Arteriovenous malformation of choroid plexus Case report
CHARLES J.
HODGE,JR., M.D., AND ROBERT B. KING, M.D.
Department of Neurosurgery, State University of New York, Upstate Medical Center, Syracuse, New York
v,' The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports. KEY WORDS choroid plexus subarachnoid hemorrhage "
9 arteriovenous malformation
9
ASCULARmalformations of the choroid plexus are an unusual cause of subarachnoid hemorrhage. This case serves to point out some of the clinical characteristics of arteriovenous malformations of the choroid plexus.
agitated state, with hallucinations but no focal neurological findings. Lumbar puncture revealed bloody cerebrospinal fluid (CSF). Her mental status improved and she was referred to the Upstate Medical Center 1 week later. Examination. On admission, the patient's vital signs were normal. She was confused, Case Report disoriented, intermittently agitated, halluA 22-year-old right-handed woman was cinating, and acutely schizophrenic. She had transferred to State University Hospital marked neck stiffness, but no dysphasia; the following her second subarachnoid hem- fundi were normal. There was decreased orrhage. She had been well until 2 years prior spontaneous movement and increased tone to admission when she experienced the first with hyperreflexia of the right leg. There were subarachnoid hemorrhage, characterized by no pathological reflexes, and sensory exheadache, stiff neck, and confusion. Bilateral amination revealed no deficit. Lumbar punccarotid angiography was normal. She was ture disclosed a pressure of 90 mm H20; the discharged from the local hospital with a CSF was cloudy and xanthochromic, with diagnosis of schizophrenia. She had remained 3700 red blood cells/mm 3, and protein of 248 well until 1 week prior to the present admis- mg%. Transfemoral cerebral angiography the sion when she again experienced sudden following day revealed an arteriovenous s,~vere bifrontal headache and stiff neck, but malformation (AVM) near the left trigone, did not lose consciousness. She was admitted supplied by the anterior and the posterior to the local hospital in a confused and lateral choroidal vessels on that side (Fig. 1).
V
J. Neurosurg. / Volume 42 / April, 1975
457
C. J. Hodge, Jr., and R. B. King
Fl6. 1. Upper Left: Left carotid angiogram, lateral view, showing an enlarged anterior choroidal artery and vascular esion (single arrow) in the region of the trigone, draining via the vein of Galen (double arrow). Upper Right: Left carotid angiogram, anteroposterior view, showing the lesion in the area of the trigone. Lower Left: Magnified left vertebral angiogram, lateral view, showing the same vascular lesion (arrow) supplied by the posterior lateral choroidal vessels. Lower Right: Pneumoencephalogram, brow down position, showing the enlarged choroid plexus projecting into the ventricular atrium (between arrows). There was early shunting to the vein of Galen. The patient was given Thorazine, and her mental status and focal findings gradually improved. Pneumoencephalography 3 weeks after admission (Fig. 1 lower right) demonstrated minimal enlargement of the left lateral ventricle and an irregular floor of the left trigone. Her mental state remained stable. Operation. Four weeks after admission, the patient underwent left parietooccipital craniotomy. A cortical incision near the midline at the parietooccipital junction exposed the left trigone. The ventricle size was normal, while the choroid plexus in the 458
trigone was enlarged and bright red. A large branch of the anterior choroidal artery coursed along the floor of the ventricle at the posterior edge of the choroid plexus; we could readily identify, clip, and divide this artery using the operating microscope at 10X magnification. Multiple small arterioles coursed to the plexus from the medial wall of the ventricle; these were coagulated and cut. We then removed the abnormal plexus from the trigone, leaving normal-appearing plexus in the temporal horn and body of the lateral ventricle in place. There was an area of staining in the ventricular floor due to previous hemorrhage.
J. Neurosurg. / Volume 42 / April, 1975
Arteriovenous malformation of choroid plexus Postoperative Course. The patient had a fluent dysphasia and right homonymous hemianopsia. The speech deficit cleared slowly until 9 days postoperatively, when she rapidly developed a decreased level of consciousness and right hemiparesis. Repeat left carotid and left vertebral angiography revealed no evidence of the previously noted AVM, but there was a large parietooccipital mass which exploration showed to be a dilated, trapped, temporal horn and porencephalic cyst at the site of the previous transcortical incision. After the second craniotomy and decompression were done, she again improved, but a shunting procedure from the temporal horn to the peritoneal cavity was necessary 5 weeks later. She has since shown continued improvement. Laboratory Studies. The choroid plexus consisted of highly vascular tissue with choroidal epithelium on the surface and numerous blood vessels of various sizes (Fig. 2). The vessels ranged from small, thin-walled channels, 50 to 100 u in diameter, up to much larger thick-walled vessels with an overall diameter of several hundred u. The outer portions of these thick-walled vessels showed a non-cellular hyalin type of degenerative change.
F~c. 2. Low power view of the operative specimen showing an abnormally increased number of variable-sized vessels in the choroid plexus. Hand E stain, • 40.
embryologic basis, since the surgical treatment of pure choroid plexus malformations should incur less deficit than treatment of a lesion embedded, even superficially, in the basal ganglia or thalamus? The 20 reported cases show consistent patterns of presentation. Five were infants, Discussion four of whom died in the neonatal period At least 20 cases of choroid plexus angioma from intraventricular hemorrhage associated or arteriovenous malformation (AVM) have with multiple congenital anomalies. been reported? -5,7,8,1~ Butler, et al.,* in McGuire, et al., 1~ reported a 3-month-old intheir discussion of 17 treated cases of vascular fant with hydrocephalus, probably secondary lesions causing mild intraventricular to episodic intraventricular hemorrhage; hemorrhage, reviewed eight cases of choroid bilateral choroid plexectomies were perplexus angioma. Doe, et al., 7 reviewed the formed and the vascular malformations idenliterature describing this lesion and added five tified bilaterally by microscopy. Two other inpostmortem cases. A single case treated with fants had bilateral lesions, and two cases were surgery was recently reported by Mat- incidental postmortem findings. T M The 13 sushima, et al. ~4 Some of the cases included remaining patients had an average age of 27 by other authors TM describing choroid plexus years; two patients were over 40 years old and AVM's have been excluded by us. Several of seven were between the ages of 14 and 20 the patients reported by Liber and Lisa ~1 years. Thus, these small angiomas tend to ocseem to have had primary choroid plexus cur in the younger age groups as do the tumors? Dandy's ~ case, in fact, was an AVM parenchymatous microangiomas? 8 Of the 20 of the lateral periventricular area which ap- patients, 69% were female. parently drained through an aneurysmallyClinical presentation is usually that of a dilated subependymal vein and shared the subarachnoid hemorrhage often without deep cerebral venous system with the choroid striking focal findings except in patients with plexus. Furthermore, it is of some importance associated intracerebral or deep nuclear clots. to separate choroid plexus vascular lesions Although these lesions have been previously from the periventricular malformations described as one of the causes of a "mild" although they are thought to have a common form of intraventricular hemorrhage, 4 38% of
J. Neurosurg. / Volume 42 / April, 1975
459
C. J. Hodge, Jr., and R. B. King the adults reported died rapidly from the initial or recurrent intraventricular or intracerebral hemorrhage. If the children are included in this group, 45% died as a direct result of bleeding. Thirty percent of the adults who survived the initial hemorrhage had identifiable recurrent hemorrhages, several of which terminated fatally, a5,17,18 Of the 18 patients with symptoms attributable to choroid plexus angiomas, the diagnosis was made antemortem in 10. Two were diagnosed at the time of operative exploration for intracerebral hematoma, seven by angiography, and one after plexectomy for hydrocephalus. Nine patients, including ours, were operated on for intracerebral hematoma and/or obliteration of the malformation; intraventricular hematomas were encountered in five of these patients and several had clots in the substance of the choroid plexus. The ventricles have often been enlarged as a result of either communicating hydrocephalus or intraventricular hematoma. In four of the patients, the malformation extended into adjacent structures, such as the thalamus, third ventricle, or temporal lobe, making complete removal more hazardous or impossible. In all but one of the cases the malformation was located primarily in the choroid glomus. Patients whose malformations have been removed have generally done well; one patient, whose lesion extended into the third ventricle, died postoperatively. In several patients, including ours, the operative approach caused the major postoperative deficit; in our patient the approach was made more difficult by the small size of the ventricles. No other report mentions the late type of postoperative obstruction of the ventricular system that occurred in our case; perhaps a formal complete choroid plexectomy at the time of the initial procedure would have avoided this problem. When an AVM or venous angioma fed by the choroidal vessels has been identified in the region of the trigone, pneumoencephalography should be performed as an important preoperative measure to delineate the size and position of the angiomatous mass within the ventricle. In the absence of an intracerebral hematoma (usually temporal lobe) to dictate the operative approach, the medial occipitoparietal approach to the trigone seems most likely to facilitate access 460
to the major feeding vessels along the posterior edge of the lesion. There is clearly no safe way into the trigone area, especially in the dominant hemisphere; however, in view of the incidence of recurrent and fatal hemorrhage from choroid plexus AVM's and venous angiomas, the risk of transcortical ventricular exposure seems warranted. References 1. Arnstein LH, Boldrey E, Naffziger HC: A case report and survey of brain tumors during the neonatal period. J Neurnsurg 8:315-319, 1951 2. Avol M, Vogel P J: Circumscribed intraventricular hematoma simulating an encapsulated neoplasm. Bull Los Angeles Neurol Soc 20:25-29, 1955 3. Bonnal S, Serratrice G, Winninger J: Angiomie art6rio-veineaux (A.A.V.) des territoires choroidiens ant6rieur et post~rieur juxtathalamique avec h~matome dans le pulvinar. Ablation partielle, l~tude des s6quelles. Neurochirurgie 6:173-185, 1960 4. Butler AB, Partain RA, Netsky MG: Primary intraventricular hemorrhage: a mild and remedial form. Neurology (Minneap) 22:675-687, 1972 5. Crawford JV, Russell DS: Cryptic arteriovenous and venous hamartomas of the brain. J Neurol Neurosurg Psychiatry 19:1-11, 1956 6. Dandy W: Benign Encapsulated Tumors of the Lateral Ventricle of the Brain: Diagnosis and Treatment. Baltimore, Williams and Wilkins, 1934 7. Doe FD, Shuangshoti S, Netsky MG: Cryptic hemangioma of the choroid plexus: a cause of intraventricular hemorrhage. Neurology (Minneap) 22:1232-1239, 1972 8. Gerlach J: Intracerebral hemorrhage caused by microangiomas. Prog Neurol Surg 3:363-396, 1969 9. Gross SW: Tumor of the left lateral ventricle with mental symptoms. J Nerv Merit Dis 89:66-70, 1939 10. Guerard M: Tumeur fongueuse dans le ventricle droit du cerveau chez une petite fille de trois ans. Bull Soc Anat Paris 8:211-214, 1833 11. Liber AF, Lisa JR: Stromal tumors of the choroid plexus. Am J Clin Pathol 10:710-735, 1940 12. Mallory TB (ed): Case records of the Massachusetts General Hospital: Case 26051. N Eng J Med 222:191-195, 1940 13. Margolis G, Odom GL, Woodhall B, et al: The role of small angiomatous malformations in the production of intracerebral hematomas. J Neurosurg 8:564-575, 1951 J. Neurosurg. / Volume 42 / April, 1975
Arteriovenous malformation of choroid plexus 14. Matsushima M, Yamamoto T, Motomochi M, et al: Papilloma and venous angioma of the choroid plexus causing primary intraventricular hemorrhage. Report of two cases. J Neurosurg 39:666-670, 1973 15. McConnell TH, Leonard JS: Microangiomatous malformations with intraventricular hemorrhage. Neurology (Minneap) 17:618620, 1967 16. McGuire TH, Greenwood J Jr, Newton BL: Bilateral angiomas of the choroid plexus. Case report. J Neurosurg 11:428-430, 1954 17. Scott WG, Simril WA, Seaman WB: Intracerebral arteriovenous malformations: their diagnosis and angiographic demonstration. Am J Roentgenol Rad Ther Nuel Med 71:762-775, 1954
J. Neurosurg. / Volume 42 / April, 1975
18. Scully F J: Internal hydrocephalus following repeated intraventricular hemorrhages. Ann Intern Med 11:684-686, 1937 19. Vianello A: Angiome art6rio-veineaux (AAV) du glomus choroidien gauche. Neuroehirurgie 15:327-332, 1969
This work was supported in part by Training Grant 5 T01 NS 05605 from the National Institute of Neurological Diseases and Stroke. Address reprint requests to: Charles J. Hodge, Jr., M.D., Department of Neurosurgery, State University of New York, Upstate Medical Center, Syracuse, New York.
a6]
CHARLES J.
HODGE,JR., M.D., AND ROBERT B. KING, M.D.
Department of Neurosurgery, State University of New York, Upstate Medical Center, Syracuse, New York
v,' The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports. KEY WORDS choroid plexus subarachnoid hemorrhage "
9 arteriovenous malformation
9
ASCULARmalformations of the choroid plexus are an unusual cause of subarachnoid hemorrhage. This case serves to point out some of the clinical characteristics of arteriovenous malformations of the choroid plexus.
agitated state, with hallucinations but no focal neurological findings. Lumbar puncture revealed bloody cerebrospinal fluid (CSF). Her mental status improved and she was referred to the Upstate Medical Center 1 week later. Examination. On admission, the patient's vital signs were normal. She was confused, Case Report disoriented, intermittently agitated, halluA 22-year-old right-handed woman was cinating, and acutely schizophrenic. She had transferred to State University Hospital marked neck stiffness, but no dysphasia; the following her second subarachnoid hem- fundi were normal. There was decreased orrhage. She had been well until 2 years prior spontaneous movement and increased tone to admission when she experienced the first with hyperreflexia of the right leg. There were subarachnoid hemorrhage, characterized by no pathological reflexes, and sensory exheadache, stiff neck, and confusion. Bilateral amination revealed no deficit. Lumbar punccarotid angiography was normal. She was ture disclosed a pressure of 90 mm H20; the discharged from the local hospital with a CSF was cloudy and xanthochromic, with diagnosis of schizophrenia. She had remained 3700 red blood cells/mm 3, and protein of 248 well until 1 week prior to the present admis- mg%. Transfemoral cerebral angiography the sion when she again experienced sudden following day revealed an arteriovenous s,~vere bifrontal headache and stiff neck, but malformation (AVM) near the left trigone, did not lose consciousness. She was admitted supplied by the anterior and the posterior to the local hospital in a confused and lateral choroidal vessels on that side (Fig. 1).
V
J. Neurosurg. / Volume 42 / April, 1975
457
C. J. Hodge, Jr., and R. B. King
Fl6. 1. Upper Left: Left carotid angiogram, lateral view, showing an enlarged anterior choroidal artery and vascular esion (single arrow) in the region of the trigone, draining via the vein of Galen (double arrow). Upper Right: Left carotid angiogram, anteroposterior view, showing the lesion in the area of the trigone. Lower Left: Magnified left vertebral angiogram, lateral view, showing the same vascular lesion (arrow) supplied by the posterior lateral choroidal vessels. Lower Right: Pneumoencephalogram, brow down position, showing the enlarged choroid plexus projecting into the ventricular atrium (between arrows). There was early shunting to the vein of Galen. The patient was given Thorazine, and her mental status and focal findings gradually improved. Pneumoencephalography 3 weeks after admission (Fig. 1 lower right) demonstrated minimal enlargement of the left lateral ventricle and an irregular floor of the left trigone. Her mental state remained stable. Operation. Four weeks after admission, the patient underwent left parietooccipital craniotomy. A cortical incision near the midline at the parietooccipital junction exposed the left trigone. The ventricle size was normal, while the choroid plexus in the 458
trigone was enlarged and bright red. A large branch of the anterior choroidal artery coursed along the floor of the ventricle at the posterior edge of the choroid plexus; we could readily identify, clip, and divide this artery using the operating microscope at 10X magnification. Multiple small arterioles coursed to the plexus from the medial wall of the ventricle; these were coagulated and cut. We then removed the abnormal plexus from the trigone, leaving normal-appearing plexus in the temporal horn and body of the lateral ventricle in place. There was an area of staining in the ventricular floor due to previous hemorrhage.
J. Neurosurg. / Volume 42 / April, 1975
Arteriovenous malformation of choroid plexus Postoperative Course. The patient had a fluent dysphasia and right homonymous hemianopsia. The speech deficit cleared slowly until 9 days postoperatively, when she rapidly developed a decreased level of consciousness and right hemiparesis. Repeat left carotid and left vertebral angiography revealed no evidence of the previously noted AVM, but there was a large parietooccipital mass which exploration showed to be a dilated, trapped, temporal horn and porencephalic cyst at the site of the previous transcortical incision. After the second craniotomy and decompression were done, she again improved, but a shunting procedure from the temporal horn to the peritoneal cavity was necessary 5 weeks later. She has since shown continued improvement. Laboratory Studies. The choroid plexus consisted of highly vascular tissue with choroidal epithelium on the surface and numerous blood vessels of various sizes (Fig. 2). The vessels ranged from small, thin-walled channels, 50 to 100 u in diameter, up to much larger thick-walled vessels with an overall diameter of several hundred u. The outer portions of these thick-walled vessels showed a non-cellular hyalin type of degenerative change.
F~c. 2. Low power view of the operative specimen showing an abnormally increased number of variable-sized vessels in the choroid plexus. Hand E stain, • 40.
embryologic basis, since the surgical treatment of pure choroid plexus malformations should incur less deficit than treatment of a lesion embedded, even superficially, in the basal ganglia or thalamus? The 20 reported cases show consistent patterns of presentation. Five were infants, Discussion four of whom died in the neonatal period At least 20 cases of choroid plexus angioma from intraventricular hemorrhage associated or arteriovenous malformation (AVM) have with multiple congenital anomalies. been reported? -5,7,8,1~ Butler, et al.,* in McGuire, et al., 1~ reported a 3-month-old intheir discussion of 17 treated cases of vascular fant with hydrocephalus, probably secondary lesions causing mild intraventricular to episodic intraventricular hemorrhage; hemorrhage, reviewed eight cases of choroid bilateral choroid plexectomies were perplexus angioma. Doe, et al., 7 reviewed the formed and the vascular malformations idenliterature describing this lesion and added five tified bilaterally by microscopy. Two other inpostmortem cases. A single case treated with fants had bilateral lesions, and two cases were surgery was recently reported by Mat- incidental postmortem findings. T M The 13 sushima, et al. ~4 Some of the cases included remaining patients had an average age of 27 by other authors TM describing choroid plexus years; two patients were over 40 years old and AVM's have been excluded by us. Several of seven were between the ages of 14 and 20 the patients reported by Liber and Lisa ~1 years. Thus, these small angiomas tend to ocseem to have had primary choroid plexus cur in the younger age groups as do the tumors? Dandy's ~ case, in fact, was an AVM parenchymatous microangiomas? 8 Of the 20 of the lateral periventricular area which ap- patients, 69% were female. parently drained through an aneurysmallyClinical presentation is usually that of a dilated subependymal vein and shared the subarachnoid hemorrhage often without deep cerebral venous system with the choroid striking focal findings except in patients with plexus. Furthermore, it is of some importance associated intracerebral or deep nuclear clots. to separate choroid plexus vascular lesions Although these lesions have been previously from the periventricular malformations described as one of the causes of a "mild" although they are thought to have a common form of intraventricular hemorrhage, 4 38% of
J. Neurosurg. / Volume 42 / April, 1975
459
C. J. Hodge, Jr., and R. B. King the adults reported died rapidly from the initial or recurrent intraventricular or intracerebral hemorrhage. If the children are included in this group, 45% died as a direct result of bleeding. Thirty percent of the adults who survived the initial hemorrhage had identifiable recurrent hemorrhages, several of which terminated fatally, a5,17,18 Of the 18 patients with symptoms attributable to choroid plexus angiomas, the diagnosis was made antemortem in 10. Two were diagnosed at the time of operative exploration for intracerebral hematoma, seven by angiography, and one after plexectomy for hydrocephalus. Nine patients, including ours, were operated on for intracerebral hematoma and/or obliteration of the malformation; intraventricular hematomas were encountered in five of these patients and several had clots in the substance of the choroid plexus. The ventricles have often been enlarged as a result of either communicating hydrocephalus or intraventricular hematoma. In four of the patients, the malformation extended into adjacent structures, such as the thalamus, third ventricle, or temporal lobe, making complete removal more hazardous or impossible. In all but one of the cases the malformation was located primarily in the choroid glomus. Patients whose malformations have been removed have generally done well; one patient, whose lesion extended into the third ventricle, died postoperatively. In several patients, including ours, the operative approach caused the major postoperative deficit; in our patient the approach was made more difficult by the small size of the ventricles. No other report mentions the late type of postoperative obstruction of the ventricular system that occurred in our case; perhaps a formal complete choroid plexectomy at the time of the initial procedure would have avoided this problem. When an AVM or venous angioma fed by the choroidal vessels has been identified in the region of the trigone, pneumoencephalography should be performed as an important preoperative measure to delineate the size and position of the angiomatous mass within the ventricle. In the absence of an intracerebral hematoma (usually temporal lobe) to dictate the operative approach, the medial occipitoparietal approach to the trigone seems most likely to facilitate access 460
to the major feeding vessels along the posterior edge of the lesion. There is clearly no safe way into the trigone area, especially in the dominant hemisphere; however, in view of the incidence of recurrent and fatal hemorrhage from choroid plexus AVM's and venous angiomas, the risk of transcortical ventricular exposure seems warranted. References 1. Arnstein LH, Boldrey E, Naffziger HC: A case report and survey of brain tumors during the neonatal period. J Neurnsurg 8:315-319, 1951 2. Avol M, Vogel P J: Circumscribed intraventricular hematoma simulating an encapsulated neoplasm. Bull Los Angeles Neurol Soc 20:25-29, 1955 3. Bonnal S, Serratrice G, Winninger J: Angiomie art6rio-veineaux (A.A.V.) des territoires choroidiens ant6rieur et post~rieur juxtathalamique avec h~matome dans le pulvinar. Ablation partielle, l~tude des s6quelles. Neurochirurgie 6:173-185, 1960 4. Butler AB, Partain RA, Netsky MG: Primary intraventricular hemorrhage: a mild and remedial form. Neurology (Minneap) 22:675-687, 1972 5. Crawford JV, Russell DS: Cryptic arteriovenous and venous hamartomas of the brain. J Neurol Neurosurg Psychiatry 19:1-11, 1956 6. Dandy W: Benign Encapsulated Tumors of the Lateral Ventricle of the Brain: Diagnosis and Treatment. Baltimore, Williams and Wilkins, 1934 7. Doe FD, Shuangshoti S, Netsky MG: Cryptic hemangioma of the choroid plexus: a cause of intraventricular hemorrhage. Neurology (Minneap) 22:1232-1239, 1972 8. Gerlach J: Intracerebral hemorrhage caused by microangiomas. Prog Neurol Surg 3:363-396, 1969 9. Gross SW: Tumor of the left lateral ventricle with mental symptoms. J Nerv Merit Dis 89:66-70, 1939 10. Guerard M: Tumeur fongueuse dans le ventricle droit du cerveau chez une petite fille de trois ans. Bull Soc Anat Paris 8:211-214, 1833 11. Liber AF, Lisa JR: Stromal tumors of the choroid plexus. Am J Clin Pathol 10:710-735, 1940 12. Mallory TB (ed): Case records of the Massachusetts General Hospital: Case 26051. N Eng J Med 222:191-195, 1940 13. Margolis G, Odom GL, Woodhall B, et al: The role of small angiomatous malformations in the production of intracerebral hematomas. J Neurosurg 8:564-575, 1951 J. Neurosurg. / Volume 42 / April, 1975
Arteriovenous malformation of choroid plexus 14. Matsushima M, Yamamoto T, Motomochi M, et al: Papilloma and venous angioma of the choroid plexus causing primary intraventricular hemorrhage. Report of two cases. J Neurosurg 39:666-670, 1973 15. McConnell TH, Leonard JS: Microangiomatous malformations with intraventricular hemorrhage. Neurology (Minneap) 17:618620, 1967 16. McGuire TH, Greenwood J Jr, Newton BL: Bilateral angiomas of the choroid plexus. Case report. J Neurosurg 11:428-430, 1954 17. Scott WG, Simril WA, Seaman WB: Intracerebral arteriovenous malformations: their diagnosis and angiographic demonstration. Am J Roentgenol Rad Ther Nuel Med 71:762-775, 1954
J. Neurosurg. / Volume 42 / April, 1975
18. Scully F J: Internal hydrocephalus following repeated intraventricular hemorrhages. Ann Intern Med 11:684-686, 1937 19. Vianello A: Angiome art6rio-veineaux (AAV) du glomus choroidien gauche. Neuroehirurgie 15:327-332, 1969
This work was supported in part by Training Grant 5 T01 NS 05605 from the National Institute of Neurological Diseases and Stroke. Address reprint requests to: Charles J. Hodge, Jr., M.D., Department of Neurosurgery, State University of New York, Upstate Medical Center, Syracuse, New York.
a6]
