J Neurosurg 74:585-589, 1991
Familial occurrence of arteriovenous malformation of the brain KAZUTOSHI YOKOYAMA, M.D., YOSHITAKA ASANO, M.D., TAKATSUGU MURAKAWA, M.D., MlTSUAKI TAKADA, M.D., TAKASHI ANDO, M.D., NOBORU SAKAI, M.D., HIROMU YAMADA, M.D., AND HITOSHI ]WATA, M.D.
Departments of Neurosurgery and Pathology'. Takayama Red Cross Hospital. and Department of Neurosurgery, Gifu University, Gifu, Japan ~" Brain arteriovenous malformations are considered to originate from a congenital maldevelopment of the brain vessels. Although there have been occasional reports suggesting a familial incidence of these lesions, data for only 10 families have been accumulated in the literature. The authors report on six such cases in three families. This high rate of occurrence of familial cases suggests an involvement of genetic factors. KEy WORDS
"
arteriovenons malformation
9 familial anomaly
RAIN arteriovenous malformations (AVM's) have been considered to originate from intrauterine maldevelopment of brain vessels. 5'7"t~In spite of the congenital nature of the disease, reports of familial occurrence have been rare; we could find only 10 such families in the literature.~-4'8'~J-13 Recently, we encountered six patients with AVM in three families. These are reported here and the literature is reviewed.
B
Case Reports
Case 1 This 50-year-old man presented for evaluation of a seizure in December, 1974. His history was noncontributory. Diagnostic angiography revealed the presence of an AVM (Fig. 1), which was totally removed in July, 1975, without neurological complication.
Case 2
FIG. 1. Left carotid angiogram in Case 1 showing an arteriovenous malformation in the left parietal region, fed by the callosomarginal and central arteries and draining into the rolandic vein.
This 16-year-old boy was the son of the patient described in Case 1 (Fig. 2). He presented with a chief complaint of convulsions, his first seizure having occurred when he was 8 years old. In May, 1978, he had a seizure, which resulted in unconsciousness. While he was being evaluated for this condition, a fight parietal AVM was revealed by right carotid angiography (Fig. 3). The lesion was totally removed; the only complication was a transient postoperative hemiparesis.
Case 3 This I l-year-old boy suddenly had a severe headache and became unconscious. On admission, he was co-
J. Neurosurg. / Volume 74/April, 1991
FIG. 2. Family tree of Case 1 (1) and Case 2 (2). Open squares = males alive; circles = females alive;filled squares = males dead; a = succumbed to apoplexy; b = history of apoplexy. 585
K. Yokoyama, et al.
FJG. 3. Right carotid angiogram in Case 2 showing an artefiovenous malformation in the right parietal region, fed by the frontopolar, eallosomarginal, and central arteries and draining into the rolandic vein.
matose and had no spontaneous respirations or brainstem responses. A lumbar puncture revealed bloody cerebrospinal fluid; a fight carotid angiogram was not diagnostic. The vertebrobasilar system was not depicted by a left retrograde brachial angiogram. He was treated conservatively and died shortly after admission. Autopsy revealed a large cerebellar hematoma and a castlike intraventricular hematoma. Enlarged tortuous vessels, hardly identifiable as arteries or veins, were seen at the margins of the cerebellar hematoma on histological examination (Fig. 4); the lesion was diagnosed as a cerebellar AVM.
Case 4 This 24-year-old woman was a cousin of the patient described in Case 3 (Fig. 5). She suffered a severe headache and became unconscious. A computerized tomography (CT) scan demonstrated a left temporal hematoma and an intraventricular hemorrhage. Left carotid angiography revealed an AVM in the left temporal lobe (Fig. 6). The AVM was totally removed at surgery, but a right homonymous hemianopsia persisted 3 months after the operation. Case 5 This 21-year-old woman presented with the chief complaints of a headache and left hemiparesis. A lumbar puncture disclosed bloody cerebrospinal fluid and right carotid angiography revealed an AVM in the right temporal lobe (Fig. 7). The artery feeding the AVM was clipped. Postoperatively, the patient suffered frequent seizures, so two more operations were performed on the AVM. Ultimately, the lesion was totally removed. Although a left hemiparesis remained postoperatively, the patient could walk without help at the time of her discharge. 586
FIo. 4. Photomicrograph of the autopsy specimen from Case 3. Enlarged tortuous blood vessels can be seen which are hardly identifiable as arteries or veins. H & E, • 10.
Case 6 This 18-year-old man was the son of the patient described in Case 5 (Fig. 8), and had a history of headaches. He suffered a seizure and became unconscious. A C T scan demonstrated a left parietal hypodense area, which was partially enhanced after administration of contrast medium. A left carotid angiogram revealed a small AVM in the left parietal region (Fig. 9 left). The AVM was totally removed without neurological complication; histological examination revealed dilated tortuous vessels (Fig. 9 right).
Discussion It is thought that AVM's are formed as congenital developmental anomalies of the blood vessels; however, their genetic origin has not yet been clarified. Arteriovenous malformations have been recognized as one group of complicating lesions in such familial brain diseases as Sturge-Weber-Dimitri disease, yon HippelLindau disease, and Osler-Weber-Rendu disease. 6 To
FIG. 5. Family tree of Case 3 (3) and Case 4 (4). Open squares = males alive; open circles = females alive; closed squares = males dead; closed circles = females dead; a = succumbed to meningitis. J. Neurosurg. / Volume 74/April, 1991
Familial occurrence of arteriovenous maltbrmation
Fl(;. 6. Left carotid angiogram in Case 4 showing an artcriovenous malfnrmation seated deeply in the temporal lobe, fed by the anterior choroidal artery and draining into the lateral atrial vein (arrow).
our knowledge, familial occurrences of brain AVM's unassociated with these diseases have been reported in only 10 families. 2"4~'~4 The previously published familial cases and the six cases reported here (a total of 29 cases in 13 families) are summarized in Table 1. Analyses of these cases were performed as follows: Age and S e x Distribution Excluding two patients whose age was not recorded, the age range was 10 to 19 years in 12 patients, 20 to 29 years in five, 30 to 39 years in six, and 40 to 49 years in two; one was aged 50 years and one aged 66 years. The average age was 27 years. The nationwide Japanese survey on cerebrospinal vascular anomalies indicated that brain AVM's become manifest most frequently in the 20- to 39-year age group; 9 thus, it appears that
Fl~. 7. Right carotid angiogram in Case 5 showing an arteriovcnous malformation in the right temporal region, fed by the lenticulostriate, precentraL central, and posterior cerebral arteries and draining into the internal cerebral vein, Trolard's vein. and the cavernous sinus.
? i !
FiG. 8. Family tree of Case 5 (5) and Case 6 (6). Squares = males alive: circles = females alive.
familial AVM cases exhibit symptoms at a somewhat younger age than do overall AVM cases. The same survey indicated that the male:female ratio of AVM cases is about 2:1. 9 The familial cases summarized in Table 1 consisted of 18 males and 11 females, indicating
FIG. 9. Case 6. Left. Left carotid angiogram showing an arteriovenous malformation (arron~ in the left parietal region, fed by the angular artery and draining into the rolandic vein. Right. Photomicrograph of the lesion showing dilated tortuous vessels. H & E, • 10. J. Neurosurg. / Volume 74/April, 1991
587
K. Yokoyama, et al. TABLE l S1onmarv qf 29.fami/ia1,4 VM cases reported m the literature* Family
Authors & Y e a r
Age Relationship Sex, (yrs)
1
Laingand Smith, 1974
sisters
2
Barre,el al., 1978
brothers
3
Snead,et aL. 1979
brothers
4
Tonnis and Large-Cosack, 1953 brothers
5
Slolland Wo]fram, 1977
6
Aberfeldand Rao, 1981
7
Boy&et al., 1985
8
Bucci,et aL, 1986
9
Yamamoto,et al., 1983
10 11 12 13
Yokoyama,et aL, 199[
father daughter sister brother father son son son niece uncle mother daughter mother daughter father son cousins mother son
F, 16 F, 19 M, 31 M, 39 M, l I M, 14 M, 17 M, ? M, ? M, 66 F, 37 F, 23 M, 32 M, 45 M, 16 M, 18 M, 20 F, 16 M, 36 F, 19 F, 36 F, 28 F, 49 M, 16 M. 50 M, l I F, 24 F, 21 M, 18
Symptoms ICH ICH ICH seizures none ICH [CH ICH ICH headache seizures ICH seizures headache headache seizures none It hemiparesis headache ICH SAH ICH ICH seizures seizures ICH ICH ICH seizures
Location rl parietal rt temporal II basal ganglia n fronte~tempora[ bilat thalamus rl lat ventricle It parietal not reported not reported It temporal It parietal It frontal It parieto-occipital n occipital rt temporal rt temporal It CPA rt thalamus It parietal rt frontal It occipital It occipital rt parieto-occipital rt parietal It parietal rt cerebellum It lat ventricle rt temporal It parietal
* AVM = aneriovenous malformation; ICH = intracranial hemorrhage; SAH = subarachnoid hemorrhage;CPA = cerebellopontineangle,
that familial A V M ' s have a tendency to occur more frequently in females than do A V M ' s in general. F a m i l i a l Incidence
Familial A V M ' s were observed in parent-child combinations in six families, in siblings in five families, a n d in cousins in two families. A m o n g the parent-child combinations, there were two mothers and daughters, one mother and son, two fathers a n d sons, and one father and daughter. In the sibling combinations, there were one sister-sister, three brother-brother, one sister-brother, and one brother-brother (with stepfathers) combination. Thus, we c a n n o t find a specific familial relationship that is particularly prone to A V M manifestation, although there is some tendency for the same sex to be affected by familial AVM. Location o f A V M
In 27 cases in which the A V M locations were described, 20 (74%) were supratentorial, five (19%) were deep-seated, and two (7%) were infratentorial. This finding is in accordance with the results of the nationwide Japanese survey2 There was no observed tendency for similar AVM locations within the same family. 588
The n u m b e r of reported familial A V M cases is too small to draw conclusions regarding the possibility of genetic factors controlling the occurrence of AVM's. However, in the fairly isolated Hida district of Japan, which has a population of about 150,000, we have personally encountered 24 patients with AVM's in the last 10 years; a m o n g these were the six cases in three families reported here. This fact is suggestive of the possibility that genetic factors may be involved in the occurrence of AVM's.
References 1. Aberfeld DC, Rao KR: Familial ancriovenous malformation of the brain. Neurology 31:184-186, 1981 2. Barre RG, Surer CG, Rosenblum WI: Familial vascular malformation or chance occurrence? Case report of two affected family members. Neurology 28:98-100, 1978 3. Boyd MC, Steinbok P, Paty DW: Familial arteriovenous malformations. Report of four cases in one family. J Neurosurg 62:597-599, 1985 4. Bucci MN, Chandler WF, Gebarski SS, et al: Multiple progressive familial thrombosed aneriovenous malformations. Neurosurgery 19:401-404, 1986 5. Handa H: [Neurosurgery.] Osaka: Nagai-~hoten, 1978 (Jpn) J. Neurosurg. / Volume 74/April, 1991
Familial occurrence of arteriovenous malformation 6. Kamiyama K, Okada H, Niizuma H, et al: [A case report: Osler-Weber-Rendu disease with cerebral aneu~,sm, cerebral arteriovenous malformation and pulmona~' arteriovenous fistula.] No Shinkei Geka 9:67-72, 1981 (Jpn) 7. Kaplan HA, Aronson SM, Browder EJ: Vascular malformations of the brain. An anatomical study. J Neurosurg 18:630-635, 1961 8. Laing JW, Smith RR: lntracranial arteriovenous malformation in sisters: a case report. J Miss State Med Assoc 15:203-206, 1974 9. Nishimoto A, Mizukawa N, Ueda K, et al: Summary of clinical survey, in: [Annual Report in 1976 of the Research Group on Cerebrospinal Vascular Anomalies.] Japanese Ministry of Public Welfare, 1977, pp 17-27 (Jpn) 10. Olivecrona A, Ladenheim J: Congenital Arteriovenous Aneurysms of Carotid and Vertebral Arterial System. Berlin: Springer, 1957 11. Snead OC, Acker JD, Morawetz R: Familial arteriovenous malformation. Ann Neurol 5:585-587, 1979
J. Neurosurg. / Volume 74/April, 199I
12. Stoll W, Wolfram A: lntrakranielle familiare Gef,'issanomalic aus hals-nases-ohrenarztlicher und neurologischer Sicht. HNO 25:7-12, 1977 13. T6nnis W, Large-Cosack H: Klinik, operative Behandlung und Prognose der arterio-ven6sen Angiome des Gehrins und seine H/iutel: ein Bericht fiber 72 FNle. Dtsch Z Nervenheilk 170:460-485, 1953 14. Yamamoto S, Ando K, Suzuki Y, et al: [Cerebral arteriovenous malformation occurring in two patients of mother-daughter combination.] Rinsho Shinkeigaku 23:908, 1983 (Jpn)
Manuscript received October 10, 1989. Accepted in final form December 20, 1990. Address reprint requests to: Kazutoshi Yokoyama, M.D., Department of Neurosurgery, Takayama Red Cross Hospital, 3-11, Tenman-cho, Takayama-Shi, Gifu-Ken 506, Japan.
589
Familial occurrence of arteriovenous malformation of the brain KAZUTOSHI YOKOYAMA, M.D., YOSHITAKA ASANO, M.D., TAKATSUGU MURAKAWA, M.D., MlTSUAKI TAKADA, M.D., TAKASHI ANDO, M.D., NOBORU SAKAI, M.D., HIROMU YAMADA, M.D., AND HITOSHI ]WATA, M.D.
Departments of Neurosurgery and Pathology'. Takayama Red Cross Hospital. and Department of Neurosurgery, Gifu University, Gifu, Japan ~" Brain arteriovenous malformations are considered to originate from a congenital maldevelopment of the brain vessels. Although there have been occasional reports suggesting a familial incidence of these lesions, data for only 10 families have been accumulated in the literature. The authors report on six such cases in three families. This high rate of occurrence of familial cases suggests an involvement of genetic factors. KEy WORDS
"
arteriovenons malformation
9 familial anomaly
RAIN arteriovenous malformations (AVM's) have been considered to originate from intrauterine maldevelopment of brain vessels. 5'7"t~In spite of the congenital nature of the disease, reports of familial occurrence have been rare; we could find only 10 such families in the literature.~-4'8'~J-13 Recently, we encountered six patients with AVM in three families. These are reported here and the literature is reviewed.
B
Case Reports
Case 1 This 50-year-old man presented for evaluation of a seizure in December, 1974. His history was noncontributory. Diagnostic angiography revealed the presence of an AVM (Fig. 1), which was totally removed in July, 1975, without neurological complication.
Case 2
FIG. 1. Left carotid angiogram in Case 1 showing an arteriovenous malformation in the left parietal region, fed by the callosomarginal and central arteries and draining into the rolandic vein.
This 16-year-old boy was the son of the patient described in Case 1 (Fig. 2). He presented with a chief complaint of convulsions, his first seizure having occurred when he was 8 years old. In May, 1978, he had a seizure, which resulted in unconsciousness. While he was being evaluated for this condition, a fight parietal AVM was revealed by right carotid angiography (Fig. 3). The lesion was totally removed; the only complication was a transient postoperative hemiparesis.
Case 3 This I l-year-old boy suddenly had a severe headache and became unconscious. On admission, he was co-
J. Neurosurg. / Volume 74/April, 1991
FIG. 2. Family tree of Case 1 (1) and Case 2 (2). Open squares = males alive; circles = females alive;filled squares = males dead; a = succumbed to apoplexy; b = history of apoplexy. 585
K. Yokoyama, et al.
FJG. 3. Right carotid angiogram in Case 2 showing an artefiovenous malformation in the right parietal region, fed by the frontopolar, eallosomarginal, and central arteries and draining into the rolandic vein.
matose and had no spontaneous respirations or brainstem responses. A lumbar puncture revealed bloody cerebrospinal fluid; a fight carotid angiogram was not diagnostic. The vertebrobasilar system was not depicted by a left retrograde brachial angiogram. He was treated conservatively and died shortly after admission. Autopsy revealed a large cerebellar hematoma and a castlike intraventricular hematoma. Enlarged tortuous vessels, hardly identifiable as arteries or veins, were seen at the margins of the cerebellar hematoma on histological examination (Fig. 4); the lesion was diagnosed as a cerebellar AVM.
Case 4 This 24-year-old woman was a cousin of the patient described in Case 3 (Fig. 5). She suffered a severe headache and became unconscious. A computerized tomography (CT) scan demonstrated a left temporal hematoma and an intraventricular hemorrhage. Left carotid angiography revealed an AVM in the left temporal lobe (Fig. 6). The AVM was totally removed at surgery, but a right homonymous hemianopsia persisted 3 months after the operation. Case 5 This 21-year-old woman presented with the chief complaints of a headache and left hemiparesis. A lumbar puncture disclosed bloody cerebrospinal fluid and right carotid angiography revealed an AVM in the right temporal lobe (Fig. 7). The artery feeding the AVM was clipped. Postoperatively, the patient suffered frequent seizures, so two more operations were performed on the AVM. Ultimately, the lesion was totally removed. Although a left hemiparesis remained postoperatively, the patient could walk without help at the time of her discharge. 586
FIo. 4. Photomicrograph of the autopsy specimen from Case 3. Enlarged tortuous blood vessels can be seen which are hardly identifiable as arteries or veins. H & E, • 10.
Case 6 This 18-year-old man was the son of the patient described in Case 5 (Fig. 8), and had a history of headaches. He suffered a seizure and became unconscious. A C T scan demonstrated a left parietal hypodense area, which was partially enhanced after administration of contrast medium. A left carotid angiogram revealed a small AVM in the left parietal region (Fig. 9 left). The AVM was totally removed without neurological complication; histological examination revealed dilated tortuous vessels (Fig. 9 right).
Discussion It is thought that AVM's are formed as congenital developmental anomalies of the blood vessels; however, their genetic origin has not yet been clarified. Arteriovenous malformations have been recognized as one group of complicating lesions in such familial brain diseases as Sturge-Weber-Dimitri disease, yon HippelLindau disease, and Osler-Weber-Rendu disease. 6 To
FIG. 5. Family tree of Case 3 (3) and Case 4 (4). Open squares = males alive; open circles = females alive; closed squares = males dead; closed circles = females dead; a = succumbed to meningitis. J. Neurosurg. / Volume 74/April, 1991
Familial occurrence of arteriovenous maltbrmation
Fl(;. 6. Left carotid angiogram in Case 4 showing an artcriovenous malfnrmation seated deeply in the temporal lobe, fed by the anterior choroidal artery and draining into the lateral atrial vein (arrow).
our knowledge, familial occurrences of brain AVM's unassociated with these diseases have been reported in only 10 families. 2"4~'~4 The previously published familial cases and the six cases reported here (a total of 29 cases in 13 families) are summarized in Table 1. Analyses of these cases were performed as follows: Age and S e x Distribution Excluding two patients whose age was not recorded, the age range was 10 to 19 years in 12 patients, 20 to 29 years in five, 30 to 39 years in six, and 40 to 49 years in two; one was aged 50 years and one aged 66 years. The average age was 27 years. The nationwide Japanese survey on cerebrospinal vascular anomalies indicated that brain AVM's become manifest most frequently in the 20- to 39-year age group; 9 thus, it appears that
Fl~. 7. Right carotid angiogram in Case 5 showing an arteriovcnous malformation in the right temporal region, fed by the lenticulostriate, precentraL central, and posterior cerebral arteries and draining into the internal cerebral vein, Trolard's vein. and the cavernous sinus.
? i !
FiG. 8. Family tree of Case 5 (5) and Case 6 (6). Squares = males alive: circles = females alive.
familial AVM cases exhibit symptoms at a somewhat younger age than do overall AVM cases. The same survey indicated that the male:female ratio of AVM cases is about 2:1. 9 The familial cases summarized in Table 1 consisted of 18 males and 11 females, indicating
FIG. 9. Case 6. Left. Left carotid angiogram showing an arteriovenous malformation (arron~ in the left parietal region, fed by the angular artery and draining into the rolandic vein. Right. Photomicrograph of the lesion showing dilated tortuous vessels. H & E, • 10. J. Neurosurg. / Volume 74/April, 1991
587
K. Yokoyama, et al. TABLE l S1onmarv qf 29.fami/ia1,4 VM cases reported m the literature* Family
Authors & Y e a r
Age Relationship Sex, (yrs)
1
Laingand Smith, 1974
sisters
2
Barre,el al., 1978
brothers
3
Snead,et aL. 1979
brothers
4
Tonnis and Large-Cosack, 1953 brothers
5
Slolland Wo]fram, 1977
6
Aberfeldand Rao, 1981
7
Boy&et al., 1985
8
Bucci,et aL, 1986
9
Yamamoto,et al., 1983
10 11 12 13
Yokoyama,et aL, 199[
father daughter sister brother father son son son niece uncle mother daughter mother daughter father son cousins mother son
F, 16 F, 19 M, 31 M, 39 M, l I M, 14 M, 17 M, ? M, ? M, 66 F, 37 F, 23 M, 32 M, 45 M, 16 M, 18 M, 20 F, 16 M, 36 F, 19 F, 36 F, 28 F, 49 M, 16 M. 50 M, l I F, 24 F, 21 M, 18
Symptoms ICH ICH ICH seizures none ICH [CH ICH ICH headache seizures ICH seizures headache headache seizures none It hemiparesis headache ICH SAH ICH ICH seizures seizures ICH ICH ICH seizures
Location rl parietal rt temporal II basal ganglia n fronte~tempora[ bilat thalamus rl lat ventricle It parietal not reported not reported It temporal It parietal It frontal It parieto-occipital n occipital rt temporal rt temporal It CPA rt thalamus It parietal rt frontal It occipital It occipital rt parieto-occipital rt parietal It parietal rt cerebellum It lat ventricle rt temporal It parietal
* AVM = aneriovenous malformation; ICH = intracranial hemorrhage; SAH = subarachnoid hemorrhage;CPA = cerebellopontineangle,
that familial A V M ' s have a tendency to occur more frequently in females than do A V M ' s in general. F a m i l i a l Incidence
Familial A V M ' s were observed in parent-child combinations in six families, in siblings in five families, a n d in cousins in two families. A m o n g the parent-child combinations, there were two mothers and daughters, one mother and son, two fathers a n d sons, and one father and daughter. In the sibling combinations, there were one sister-sister, three brother-brother, one sister-brother, and one brother-brother (with stepfathers) combination. Thus, we c a n n o t find a specific familial relationship that is particularly prone to A V M manifestation, although there is some tendency for the same sex to be affected by familial AVM. Location o f A V M
In 27 cases in which the A V M locations were described, 20 (74%) were supratentorial, five (19%) were deep-seated, and two (7%) were infratentorial. This finding is in accordance with the results of the nationwide Japanese survey2 There was no observed tendency for similar AVM locations within the same family. 588
The n u m b e r of reported familial A V M cases is too small to draw conclusions regarding the possibility of genetic factors controlling the occurrence of AVM's. However, in the fairly isolated Hida district of Japan, which has a population of about 150,000, we have personally encountered 24 patients with AVM's in the last 10 years; a m o n g these were the six cases in three families reported here. This fact is suggestive of the possibility that genetic factors may be involved in the occurrence of AVM's.
References 1. Aberfeld DC, Rao KR: Familial ancriovenous malformation of the brain. Neurology 31:184-186, 1981 2. Barre RG, Surer CG, Rosenblum WI: Familial vascular malformation or chance occurrence? Case report of two affected family members. Neurology 28:98-100, 1978 3. Boyd MC, Steinbok P, Paty DW: Familial arteriovenous malformations. Report of four cases in one family. J Neurosurg 62:597-599, 1985 4. Bucci MN, Chandler WF, Gebarski SS, et al: Multiple progressive familial thrombosed aneriovenous malformations. Neurosurgery 19:401-404, 1986 5. Handa H: [Neurosurgery.] Osaka: Nagai-~hoten, 1978 (Jpn) J. Neurosurg. / Volume 74/April, 1991
Familial occurrence of arteriovenous malformation 6. Kamiyama K, Okada H, Niizuma H, et al: [A case report: Osler-Weber-Rendu disease with cerebral aneu~,sm, cerebral arteriovenous malformation and pulmona~' arteriovenous fistula.] No Shinkei Geka 9:67-72, 1981 (Jpn) 7. Kaplan HA, Aronson SM, Browder EJ: Vascular malformations of the brain. An anatomical study. J Neurosurg 18:630-635, 1961 8. Laing JW, Smith RR: lntracranial arteriovenous malformation in sisters: a case report. J Miss State Med Assoc 15:203-206, 1974 9. Nishimoto A, Mizukawa N, Ueda K, et al: Summary of clinical survey, in: [Annual Report in 1976 of the Research Group on Cerebrospinal Vascular Anomalies.] Japanese Ministry of Public Welfare, 1977, pp 17-27 (Jpn) 10. Olivecrona A, Ladenheim J: Congenital Arteriovenous Aneurysms of Carotid and Vertebral Arterial System. Berlin: Springer, 1957 11. Snead OC, Acker JD, Morawetz R: Familial arteriovenous malformation. Ann Neurol 5:585-587, 1979
J. Neurosurg. / Volume 74/April, 199I
12. Stoll W, Wolfram A: lntrakranielle familiare Gef,'issanomalic aus hals-nases-ohrenarztlicher und neurologischer Sicht. HNO 25:7-12, 1977 13. T6nnis W, Large-Cosack H: Klinik, operative Behandlung und Prognose der arterio-ven6sen Angiome des Gehrins und seine H/iutel: ein Bericht fiber 72 FNle. Dtsch Z Nervenheilk 170:460-485, 1953 14. Yamamoto S, Ando K, Suzuki Y, et al: [Cerebral arteriovenous malformation occurring in two patients of mother-daughter combination.] Rinsho Shinkeigaku 23:908, 1983 (Jpn)
Manuscript received October 10, 1989. Accepted in final form December 20, 1990. Address reprint requests to: Kazutoshi Yokoyama, M.D., Department of Neurosurgery, Takayama Red Cross Hospital, 3-11, Tenman-cho, Takayama-Shi, Gifu-Ken 506, Japan.
589
