified by various authors [3,12,32,40,41]. The classification that we believe best conforms to what is seen histologically divides the vascular malformation into three types: capillary telangiectases, venous malformations including cavernous and racemose angioma, and the at- Figure 6. Case .3. Section of excised mass showing the proliferation of many vessels of various thickness (hematoxylin and eosin, × 102A Surg Neurol 1985;23:431-9 435 teriovenous malformations. The vast majority of these vascular malformations are arteriovenous malformations. Beside the classical arteriovenous malformations, the "cryptic" arteriovenous malfi3rmations are clinically silent, small lesions measuring 2 - 3 cm in maximum size, and are angiographically occult. Their true incidence is still unknown, but their ratio to the classical malformation is 48:5, as detected on autopsy of 48 cases by McCormick and Nofzinger [31]. The risk of initial bleeding is greater with small "cryptic" arteriovenous malformations [ 15,30,43]. They usually give rise to signs and symptoms when they bleed, which results in massive intracerebral hematomas. In rare instances these lesions present with neurological disorders, but do not show any clinical evidence of intracranial hemorrhage. We have reviewed the clinical, radiologic, and histologic findings of 47 cases in the literature as examples of such an uncommon entity, and our cases l, 2, and 3 meet these criteria. Table 1 summarizes the clinical, radiographic, and pathologic features of these 50 cases. There was a 22 : 19 female predominance. In 9 of the 50 cases these data were not given. Two children, 4- and 6-yearold girls, were the youngest patients to be diagnosed in this series, whereas the eldest was a woman of 60 years. Average age at the time of diagnosis was 30 years, and nearly 70% of patients had their first symptom before they were age 30 years. These arteriovenous malformations presented as seizures in 75% of the cases, headaches in 16%, hemiparesis in 4%, ataxia in 2%, and dizziness and vertigo in 2%. Twenty (38%) lesions were located in the temporal lobe, 34% in the frontal lobe, 436 Surg Neurol 1985;23:431-9 H a s h i m et al T a b l e 1. Details of Angiographically Occult Arteriovenous Malformations in 50 Cases with No Clinical Evidence of lntracrania/ Hemorrhage Reference Year Author Age~/Sex Clinical presentation Skull x-ray EEG lsotope scan 1956 14/M Seizures Normal A -- 1965 38/M 3l/F 40/M 45/M 46/M 46/F TL seizures TL seizures TL seizures TL seizures TL seizures Headaches Normal Normal Normal Normal Normal Calcification A A A A A N ------- Paterson and McKissock [38] 1960 Edgar and Baldwin [ 11 ] Kamrin and Buchsbaum [19] 1976 Kendall and Claveria [20] 1977 Dyck [10] 1977 Kramer and Wing [22] 47/F - - 4/F Focal seizures Normal 29/M Seizures 22/F 1977 Lukin et al [27] 60/F Focal seizures Headaches Hemiparesis Seizures Seizures Seizures Seizures Headaches Headaches Focal seizures 1978 24/F Headaches 11/F 37/F Bell et al [4] 1978 Golden and Kramer [ 14] 1979 Becker et al [3] 32/F 38/M 47/F 55/F 36/F 32/F 20/F 6/F 22/F 18/F 29/M 1 8 / M 1979 Leblanc et al [25] ---- - 1980 Jabbari et al [18] 1981 Maehara and Tasaka [29] 1982 Wharen et al [54] Normal A Angiography Site of lesion Enhanced Normal Lt frontal Normal Normal Normal Normal Normal Mass Rt temporal Lt temporal Rt temporal Rt temporal Rt temporal Suprasellar ------- -- Nonenhanced Normal Rt temporal A Enhanced -- Calcification CT scan -- - - ----------- Enhanced Enhanced Enhanced Enhanced Enhanced Enhanced Enhanced Enhanced Enhanced Enhanced A N Enhanced - - - ------ - - Mass Lt parietal Normal Rt temporal Normal Mass Normal Normal Mass Mass Mass Mass Mass Mass Lt parietal Lt parietal Rt parietal Temporal Temporal Temporal Temporal Frontal Frontal Lt parietal Pathology Vessels occluded by connective tissue. Thrombosed vessels with basophilic hyaline and calcium deposition. Irregular vessels. Complete thrombosis. Calcification and hemosiderin. Partial thrombosis of small vessels. Fibrosis and loci of old hemorrhage. Tangle of abnormal small vessels containing thrombosis. Calcification TL seizures Normal Focal seizures Normal TL seizures Normal Focal seizures Normal Hemiparesis Normal Headaches Normal Focal seizures Normal A N A A A N -N N A N A N A Normal Rt lateral ventricle Nonenhanced Normal Rt temporal Enhanced Normal Rt parietal Rt temporal Enhanced Mass Lt frontal Enhanced Mass Enhanced Normal Rt frontal Enhanced Normal Lt frontal - Mass Rt frontal Focal seizures Headaches Focal seizures Headaches A -A N A A A A Enhanced Enhanced Enhanced Enhanced Normal Normal Normal Normal -- Enhanced Normal Thrombosis and recanalization, and also calcification. Partial thrombosis, Lt parietal Lt frontal evidence of old Rt frontal hemorrhage and calcification. Rt temporoparietal Lt parietal --- Normal Normal Mass Mass Hyalinized and calcified vessels with thrombosis and hemosiderin. Normal Normal Normal Normal Focal seizures Calcification Focal seizures -Focal seizures -~ Focal seizures -Ataxia Normal -- w - - Enhanced Enhanced Enhanced Enhanced A -- N -- Enhanced Enhanced -- Enhanced Enhanced Enhanced calcification Enhanced Enhanced calcification - - 32/M 40/F TL seizures Seizures 30/M 25/M 15/M Seizures TL seizures Normal Focal seizures Normal m 29/M 42/F TL seizures TL seizures N N Lt frontal Lt temporal Lt frontal Lt cerebellum Normal Lt temporal Normal Frontal Thrombosis. Thrombosed small vesse]s. Normal Normal A A - -- --- Normal Frontal Mass Lt temporal Mass Lt parietal Normal Rt temporal Normal Rt temporal Thrombosis with recanalization and hemosiderin deposition. (continued) Occult Arteriovenous Malformations Surg Neurol 1985;23:431-9 437 Table 1. ~continued) Reference Author Age~/Sex Clinical presentation Skull x-ray EEG Isotope scan CT scan Angiography Site of lesion Pathology C h i n and H a r p e r 43/M 21/M 38/F 30/M TL seizures TL seizures Focal seizures Seizures Normal Normal Normal Normal A N A A ----- Enhanced Enhanced Nonenhanced Enhanced Normal Mass Normal Mass Lt t e m p o r a l 3rd v e n t r i c l e R t frontal R t frontal Old thrombosis. 25/M 25/F Focal seizures Dizziness A A N A Enhanced Enhanced Normal Mass Rt frontal Lt frontal 31/M Seizures Normal Calcification Normal N A Enhanced Normal Lt t e m p o r o parietal Year 1983 [6] 1985 P r e s e n t study Abbreviations: EEG = electroencephalography; CT = computed tomography; N = normal; A - abnormal; TL right; - - = not mentioned in the reports. "In years. 18% in the parietal, 4 % in the ventricles, 2 % in the temporoparietal, 2 % in the temporooccipital, 2 % in the sellar region, and 2 % in the cerebellum. Plain x-ray films rarely show abnormal calcification related to an arteriovenous malformation. Dandy [9] diagnosed two cases of arteriovenous malformation by plain x-ray films of the skull: one by the presence o f intracerebral calcification and the other by the large meningeal vascular markings. Calcification may be very faint and only seen in retrospect. The most common findings are little specks and a few flecks of calcification, curvilinear or ringlike, suggesting that blood vessels are most typical of an arteriovenous malformation [40]. Plain x-ray films have shown similar abnormal calcifications in 16% of the cases reported by Wharen et al [54], in 2 4 % of the cases reported by Paterson and McKissock [38], and in 29.5% of the cases reported by Rumbaugh and Potts [42]. In the present group, x-ray films of the skull of 35 cases have been reported, of which five (14.2%) demonstrated calcification. Electroencephalograms are reported in 31 cases, of which 21 (67%) demonstrated abnormalities including spike-and-wave or slow-wave activities. The role of electroencephalography in the diagnosis of this entity is only supportive, but is nonspecific. Radionuclide brain scan was reported in 16, of which 10 (62%) demonstrated increased isotope accumulation. The more specific features of isotope scan in classical arteriovenous malformations reflect the increased blood flow and would clearly be absent in the occult group under discussion. Negative results have also been attributed to these small lesions because of their location, either deep in the midline of the brain or in parts of the brain situated near the basis of the skull including the posterior fossa [53]. Angiography is reported in all 50 cases, and has failed to demonstrate the characteristic features of an arteriovenous malformation, but has shown the presence of an T h r o m b o s i s with hyaline and calcium deposition. temporal h)be (seizures); Lt = left; Rt = avascular mass in 19 (38%) of the 50 cases. Several factors could account for the nonopacification of an arteriovenous malformation on angiography. First, technical reasons should be counted as responsible for nonopacification [4,15,19]. The phase of abnormal vascular filling may be missed unless serial angiography is performed to detect abnormally rapid or slow circulation times, commonly present in arteriovenous malformations. Failure to opacify the appropriate feeding artery to an arteriovenous malformation is another major cause of nonvisualization. Thus, arteriovenous malformations in an area of the brain supplied jointly by two major arteries such as middle and posterior cerebral arteries may fill from one artery only. In these cases carotid angiography might be normal, whereas vertebral angiography would demonstrate the lesion [8,36,39]. On the other hand, some anomalies may not show abnormal vascularity on angiography because they are anatomically separate from the main vascular supply of the brain. Cavernous angiomas fall into this category [3,6,23, 29,33,41,44]. Some of the arteriovenous malformations are so small that they may pass undetected, because there is lack of adequately sized afferent vessels to the malformation. Thus a sufficient quantity of radiopaque medium cannot enter the malformation [3,8,19,22, 37,5O]. In an arteriovenous malformation which has bled, the circulation time becomes slower than normal, and if the local intracortical hematoma is formed, it either compresses or causes destruction of the anomaly [2,4,7, 19,23,40,44,50]. Nukui et al [35] have reported a convincing case of a small arteriovenous malformation in a 26-year-old man with a small intracerebral hematoma. The patient was treated conservatively, and angiography performed 3 months after the first study demonstrated complete disappearance of the arteriovenous malformation. 438 Surg Neurol 1985;23:431-9 Thrombosis is considered as the most probable cause. Partial spontaneous thrombosis was first documented in 1949 by Norldn [34], and if extensive, will diminish the flow and prevent the vessel filling with sufficient contrast medium to appear radiopaque. Similar cases of spontaneously thrombosed arteriovenous malformations have also been reported [7,10,12,17,22,24,26,28,35,45, 47-49,51]. Various hypotheses have been made to explain why some arteriovenous malformations spontaneously thrombose. Abnormal vessels in the arteriovenous malformations might have a propensity for thrombosis greater than that o f the adjacent normal vessels [48,49]. Kushner and Alexander [24] postulated that an embolus could initiate the thrombosis o f an arteriovenous malformation. Terao et al [50] stated that stagnant or slow flow in an angioma can lead to thrombosis in the lesion. Dyck [10] has proposed that the intravascular turbulence due to increased elongation and tortuosity o f the lesion resulted in spontaneous thrombosis o f an arteriovenous malformation, in this case of a 4-year-old girl. Shuey et al [47] suggested that a hypercoagulable state may initiate the thrombosis o f an arteriovenous malformation. They found marked female predominance; most o f these females were in a hormonally active age range. It should be considered also that thrombosis does not entirely account for the presence o f the angiographically occult lesions. Becker et al [3] found bright red and pulsatile bleeding at operation in their case 11, which was angiographically occult. Similar cases have been reported with patent vascular channels, and it has been postulated that nonvisualization on angiography is due to the stagnant flow, which does not allow sufficient iodine accumulation for radiographic identification [6,22,52]. Histology of all the cases in Table 1 showed partial or complete thrombosis with foci o f old hemorrhage in a majority o f the cases. Depending on the duration of hemorrhage, histology has shown various degrees of thrombosis, fibrosis, calcification, and hyalinization. Computed tomographic scanning may provide important clues regarding the presence o f angiographically occult arteriovenous malformations [14,20,22,25,27, 28,47,50]. Computed tomography scans have been performed in 42 (84%) of the 50 cases (Table 1), and 39 (93%) cases have shown the findings of a mass of increased attenuation, which enhanced slightly with contrast infusion. T h r e e (7%) of the cases have not shown enhancement after contrast infusion. Typically an arteriovenous malformation is o f slightly increased attenuation, corresponding to that of circulating blood, which is proportional to the hemoglobin level and equivalent to 28 EMI units with a hemoglobin o f 15 g/dL [4]. Golden and Kramer [ 14] have also noted that the density of a lesion on a noninfused computed tomography Hashim et al scan was relatively high, 2 0 - 3 5 on the EMI scale, consistent with partially thrombosed vascular channels. In addition, computed tomography scans can demonstrate extravascular accumulations, which also contribute to contrast enhancement [22]. N o enhancement would be observed if the thrombosis of an arteriovenous malformation were so extensive that the vascular channels could not opacify [4,20]. Patients presenting with headaches or seizures should undergo this procedure early in the course of their neurological investigation. Caution is advised that all the angiographically avascular lesions demonstrable by computed tomography scan are not vascular malformations. The greatest problem is usually differentiating these lesions from partially calcified, avascular low-grade gliomas [6,22]. Biopsy, however, is the only way to establish the diagnosis with certainty. Deeply situated lesions may be approached with the aid o f the operating microscope, and if frozen section demonstrates an arteriovenous malformation, total excision should follow. References 1. Bagley C Jr. Spontaneous cerebral hemorrhage. Discussion of four types, with surgical consideration. Arch Neurol Psychiatry 1932;27:1133-74. 2. Beck DJK. Operable intracranial hemorrhage. Proc R Soc Med 1954;47:700-1. 3. Becker DH, Townsend JJ, Kramer RA, Newton TH. Occult cerebrovascular malformations. A series of 18 histologically verified cases with negative angiography. Brain 1979;102:249-87. 4. Bell BA, Kendall BE, Symon L. 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