Arteriovenous Malformations Locations and Evolution in the Fetal Brain Christine H. Comstock, MD, Janet S. Kirk.t MO
Almost all cerebral arteriovenous malformations in the fetus involve the vein of Galen, although occasionally they may involve the frontal area of the brain instead. In all reported cases arteriovenous malformations have presented some time after 30 weeks as a sonolucent oval lesion located in the midline behind the third
A
rteriovenous malformations (AVMs) of the fetus and neonate, with only occasional exceptions, involve the vein of Galen. These are "end-to-end' aneurysms in which the artery and vein connect without intervening capillaries. Blood flow through the brain is markedly increased, straining the heart. Unfortunately, the outcome of neonates born with a vein of Galen aneurysm is usually poor. This is particularly disturbing to parents who have been informed that a previous scan was normal. Recognition of the characteristic prognostic features and rapid and definitive diagnosis help in the counselling of these parents.
METHODS All cases of cerebral AVMs detected in 25,000 fetal scans were reviewed to determine how and when they first appeared and what ultrasound features they shared. The scans included evaluation of the size and appearance of the calvarium, lateral and third ventricles, cerebellum, cisterna magna, neck vessels, and Received July 6, 1990, from the William Beaumont Hospital, Division of Fetal Imaging, Department of ObstetriG and Gynecology, Royal Oak, Michigan .Revised manuscript accepted for publication December 5, 1990. Address correspondence and reprint requests to Dr. Christine H. Comstock: William Beaumont Hospital. Division of Fetal Imaging,. Department of Obstetrics and Gynecology. 3601 W. Thirteenth Mile Road, Royal Oak, Ml 48073.
ventricle. Previous scans have been normal. Evidence of high output failure such as cardiomegaly, enlarged neck veins, or hydrops predicts a poor outcome. KEY woRos: aneurysm, fetal, cerebral; Galen, fetal aneurysms; cardiomegaly, fetal; heart, fetal; neck, fetal. (/ Ultraso1111d Med 10: 361, 1991)
heart (including the great vessels). Pulsed Doppler was used to determine the presence of blood flow within a lesion if flow was not apparent on B-mode. The scanners used were manufactured by General Electric (RT3000, Milwaukee, WI) or Acuson (Mountain View, CA).
RESULTS Four fetuses of 25,000 had evidence of cerebral AVMs. Two fetuses had been referred for a suspected intracerebral lesion; AVMs in the other two were discovered at a return visit for evaluation of fetal size. All four had had normal scans at an earlier gestational age. One infant had a normal scan elsewhere at 20 weeks, but had developed a 5-cm AVM of the left frontal lobe by 34 weeks (Fig. 1). There were multiple blood vessels around the larger sonolucent lesion and over the surface of the cerebellum. Turbulence and arterial blood flow were noted in various locations within this large lesion . The other three infants had vein of Galen aneurysms with the typical midline location behind the third ventricle. One had a normal scan at 25 weeks and an abnormal scan at 37 weeks, at which time an oval central cystic lesion was identified (Fig. 2). The second had normal scans at 27 weeks and 33 weeks, but by 37 weeks a 3·cm vein of Galen aneurysm was visible (Fig. 3). This latter fetus was a growth· retarded twin in a monochorionic diamniotic pregnancy. The fourth
© 1991 by the American Institute of Ultrasound in Medicine• J Ultrasound Med 10:361- 365, 1991•0278· 4927/ 91 / $3.50
362
ARTERIOVENOUS MALFORMATIONS
J Ultrasound Med 10:361- 365, 1991
Figure 1 Frontal AVM in a 34Tweek fetus. The numerous sonolucent areas within the little remaining solid tissue are abnormal vessels. V, ventricle. appeared normal at 19 weeks, but at 30 weeks a typical vein of Galen aneurysm was quickly identified with color Doppler (Fig. 4). All four AVMs were sonolucent with obvious dilated feeding vessels around their walls. The three vein of Galen·aneurysms were oval; one had the typical "cigar" shape. All four fetuses had normal head circumferences throughout the pregnancy. Hydrocephalus was variT Figure 2 Typical appearance of a vein of Galen aneurysm with oval shape and central location.
Figure 3 Vein of Galen aneurysm with dilated blood vessels
(arrows) around a central lucent area.
able: severe in the fetus with the 5 ~ cm frontoparietal lesion noted at 34 weeks, not present in two others, and mild in the infant whose lesion became visible between 25 and 37 weeks. Generalized cardiomegaly was present in the fetus with the frontoparietal AVM (Fig. 5). In one fetus with a vein of Galen aneurysm (discovered at 37 weeks) there was marked enlargement of the right ventricle, slight enlargement of the right atrium, tricuspid insuf· ficiency, enlargement of the pulmonary artery, and apparent narrowing of the aortic arch. At autopsy this fetus was found to have coarctation of the aorta. The Figure 4 Color Doppler shows communication of the aneuT rysm with the straight sinus (axial view).
J Ultrasound Med 10:361- 365, 1991
COMSTOCK AND KIRK
363
Figure S A transverse view of the heart shows that it is enlarged and occupies most of the chest. S, spine.
right ventricle of another fetus was enlarged, and there was increased velocity over the aortic valve. The arch appeared normal. There was no autopsy. The heart of the third fetus with a vein of Galen aneurysm could not be seen well enough to comment (but was enlarged at autopsy). Neck veins were enlarged in all four (Fig. 6). None of them had hydrops, but one had mild polyhydramnios. Flow within the lesion could be seen on B-mode in the large left frontal lesion, but Doppler was needed to detect it in the smaller vein of Galen aneurysms (Figs. 4, 7). The antenatal findings were confirmed by neonatal ultrasound examinations. All four newborns died within several days of birth of intractable heart failure and disseminated intravascular coagulation. Autopsies Figure 6 Very enlarged neck veins (arrows). Coronal view with to head to the right.
Figure 7 Flow within a vein of Galen aneurysm is demonstrated by Doppler.
were performed on three of the four. At autopsy, the sizes of the AVMs closely matched those reported by ultrasound..
DISCUSSION The two internal cerebral veins unite just posterior to the pineal gland to form the great vein of Galen, which then courses posteriorly to empty into the straight sinus. Aneurysms of this vein are actually end-to-end anastomoses of a major artery to a vein without the usual intervening capillaries. In Gold's series one or both of the posterior cerebral arteries communicated directly with the vein of Galen. In five of nine infants the superior cerebellar artery was also involved as were the anterior and middle cerebral arteries in three of nine cases. 9 Hoffman 2 reports a different supply in his series: in neonates the anterior cerebral, lenticulostriate, thalamic perforating, and anterior and posterior choroidal arteries suppled into the vein of Galen. Seven cases of in utero diagnosis of vein of Galen aneurysms have been previously reported. 3" 9 The appearance and locations were similar to the three vein of Galen aneurysms described in this series: a central oval or tubular cystic area just above and behind the thalamus, usually not exceeding 2.5 cm in its smallest diameter. Often there were heterogeneous cystic areas around the larger lucent area, which represented dilated blood vessels. The AVM in the frontal lobe reported here is not
364
ARTERIOVENOUS MALFORMATIONS
typical of a fetal AVM in location or size, since all other reported fetal aneurysms have been smaller and have been related to the vein of Galen. This reflects the experience with the pediatric population: AVMs presenting in the newborn almost always involve the vein of Galen. 2 Occipital, frontal, or parietal AVMs typically present later in childhood. 10 From our experience, it appears that AVMs may not become visible until the third trimester. In all four cases in this series the brain appeared normal in the second trimester and even as late as 33 weeks. Late appearance was also seen in a case reported by Mao; 4 a vein of Galen aneurysm was first identified at 38 weeks after a normal scan at 33 weeks. Vintzileos reported one at 37 weeks after a normal scan at 22 weeks.6 None of the previously reported cases have been identified earlier than 32 weeks gestation. Occasionally, turbulent flow within a lesion can be seen without resorting to Doppler scanning. Doppler evaluation can show arterial and/ or venous flow depending on the area within the tubular structure sampled.' Apparently, brain anoxia may exist in utero since microinfarcts and periventricular leukomalacia have been reported at birth, 6•7•11•12 due to either decreased blood supply or pressure necrosis. Appearance of the cerebral ventricles is variable. Only 1 of 45 neonates with vein of Galen aneurysms had hydrocephalus in Hoffman's series. 2 Manifestations of hydrocephalus were the major findings in children presenting after the newborn period (between 3 weeks and 11 months), 1•1•13 but not in newborns. Three of seven of the previously reported antenatal cases had hydrocephalus, but their lesions were no different in size than those who did not have hydrocephalus. Heart failure, rather than hydrocephalus, is the major finding in symptomatic newborns. The antenatal appearance of the heart is variable, but generalized cardiomegaly or right ventricular enlargement is the rule. In all of our cases the neck veins were also enlarged, reflecting increased right heart output. The outcome of cases detected in utero or in the early neonatal period is usually poor if there is evidence of heart failure. 2 Only one fetus of the six antenatal cases previously reported with heart enlargement has sur ~ vived. 6 Myocardial infarction due to markedly reduced coronary blood flow can add to intraoperative problems.2 The prognosis is better for those neonates who have no evidence of heart failure at birth ..l Apparently, if the AVM develops later in neonatal life, or if the lesion is so small that it remains undetected up to that point, outcome appears to be somewhat better. That is, prog· nosis appears to be related to heart failure, not the size of the lesion.
JUltrasound Med 10:361- 365, 1991
Heart enlargement should not be ascribed to high output failure alone until a fetal echocardiogram is performed. As in the case of any identified abnormality, there is sometimes an additional one, as in the one fetus here in which there was a significant coarctation of the aorta. Coarctation of the aorta and transposition of the great vessels occur with increased frequency in infants with vein of Galen aneurysm. tu! Although right ventricular enlargement could have been easily attributed to high output failure alone, narrowing of the aortic arch suggested that some of the right ventricular dilatation was due to coarctation. However, often this narrowing is not seen in the fetus with coarctation; therefore, right heart enlargement might be the result of the AVM only or of coarctation as well. Resulting cardiac failure with asdtes and pleural effusions has produced hypoplastic lungs. 7 Massive hydrops has been reported as early as 31 weeks in two fetuses in which the actual intracerebral lesion was not identified until after birth.16 Hepatomegaly appears to be the rule if there is evidence for congestive heart failure . In summary, it appears that fetal AVMs may develop in or enlarge to a detectable size over a short period of time, usually in the third trimester. In fact, to date no vein of Galen aneurysm has yet been reported prior to 30 weeks gestation. Although almost all cerebral AVMs in the neonate and the fetus involve the vein of Galen, occasionally they may be located elsewhere in the brain. Consequently, all intracerebral sonolucent lesions not obviously part of a ventricle should be evaluated for blood flow. The fetal brain should also be carefully examined for an aneurysm in cases of hydrops or when the heart and neck veins are enlarged. If there is heart failure in the absence of underlying cardiac anomalies, outcome is generally poor. Color Doppler aids in quick diagnosis and identification of the supplying branches.
REFERENCES 1. Gold AP, Ransohoff J, Carter 5: Vein of Galen malfor ~ mation. Acta Neurol Scand 40:p.5 Suppl. 11, 1964 2. Hoffman HJ, Chuang S, Hendrick EB, et al: Aneurysms of the vein of Galen.J Neurosurg 57:316, 1982 3. Hirsch JH, Cyr 0, Heidrun E, et al: Ultrasonographic diagnosis of an aneurysm of the vein of Galen in utero by duplex scanning. J Ultrasound Med 2:231, 1983
4. Mao K, Adams J: Antenatal diagnosis of intracranial arteriovenous fistula by ultrasonography. Case Report. Br J Obstet Gynaecol 90:872, 1983 5. Mendelsohn DB, Hertzanu Y, Butterworth A: In utero diagnosis of a vein of Galen aneurysm by ultrasound. Neuroradiology 26:417, 1984
COMSTOCK AND KIRK
J Ultrasound Med 10:361-365, 1991
6. Vintzileos AM, Eisenfeld LI, Campbell WA, et al: Prenatal ultrasonic diagnosis of arteriovenous malformation of the vein of Galen. Am J Perinatology 3:209, 1986 7. Reiter AA, Huhta JC, Carpenter FJ, et al: Prenatal diagnosis of arteriovenous malformation of the vein of Galen. J Clin Ultrasound 14:623, 1986 8. Rizzo G, Arduini D, Colosimo C, et al: Abnormal fetal cerebral blood flow velocity waveforms as a sign of an aneurysm of the vein of Galen. Fetal Therapy 2:75, 1987 9. Jeanty P, Kepple D, Roussis P, et al: In utero detection of cardiac failure from an aneurysm of the vein of Galen. Am J Ob Gyn 163:50, 1990 10. Lagos JC, Riley HD: Congenital intracranial vascular malformations in children. Arch Dis Childhood 46:285, 1971 11 . Norman MG, Becker LE: Cerebral damage in neonates,
12. 13. '14.
15. 16.
365
resulting from arteriovenous malformation of the vein of Galen. J Neurol Neurosurg Psychiatry 37:252, 1974 Gomez MR. Whitten CF, Nolke A, et al: Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Pediatrics 32:400, 1963 Montoya G, Dohn OF, Mercer RD: Arteriovenous ma!· formation of the vein of Galen as a cause of heart failure and hydrocephalus in infants. Neurology 21:1054, 1971 Watson DG, Smith RR, Brann AW: Arteriovenous malformation of the vein of Galen. Am J Dis Child 130:520, 1976 Warkany J: Cerebrovascular malformations. Congenital Malform 249, 1971 Johnson W, Berry JM, Einzig S, et al: Doppler findings in nonimmune hydrops fetalis and cerebral arteriovenous malformation. Am Heart J 5:1138, 1988
Almost all cerebral arteriovenous malformations in the fetus involve the vein of Galen, although occasionally they may involve the frontal area of the brain instead. In all reported cases arteriovenous malformations have presented some time after 30 weeks as a sonolucent oval lesion located in the midline behind the third
A
rteriovenous malformations (AVMs) of the fetus and neonate, with only occasional exceptions, involve the vein of Galen. These are "end-to-end' aneurysms in which the artery and vein connect without intervening capillaries. Blood flow through the brain is markedly increased, straining the heart. Unfortunately, the outcome of neonates born with a vein of Galen aneurysm is usually poor. This is particularly disturbing to parents who have been informed that a previous scan was normal. Recognition of the characteristic prognostic features and rapid and definitive diagnosis help in the counselling of these parents.
METHODS All cases of cerebral AVMs detected in 25,000 fetal scans were reviewed to determine how and when they first appeared and what ultrasound features they shared. The scans included evaluation of the size and appearance of the calvarium, lateral and third ventricles, cerebellum, cisterna magna, neck vessels, and Received July 6, 1990, from the William Beaumont Hospital, Division of Fetal Imaging, Department of ObstetriG and Gynecology, Royal Oak, Michigan .Revised manuscript accepted for publication December 5, 1990. Address correspondence and reprint requests to Dr. Christine H. Comstock: William Beaumont Hospital. Division of Fetal Imaging,. Department of Obstetrics and Gynecology. 3601 W. Thirteenth Mile Road, Royal Oak, Ml 48073.
ventricle. Previous scans have been normal. Evidence of high output failure such as cardiomegaly, enlarged neck veins, or hydrops predicts a poor outcome. KEY woRos: aneurysm, fetal, cerebral; Galen, fetal aneurysms; cardiomegaly, fetal; heart, fetal; neck, fetal. (/ Ultraso1111d Med 10: 361, 1991)
heart (including the great vessels). Pulsed Doppler was used to determine the presence of blood flow within a lesion if flow was not apparent on B-mode. The scanners used were manufactured by General Electric (RT3000, Milwaukee, WI) or Acuson (Mountain View, CA).
RESULTS Four fetuses of 25,000 had evidence of cerebral AVMs. Two fetuses had been referred for a suspected intracerebral lesion; AVMs in the other two were discovered at a return visit for evaluation of fetal size. All four had had normal scans at an earlier gestational age. One infant had a normal scan elsewhere at 20 weeks, but had developed a 5-cm AVM of the left frontal lobe by 34 weeks (Fig. 1). There were multiple blood vessels around the larger sonolucent lesion and over the surface of the cerebellum. Turbulence and arterial blood flow were noted in various locations within this large lesion . The other three infants had vein of Galen aneurysms with the typical midline location behind the third ventricle. One had a normal scan at 25 weeks and an abnormal scan at 37 weeks, at which time an oval central cystic lesion was identified (Fig. 2). The second had normal scans at 27 weeks and 33 weeks, but by 37 weeks a 3·cm vein of Galen aneurysm was visible (Fig. 3). This latter fetus was a growth· retarded twin in a monochorionic diamniotic pregnancy. The fourth
© 1991 by the American Institute of Ultrasound in Medicine• J Ultrasound Med 10:361- 365, 1991•0278· 4927/ 91 / $3.50
362
ARTERIOVENOUS MALFORMATIONS
J Ultrasound Med 10:361- 365, 1991
Figure 1 Frontal AVM in a 34Tweek fetus. The numerous sonolucent areas within the little remaining solid tissue are abnormal vessels. V, ventricle. appeared normal at 19 weeks, but at 30 weeks a typical vein of Galen aneurysm was quickly identified with color Doppler (Fig. 4). All four AVMs were sonolucent with obvious dilated feeding vessels around their walls. The three vein of Galen·aneurysms were oval; one had the typical "cigar" shape. All four fetuses had normal head circumferences throughout the pregnancy. Hydrocephalus was variT Figure 2 Typical appearance of a vein of Galen aneurysm with oval shape and central location.
Figure 3 Vein of Galen aneurysm with dilated blood vessels
(arrows) around a central lucent area.
able: severe in the fetus with the 5 ~ cm frontoparietal lesion noted at 34 weeks, not present in two others, and mild in the infant whose lesion became visible between 25 and 37 weeks. Generalized cardiomegaly was present in the fetus with the frontoparietal AVM (Fig. 5). In one fetus with a vein of Galen aneurysm (discovered at 37 weeks) there was marked enlargement of the right ventricle, slight enlargement of the right atrium, tricuspid insuf· ficiency, enlargement of the pulmonary artery, and apparent narrowing of the aortic arch. At autopsy this fetus was found to have coarctation of the aorta. The Figure 4 Color Doppler shows communication of the aneuT rysm with the straight sinus (axial view).
J Ultrasound Med 10:361- 365, 1991
COMSTOCK AND KIRK
363
Figure S A transverse view of the heart shows that it is enlarged and occupies most of the chest. S, spine.
right ventricle of another fetus was enlarged, and there was increased velocity over the aortic valve. The arch appeared normal. There was no autopsy. The heart of the third fetus with a vein of Galen aneurysm could not be seen well enough to comment (but was enlarged at autopsy). Neck veins were enlarged in all four (Fig. 6). None of them had hydrops, but one had mild polyhydramnios. Flow within the lesion could be seen on B-mode in the large left frontal lesion, but Doppler was needed to detect it in the smaller vein of Galen aneurysms (Figs. 4, 7). The antenatal findings were confirmed by neonatal ultrasound examinations. All four newborns died within several days of birth of intractable heart failure and disseminated intravascular coagulation. Autopsies Figure 6 Very enlarged neck veins (arrows). Coronal view with to head to the right.
Figure 7 Flow within a vein of Galen aneurysm is demonstrated by Doppler.
were performed on three of the four. At autopsy, the sizes of the AVMs closely matched those reported by ultrasound..
DISCUSSION The two internal cerebral veins unite just posterior to the pineal gland to form the great vein of Galen, which then courses posteriorly to empty into the straight sinus. Aneurysms of this vein are actually end-to-end anastomoses of a major artery to a vein without the usual intervening capillaries. In Gold's series one or both of the posterior cerebral arteries communicated directly with the vein of Galen. In five of nine infants the superior cerebellar artery was also involved as were the anterior and middle cerebral arteries in three of nine cases. 9 Hoffman 2 reports a different supply in his series: in neonates the anterior cerebral, lenticulostriate, thalamic perforating, and anterior and posterior choroidal arteries suppled into the vein of Galen. Seven cases of in utero diagnosis of vein of Galen aneurysms have been previously reported. 3" 9 The appearance and locations were similar to the three vein of Galen aneurysms described in this series: a central oval or tubular cystic area just above and behind the thalamus, usually not exceeding 2.5 cm in its smallest diameter. Often there were heterogeneous cystic areas around the larger lucent area, which represented dilated blood vessels. The AVM in the frontal lobe reported here is not
364
ARTERIOVENOUS MALFORMATIONS
typical of a fetal AVM in location or size, since all other reported fetal aneurysms have been smaller and have been related to the vein of Galen. This reflects the experience with the pediatric population: AVMs presenting in the newborn almost always involve the vein of Galen. 2 Occipital, frontal, or parietal AVMs typically present later in childhood. 10 From our experience, it appears that AVMs may not become visible until the third trimester. In all four cases in this series the brain appeared normal in the second trimester and even as late as 33 weeks. Late appearance was also seen in a case reported by Mao; 4 a vein of Galen aneurysm was first identified at 38 weeks after a normal scan at 33 weeks. Vintzileos reported one at 37 weeks after a normal scan at 22 weeks.6 None of the previously reported cases have been identified earlier than 32 weeks gestation. Occasionally, turbulent flow within a lesion can be seen without resorting to Doppler scanning. Doppler evaluation can show arterial and/ or venous flow depending on the area within the tubular structure sampled.' Apparently, brain anoxia may exist in utero since microinfarcts and periventricular leukomalacia have been reported at birth, 6•7•11•12 due to either decreased blood supply or pressure necrosis. Appearance of the cerebral ventricles is variable. Only 1 of 45 neonates with vein of Galen aneurysms had hydrocephalus in Hoffman's series. 2 Manifestations of hydrocephalus were the major findings in children presenting after the newborn period (between 3 weeks and 11 months), 1•1•13 but not in newborns. Three of seven of the previously reported antenatal cases had hydrocephalus, but their lesions were no different in size than those who did not have hydrocephalus. Heart failure, rather than hydrocephalus, is the major finding in symptomatic newborns. The antenatal appearance of the heart is variable, but generalized cardiomegaly or right ventricular enlargement is the rule. In all of our cases the neck veins were also enlarged, reflecting increased right heart output. The outcome of cases detected in utero or in the early neonatal period is usually poor if there is evidence of heart failure. 2 Only one fetus of the six antenatal cases previously reported with heart enlargement has sur ~ vived. 6 Myocardial infarction due to markedly reduced coronary blood flow can add to intraoperative problems.2 The prognosis is better for those neonates who have no evidence of heart failure at birth ..l Apparently, if the AVM develops later in neonatal life, or if the lesion is so small that it remains undetected up to that point, outcome appears to be somewhat better. That is, prog· nosis appears to be related to heart failure, not the size of the lesion.
JUltrasound Med 10:361- 365, 1991
Heart enlargement should not be ascribed to high output failure alone until a fetal echocardiogram is performed. As in the case of any identified abnormality, there is sometimes an additional one, as in the one fetus here in which there was a significant coarctation of the aorta. Coarctation of the aorta and transposition of the great vessels occur with increased frequency in infants with vein of Galen aneurysm. tu! Although right ventricular enlargement could have been easily attributed to high output failure alone, narrowing of the aortic arch suggested that some of the right ventricular dilatation was due to coarctation. However, often this narrowing is not seen in the fetus with coarctation; therefore, right heart enlargement might be the result of the AVM only or of coarctation as well. Resulting cardiac failure with asdtes and pleural effusions has produced hypoplastic lungs. 7 Massive hydrops has been reported as early as 31 weeks in two fetuses in which the actual intracerebral lesion was not identified until after birth.16 Hepatomegaly appears to be the rule if there is evidence for congestive heart failure . In summary, it appears that fetal AVMs may develop in or enlarge to a detectable size over a short period of time, usually in the third trimester. In fact, to date no vein of Galen aneurysm has yet been reported prior to 30 weeks gestation. Although almost all cerebral AVMs in the neonate and the fetus involve the vein of Galen, occasionally they may be located elsewhere in the brain. Consequently, all intracerebral sonolucent lesions not obviously part of a ventricle should be evaluated for blood flow. The fetal brain should also be carefully examined for an aneurysm in cases of hydrops or when the heart and neck veins are enlarged. If there is heart failure in the absence of underlying cardiac anomalies, outcome is generally poor. Color Doppler aids in quick diagnosis and identification of the supplying branches.
REFERENCES 1. Gold AP, Ransohoff J, Carter 5: Vein of Galen malfor ~ mation. Acta Neurol Scand 40:p.5 Suppl. 11, 1964 2. Hoffman HJ, Chuang S, Hendrick EB, et al: Aneurysms of the vein of Galen.J Neurosurg 57:316, 1982 3. Hirsch JH, Cyr 0, Heidrun E, et al: Ultrasonographic diagnosis of an aneurysm of the vein of Galen in utero by duplex scanning. J Ultrasound Med 2:231, 1983
4. Mao K, Adams J: Antenatal diagnosis of intracranial arteriovenous fistula by ultrasonography. Case Report. Br J Obstet Gynaecol 90:872, 1983 5. Mendelsohn DB, Hertzanu Y, Butterworth A: In utero diagnosis of a vein of Galen aneurysm by ultrasound. Neuroradiology 26:417, 1984
COMSTOCK AND KIRK
J Ultrasound Med 10:361-365, 1991
6. Vintzileos AM, Eisenfeld LI, Campbell WA, et al: Prenatal ultrasonic diagnosis of arteriovenous malformation of the vein of Galen. Am J Perinatology 3:209, 1986 7. Reiter AA, Huhta JC, Carpenter FJ, et al: Prenatal diagnosis of arteriovenous malformation of the vein of Galen. J Clin Ultrasound 14:623, 1986 8. Rizzo G, Arduini D, Colosimo C, et al: Abnormal fetal cerebral blood flow velocity waveforms as a sign of an aneurysm of the vein of Galen. Fetal Therapy 2:75, 1987 9. Jeanty P, Kepple D, Roussis P, et al: In utero detection of cardiac failure from an aneurysm of the vein of Galen. Am J Ob Gyn 163:50, 1990 10. Lagos JC, Riley HD: Congenital intracranial vascular malformations in children. Arch Dis Childhood 46:285, 1971 11 . Norman MG, Becker LE: Cerebral damage in neonates,
12. 13. '14.
15. 16.
365
resulting from arteriovenous malformation of the vein of Galen. J Neurol Neurosurg Psychiatry 37:252, 1974 Gomez MR. Whitten CF, Nolke A, et al: Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Pediatrics 32:400, 1963 Montoya G, Dohn OF, Mercer RD: Arteriovenous ma!· formation of the vein of Galen as a cause of heart failure and hydrocephalus in infants. Neurology 21:1054, 1971 Watson DG, Smith RR, Brann AW: Arteriovenous malformation of the vein of Galen. Am J Dis Child 130:520, 1976 Warkany J: Cerebrovascular malformations. Congenital Malform 249, 1971 Johnson W, Berry JM, Einzig S, et al: Doppler findings in nonimmune hydrops fetalis and cerebral arteriovenous malformation. Am Heart J 5:1138, 1988
