Aneurysms of the vein of Galen

Experience at The Hospital for Sick Children, Toronto

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✓ A study of the literature published between 1937 and 1981 revealed 128 aneurysms of the vein of Galen. Their clinical course and management are reviewed. During the years 1950 to 1980, 29 patients with an aneurysm of the vein of Galen were seen at The Hospital for Sick Children. In 14 of these patients surgical obliteration of their aneurysm was attempted, and in six this proved successful.

Abstract

✓ A study of the literature published between 1937 and 1981 revealed 128 aneurysms of the vein of Galen. Their clinical course and management are reviewed. During the years 1950 to 1980, 29 patients with an aneurysm of the vein of Galen were seen at The Hospital for Sick Children. In 14 of these patients surgical obliteration of their aneurysm was attempted, and in six this proved successful.

Although Steinheil54 made initial reference to an aneurysm of the vein of Galen in 1895, the first comprehensive description of the condition and the first attempt at treatment was published in a case report by Jaeger, et al., in 1937.26 In 1947, Oscherwitz and Davidoff40 were the first to approach an aneurysm of the vein of Galen intracranially. Boldrey and Miller6 in 1949 clipped the posterior cerebral arteries in an attempt to deal with an aneurysm of the vein of Galen.

Gold, et al.,20 firmly established the clinical features of aneurysms of the vein of Galen in 1964. They divided the clinical presentation into three characteristic age groups: that of the neonate, that of the infant, and that of the older child or adult. In neonates, congestive heart failure typically appeared shortly after birth; this was frequently cyanotic in type, and usually refractory to digitalis therapy. The infants presented with hydrocephalus or seizures, and older children or adults complained of headaches and/or signs and symptoms of subarachnoid hemorrhage (SAH).

In 1959, Silverman, et al.,49 first recognized congestive heart failure as the result of an aneurysm of the vein of Galen in a neonate. In patients with a large arteriovenous communication such as an aneurysm of the vein of Galen, there is a tendency to increased cardiac output as well as an increase of venous return to the heart. This results in pulmonary hypertension and progressive and intractable heart failure.25 Furthermore, because of the low diastolic pressure as the result of a large arteriovenous communication, there is reduced coronary blood flow, since coronary flow occurs predominantly during diastole. This leads to myocardial ischemia.

In addition to the intractable heart failure in these neonates, the tremendous flow of blood through the fistula deprives the cerebrum of blood and leads to gross parenchymal damage to the brain.39

Review of the Literature

Since 1937, 128 patients with aneurysms of the vein of Galen have been described in the literature in sufficient detail to firmly establish the clinical presentation and management.1–67 These 128 patients consisted of 45 neonates who were diagnosed within the first 2 weeks of life, 36 infants who presented between 3 weeks and 11 months of age, and 47 older children and adults who came for evaluation between 1 and 54 years of age.

Forty-three of the 45 neonates presented in heart failure (Table 1). Only one had hydrocephalus at the time of presentation, and one neonate had suffered an SAH. Only two of the 36 infants had heart failure, but 33 had hydrocephalus and one presented with an SAH. The characteristic presentation in the 47 older children and adults was that of SAH, which occurred in 18 of them. A further 14 presented with hydrocephalus, and only one had heart failure. Seven exhibited neurological deterioration, which was due mainly to the “steal” phenomenon, producing evidence of dementia and focal neurological deficit. In some patients, compression of brain parenchyma by the aneurysm also led to neurological deterioration. Seven patients presented with evidence of cranial venous hypertension and were described as being troubled by repeated bouts of epistaxis as well as showing evidence of distended veins about their scalp and face.

TABLE 1

Presenting symptoms in 128 cases of aneurysm of the vein of Galen

Presenting SymptomsNeonatesInfantsOlder Children & Adults
heart failure4321
hydrocephalus13314
hemorrhage1118
neurological deterioration007
cranial venous hypertension007
total cases453647

Surgical treatment was carried out in 54 of these 128 patients (Table 2). Untreated patients as a group did badly; none was reported as normal. Of the 54 patients who were treated, many were treated in a very primitive fashion in the early years, such as the original case of Jaeger, et al.,26 which was treated by carotid artery ligation. Despite this, 26 of the 54 treated patients were normal.

TABLE 2

Management and results in 128 cases of aneurysm of the vein of Galen

Age GroupNo. of CasesTreatedUntreated
NormalImpairedDeadNormalImpairedUnknownDead  
neonates4513404033
infants36104802111
older children & adults47155406116
total1282612160121250

Summary of Cases

We have reviewed the clinical course of patients brought to The Hospital for Sick Children during the years 1950 to 1980, with aneurysms of the vein of Galen. A total of 29 patients were seen with this condition, 21 of these during the last decade. The literature indicates a sex incidence of two boys to one girl;44 this was certainly true at our institution, where 20 of the 29 patients were male. Sixteen of the 29 patients were neonates, eight were infants, and five were older children.

Presenting Features

The neonates typically were brought to the hospital in heart failure, with 14 of the 16 presenting in this fashion (Table 3). One neonate died of a massive SAH. One neonate was born prematurely, and had a computerized tomography (CT) scan to rule out intraventricular hemorrhage. An aneurysm of the vein of Galen was noted on the scan and was confirmed angiographically. This child is now 2 years of age and remains normal despite not having been treated.

TABLE 3

Presenting symptoms in 29 cases of aneurysm of the vein of Galen

Presenting SymptomsNeonatesInfantsOlder Children
heart failure1400
hydrocephalus062
hemorrhage111
neurological deterioration012
serendipity100
total cases1685

Of the eight infants, six presented with progressive enlargement of their head and a diagnosis of hydrocephalus. One infant had a massive SAH that resulted in death. One infant was brought in with a progressive hemiparesis and unsteadiness which was due to compression of the midbrain by the aneurysm.

Two of the five older children presented with hydrocephalus. One 8-year-old child died of a massive SAH. Two older children exhibited progressive neurological deterioration, in the form of seizures in one and a progressive dementia in the other.

Angiographic Studies

We reviewed the angiographic studies on these patients and found four prominent patterns. In the neonates, we found that the feeding vessels entered the aneurysm at its anterosuperior border, and consisted usually of both anterior cerebral arteries, the lenticulostriate arteries, the thalamic perforating arteries, and both anterior and posterior choroidal arteries. Occasionally, the superior cerebellar arteries were also involved in feeding the aneurysm. The aneurysms were moderate in size, and drained by a huge straight sinus and lateral sinuses (Fig. 1).

Fig. 1.
Fig. 1.

Left: Drawing of an aneurysm of the vein of Galen in a neonate, showing feeding vessels: the anterior cerebral arteries, lenticulostriate arteries, thalamic perforating arteries, and anterior and posterior choroidal arteries. Right: Lateral angiogram of a neonate with an aneurysm of the vein of Galen, showing pattern illustrated left.

Predominantly in infants, the feeding vessel was situated inferiorly and laterally, and consisted of one posterior choroidal artery (Fig. 2). In infants and older children, the feeding vessels were usually located anteriorly and superiorly and included one or both posterior choroidal arteries and one or both anterior cerebral arteries (Fig. 3). In infants with hydrocephalus, the aneurysms were frequently huge and round, with poorly visualized outflow tracts (Fig. 2).

Fig. 2.
Fig. 2.

Drawing showing the anteroposterior view of an aneurysm of the vein of Galen in an infant. The aneurysm is being fed by one posterior choroidal artery.

Fig. 3.
Fig. 3.

Drawing (left) and lateral carotid arteriogram (right) of an infant with an aneurysm of the vein of Galen. The aneurysm is fed by one anterior cerebral and one posterior choroidal artery.

Predominantly in older children, the feeding vessels consisted of an angiomatous network arising mainly from the posterior choroidal arteries and thalamic perforating arteries and directly entering the aneurysm. The aneurysms were not large, and were drained by a well visualized venous outflow through the straight sinus and transverse sinuses (Fig. 4).

Fig. 4.
Fig. 4.

Left: Drawing of a typical angiomatous network arising from the posterior choroidal arteries and thalamic perforating vessels feeding into an aneurysm of the vein of Galen in an older child. Right: Lateral carotid angiogram of 14-year-old child with an aneurysm of the vein of Galen, showing pattern illustrated left.

Surgical Management

Fourteen of the 29 children underwent craniotomy, and an attempt was made to obliterate the aneurysm of the vein of Galen. In 11 patients this was carried out by a transcallosal route, in two by a subtemporal route, and in one by a transtentorial route.

Only one of the older children had surgical management of his aneurysm. This was carried out by a transcallosal approach in 1953. The patient did badly and died postoperatively. Six of the eight infants were treated by direct surgical attack on their aneurysm, and in five this was completely successful. The only death in this group occurred in 1963, prior to the routine utilization of the microscope.

Our worst results occurred among the neonates. These were all critically ill and in congestive heart failure. The aneurysms were fed by numerous vessels, and we believed that the surgery might be made easier by using deep hypothermia, cardiac arrest, and cardiopulmonary bypass. This was done in four neonates, and all four died on the operating table. In two neonates, hypotension was used as an adjunct to our anesthetic management during surgery; both of these patients had cardiac arrest and died on the table.

We subsequently discovered that myocardial infarction is common in these neonates due to the markedly reduced coronary blood flow. Adding hypotension to their anesthetic regime during surgical treatment just increases the risk of myocardial infarction, since the lowered blood pressure reduces diastolic blood pressure to near zero levels. This low diastolic pressure severely impairs coronary blood flow and thus led to the operative deaths in these neonates.

In our one surviving neonate, we avoided hypotension and had no difficulty with the child's heart during surgery. Furthermore, with reduction of flow through his fistula, the evidence of myocardial ischemia, including the inverted S-T segments that we saw on his electrocardiogram preoperatively, completely reversed. His cardiac size on chest x-ray decreased and his signs and symptoms of congestive heart failure completely abated.

Results of Management

The results of management are summarized in Table 4. The 16 neonates did poorly. Only one of the seven surgically treated neonates is alive, and this child is left with a hemiparesis. The eight infants did well. Six were treated surgically and five of these are normal. Our older children did poorly. One died postoperatively after an unsuccessful attempt in 1953 to deal with her aneurysm. One child was treated unsuccessfully with particulate emboli, and displays a progressive dementia. Three of the older children have not had their aneurysm treated. Of these, one has died, one is severely impaired, and one has been lost to follow-up study.

TABLE 4

Management and results in 29 cases of aneurysm of the vein of Galen

Age GroupNo. of CasesTreatedUntreated   
NormalImpairedDeadNormalImpairedUnknownDead  
neonates16017*100 
infants8501000 
older children501*1011 
total29529111 

One neonate and one older child treated only by embolization.

Discussion

In most arteriovenous malformations, excision of the lesion is the treatment of choice. However, in the case of aneurysms of the vein of Galen, there is basically a fistulous tract from the arterial side into the vein. Thus, all that is necessary is occlusion of the fistula. Once this is done, the aneurysm progressively shrinks to become a normal vein of Galen.

Aneurysms of the vein of Galen, although rare, are being seen with increasing frequency due to better diagnostic techniques and the awareness among pediatricians and cardiologists that the entity exists. In neonates, early treatment is mandatory for two reasons: 1) the tremendous flow through the aneurysm steals blood away from the cerebral parenchyma and leads to massive infarction of the brain; and 2) the tremendous flow through the aneurysm produces the hemodynamic changes that lead to myocardial ischemia and infarction. Early and effective reduction in flow through the aneurysm reduces the steal phenomenon and therefore prevents progressive cerebral ischemia. It also improves the hemodynamic situation of the heart and thus ameliorates the congestive heart failure.

Ideally in neonates, embolism with glue28 can be used to reduce flow sufficiently to bring the child out of heart failure. If this can be done, surgery can be delayed until the child is larger and stronger. On the other hand, if this does not prove feasible it is possible to surgically obliterate many of the feeders in the neonate with congestive failure providing that the anesthetic techniques does not include hypotension, which invariably aggravates myocardial ischemia.

In the infant with a single feeder, it is a simple matter to ligate it surgically or to occlude it by catheter with a detachable balloon or glue. In the older child with an angiomatous network feeding the aneurysm, surgical obliteration is difficult if not impossible, but embolism with glue may become the treatment of choice.

Aneurysms of the vein of Galen were previously regarded as a rare and curious surgical lesion. They then became a therapeutic engima. Moder investigation and management allows for satisfactory treatment in many of these patients.

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Article Information

Address reprint requests to: Harold J. Hoffman, M.D., Division of Neurosurgery, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.

© AANS, except where prohibited by US copyright law.

Headings

Figures

  • View in gallery

    Left: Drawing of an aneurysm of the vein of Galen in a neonate, showing feeding vessels: the anterior cerebral arteries, lenticulostriate arteries, thalamic perforating arteries, and anterior and posterior choroidal arteries. Right: Lateral angiogram of a neonate with an aneurysm of the vein of Galen, showing pattern illustrated left.

  • View in gallery

    Drawing showing the anteroposterior view of an aneurysm of the vein of Galen in an infant. The aneurysm is being fed by one posterior choroidal artery.

  • View in gallery

    Drawing (left) and lateral carotid arteriogram (right) of an infant with an aneurysm of the vein of Galen. The aneurysm is fed by one anterior cerebral and one posterior choroidal artery.

  • View in gallery

    Left: Drawing of a typical angiomatous network arising from the posterior choroidal arteries and thalamic perforating vessels feeding into an aneurysm of the vein of Galen in an older child. Right: Lateral carotid angiogram of 14-year-old child with an aneurysm of the vein of Galen, showing pattern illustrated left.

References

1.

Agee OFMusella RTweed CG: Aneurysm of the great vein of Galen. Report of two cases. J Neurosurg 31:3463511969J Neurosurg 31:

2.

Alpers BJForster FM: Arteriovenous aneurysms of great cerebral vein and arteries of circle of Willis. Formation by junction of the great cerebral vein and the straight sinus and by the choroidal arteries and anomalous branches of the posterior cerebral arteries. Arch Neurol Psychiatry 54:1811851945Arch Neurol Psychiatry 54:

3.

Amacher ALShillito J Jr: The syndromes and surgical treatment of aneurysms of the great vein of Galen. J Neurosurg 39:89981973J Neurosurg 39:

4.

Askenasy HMHerzberger EEWijsenbeek HS: Hydrocephalus with vascular malformations of the brain. A preliminary report. Neurology 3:2132201953Neurology 3:

5.

Bartal ADSchiffer JMGoodwin DR: Excision of arteriovenous malformation of the vein of Galen complicated by congestive heart failure. Neurochirurgia (Stuttg) 17:16231974Neurochirurgia (Stuttg) 17:

6.

Boldrey EMiller ER: Arteriovenous fistula (aneurysm) of the great cerebral vein (of Galen) and circle of Willis. Report on two patients treated by ligation. Arch Neurol Psychiatry 62:7787831949Arch Neurol Psychiatry 62:

7.

Boynton RCMorgan BC: Cerebral arteriovenous fistula with possible hereditary telangiectasia. Am J Dis Child 125:991011973Am J Dis Child 125:

8.

Carroll CPHJakoby RK: Neonatal congestive heart failure as the presenting symptom of cerebral arteriovenous malformation. J Neurosurg 25:1591631966J Neurosurg 25:

9.

Carson LVBrooks BSEl Gammal Tet al: Adult arteriovenous malformation of the vein of Galen: a case report with pre- and postoperative computed tomographic findings. Neurosurgery 7:4954981980Neurosurgery 7:

10.

Claireaux AENewman CGH: Arteriovenous aneurysm of the great vein of Galen with heart failure in the neonatal period. Arch Dis Child 35:6056121960Arch Dis Child 35:

11.

Cohen MMKristiansen KHval E: Arteriovenous malformations of the great vein of Galen. Neurology 4:1241271954Neurology 4:

12.

Copty MBédard FTurcotte JF: Successful removal of an entire calcified aneurysm of the vein of Galen. Surg Neurol 14:3964001980Surg Neurol 14:

13.

Corrin B: Three cases of intracranial vascular malformations in infants. J Clin Pathol 12:4124181959Corrin B: Three cases of intracranial vascular malformations in infants. J Clin Pathol 12:

14.

Couture AFerran JLSenac JPCTet al: Image ultrasonore d'un aneurysme de la veine de Galien. Arch Fr Pediatr 38:55571981Arch Fr Pediatr 38:

15.

Cunliffe PN: Cerebral arteriovenous aneurysm presenting with heart failure. Report of three cases. Br Heart J 36:9199231974Cunliffe PN: Cerebral arteriovenous aneurysm presenting with heart failure. Report of three cases. Br Heart J 36:

16.

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