J Neurosurg 75:947-949, 1991
A sacral dural arteriovenous fistula presenting with an intermittent myelopathy aggravated by menstruation Case report DONG-IK KIM, M.D., IN-SuP CHOI, M.D., AND ALEX BERENSTEIN,M.D.
Interventional Neuroradiology Section, Department of Radiology, New York University, New York, New York, and Department qf Diagnostic Radiology, Yonsei University College of Medicine, Seoul, South Korea
t/ The case is reported of a woman with a spinal dural arteriovenous fistula whose intermittent myelopathy became aggravated with menstruation. Her symptoms recurred in spite of successful acrylic embolization of the lateral sacral arteriovenous fistula. Repeat angiography showed venous drainage from the uterus toward the medullary vein. Total abdominal hysterectomycured her symptoms. The pathophysiologicalbasis for this peculiar clinical manifestation and its management are discussed. KEy WORDS
'
hysterectomy
spinal anomaly 9 menstruation
.
S
P|NAL dural arteriovenous (AV) fistulas have been recognized as an acquired AV shunt that presents as a progressive myelopathy secondary to venous hypertension of medullary veins. The anatomicopathological lesion consists of a feeding dural artery, an AV fistulous nidus, and an arterialized intradural draining vein. 4'5"t~ The symptoms include a slowly progressive myelopathy and/or radiculopathy with varying degrees of spastic or flaccid paraparesis, muscle atrophy, sphincter disturbances, and dorsal-column sensory signs. Neurological deterioration has been associated with high intraspinal venous pressure with a reduced AV pressure gradient leading to hypoxic damage of the spinal cord. 8'~~ This intraspinal venous pressure could also be influenced by various hemodynamic factors?8'~6 Deterioration can be stabilized or reversed by therapeutic interventions such as embolization and/or surgical obliteration of the dural AV fistulaJ '6''~ 16 We report a case in which the patient developed intermittent myelopathy during her menstrual cycle from a dural AV fistula. The case prompted consideration of the hemodynamic aspect of myelopathy associated with spinal dural AV fistula and its proper management. Case Report
This 46-year-old woman presented with a few months' history of intermittent episodes of weakness J. Neurosurg. / Volume 75 /December, 1991
arteriovenous fistula
venous drainage
9
and a cold sensation in both legs at the beginning of her menstrual periods. She usually regained function in about 2 hours. She occasionally experienced a burning sensation on the soles of her feet. Her neurological examination on admission revealed mild weakness (4/5) of the proximal muscles of the left lower extremity. The fight patellar and both Achilles reflexes were absent, and superficial sensation below the knees was diminished bilaterally. A thoracolumbar myelogram revealed scalloped filling defects in the region of the conus medullaris, consistent with dilated veins of spinal AV malformation. Computerized tomography (CT)-myelography demonstrated a slight expansion of the lower thoracic spinal cord surrounded by multiple tiny filling defects. Selective spinal angiography revealed a spinal dural AV fistula from the left lateral sacral artery draining toward the spinal canal via the ilium terminale vein (Fig. 1 left). The artery feeding the lumbar enlargement originated from the left L-2 artery. Slow flow in the anterior spinal artery was noted. Operation. Prior to embolization, the proximal segment of the left internal iliac artery posterior division was protected by placement of a Gianturco coil in the vessel. The fistula was successfully embolized with 0.15 ml ofisobutyl 2-cyanoacrylate mixture using the "push" techniqueJ LA control angiogram of both internal iliac
947
D. I. Kim, I. S. Choi, and A. Berenstein arteries verified complete closure of the AV fistula (Fig. l righl). Postoperative ('our.so. lmmediatelv after embolization, there was significant improvement in the patient's neurological status and she had no episode of weakness for one subsequent menstrual cycle. She then began to develop transient weakness in the lower extremitics similar to those prior to embolization, although not as severe; these events were related to her menstrual cycles. Repeat spinal angiography performed 2 months after embolization confirmed exclusion of the fistula and normal circulation time through the artery feeding the lumbar enlargement. The muscular branches of both uterine arteries were still tortuous and hypertrophied, and an intense persistent capillary blush was noted in the corpus uterus (Fig. 2A). In the later phase, venous drainage into the same ilium terminale vein through the sacral vein was seen (Fig. 2B). A decision was made to recommend a hysterectomy so that the venous drainage into the sacral venous system would be reduced. One month later, the patient underwent a total abdominal hysterectomy and bilateral salphingo-oophorectomy. A large collection of aberrant vessels including large dilated varicose veins were noted on the left pelvic wall extraperitoneally. At pathological examination, the uterus and ovaries were unremarkable. Dramatic improvement of the patient's neurological symptoms followed. At her recent 5-year follow-up examination, she was found to be symptomfree.
Discussion This case raises several important issues for consideration. These include the basic pathophysiological mechanisms of the symptoms of spinal dural AV fistulas and their hemodynamie relationship to the spinal cord venous circulation. Normally, venous drainage of the spinal cord begins from its intramedullary portion of the medullary veins, pierces the dura, and exits toward the epidural venous plexus. There is usually no retrograde reflux from the epidural vein to the intradural vein. 7~~ It has been widely accepted that, in most patients harboring a spinal dural AV fistula, there is a dural branch (or branches) of the spinal ramus of the intercostal or lumbar segmental artery that supplies the actual fistula in the dura. Blood flow through the fistula runs toward the medullary veins and drains into the coronal and/or longitudinal venous plexus of the spinal cord, which forms the arterialized complex of vessels seen on the surface of" the cord. 4's~~>~6 This venous dilatation and stagnation may also be explained by the presence of a defect in the outflow to the epidural venous system. L~,~ Therefore, the direct cause of hypoxic myelopathy is a decreased intramedullav AV pressure gradient due to raised pressure in the perimedullary venous system and/ or by outflow obstruction? ~ This phenomenon has been confirmed by Hassler, et al., ~ who, in a direct 948
FJ(i. 1. Let~: Selective arteriogram revealing a fistulous shunt (small arrow.~J from the left lateral sacral artery (long arrow), draining toward the spinal canal through the dilated filum terminalc vein (curved arrowsj. Ri~hl." Postembolization angiogram verified complete closure of the arteriovenous fistula.
measurement of intravascular pressure in the draining veins, found that it was about 70% of systemic arterial pressure. Venous hypertension in the absence of normal epidural venous drainage can also be influenced by various hemodynamic factors. Exercise or certain postures which temporarily induce systemic arterial or venous hypertension exacerbate the symptoms in 42% to 70% of patients with a diagnosis of spinal dural AV fistula/'t6 Other reported aggravating factors are trauma, surgery, angiography, lumbar puncture, pregnancy, and systemic arterial hypertension. 2~~~2~4-~ The precipitating factor that was unique in this case was the onset of menstruation. Myelopathy was consistently preceded by menstruation, even after successful fistula embolization. It is well known that the vertebral veins, with their rich, valveless ramification and connections, offer an important alternative route of venous drainage from the pelvis and lower extremities. Injection experiments with simulated abdominal straining showed venous flow from the pelvic veins was into the paravertebral venous system) Under certain circumstances, spinal medullary veins might be filled retrogradely from the epidural venous plexus in spite of a valve-like barrier at the dura. The retrograde filling of intradural veins, occasionally observed above an obstruction of epidural veins due to spinal stenosis, has been reported in a series of lumbar and cervical epidural venograms. 9~8~9 As in the case of long-standing occlusion of the inferior vena cava, the diversion of significant venous drainage into the epidural venous plexus can produce symptomatic spinal venous hypertension.~ A case was also reported J. Neurosurg. / Volume 75 / December, 1991
Myelopathy aggravaled by menstruation
FIG. 2. FolIow-up angiograms obtained 2 months alicr embolization. A: The muscular branches of the lefl uterine artery (curved arnm) were tortuous and hypertrophied. An intense capillary blush was noted. B: Late venous phase showing persistent staining in the uterine musculature which drains only into the ilium terminale vein through a sacral venous collateral vessel (curved arrow.s). The left hypogastric vein, which is the normal route of uterine venous drainage, is not opacified.
in which a posttraumatic pelvic AV fistula caused progressive paraplegia because of voluminous shunting into the epidural venous system after surgical obliteration of the usual pelvic venous pathways. :~ One possible explanation in our patient is that the uterine hyperemia during the menstrual periods increased the venous return to an already compromised pelvic venous system, which in turn drained into the medullary vein through a sacral venous collateral route. This phenomenon is supported not only by a repeat angiogram which disclosed persistent uterine hyperemia with aberrant drainage into the ilium tcrminale vein, but also by the surgically verified pathological condition in the pelvic veins, The combined treatment of closure of the spinal dural fistula by embolizafion and surgical removal of the uterus completely cured the patient's neurological dysfunction. Early recognition of the pathophysiology of symptoms based on the functional vascular anatomy and physiology played a significant role in the proper management of this lesion. References i. Aboulker J, Bar D, Marsault C, et al: Intraspinal venous hypertension caused by multiple abnormalities of the caval system. A major cause of spinal cord problems. Chirurgie 103:i003-1015, 1977 2. Awad IA, Barnett GH: Neurological deterioration in a patient with a spinal arteriovenous malformation followmg lumbar puncture. Case report. J Neurosurg 72: 650-653, 1990 3. Batson OV: The vertebral vein system. Caldweli lecture,
J. Neurosurg / Volume 75 /December, 1991
1956. AJR 78:195-212, 1957 4. Benhaiem N, Pottier J, Hurth M: Arteriovenous fistulae of the meninges draining into the spinal veins. A histological study of 28 cases. Acta Neuropalhol 62:103-111. I983 5. Bcrcnstein A, Lasjaunias P: Spine and spinal cord vascular lesions, in Berenstein A, Lasjaunias P (eds): Surgical Neuroangiography, Vol 4. Berlin: Springer-Verlag (In press) 6. Burguet JL, Dietemann Jr,, Wackenheim A, et al: Sacral meningeal arteriovenous fistula fed by branches of the hypogastric arteries and drained through medullau vein. Neuroradiology 27:232-237, 1985 7. Gillilan LA: Veins of the spinal cord. Anatomic details; suggested clinical applications. Neurology 20:860-868, 1970 8. Hassler W, Thron A, Grote EH: Hemodynamics of spinal dural arteriovenous fistulas. An intraoperative sludy. J Neurosurg 70:360-370, 1989 9. Ike BW, Thijssen HOM, Chevrot A, el al: Collateral pathways in lumbar epidural venography. Report of three cases. Neuroradiology 24:91-96, 1982 10. Kendall BE, Logue V: Spinal epidural angiomatous malformations draining into intrathecal veins. Neuroradiology 13:I81-189, 1977 11. Lasjaunias P, Berenstein A: Technical aspects of surgical neuroangiography, in Lasjaunias P, Berenstein A (eds): Surgical Neuroangiography, Vol 2. Endovascular Treatment of Craniofacial Lesions. Berlin: Springer-Verlag, 1987, pp 29-40 12. Madsen JR. Heros RC: Spinal arteriovenous malformations and neurogenic claudieation. Report of two cases. J Neurosurg 68:793-797, 1988 13. Merland JJ, Riche MC, Chiras J: lntraspinal extramedullau arteriovenous fistulae draining into the medullary veins. J Neuroradiol 7:271-320, t980 14. Morgan MK, Marsh WR: Management of spinal dural arleriovenous malformations. J Neurosurg 70:832-836, 1989 15. Rosenblum B, Oldfield EH, Doppman JL, et al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM's in 81 patients. J Neurosurg 67:795-802, 1987 16. Symon L, Kuyama H, Kendall B: Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60:238-247, 1984 17. Tadi6 M, Hemet J, Freger P, et al: Morphological and functional anatomy of spinal cord veins. J Neuroradiol 12:3-20, 1985 18. Thrron J: Cervicovertebral phlebography: pathological results. Radiology 118:73-81, 1976 19. Thrron J, Houtteville JP, Ammerich H, et ah Lumbar phlebography by catheterization of the lateral sacral and ascending lumbar veins with abdominal compression. Neuroradiology 11:175-182, 1976 20. Weingrad DN, Doppman JL, Chretien PB, et al: Paraplegia due to posttraumatic pelvic arteriovenous fistula treated by surgery and embolization. Case report. J Neurosurg 50:805-810, 1979 Manuscript received January 3, 1991. Accepted in final form May 29, 199t. Address rept:int requests to: Dong-Ik Kim, M.D., Interventional Neuroradiology Section, Department of Radiology, New York University, 560 First Avenue, New York, New York 10016.
949
A sacral dural arteriovenous fistula presenting with an intermittent myelopathy aggravated by menstruation Case report DONG-IK KIM, M.D., IN-SuP CHOI, M.D., AND ALEX BERENSTEIN,M.D.
Interventional Neuroradiology Section, Department of Radiology, New York University, New York, New York, and Department qf Diagnostic Radiology, Yonsei University College of Medicine, Seoul, South Korea
t/ The case is reported of a woman with a spinal dural arteriovenous fistula whose intermittent myelopathy became aggravated with menstruation. Her symptoms recurred in spite of successful acrylic embolization of the lateral sacral arteriovenous fistula. Repeat angiography showed venous drainage from the uterus toward the medullary vein. Total abdominal hysterectomycured her symptoms. The pathophysiologicalbasis for this peculiar clinical manifestation and its management are discussed. KEy WORDS
'
hysterectomy
spinal anomaly 9 menstruation
.
S
P|NAL dural arteriovenous (AV) fistulas have been recognized as an acquired AV shunt that presents as a progressive myelopathy secondary to venous hypertension of medullary veins. The anatomicopathological lesion consists of a feeding dural artery, an AV fistulous nidus, and an arterialized intradural draining vein. 4'5"t~ The symptoms include a slowly progressive myelopathy and/or radiculopathy with varying degrees of spastic or flaccid paraparesis, muscle atrophy, sphincter disturbances, and dorsal-column sensory signs. Neurological deterioration has been associated with high intraspinal venous pressure with a reduced AV pressure gradient leading to hypoxic damage of the spinal cord. 8'~~ This intraspinal venous pressure could also be influenced by various hemodynamic factors?8'~6 Deterioration can be stabilized or reversed by therapeutic interventions such as embolization and/or surgical obliteration of the dural AV fistulaJ '6''~ 16 We report a case in which the patient developed intermittent myelopathy during her menstrual cycle from a dural AV fistula. The case prompted consideration of the hemodynamic aspect of myelopathy associated with spinal dural AV fistula and its proper management. Case Report
This 46-year-old woman presented with a few months' history of intermittent episodes of weakness J. Neurosurg. / Volume 75 /December, 1991
arteriovenous fistula
venous drainage
9
and a cold sensation in both legs at the beginning of her menstrual periods. She usually regained function in about 2 hours. She occasionally experienced a burning sensation on the soles of her feet. Her neurological examination on admission revealed mild weakness (4/5) of the proximal muscles of the left lower extremity. The fight patellar and both Achilles reflexes were absent, and superficial sensation below the knees was diminished bilaterally. A thoracolumbar myelogram revealed scalloped filling defects in the region of the conus medullaris, consistent with dilated veins of spinal AV malformation. Computerized tomography (CT)-myelography demonstrated a slight expansion of the lower thoracic spinal cord surrounded by multiple tiny filling defects. Selective spinal angiography revealed a spinal dural AV fistula from the left lateral sacral artery draining toward the spinal canal via the ilium terminale vein (Fig. 1 left). The artery feeding the lumbar enlargement originated from the left L-2 artery. Slow flow in the anterior spinal artery was noted. Operation. Prior to embolization, the proximal segment of the left internal iliac artery posterior division was protected by placement of a Gianturco coil in the vessel. The fistula was successfully embolized with 0.15 ml ofisobutyl 2-cyanoacrylate mixture using the "push" techniqueJ LA control angiogram of both internal iliac
947
D. I. Kim, I. S. Choi, and A. Berenstein arteries verified complete closure of the AV fistula (Fig. l righl). Postoperative ('our.so. lmmediatelv after embolization, there was significant improvement in the patient's neurological status and she had no episode of weakness for one subsequent menstrual cycle. She then began to develop transient weakness in the lower extremitics similar to those prior to embolization, although not as severe; these events were related to her menstrual cycles. Repeat spinal angiography performed 2 months after embolization confirmed exclusion of the fistula and normal circulation time through the artery feeding the lumbar enlargement. The muscular branches of both uterine arteries were still tortuous and hypertrophied, and an intense persistent capillary blush was noted in the corpus uterus (Fig. 2A). In the later phase, venous drainage into the same ilium terminale vein through the sacral vein was seen (Fig. 2B). A decision was made to recommend a hysterectomy so that the venous drainage into the sacral venous system would be reduced. One month later, the patient underwent a total abdominal hysterectomy and bilateral salphingo-oophorectomy. A large collection of aberrant vessels including large dilated varicose veins were noted on the left pelvic wall extraperitoneally. At pathological examination, the uterus and ovaries were unremarkable. Dramatic improvement of the patient's neurological symptoms followed. At her recent 5-year follow-up examination, she was found to be symptomfree.
Discussion This case raises several important issues for consideration. These include the basic pathophysiological mechanisms of the symptoms of spinal dural AV fistulas and their hemodynamie relationship to the spinal cord venous circulation. Normally, venous drainage of the spinal cord begins from its intramedullary portion of the medullary veins, pierces the dura, and exits toward the epidural venous plexus. There is usually no retrograde reflux from the epidural vein to the intradural vein. 7~~ It has been widely accepted that, in most patients harboring a spinal dural AV fistula, there is a dural branch (or branches) of the spinal ramus of the intercostal or lumbar segmental artery that supplies the actual fistula in the dura. Blood flow through the fistula runs toward the medullary veins and drains into the coronal and/or longitudinal venous plexus of the spinal cord, which forms the arterialized complex of vessels seen on the surface of" the cord. 4's~~>~6 This venous dilatation and stagnation may also be explained by the presence of a defect in the outflow to the epidural venous system. L~,~ Therefore, the direct cause of hypoxic myelopathy is a decreased intramedullav AV pressure gradient due to raised pressure in the perimedullary venous system and/ or by outflow obstruction? ~ This phenomenon has been confirmed by Hassler, et al., ~ who, in a direct 948
FJ(i. 1. Let~: Selective arteriogram revealing a fistulous shunt (small arrow.~J from the left lateral sacral artery (long arrow), draining toward the spinal canal through the dilated filum terminalc vein (curved arrowsj. Ri~hl." Postembolization angiogram verified complete closure of the arteriovenous fistula.
measurement of intravascular pressure in the draining veins, found that it was about 70% of systemic arterial pressure. Venous hypertension in the absence of normal epidural venous drainage can also be influenced by various hemodynamic factors. Exercise or certain postures which temporarily induce systemic arterial or venous hypertension exacerbate the symptoms in 42% to 70% of patients with a diagnosis of spinal dural AV fistula/'t6 Other reported aggravating factors are trauma, surgery, angiography, lumbar puncture, pregnancy, and systemic arterial hypertension. 2~~~2~4-~ The precipitating factor that was unique in this case was the onset of menstruation. Myelopathy was consistently preceded by menstruation, even after successful fistula embolization. It is well known that the vertebral veins, with their rich, valveless ramification and connections, offer an important alternative route of venous drainage from the pelvis and lower extremities. Injection experiments with simulated abdominal straining showed venous flow from the pelvic veins was into the paravertebral venous system) Under certain circumstances, spinal medullary veins might be filled retrogradely from the epidural venous plexus in spite of a valve-like barrier at the dura. The retrograde filling of intradural veins, occasionally observed above an obstruction of epidural veins due to spinal stenosis, has been reported in a series of lumbar and cervical epidural venograms. 9~8~9 As in the case of long-standing occlusion of the inferior vena cava, the diversion of significant venous drainage into the epidural venous plexus can produce symptomatic spinal venous hypertension.~ A case was also reported J. Neurosurg. / Volume 75 / December, 1991
Myelopathy aggravaled by menstruation
FIG. 2. FolIow-up angiograms obtained 2 months alicr embolization. A: The muscular branches of the lefl uterine artery (curved arnm) were tortuous and hypertrophied. An intense capillary blush was noted. B: Late venous phase showing persistent staining in the uterine musculature which drains only into the ilium terminale vein through a sacral venous collateral vessel (curved arrow.s). The left hypogastric vein, which is the normal route of uterine venous drainage, is not opacified.
in which a posttraumatic pelvic AV fistula caused progressive paraplegia because of voluminous shunting into the epidural venous system after surgical obliteration of the usual pelvic venous pathways. :~ One possible explanation in our patient is that the uterine hyperemia during the menstrual periods increased the venous return to an already compromised pelvic venous system, which in turn drained into the medullary vein through a sacral venous collateral route. This phenomenon is supported not only by a repeat angiogram which disclosed persistent uterine hyperemia with aberrant drainage into the ilium tcrminale vein, but also by the surgically verified pathological condition in the pelvic veins, The combined treatment of closure of the spinal dural fistula by embolizafion and surgical removal of the uterus completely cured the patient's neurological dysfunction. Early recognition of the pathophysiology of symptoms based on the functional vascular anatomy and physiology played a significant role in the proper management of this lesion. References i. Aboulker J, Bar D, Marsault C, et al: Intraspinal venous hypertension caused by multiple abnormalities of the caval system. A major cause of spinal cord problems. Chirurgie 103:i003-1015, 1977 2. Awad IA, Barnett GH: Neurological deterioration in a patient with a spinal arteriovenous malformation followmg lumbar puncture. Case report. J Neurosurg 72: 650-653, 1990 3. Batson OV: The vertebral vein system. Caldweli lecture,
J. Neurosurg / Volume 75 /December, 1991
1956. AJR 78:195-212, 1957 4. Benhaiem N, Pottier J, Hurth M: Arteriovenous fistulae of the meninges draining into the spinal veins. A histological study of 28 cases. Acta Neuropalhol 62:103-111. I983 5. Bcrcnstein A, Lasjaunias P: Spine and spinal cord vascular lesions, in Berenstein A, Lasjaunias P (eds): Surgical Neuroangiography, Vol 4. Berlin: Springer-Verlag (In press) 6. Burguet JL, Dietemann Jr,, Wackenheim A, et al: Sacral meningeal arteriovenous fistula fed by branches of the hypogastric arteries and drained through medullau vein. Neuroradiology 27:232-237, 1985 7. Gillilan LA: Veins of the spinal cord. Anatomic details; suggested clinical applications. Neurology 20:860-868, 1970 8. Hassler W, Thron A, Grote EH: Hemodynamics of spinal dural arteriovenous fistulas. An intraoperative sludy. J Neurosurg 70:360-370, 1989 9. Ike BW, Thijssen HOM, Chevrot A, el al: Collateral pathways in lumbar epidural venography. Report of three cases. Neuroradiology 24:91-96, 1982 10. Kendall BE, Logue V: Spinal epidural angiomatous malformations draining into intrathecal veins. Neuroradiology 13:I81-189, 1977 11. Lasjaunias P, Berenstein A: Technical aspects of surgical neuroangiography, in Lasjaunias P, Berenstein A (eds): Surgical Neuroangiography, Vol 2. Endovascular Treatment of Craniofacial Lesions. Berlin: Springer-Verlag, 1987, pp 29-40 12. Madsen JR. Heros RC: Spinal arteriovenous malformations and neurogenic claudieation. Report of two cases. J Neurosurg 68:793-797, 1988 13. Merland JJ, Riche MC, Chiras J: lntraspinal extramedullau arteriovenous fistulae draining into the medullary veins. J Neuroradiol 7:271-320, t980 14. Morgan MK, Marsh WR: Management of spinal dural arleriovenous malformations. J Neurosurg 70:832-836, 1989 15. Rosenblum B, Oldfield EH, Doppman JL, et al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM's in 81 patients. J Neurosurg 67:795-802, 1987 16. Symon L, Kuyama H, Kendall B: Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60:238-247, 1984 17. Tadi6 M, Hemet J, Freger P, et al: Morphological and functional anatomy of spinal cord veins. J Neuroradiol 12:3-20, 1985 18. Thrron J: Cervicovertebral phlebography: pathological results. Radiology 118:73-81, 1976 19. Thrron J, Houtteville JP, Ammerich H, et ah Lumbar phlebography by catheterization of the lateral sacral and ascending lumbar veins with abdominal compression. Neuroradiology 11:175-182, 1976 20. Weingrad DN, Doppman JL, Chretien PB, et al: Paraplegia due to posttraumatic pelvic arteriovenous fistula treated by surgery and embolization. Case report. J Neurosurg 50:805-810, 1979 Manuscript received January 3, 1991. Accepted in final form May 29, 199t. Address rept:int requests to: Dong-Ik Kim, M.D., Interventional Neuroradiology Section, Department of Radiology, New York University, 560 First Avenue, New York, New York 10016.
949
