Acta Pzdiatr Scand 67: 529-532, 1978
CASE REPORT
MALFORMATION O F THE GREAT VEIN O F GALEN WITH NEONATAL HEART FAILURE Report of Two Cases J. EIDE and M. FgLLING From the Gade Institute, Department of Pathology, and the Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway
ABSTRACT. Eide, J. and Falling, M. (The Gade Institute, Department of Pathology, and the Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway). Malformation of the great vein of Galen with neonatal heart failure. Report of two cases. Acta Paediatr Scand, 67: 529, 1978.-The clinical and pathological findings in two neonates with the malformation of the great vein of Galen are given. They both reported with serious neonatal heart failure suggesting congenital heart disease. In one of them cardiac catheterization revealed a foetal pattern of circulation causing cyanosis. A bruit and in one of them a thrill over the skull gave the clinical diagnosis of an intracranial arteriovenous aneurysm. They died 48 and 144 hours after birth in spite of medical treatment. The outlook for patients having malformation of the great vein of Galen and suffering neonatal heart failure treated conservatively, seems hopeless. KEY WORDS: Arteriovenous aneurysms, malformation of the great vein of Galen, neonatal heart, failure
The vein of Galen malformation is said to be present when one or more major branches of arteries of the carotid or vertebral system feed directly into a hugely dilated vein of Galen (5, 13), which functions as an arteriovenous aneurysm, short-circuiting varying and sometimes large volumes of blood, and giving rise to heart failure and/or various neurological symptoms ( 5 , 7, 8, 16). In the neonatal period it may cause fatal heart failure. The diagnosis is usually made post mortem, as the symptoms closely mimic a serious congenital heart defect (1, 5). During the last 7 years we have seen two cases, and report the clinical and post-mortem findings, as they may contribute to the clinical diagnosis of future cases and thus open up the possibility of adequate treatment.
CASE REPORTS
Patient I A. H., a newborn female, was born after 40 weeks’ gestation. The mother had had one previous first trimester
35-782874
abortion. She had been given diazepam in the third month of pregnancy because of vaginal haemorrhage, and an antibiotic in the 7th month for urinary infection. The labour was normal and lasted for 7 hours. Birth weight was 3 150 g, and crown-heel length 48 cm. The head circumference measured 34 cm. The child was cyanotic, with tachycardia, tachypnoea, and hepatomegaly from birth. A grade 2-316 systolic murmur that later disappeared was heard in the third intercostal space on the left side of the sternum. Electrocardiogram and chest X-ray indicated cardiomegaly with a right ventricular and right atrial predominance. Cardiac catheterization was performed. The left side of the heart was not entered by the catheter. Right atrial pressure was high, and the right ventricular and pulmonary arterial pressure were at systemic levels. Right ventricular angiography showed an enlarged right ventricle, widely open ductus arteriosus and right to left shunting to the descending aorta. The pulmonary circulation was very slow, and the left side of the heart could not be visualized until 5 seconds after the contrast injection. The findings were misinterpreted as hypoplastic left heart syndrome. The day after catheterization a loud bruit was heard over the skull, and an intracranial arteriovenous malformation was suggested as the cause of the cardiac failure. The child died 48 hours after birth, not responding to medical treatment. Autopsy (0.553159) revealed a malformation of the vein of Galen (Fig. 1) bilaterally fed by branches of the posActa Paediatr Scund 67
530
J . Eide and M . Fdling
Fig. 2. T. B. Chest X-ray, anterior view, showing marked cardiac enlargement.
Fig. I . A. H. Pathological specimen. Base of brain, the cerebellum and brain stem removed. Tortuous vessels can be seen on the right side connecting the posterior cerebral artery to the dilated vein of Galen (urrow).
terior cerebral arteries, 3 on the right side and 1 on the left. The vein showed a large sac-like dilatation with compression of surrounding brain structures. The heart showed no congenital defects, but marked right ventricular and atrial hypertrophy and dilatation. The calibre of the aortic arch, the brachiocephalic trunk, the common, internal and external carotid arteries were enlarged, and the ductus arteriosus was open. The lungs showed incipient bronchopneumonia, and the lungs, liver, spleen and kidneys evidence of passive congestion. Patient 2
T. B., a newborn male, was born after40 weeks' gestation. Labour exceeded 24 hours, but was uncomplicated. The infant weighed 3600 g and had a crown-heel length of 55 cm. Head circumference was 35 cm. Apgar score was 9 after 1 and 5 min. Progressive respiratory distress developed 48 hours after birth. Chest X-ray showed cardiomegaly, and the infant was transferred to this hospital. At admission he was in severe heart failure with enlarged liver, 4 cm below the costal margin. No cyanosis. Heart rate was lSO/min with a normal femoral pulse, and blood pressure 65/40 in upper and lower limbs. Respiratory frequency increased from 70/min to 95/min during the ensuing 6 hours. A grade 2-3/6 systolic murmur was heard along the left costal margin. The electrocardiogram showed QRS-complexes within normal limits, and pActu Pardiatr Scand 67
waves suggesting right atrial enlargement. Chest X-ray revealed an enlarged heart, with predominance of the right side (Fig. 2). A loud, coarse, intracranial continuous bruit anda,thrill over the skull led to the clinical diagnosis of a large mtracranial arteriovenous aneurysm. The neurosurgeon was consulted, but the lesion was considered inoperable because of the child's clinical condition. Heart catheterization and cerebral angiography were therefore not performed. The progressive heart failure did not respond to treatment, and he died 144 hours after birth. Aufopsy (0.250/76) revealed a malformation of the vein of Galen with a huge, sac-like dilatation that made large impressions on the medial side of the hemispheres, and compressed the roof of the midbrain, the posterior part of the corpus callosum, and the superior part of the cerebellum. The ventricular system of the brain did not seem to be dilated. Three to four branches of the posterior cerebral arteries on each side fed into the aneurysm (Fig. 3). The torcula Herophilii, the straight and sigmoid sinuses were dilated, as were the grooves for the sinuses on the internal surface of the skull. The heart showed enlargement, predominantly on the right side. Dilatation of the pulmonary artery, the aorta and the neck arteries were noted. The ductus arteriosus was patent, and no congenital heart defects were found.
DISCUSSION A widely dilated, sac-like vein of Galen fed directly from few large branches of the pos-
Malformation of the great vein of Galen
53 1
cranial tumours (4), and 13.9% of all intracranial aneurysms (14). Gold et al. (5) were able to find 35 cases in the literature and reported another 5. Amacher & Shillito (1) in their review from 1973 accepted 37 cases after critical analysis of reports in the English language, considering only the solitary aneurysms, and not the secondary dilatations, in which an angiomatous malformation drains through the Galenic system (1 1). Eleven cases belonged to the neonatal heart failure group. A loud intracranial bruit is of major diagnostic importance in the symptomatic infant and older childredadult groups, but has Fig. 3 . T. B. Pathological specimen. Base of brain and previously been demonstrated only in one cerebellum, posterior view. The aneurysm of the vein of child of the neonatal heart failure group (1, 5). Galen is filled with water from a catheter to demonstrate In both our cases a loud intracranial bruit and its size. in the second case an additional thrill over the skull were present. Cardiac catheterization of tenor cerebral arteries giving considerable patient 1 revealed a foetal pattern of circulashunting of blood through the arteriovenous tion which has been described in this condition aneurysm, and rapidly progressing heart fail- by others causing cyanosis (15). In patient 2 ure, are characteristic features of the malfor- cyanosis was absent. This sign in combination mation of the vein of Galen in neonates (1, 5). with right heart enlargement suggested an exThree clinical syndromes are generally re- tracardiac cause of heart insufficiency, and cognized with this aneurysm: Fatal heart fail- this led to the finding of the diagnostically imure in the neonatal period usually without portant intracranial bruit. A cerebral angioclinical recognition of the arteriovenous aneu- gram that might have given the precise diagrysm (the neonatal heart failure group), slight- nosis of the malformation was not undertaken; ly older infants developing hydrocephalus, in case 1 because of rapidly deteriorating heart seizures or other neurological symptoms (the failure, in case 2 because of the seemingly symptomatic infant group), and older children hopeless outlook. or adults with headaches and/or signs of subUsually the malformation is not associated arachnoid haemorrhage (the older infantladult with other congenital defects, as in our cases, group) (5). In addition, one infant with mild but supernumerary digits, hypospadia, and heart failure in the neonatal period, later de- transposition of the great vessels have been veloping hydrocephalus, has been placed in reported by Claireaux & Newman ( 2 ) , and yet another group (1). Hirano & Solomon (9). Both our patients belong to the neonatal Surgical treatment has been rewarding for heart failure group. the symptomatic infant and the older children/ The frequency of this malformation is not adult group. The technical procedure and the precisely known. It seems comparatively low results have been reviewed by Gold et al. (3, but is not insignificant: 15.4% of the con- and Amacher & Shillito (1). Usually a right genital intracranial arteriovenous malforma- parietooccipital craniotomy is performed tions in Lagos & Riley’s (10) series, 50% in through which the dilated vein of Galen is isoGold et al. (5); the arteriovenous aneurysms lated by ligating the feeder arteries. comprising about 1.4% of all verified intraThe question of surgical treatment of paActa Paediatr Scand 67
532
J. Eide and M . Fdling
tients belonging to the neonatal heart failure group has emerged only recently, as the condition has only rarely been diagnosed before death. One such case, reported by Gomez et al. (6), was treated with ligature of the right common carotid artery, later with ligature of the left external carotid artery, and recovered from the heart failure. However, the cerebral condition and subsequent course were not mentioned. One patient was reported by Amacher & Shillito ( l ) , and was diagnosed clinically by an intracranial bruit, cerebral angiography, and cardiac catheterization. Craniotomy and partial ligation of the feeder arteries was carried out on the fourth day of life in spite of serious heart failure. The infant died 18 hours later of heart failure that did not respond to intensive measures. The major postoperative hazard in this clinical group seems to be progressive heart failure following closure of the shunt. Immediate phlebotomy, digitalization, and rigid fluid control may be mandatory (5). The effectiveness of surgery in the neonatal heart failure group remains to be settled, as the evidence so far is very limited. However, it seems reasonable to try surgical measures, as the evidence points to an invariable fatal outcome in conservatively treated cases. One also has to consider rewarding results of surgery with other forms of intracranial arteriovenous aneurysms, and with the same malformation in other age groups, as shown by Amacher & Shillito ( l ) , Gold et al. (3,and Cronqvist et al. (3). Diagnosis depends on examination for and awareness of the significance of an intracranial bruit, when examining neonates with heart failure and suspected congenital heart disease. The bruit is loud and pulse synchronous and differs from the soft bruits that may be heard in normal children (12).
Acta Puediutr Scand 67
REFERENCES 1. Amacher, A . L. & Shillito, J.: The syndromes and
surgical treatment of aneurysms of the great vein of Galen. J Neurosurg, 39: 89, 1973. 2. Claireaux, A. E. & Newman, C. G. H.: Arteriovenous aneurysms of the great vein of Galen with heart failure in the neonatal period. Arch Dis Child, 35: 605, 1960. 3. Cronqvist, S., Granholm, L. & Lu n d st r ~ m ,N. R.: Hydrocephalus and congestive heart failure caused by intracranial arteriovenous malformations in infants. J Neurosurg, 36: 249, 1972. 4. Dandy, W. E.: Arteriovenous aneurysm of the brain. Arch Surg, 17: 190, 1928. 5. Gold, A. P., Ransohoff, J. & Carter, S.: Vein of Galen malformation. Acta Neurol Scand, Suppl. 11, 40: 1, 1964. 6. Gomez, M. R., Witten, C. F., Nolke, A., Bernstein, J. & Sterling Meyer, J.: Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Pediatrics, 31: 400, 1963. 7. Holman, E.: Abnormal arteriovenous communications. Great variability of effects with particular reference to delayed development of cardiac failure. Circulation, 32: 1001, 1965. 8. Holman, E.: Reflections on arteriovenous fistulas. Ann Thorac Surg, 11,2: 176, 1971. 9. Hirano, A. & Solomon, S.: Al-teriovenous aneurysm of the vein of Galen. Arch Neurol, 3: 589, 1960. 10. Lagos, J. C. & Riley, H. D.: Congenital intracranial vascular malformation in children. Arch Dis Child, 46: 285, 1971. 11. Litvak, J., Yahr, M. D. & Ransohoff, J.: Aneurysms of the great vein of Galen and midline cerebral arteriovenous anomalies. J Neurosurg, 17: 945, 1960. 12. Mace, J. W., Peters, E. R. & Mathies, A. W.: Cranial bruits in purulent meningitis in childhood. N Engl J Med, 278: 1420, 1968. 13. Russel, D. S. & Nevin, S.: Aneurysm of the great vein of Galen causing internal hydrocephalus: Report of two cases. J Pathol, 51: 375, 1940. 14. Sedzimir, C. B. & Robinson, J.: Intracranial haemorrhage in children and adolescents. J Neurosurg, 38: 269, 1973. 15. Stern, L.: Congestive heart failure secondary to cerebral arteriovenous aneurysm in the newborn infant. Am J Dis Child, 115: 581, 1968. 16. Wallace, J. M., Nashold, B. S. & Slewka, P.: Hemodynamic effects of cerebral arteriovenous aneurysms. Circulation, 31: 696, 1965. Submitted Jan. 24, 1977 Accepted Jan. 10, 1978
(J. E.) Department of Pathology Central Hospital of Vest-Agder 4600 Kristiansand Norway
CASE REPORT
MALFORMATION O F THE GREAT VEIN O F GALEN WITH NEONATAL HEART FAILURE Report of Two Cases J. EIDE and M. FgLLING From the Gade Institute, Department of Pathology, and the Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway
ABSTRACT. Eide, J. and Falling, M. (The Gade Institute, Department of Pathology, and the Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway). Malformation of the great vein of Galen with neonatal heart failure. Report of two cases. Acta Paediatr Scand, 67: 529, 1978.-The clinical and pathological findings in two neonates with the malformation of the great vein of Galen are given. They both reported with serious neonatal heart failure suggesting congenital heart disease. In one of them cardiac catheterization revealed a foetal pattern of circulation causing cyanosis. A bruit and in one of them a thrill over the skull gave the clinical diagnosis of an intracranial arteriovenous aneurysm. They died 48 and 144 hours after birth in spite of medical treatment. The outlook for patients having malformation of the great vein of Galen and suffering neonatal heart failure treated conservatively, seems hopeless. KEY WORDS: Arteriovenous aneurysms, malformation of the great vein of Galen, neonatal heart, failure
The vein of Galen malformation is said to be present when one or more major branches of arteries of the carotid or vertebral system feed directly into a hugely dilated vein of Galen (5, 13), which functions as an arteriovenous aneurysm, short-circuiting varying and sometimes large volumes of blood, and giving rise to heart failure and/or various neurological symptoms ( 5 , 7, 8, 16). In the neonatal period it may cause fatal heart failure. The diagnosis is usually made post mortem, as the symptoms closely mimic a serious congenital heart defect (1, 5). During the last 7 years we have seen two cases, and report the clinical and post-mortem findings, as they may contribute to the clinical diagnosis of future cases and thus open up the possibility of adequate treatment.
CASE REPORTS
Patient I A. H., a newborn female, was born after 40 weeks’ gestation. The mother had had one previous first trimester
35-782874
abortion. She had been given diazepam in the third month of pregnancy because of vaginal haemorrhage, and an antibiotic in the 7th month for urinary infection. The labour was normal and lasted for 7 hours. Birth weight was 3 150 g, and crown-heel length 48 cm. The head circumference measured 34 cm. The child was cyanotic, with tachycardia, tachypnoea, and hepatomegaly from birth. A grade 2-316 systolic murmur that later disappeared was heard in the third intercostal space on the left side of the sternum. Electrocardiogram and chest X-ray indicated cardiomegaly with a right ventricular and right atrial predominance. Cardiac catheterization was performed. The left side of the heart was not entered by the catheter. Right atrial pressure was high, and the right ventricular and pulmonary arterial pressure were at systemic levels. Right ventricular angiography showed an enlarged right ventricle, widely open ductus arteriosus and right to left shunting to the descending aorta. The pulmonary circulation was very slow, and the left side of the heart could not be visualized until 5 seconds after the contrast injection. The findings were misinterpreted as hypoplastic left heart syndrome. The day after catheterization a loud bruit was heard over the skull, and an intracranial arteriovenous malformation was suggested as the cause of the cardiac failure. The child died 48 hours after birth, not responding to medical treatment. Autopsy (0.553159) revealed a malformation of the vein of Galen (Fig. 1) bilaterally fed by branches of the posActa Paediatr Scund 67
530
J . Eide and M . Fdling
Fig. 2. T. B. Chest X-ray, anterior view, showing marked cardiac enlargement.
Fig. I . A. H. Pathological specimen. Base of brain, the cerebellum and brain stem removed. Tortuous vessels can be seen on the right side connecting the posterior cerebral artery to the dilated vein of Galen (urrow).
terior cerebral arteries, 3 on the right side and 1 on the left. The vein showed a large sac-like dilatation with compression of surrounding brain structures. The heart showed no congenital defects, but marked right ventricular and atrial hypertrophy and dilatation. The calibre of the aortic arch, the brachiocephalic trunk, the common, internal and external carotid arteries were enlarged, and the ductus arteriosus was open. The lungs showed incipient bronchopneumonia, and the lungs, liver, spleen and kidneys evidence of passive congestion. Patient 2
T. B., a newborn male, was born after40 weeks' gestation. Labour exceeded 24 hours, but was uncomplicated. The infant weighed 3600 g and had a crown-heel length of 55 cm. Head circumference was 35 cm. Apgar score was 9 after 1 and 5 min. Progressive respiratory distress developed 48 hours after birth. Chest X-ray showed cardiomegaly, and the infant was transferred to this hospital. At admission he was in severe heart failure with enlarged liver, 4 cm below the costal margin. No cyanosis. Heart rate was lSO/min with a normal femoral pulse, and blood pressure 65/40 in upper and lower limbs. Respiratory frequency increased from 70/min to 95/min during the ensuing 6 hours. A grade 2-3/6 systolic murmur was heard along the left costal margin. The electrocardiogram showed QRS-complexes within normal limits, and pActu Pardiatr Scand 67
waves suggesting right atrial enlargement. Chest X-ray revealed an enlarged heart, with predominance of the right side (Fig. 2). A loud, coarse, intracranial continuous bruit anda,thrill over the skull led to the clinical diagnosis of a large mtracranial arteriovenous aneurysm. The neurosurgeon was consulted, but the lesion was considered inoperable because of the child's clinical condition. Heart catheterization and cerebral angiography were therefore not performed. The progressive heart failure did not respond to treatment, and he died 144 hours after birth. Aufopsy (0.250/76) revealed a malformation of the vein of Galen with a huge, sac-like dilatation that made large impressions on the medial side of the hemispheres, and compressed the roof of the midbrain, the posterior part of the corpus callosum, and the superior part of the cerebellum. The ventricular system of the brain did not seem to be dilated. Three to four branches of the posterior cerebral arteries on each side fed into the aneurysm (Fig. 3). The torcula Herophilii, the straight and sigmoid sinuses were dilated, as were the grooves for the sinuses on the internal surface of the skull. The heart showed enlargement, predominantly on the right side. Dilatation of the pulmonary artery, the aorta and the neck arteries were noted. The ductus arteriosus was patent, and no congenital heart defects were found.
DISCUSSION A widely dilated, sac-like vein of Galen fed directly from few large branches of the pos-
Malformation of the great vein of Galen
53 1
cranial tumours (4), and 13.9% of all intracranial aneurysms (14). Gold et al. (5) were able to find 35 cases in the literature and reported another 5. Amacher & Shillito (1) in their review from 1973 accepted 37 cases after critical analysis of reports in the English language, considering only the solitary aneurysms, and not the secondary dilatations, in which an angiomatous malformation drains through the Galenic system (1 1). Eleven cases belonged to the neonatal heart failure group. A loud intracranial bruit is of major diagnostic importance in the symptomatic infant and older childredadult groups, but has Fig. 3 . T. B. Pathological specimen. Base of brain and previously been demonstrated only in one cerebellum, posterior view. The aneurysm of the vein of child of the neonatal heart failure group (1, 5). Galen is filled with water from a catheter to demonstrate In both our cases a loud intracranial bruit and its size. in the second case an additional thrill over the skull were present. Cardiac catheterization of tenor cerebral arteries giving considerable patient 1 revealed a foetal pattern of circulashunting of blood through the arteriovenous tion which has been described in this condition aneurysm, and rapidly progressing heart fail- by others causing cyanosis (15). In patient 2 ure, are characteristic features of the malfor- cyanosis was absent. This sign in combination mation of the vein of Galen in neonates (1, 5). with right heart enlargement suggested an exThree clinical syndromes are generally re- tracardiac cause of heart insufficiency, and cognized with this aneurysm: Fatal heart fail- this led to the finding of the diagnostically imure in the neonatal period usually without portant intracranial bruit. A cerebral angioclinical recognition of the arteriovenous aneu- gram that might have given the precise diagrysm (the neonatal heart failure group), slight- nosis of the malformation was not undertaken; ly older infants developing hydrocephalus, in case 1 because of rapidly deteriorating heart seizures or other neurological symptoms (the failure, in case 2 because of the seemingly symptomatic infant group), and older children hopeless outlook. or adults with headaches and/or signs of subUsually the malformation is not associated arachnoid haemorrhage (the older infantladult with other congenital defects, as in our cases, group) (5). In addition, one infant with mild but supernumerary digits, hypospadia, and heart failure in the neonatal period, later de- transposition of the great vessels have been veloping hydrocephalus, has been placed in reported by Claireaux & Newman ( 2 ) , and yet another group (1). Hirano & Solomon (9). Both our patients belong to the neonatal Surgical treatment has been rewarding for heart failure group. the symptomatic infant and the older children/ The frequency of this malformation is not adult group. The technical procedure and the precisely known. It seems comparatively low results have been reviewed by Gold et al. (3, but is not insignificant: 15.4% of the con- and Amacher & Shillito (1). Usually a right genital intracranial arteriovenous malforma- parietooccipital craniotomy is performed tions in Lagos & Riley’s (10) series, 50% in through which the dilated vein of Galen is isoGold et al. (5); the arteriovenous aneurysms lated by ligating the feeder arteries. comprising about 1.4% of all verified intraThe question of surgical treatment of paActa Paediatr Scand 67
532
J. Eide and M . Fdling
tients belonging to the neonatal heart failure group has emerged only recently, as the condition has only rarely been diagnosed before death. One such case, reported by Gomez et al. (6), was treated with ligature of the right common carotid artery, later with ligature of the left external carotid artery, and recovered from the heart failure. However, the cerebral condition and subsequent course were not mentioned. One patient was reported by Amacher & Shillito ( l ) , and was diagnosed clinically by an intracranial bruit, cerebral angiography, and cardiac catheterization. Craniotomy and partial ligation of the feeder arteries was carried out on the fourth day of life in spite of serious heart failure. The infant died 18 hours later of heart failure that did not respond to intensive measures. The major postoperative hazard in this clinical group seems to be progressive heart failure following closure of the shunt. Immediate phlebotomy, digitalization, and rigid fluid control may be mandatory (5). The effectiveness of surgery in the neonatal heart failure group remains to be settled, as the evidence so far is very limited. However, it seems reasonable to try surgical measures, as the evidence points to an invariable fatal outcome in conservatively treated cases. One also has to consider rewarding results of surgery with other forms of intracranial arteriovenous aneurysms, and with the same malformation in other age groups, as shown by Amacher & Shillito ( l ) , Gold et al. (3,and Cronqvist et al. (3). Diagnosis depends on examination for and awareness of the significance of an intracranial bruit, when examining neonates with heart failure and suspected congenital heart disease. The bruit is loud and pulse synchronous and differs from the soft bruits that may be heard in normal children (12).
Acta Puediutr Scand 67
REFERENCES 1. Amacher, A . L. & Shillito, J.: The syndromes and
surgical treatment of aneurysms of the great vein of Galen. J Neurosurg, 39: 89, 1973. 2. Claireaux, A. E. & Newman, C. G. H.: Arteriovenous aneurysms of the great vein of Galen with heart failure in the neonatal period. Arch Dis Child, 35: 605, 1960. 3. Cronqvist, S., Granholm, L. & Lu n d st r ~ m ,N. R.: Hydrocephalus and congestive heart failure caused by intracranial arteriovenous malformations in infants. J Neurosurg, 36: 249, 1972. 4. Dandy, W. E.: Arteriovenous aneurysm of the brain. Arch Surg, 17: 190, 1928. 5. Gold, A. P., Ransohoff, J. & Carter, S.: Vein of Galen malformation. Acta Neurol Scand, Suppl. 11, 40: 1, 1964. 6. Gomez, M. R., Witten, C. F., Nolke, A., Bernstein, J. & Sterling Meyer, J.: Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Pediatrics, 31: 400, 1963. 7. Holman, E.: Abnormal arteriovenous communications. Great variability of effects with particular reference to delayed development of cardiac failure. Circulation, 32: 1001, 1965. 8. Holman, E.: Reflections on arteriovenous fistulas. Ann Thorac Surg, 11,2: 176, 1971. 9. Hirano, A. & Solomon, S.: Al-teriovenous aneurysm of the vein of Galen. Arch Neurol, 3: 589, 1960. 10. Lagos, J. C. & Riley, H. D.: Congenital intracranial vascular malformation in children. Arch Dis Child, 46: 285, 1971. 11. Litvak, J., Yahr, M. D. & Ransohoff, J.: Aneurysms of the great vein of Galen and midline cerebral arteriovenous anomalies. J Neurosurg, 17: 945, 1960. 12. Mace, J. W., Peters, E. R. & Mathies, A. W.: Cranial bruits in purulent meningitis in childhood. N Engl J Med, 278: 1420, 1968. 13. Russel, D. S. & Nevin, S.: Aneurysm of the great vein of Galen causing internal hydrocephalus: Report of two cases. J Pathol, 51: 375, 1940. 14. Sedzimir, C. B. & Robinson, J.: Intracranial haemorrhage in children and adolescents. J Neurosurg, 38: 269, 1973. 15. Stern, L.: Congestive heart failure secondary to cerebral arteriovenous aneurysm in the newborn infant. Am J Dis Child, 115: 581, 1968. 16. Wallace, J. M., Nashold, B. S. & Slewka, P.: Hemodynamic effects of cerebral arteriovenous aneurysms. Circulation, 31: 696, 1965. Submitted Jan. 24, 1977 Accepted Jan. 10, 1978
(J. E.) Department of Pathology Central Hospital of Vest-Agder 4600 Kristiansand Norway
