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Receive exclusive offers and updates from Oxford Academic. Related articles in Google Scholar. Citing articles via Google Scholar. Looking for your next opportunity? View all jobs. In some cases, embolization has been used as an adjunct to surgical resection. Embolization is contraindicated in cases where a spinal cord artery radiculomedullary artery arises from the same pedicle as the feeder. Attempts with endovascular treatment in these cases may result in either inadequate embolization or spinal cord ischemia if the medullary artery is occluded [ 5 - 6 ].
Prognosis after treatment directly correlates with duration and severity of pre-operative symptoms 6, 8, Otherwise, there has been an inconsistency in the literature regarding prognosis after treatment. They are extremely rare, with only a few cases reported in the literature [ 14 ]. They are also more prevalent at the conus medullaris and cauda equina [ 14 ].
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Ventral intradural AVFs originate from the anterior spinal artery [ 14 , 15 ]. The fistulous connection lies completely outside the cord parenchyma and pia matter in the subarachnoid space ventral to the cord at the midline.
Blood flow through these AVFs is rapid and they may have flow-related aneurysms and venous hypertension [ 15 ]. In contrast to the dorsal types, ventral intradural AVFs may present as congenital lesions, but there is evidence supporting an acquired etiology to these lesions. They can be further subdivided into 3 distinct types based on feeding vessel size, shunt volume and drainage pattern [ 11 , 15 ]. Type A — Small with a single feeder and low shunt volume.
The feeding artery and draining vein are not significantly dilated. Hemodynamic features are similar to dorsal intradural AVFs. Type B — These are of an intermediate size with a major feeder from anterior spinal artery as well as smaller feeders at the level of the fistula.
Endovascular Treatment of Spinal Vascular Malformations
Type C — These are giant lesions with multi-pediculated and massively dilated venous channels and large shunt volumes. Hemodynamic features are similar to intramedullary AVMs. They originate from the anterior spinal artery, with a direct fistulous connection to the engorged venous drainage system. There are no capillaries between the artery and the venous network. The pathology is similar to dorsal intradural AVFs with venous hypertension a common finding. However, the cause of the venous hypertension appears to be me more from vascular steal and mechanical compression [ 15 ] than from slow flow and venous congestion.
As opposed to the dorsal AVFs, symptoms are thought to be produced by vascular steal and mechanical compression from engorged veins or by subarachnoid or intraparenchymal hemorrhage. Symptoms are usually progressive in nature, with myelopathy the most common finding.
Cases in which a patient may have an acute presentation or an acute exacerbation of baseline symptoms are usually a result of hemorrhage. Like their dorsal counterparts, T2 prolongation in the parenchyma may be noted with flow voids on the ventral aspect of the cord or thecal sac. However, it is difficult to determine the type of AVF or differentiate between the subtypes of ventral AVFs and spinal angiography remains the standard for diagnosis.
Figure 3. Catheterization of the anterior spinal artery cements the diagnosis of ventral intradural AVFs. Figure 4. Spinal angiography showing an AVF fed by an anterior spinal artery at the thoracic level.
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Delayed images show the perispinal venous drainage of the fistula. Treatment modality depends on the subtype of the ventral intradural AVFs. Types A and B are often treated surgically, while Type C lesions are almost always treated via endovascular embolization [ 13 - 15 ]. This is feasible when they are located at the conus or cauda equina but may prove difficult in higher lesions and necessitate an anterior or anterolateral approach for treatment [ 14 ]. The target for surgery is the fistulous connection. Care must be taken to preserve the patency of the anterior spinal artery [ 2 ].
Endovascular embolization is often of limited use in these lesions due to the involvement of the anterior spinal artery, which is difficult to catheterize and navigate. For Type C lesions, however, endovascular treatment via embolization or detachable balloon occlusion appears to be the only safe course of action secondary to the large size of the lesion and easy catheterization of the severely dilated anterior spinal artery [ 2 , 13 - 14 ].
Treatment usually results in stabilization of symptoms. Secondary to the paucity of these cases in the literature, definitive prognostic figures are not available. Extradural-Intradural Arteriovenous Malformation is rare and very complex. It contains an intramedullary nidus which may take up the entire spinal canal at the occupied level. It could involve bony, extradural, intradural, and intramedullary tissue.
This is a high-flow system with multiple feeding and draining vessels. The cause of this malformation is thought to be a problem with embryogenesis [ 2 , 15 , 37 ]. Adolescents and young adults are the most affected by this type of AVM. Patients usually present with pain or progressive myelopathic symptoms from spinal cord compression, venous hypertension, or vascular steal. Intramedullary or subarachnoid hemorrhage could also lead to meningismus or acute pain [ 15 , 37 ]. Flow voids can be seen on T1 weighted imaging. On T2 weighted imaging, hyperintensity and cord expansion are noted, which may be associated with venous hypertension.
Appearance of subarachnoid or intraparenchymal bleeding on MRI varies depending on whether it is acute or chronic blood. In extradural-intradural AVM, the extension of the vessels into the paraspinal tissue can be found on MRI [ 2 , 15 , 37 ]. The goal for treating extradural-intradural AVM is no different than any other type of AVM—obliteration of the nidus without causing damage to the spinal cord.
However, treatment is very difficult and involves a multidisciplinary approach. A common strategy is to embolize the multiple feeding arteries followed by resecting the nidus if possible.
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Complete resection without neurological deficits is extremely difficult [ 15 , 20 , 37 ]. Many cases of extradural-intradural AVM are inoperable. There are only a few case reports that relate successful resection of nidus with pre-operative embolization.
No long term outcome data is available for this disorder [ 20 ]. A spinal intramedullary AVM is formed by multiple abnormal vessels constituting a nidus with a feeding artery and a draining vein. The nidus may be entirely intramedullary in location, intra and extramedullary or may be located in the region of conus medullaris. The intramedullary AVMs resemble the intracranial AVMs closely, in that they are located within the parenchyma and have distinct multiple feeding arteries from either the anterior or posterior spinal arteries and draining veins.
These lesions are most often located in the cervico-thoracic area. Another distinct feature of the intramedullary AVMs is the association with spinal aneurysms. Djindjian and colleagues suggested classifying them into types based on the volume of spinal cord involved.