British Journal of Radiology (2004) 77, 969-973
© 2004 British Institute of Radiology
doi: 10.1259/bjr/30760081
Angiography-induced closure of perimedullary spinal arteriovenous fistula
K Aydin, MD1,
S Sencer, MD1,
A Sencer, MD2,
E Terzibasioglu, MD1 and
O Minareci, MD1
Departments of 1 Radiology and 2 Neurosurgery, Neuroradiology Division, Istanbul University, Istanbul Medical School, Capa, Istanbul, Turkey
Correspondence: Dr Kubilay Aydin, Yan
kses sokak, Tempo 2 Apt. Daire: 15, Yenimahalle/Bakrköy, Istanbul/Turkey
 |
Abstract
|
|---|
Type 4 spinal vascular malformations are called perimedullary arteriovenous fistulae, in which there is a shunt between a radicular artery and intradural veins. We report the spinal MR imaging and angiography findings of the angiography-induced closure of a type 4 spinal vascular malformation.
|
Introduction
|
|---|
Vascular malformations of spinal cord are classified into four types, according to their anatomy and angiographic features [1–3]. Type 1 and 4 spinal vascular malformations are actually arteriovenous fistulae (AVFs). Type 1 malformations are dural AVFs, in which there is a direct shunt between a dural branch of dorsospinal artery and an intradural vein. As its names implies, dural AVFs are located in the dural covering of a nerve root or in the adjacent spinal dura. In type 4 spinal vascular malformations, which are called perimedullary AVFs, there is a shunt between a branch of a radicular artery and intradural veins. The localization of perimedullary AVFs is intradural.
We report the spinal MRI and digital subtraction angiography findings in a case of spinal perimedullary AVF, which showed spontaneous closure after the diagnostic angiography.
|
Case report
|
|---|
A 29-year-old female presented with progressive weakness in the lower extremities for 9 months, and urinary incontinence for 2 months. At admission, physical examination revealed bilateral motor weakness in the lower extremities. The patellar and achilles tendon reflexes were diminished in the lower extremities. There was sensory deficit below the T9 level. There was no motor or sensory deficit in the upper extremities. Cranial nerves were intact.
MRI of the spine was performed to evaluate the neurological symptoms. Sagittal T2 weighted images revealed hyperintense signal intensity changes in the lower thoracic cord and serpentine signal voids, which were located posterior to the cord between the levels of T7 and L1 vertebrae (Figure 1
). Sagittal T1 weighted and axial T2 weighted images demonstrated the intradural signal voids, representing the enlarged vessels. The dilated intradural vessels, including a venous aneurysm were compressing the cord. With an initial diagnosis of spinal vascular malformation, spinal angiography was performed. The selective injection of left 12th intercostal artery showed a minimally enlarged posterolateral radicular artery with early arteriovenous shunt into tortous intradural veins, which was consistent with a diagnosis of perimedullary AVF (Figure 2). The left 12th intercostal injection also demonstrated another radiculomedullary artery leading to the artery of Adamchiewicz. The patient declined immediate embolisation of the AVF. Embolisation was planned for a later date, and during the weeks following the spinal angiography, the patient noticed considerable improvement in the neurological symptoms. On re-admission, spinal angiography including injection into all the intercostal and lumbar arteries revealed the disappearance of cord AVF (Figure 3). Spinal MR study was repeated to investigate the angiographic disappearance of AVF (Figure 4). T1 and T2 weighted sagittal and axial images demonstrated the thombosis of the enlarged, tortuous intradural vessels. The patient was discharged without any medication and her neurological symptoms and signs showed progressive improvement in the following months. Spinal angiography performed 6 months after the previous angiography was normal.
View larger version (145K):
[in this window]
[in a new window]
|
Figure 1. Spinal MR images. (a) Sagittal T2 weighted image of the thoracic spinal cord reveals enlarged, tortuous intradural veins. There is hyperintense signal intensity change in the lower thoracic cord (arrow). (b) Post-contrast sagittal T1 weighted image shows the pial enhancement in the lower thoracic regions and enlarged intradural veins.
|
|
View larger version (119K):
[in this window]
[in a new window]
|
Figure 2. Angiography images of the selective injection of left thoracal 12th intercostal artery. (a) An early arterial phase image reveals the minimally enlarged posterolateral radiculomedullary artery (double arrows) feeding the fistula. The sudden change in the calibre of feeding artery demonstrates the point of the fistula (arrow). (b) Close-up image of another injection into left 12th intercostal artery shows the point of fistula (arrow) and also faint filling of the artery of Adamchiewicz from another radiculomedullary artery (open arrows). (c) Another angiography image demonstrates the artery of Adamchiewicz (white arrow) and arteriovenous fistula. (d) A late phase angiography image shows the filling of enlarged, tortuous intramedullary veins (white arrows).
|
|
View larger version (104K):
[in this window]
[in a new window]
|
Figure 3. Follow up angiography. Selective injection of thoracal 12th intercostal artery reveals the disappearance of the arteriovenous fistula (AVF). The radiculomedullary artery which was previously feeding the AVF was thrombosed (white arrow). Note the normal filling of anterior radiculomedullary artery (black arrows), which gives rise to the artery of Adamchiewicz (open arrows).
|
|
View larger version (111K):
[in this window]
[in a new window]
|
Figure 4. Follow up MR images demonstrate the thrombosis of arteriovenous fistula (AVF). (a) Sagittal T1 weighted image of the thoracic cord shows the hyperintense and isointense (compared with the intensity of the cord) thrombi in the enlarged intradural veins. (b) Sagittal T2 weighted image reveals the thrombosis of the enlarged dilated intradural veins. Mixed signal intensity on T2 and T1 weighted imaging is likely to be due to a mixture of breakdown products of haemoglobin within thrombus.
|
|
|
Discussion
|
|---|
Perimedullary AVFs are relatively rare form of spinal arteriovenous malformations (AVMs). They constitute 8–19% of the spinal vascular malformations [4]. Direct arteriovenous shunt between the radiculomedullary artery(ies) and intradural spinal vein(s) creates perimedullary AVFs. Perimedullary AVFs are located in or on the spinal cord. The lack of a nidus differentiates it from the true spinal AVMs (type 2 and 3 spinal vascular malformations). The involvement of arteries feeding the cord and the intradural location of arteriovenous shunt differentiate perimedullary AVFs from dural AVFs. Perimedullary AVFs have been classified into three subtypes, according to shunt flow and degree of vascular enlargement [1]. In type 1 perimedullary AVF, there is a slow-flow, single shunt between a non-dilated anterior or posterolateral spinal artery and a spinal vein. The mass effect in type 1 fistulae is not significant. The arterial flow in type 2 AVFs is greater than that of type 1 lesions. One or two arteries with medium dilatation feed type 2 lesions. Increased shunt flow causes dilated, tortuous intradural veins. Type 3 AVFs, called giant perimedullary AVFs, have multiple, high flow dilated feeding arteries and giant dilatation of draining veins. Minimally dilated, feeding posterior radiculomedullary artery and dilated, tortuous draining veins in our case fit the diagnosis of type 2 perimedullary AVF.
Patients with perimedullary AVFs usually present with progressive or acute neurological deficits, subarachnoid haemorrhage or radiculopathy [5, 6]. Our case presented with myelopathy. Three hypotheses have been proposed to explain the progressive myeloradiculopathy in the patients with perimedullary AVF. The first possible explanation is the steal of the arterial feed of spinal cord by the AVF. In another hypothesis, venous hypertension and cord ischaemia, due to the venous congestion cause neurological deficits [7]. Compression of the spinal cord and nerve roots by the dilated vascular structures may result in myeloradiculopathy. In MR images of our case, there was minimal signal intensity change which might imply cord oedema in the spinal cord. Compression of the thoracic cord by the hypertrophied vessels was evident on the MR images in our case. The lack of signal intensity changes in the cord could not exclude the possibility of venous hypertension. Regression of the symptoms, despite of persistence of thrombosed dilated vascular structures, indicated that the cord compression by the enlarged vessels was not the only reason for myelopathy in our case. Subarachnoid haemorrhage is a frequent clinical presentation, especially in cases with type 3 AVFs. There was no history of haemorrhage in our case. Because of the progressive neurological deficits and possibility of subarachoid haemorrhage, the aim of the treatment of perimedullary AVFs is the complete closure of the fistula. Endovascular embolisation and surgery are the treatment modalities for the patients with perimedullary AVFs [5, 6]. Polyvinyl alcohol and other liquid embolic agents, detachable and non-detachable latex balloons, glue and coils can be used in the endovascular embolisation. Surgery is indicated for the cases, in which endovascular therapy is partial or unsuccessful. Two cases of spinal dural AVF with spontaneous closure during their follow-up have been reported [8, 9]. To our knowledge, spontaneous or angiography induced closure of perimedullary spinal AVF has not been reported in English literature. In cases with intracranial dural AVF, angiography-induced thrombosis of the fistula has been reported. Similarly, diagnostic angiography might have induced the thrombosis of AVF in our case. Slowing of the shunt flow in AVF caused by the selective catheterization of the feeding artery and thrombogenic effect of the contrast media might be the reason for thombosis of AVF.
In conclusion, although spontaneous or angiography induced closure is a known phenomenon in intracranial and spinal dural AVFs, it has not been reported in perimedullary AVF before, and we report a case of thrombosis of perimedullary AVF which appears to have been precipitated by diagnostic angiography.
Received for publication November 13, 2003.
Revision received April 13, 2004.
Accepted for publication May 18, 2004.
|
References
|
|---|
- Anson JA, Spetzler RF. Classification of spinal arteriovenous malformations and complications for treatment. Barrow Neurol Inst Q 1992;8:2–8.
- Rosenblum B, Oldfield EH, Doppman JL, Di Chiro G. Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM's in 81 patients. J Neurosurg 1987;67:795–802.[Medline]
- Barrow DL, Colohan ART, Dawson R. Intradural perimedullary arteriovenous fistulas (type IV spinal cord arteriovenous malformations). J Neurosurg 1994;81:221–9.[Medline]
- Hurst RW. Vascular disorders of the spine and spinal cord. In: Atlas SW, editor. Magnetic resonance imaging of the brain and spine (3rd edn). Philedelphia: Lippicott Williams and Wilkins, 2002;1825–54.
- Ricolfi F, Gobin PY, Aymard A, Brunelle F, Gaston A, Merland JJ. Giant perimedullary arteriovenous fistulas of the spine: radiologic features and endovascular treatment. AJNR Am J Neuroradiol 1997;18:677–87.[Abstract]
- Mourier KL, Gobin YP, George B, Lot G, Merland JJ. Intradural perimedullary arteriovenous fistulae: results of surgical and endovascular treatment of 35 cases. Neurosurgery 1993;32:885–91.[Medline]
- Halbach VV, Higashida RT, Hieshima GB, Norman D. Normal perfusion pressure breakthrough occurring during treatment of carotid and vertebral fistulas. AJNR Am J Neuroradiol 1987;8:751–6.[Abstract]
- Meder JF, Devaux B, Merland JJ, Fredy D. Spontaneous disappearance of a spinal dural arteriovenous fistula. AJNR Am J Neuroradiol 1995;16:2058–62.[Abstract]
- Renowden SA, Molyneux AJ. Case report: spontaneous thrombosis of a spinal dural AVM (Foix-Alajouanine syndrome)-magnetic resonance appearance. Clin Radiol 1993;47:134–6.[CrossRef][Medline]
Top
Abstract
Introduction
