Enlargement of an arteriovenous malformation documented by angiography Case report
ROBERT F. SeETZLER, M.D., AND CHARLES B. WILSON, M.D. Department of Neurological Surgery, University of California School of Medicine, San Francisco, California The authors present a case in which an enlarging arteriovenous malformation was documented angiographically. Enlargement of the malformation concurrent with the appearance of basilar artery insufficiencywas ascribed to a sump effect (steal) by the arteriovenous shunt. KEvWoRos 9 arteriovenous m a l f o r m a t i o n arterial insufficiency
9 basilar artery
9
was found (Fig. 1). Headaches were her only symptom; the neurological examination was normal. She was treated with Dilantin and did well until December, 1973, when she developed marked unsteadiness of gait and drop attacks without loss of consciousness. Angiography demonstrated that the right parietal AVM had greatly enlarged, with contributions from the left carotid and vertebral systems (Figs. 2 and 3). At physical examination the patient was alert and cooperative with normal mental C a s e Report status. The cranial nerves were normal, but A 49-year-old woman was well until 1968 bruits were detected in the cervical carotid when she experienced a generalized seizure. area bilaterally. She demonstrated difficulty In January, 1971, she suffered two left-sided with tandem gait, mild clumsiness of the right seizures that became generalized, followed by arm, and slight increase in the deep tendon severe headaches. Evaluation included a lum- reflexes in the right upper extremities combar puncture with an opening pressure of 250 pared to the left. Sensory examination, inmm H20 and bloody cerebrospinal fluid cluding two-point discrimination and (CSF). At angiography a right parietal AVM graphesthesia, was completely normal. ,E are reporting a patient in whom an untreated arteriovenous malformation (AVM) increased dramatically in size accompanied by the development of basilar artery insufficiency over a 3-year period. Although progressive enlargement of AVM's is known to produce symptoms, its relationship to basilar artery insufficiency has been rarely documented.
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J. Neurosurg. / Volume 43 / December, 1975
767
R. F. Spetzler and C. B. Wilson
F~. 1. Lateral selective internal carotid angiograms, January, 1971. The AVM can be seen with feeding vessels and venous drainage.
F~G. 2. Lateral selective internal carotid angiograms, December, 1973. The AVM is much enlarged, with marked dilatation of the feeding vessels (arrows) and more extensive venous drainage than found previously.
Discussion
The report by Paterson and McKissock~ provides indirect evidence for the progressive This woman's symptoms were attributed to enlargement of vascular malformations. In a forward vertebral steal phenomenon. The their series of 110 cases, the older patients AVM, by offering low peripheral resistance, harbored larger malformations at diagnosis. caused intermittent basilar artery insufficien- Potter 5 first reported enlargement of an cy. Olivecrona and Riives3 first proposed AVM. His patient, a 22-year-old man, ischemia as a mechanism that produced presented with intracranial hemorrhage; a symptoms in the presence of high-flow second angiogram showed enlargement of the arteriovenous shunts. AVM. His case differs from ours in that his 768
J. Neurosurg. / Volume 43 / December, 1975
AVM enlargement shown by angiography and progressive enlargement of the malformation. In our case, the enlargement appears to be the consequence of progressive dilatation of pre-existing abnormal vessels.
References
F~G. 3. Selective vertebral angiogram demonstrating AVM and venous drainage. patient presented with an intracerebral clot, with the possibility that the clot compressed and initially occluded a portion of the A V M . Nori+n ~ described a p a t i e n t in w h o m angiography demonstrated only a small A V M but who had a considerably larger and partially thrombosed lesion at operation. Paterson and McKissock, 4 and H a m b y 1 suggested that an initial rupture forming an aneurysmal varix m a y produce a larger shunt
J. Neurosurg. / Volume 43 / December, 1975
1. Hamby WB: The pathology of supra-tentorial angiomas. J Neurosurg 15:65-75, 1958 2. Norl6n G: Arteriovenous aneurysms of the brain. Report of ten cases of total removal of the lesion. J Neurosurg 6:475-494, 1949 3. Olivecrona H, Riives J: Arteriovenous aneurysms of the brain. Their diagnosis and treatment. Arch Neurol Psychiatry 59:576-602, 1948 4. Paterson JH, McKissock W: A clinical survey of intracranial angiomas with special reference to their mode of progression and surgical treatment: a report of 110 cases. Brain 79:233-266, 1956 5. Potter JM: Angiomatous malformations of the brain: their nature and prognosis. Ann R Coil Surg 16:227-243, 1955
This work was supported in part by NINCDS Training Grant 5593. Address reprint requests to." Robert F. Spetzler, M.D., Department of Neurological Surgery, University of California School of Medicine, San Francisco, California 94143.
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ROBERT F. SeETZLER, M.D., AND CHARLES B. WILSON, M.D. Department of Neurological Surgery, University of California School of Medicine, San Francisco, California The authors present a case in which an enlarging arteriovenous malformation was documented angiographically. Enlargement of the malformation concurrent with the appearance of basilar artery insufficiencywas ascribed to a sump effect (steal) by the arteriovenous shunt. KEvWoRos 9 arteriovenous m a l f o r m a t i o n arterial insufficiency
9 basilar artery
9
was found (Fig. 1). Headaches were her only symptom; the neurological examination was normal. She was treated with Dilantin and did well until December, 1973, when she developed marked unsteadiness of gait and drop attacks without loss of consciousness. Angiography demonstrated that the right parietal AVM had greatly enlarged, with contributions from the left carotid and vertebral systems (Figs. 2 and 3). At physical examination the patient was alert and cooperative with normal mental C a s e Report status. The cranial nerves were normal, but A 49-year-old woman was well until 1968 bruits were detected in the cervical carotid when she experienced a generalized seizure. area bilaterally. She demonstrated difficulty In January, 1971, she suffered two left-sided with tandem gait, mild clumsiness of the right seizures that became generalized, followed by arm, and slight increase in the deep tendon severe headaches. Evaluation included a lum- reflexes in the right upper extremities combar puncture with an opening pressure of 250 pared to the left. Sensory examination, inmm H20 and bloody cerebrospinal fluid cluding two-point discrimination and (CSF). At angiography a right parietal AVM graphesthesia, was completely normal. ,E are reporting a patient in whom an untreated arteriovenous malformation (AVM) increased dramatically in size accompanied by the development of basilar artery insufficiency over a 3-year period. Although progressive enlargement of AVM's is known to produce symptoms, its relationship to basilar artery insufficiency has been rarely documented.
w
J. Neurosurg. / Volume 43 / December, 1975
767
R. F. Spetzler and C. B. Wilson
F~. 1. Lateral selective internal carotid angiograms, January, 1971. The AVM can be seen with feeding vessels and venous drainage.
F~G. 2. Lateral selective internal carotid angiograms, December, 1973. The AVM is much enlarged, with marked dilatation of the feeding vessels (arrows) and more extensive venous drainage than found previously.
Discussion
The report by Paterson and McKissock~ provides indirect evidence for the progressive This woman's symptoms were attributed to enlargement of vascular malformations. In a forward vertebral steal phenomenon. The their series of 110 cases, the older patients AVM, by offering low peripheral resistance, harbored larger malformations at diagnosis. caused intermittent basilar artery insufficien- Potter 5 first reported enlargement of an cy. Olivecrona and Riives3 first proposed AVM. His patient, a 22-year-old man, ischemia as a mechanism that produced presented with intracranial hemorrhage; a symptoms in the presence of high-flow second angiogram showed enlargement of the arteriovenous shunts. AVM. His case differs from ours in that his 768
J. Neurosurg. / Volume 43 / December, 1975
AVM enlargement shown by angiography and progressive enlargement of the malformation. In our case, the enlargement appears to be the consequence of progressive dilatation of pre-existing abnormal vessels.
References
F~G. 3. Selective vertebral angiogram demonstrating AVM and venous drainage. patient presented with an intracerebral clot, with the possibility that the clot compressed and initially occluded a portion of the A V M . Nori+n ~ described a p a t i e n t in w h o m angiography demonstrated only a small A V M but who had a considerably larger and partially thrombosed lesion at operation. Paterson and McKissock, 4 and H a m b y 1 suggested that an initial rupture forming an aneurysmal varix m a y produce a larger shunt
J. Neurosurg. / Volume 43 / December, 1975
1. Hamby WB: The pathology of supra-tentorial angiomas. J Neurosurg 15:65-75, 1958 2. Norl6n G: Arteriovenous aneurysms of the brain. Report of ten cases of total removal of the lesion. J Neurosurg 6:475-494, 1949 3. Olivecrona H, Riives J: Arteriovenous aneurysms of the brain. Their diagnosis and treatment. Arch Neurol Psychiatry 59:576-602, 1948 4. Paterson JH, McKissock W: A clinical survey of intracranial angiomas with special reference to their mode of progression and surgical treatment: a report of 110 cases. Brain 79:233-266, 1956 5. Potter JM: Angiomatous malformations of the brain: their nature and prognosis. Ann R Coil Surg 16:227-243, 1955
This work was supported in part by NINCDS Training Grant 5593. Address reprint requests to." Robert F. Spetzler, M.D., Department of Neurological Surgery, University of California School of Medicine, San Francisco, California 94143.
769
