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Paravertebral arteriovenous malformations with epidural drainage: clinical spectrum, imaging features, and results of treatment.
BACKGROUND AND PURPOSE: Arteriovenous malformations (AVMs) of the spine or spinal cord can be characterized as spinal cord AVMs, spinal cord and dural arteriovenous fistulas, and AVMs occurring outside the dura but draining into the epidural veins. The purpose of this study was to review the clinical spectrum, imaging features, and results of treatment of paravertebral arteriovenous malformations (PVAVMs) with epidural drainage.
METHODS: The clinical records and images of 10 patients with PVAVMs were analyzed retrospectively for clinical presentation, MR findings, angioarchitecture, pathophysiology, treatment efficacy, and clinical follow-up.
RESULTS: Seven patients had myelopathy. The MR findings for three of these patients showed spinal cord hyperintensity on T2-weighted sequences and prominent perimedullary vessels. Angiography, performed in two of the three patients, showed evidence of reflux into the perimedullary veins from the PVAVMs. Each of these two patients underwent surgical clipping of the radicular vein leading to the perimedullary veins. In three of the seven patients, there were large epidural veins compressing the cord. Angiography performed in these patients showed large PVAVMs with multiple feeders, which were treated by a combination of transarterial and transvenous embolization. One of the seven patients had an associated spinal cord arteriovenous malformation. In three patients with incidental PVAVMs, cure was achieved by using a combination of coils and liquid adhesives by the endovascular route.
CONCLUSION: The clinical presentation of PVAVMs is variable, and symptomatic lesions are the result of compression by epidural veins or of congestive myelopathy. A clear understanding of the anatomy and pathophysiology is necessary to plan treatment. Endovascular techniques are capable of curing the malformation, alleviating the symptoms, or both in a significant proportion of these lesions.
METHODS: The clinical records and images of 10 patients with PVAVMs were analyzed retrospectively for clinical presentation, MR findings, angioarchitecture, pathophysiology, treatment efficacy, and clinical follow-up.
RESULTS: Seven patients had myelopathy. The MR findings for three of these patients showed spinal cord hyperintensity on T2-weighted sequences and prominent perimedullary vessels. Angiography, performed in two of the three patients, showed evidence of reflux into the perimedullary veins from the PVAVMs. Each of these two patients underwent surgical clipping of the radicular vein leading to the perimedullary veins. In three of the seven patients, there were large epidural veins compressing the cord. Angiography performed in these patients showed large PVAVMs with multiple feeders, which were treated by a combination of transarterial and transvenous embolization. One of the seven patients had an associated spinal cord arteriovenous malformation. In three patients with incidental PVAVMs, cure was achieved by using a combination of coils and liquid adhesives by the endovascular route.
CONCLUSION: The clinical presentation of PVAVMs is variable, and symptomatic lesions are the result of compression by epidural veins or of congestive myelopathy. A clear understanding of the anatomy and pathophysiology is necessary to plan treatment. Endovascular techniques are capable of curing the malformation, alleviating the symptoms, or both in a significant proportion of these lesions.
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