Concurrent intracranial and spinal cord arteriovenous malformations

1975 ◽  
Vol 43 (1) ◽  
pp. 104-107 ◽  
Author(s):  
Cecil J. Hash ◽  
Charles B. Grossman ◽  
Henry A. Shenkin

✓ The authors report the case of a patient with subarachnoid hemorrhage in whom an intracranial dural arteriovenous malformation coexisted with a spinal arteriovenous malformation. The latter was considered to be the source of the hemorrhage by clinical and radiographic criteria. It is concluded that patients with subarachnoid hemorrhage who show no suitable intracranial source for their bleed in some instances should be investigated for a spinal origin of hemorrhage.

1973 ◽  
Vol 39 (5) ◽  
pp. 652-655 ◽  
Author(s):  
Anthony D. Oliver ◽  
Charles B. Wilson ◽  
Edwin B. Boldrey

✓ Two cases of spinal arteriovenous malformation (AVM) are reported because of a previously unobserved clinical feature: recurrent transient postprandial paresis of the legs. The authors believe the paresis was caused by chronic shunting of blood away from the cord and into the low-resistance AVM. Symptomatic cord ischemia might then be precipitated by vasodilatation in other areas of the body such as the splanchnic, brachial, or uterine vessels. We believe that in some instances this mechanism should be considered as an explanation for episodic neurological deficits seen in association with spinal AVM's.


1977 ◽  
Vol 47 (6) ◽  
pp. 965-968 ◽  
Author(s):  
Dwight Parkinson ◽  
Michael West

✓ A patient presented with spontaneous subarachnoid hemorrhage (SAH) from a cerebral arteriovenous malformation (AVM) which was later totally removed at surgery. The patient presented again with a new SAH from a spinal AVM that was also totally removed at surgery. Coexistence of spinal and cerebral arteriovenous malformations are exceedingly rare and hemorrhage from each is not previously reported. This case emphasizes the importance of investigating the spinal canal in otherwise unexplained spontaneous SAH.


1994 ◽  
Vol 81 (4) ◽  
pp. 620-623 ◽  
Author(s):  
Ghaus M. Malik ◽  
Asim Mahmood ◽  
Bharat A. Mehta

✓ Intracranial arteriovenous malformations (AVM's) have been classified as pure pial, pure dural, and mixed pial and dural. Dural AVM's are relatively uncommon, with 377 cases documented up to 1990. These lesions were believed to be situated within the walls of the sinuses, but during the last decade researchers discovered a small subgroup of dural AVM's in extrasinusal locations such as the skull base and tentorium. Two of the 17 patients who were studied between 1976 and 1993 had dural AVM's that were entirely intraosseous except for their venous drainage, which was via the dural venous sinuses. Although such intraosseous dural AVM's have not been previously described, the authors elected to group these malformations with dural AVM's because their venous drainage was intracranial and angiograms revealed identical features.


1984 ◽  
Vol 60 (2) ◽  
pp. 238-247 ◽  
Author(s):  
Lindsay Symon ◽  
Hideyuki Kuyama ◽  
Brian Kendall

✓ The clinical and angiographic findings of 55 patients with a spinal dural arteriovenous malformation (AVM) are reviewed, and the results of surgery assessed. The symptoms of dural AVM are usually gradual in onset, and hemorrhage from this type of AVM is less common than in true spinal cord angiomas. Other clinical features and the myelographic findings are similar to those of spinal cord angiomas. On angiography, the nidus of dural AVM's usually projected lateral to the spinal cord. Clipping of communicating vessels between the AVM and the coronal plexus was carried out in 50 patients, and decompressive laminectomy only in five cases. Surgery led to improvement of disturbed gait or arrest of a previously progressive course in 85% of those managed by clipping communicating vessels. The pathophysiology and surgical treatment of dural AVM's are discussed.


1977 ◽  
Vol 47 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Hiroshi Matsumura ◽  
Yasumasa Makita ◽  
Kuniyuki Someda ◽  
Akinori Kondo

✓ We have operated on 12 of 14 cases of arteriovenous malformation (AVM) in the posterior fossa since 1968, with one death. The lesions were in the cerebellum in 10 cases (three anteromedial, one central, three lateral, and three posteromedial), and in the cerebellopontine angle in two; in two cases the lesions were directly related to the brain stem. The AVM's in the anterior part of the cerebellum were operated on through a transtentorial occipital approach.


1975 ◽  
Vol 42 (4) ◽  
pp. 457-461 ◽  
Author(s):  
Charles J. Hodge ◽  
Robert B. King

✓ The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports.


1979 ◽  
Vol 51 (5) ◽  
pp. 715-717 ◽  
Author(s):  
Shunro Endo ◽  
Keiji Koshu ◽  
Jiro Suzuki

✓ The authors report a case of infratentorial arteriovenous malformation that regressed spontaneously within 25 months without bleeding episodes or surgical intervention. The patient's clinical symptoms, left-sided tinnitus, cranial bruit, and right homonymous hemianopsia, disappeared completely over the same period.


2001 ◽  
Vol 95 (2) ◽  
pp. 346-349 ◽  
Author(s):  
Francisco A. Ponce ◽  
Patrick P. Han ◽  
Robert F. Spetzler ◽  
Alexa Canady ◽  
Iman Feiz-Erfan

✓ Wyburn-Mason syndrome is a rare condition associated with multiple cerebral arteriovenous malformations. The disease, also called retinoencephalofacial angiomatosis, includes lesions of the retina, brain, and skin. This disorder stems from a vascular dysgenesis of the embryological anterior plexus early in the gestational period when the primitive vascular mesoderm is shared by the involved structures. The timing of the insult to the embryonic tissue determines which structures are affected. Extensions of the lesions vary widely but cutaneous lesions are unusual. Among reports in the literature, only three cases appear to have manifested without retinal involvement. The authors report the fourth case of Wyburn-Mason syndrome in which there was no retinal involvement and the first to involve neither the retina nor the face.


1986 ◽  
Vol 64 (2) ◽  
pp. 322-324 ◽  
Author(s):  
T. S. Park ◽  
Wayne S. Cail ◽  
Johnny B. Delashaw ◽  
John Kattwinkel

✓ A 2-day-old neonate with a spinal cord arteriovenous malformation developed severe paraparesis. The abrupt neurological deterioration was not associated with hemorrhage or aneurysmal dilatation. Ischemic damage of the spinal cord is suggested as the cause of the clinical manifestation.


2002 ◽  
Vol 96 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Robert F. Spetzler ◽  
Paul W. Detwiler ◽  
Howard A. Riina ◽  
Randall W. Porter

The literature on spinal vascular malformations contains a great deal of confusing terminology. Some of the nomenclature is inconsistent with the lesions described. Based on the experience of the senior author (R.F.S.) in the treatment of more than 130 spinal cord vascular lesions and based on a thorough review of the relevant literature, the authors propose a modified classification system for spinal cord vascular lesions. Lesions are divided into three primary or broad categories: neoplasms, aneurysms, and arteriovenous lesions. Neoplastic vascular lesions include hemangioblastomas and cavernous malformations, both of which occur sporadically and familially. The second category consists of spinal aneurysms, which are rare. The third category, spinal cord arteriovenous lesions, is divided into arteriovenous fistulas and arteriovenous malformations (AVMs). Arteriovenous fistulas are subdivided into those that are extradural and those that are intradural, with intradural lesions categorized as either dorsal or ventral. Arteriovenous malformations are subdivided into extradural-intradural and intradural malformations. Intradural lesions are further divided into intramedullary, intramedullary-extramedullary, and conus medullaris, a new category of AVM. This modified classification system for vascular lesions of the spinal cord, based on pathophysiology, neuroimaging features, intraoperative observations, and neuroanatomy, offers several advantages. First, it includes all surgical vascular lesions that affect the spinal cord. Second, it guides treatment by classifying lesions based on location and pathophysiology. Finally, it eliminates the confusion produced by the multitude of unrelated nomenclatural terms found in the literature.


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