Spinal dural arteriovenous fistula formation after scoliosis surgery: case report

Clay M. Elswick Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Search for other papers by Clay M. Elswick in
jns
Google Scholar
PubMed
Close
 MD
,
Siri Sahib S. Khalsa Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Search for other papers by Siri Sahib S. Khalsa in
jns
Google Scholar
PubMed
Close
 MD
,
Yamaan S. Saadeh Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Search for other papers by Yamaan S. Saadeh in
jns
Google Scholar
PubMed
Close
 MD
,
Aditya S. Pandey Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Search for other papers by Aditya S. Pandey in
jns
Google Scholar
PubMed
Close
 MD
, and
Mark E. Oppenlander Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Search for other papers by Mark E. Oppenlander in
jns
Google Scholar
PubMed
Close
 MD
Full access

Spinal dural arteriovenous fistulas are diagnostically challenging lesions, and they are not well described in patients with a history of a spinal deformity correction. The authors present the challenging case of a 74-year-old woman who had previously undergone correction of a spinal deformity with subsequent revision. Several years after the last deformity operation, she developed a progressive myelopathy with urinary incontinence over a 6-month period. After evaluation at the authors’ institution, an angiogram was obtained, demonstrating a fistula at the T12–L1 region. Surgical ligation of the fistula was performed with subsequent improvement of the neurological symptoms. This case is thought to represent the first fistula documented in an area of the spine that had previously been operated on, and to the authors’ knowledge, it is the first case report to be associated with spinal deformity surgery. A brief historical overview and review of the pathophysiology of spinal dural arteriovenous fistulas is also included.

ABBREVIATIONS

AVF = arteriovenous fistula; AVM = arteriovenous malformation; dAVF = dural AVF; ICG = indocyanine green.

Spinal dural arteriovenous fistulas are diagnostically challenging lesions, and they are not well described in patients with a history of a spinal deformity correction. The authors present the challenging case of a 74-year-old woman who had previously undergone correction of a spinal deformity with subsequent revision. Several years after the last deformity operation, she developed a progressive myelopathy with urinary incontinence over a 6-month period. After evaluation at the authors’ institution, an angiogram was obtained, demonstrating a fistula at the T12–L1 region. Surgical ligation of the fistula was performed with subsequent improvement of the neurological symptoms. This case is thought to represent the first fistula documented in an area of the spine that had previously been operated on, and to the authors’ knowledge, it is the first case report to be associated with spinal deformity surgery. A brief historical overview and review of the pathophysiology of spinal dural arteriovenous fistulas is also included.

Spinal vascular malformations are relatively uncommon lesions of the spinal cord. They represent 3%–4% of all mass lesions of the spinal cord2 and can be a major source of neurological morbidity. Patients with these lesions may present with pain, paresthesias, paresis, radiculopathy, myelopathy, hemorrhage, and bowel/bladder dysfunction.18 Spinal vascular malformations have historically been challenging to identify and treat, but with advances in surgical and endovascular techniques, successful treatment of these lesions has become increasingly common with less treatment-related morbidity.

Spinal dural arteriovenous fistulas (dAVFs) are a subtype of spinal vascular malformations that have a direct arterial-to-venous shunt. Although the exact etiology of spinal dAVFs is not well understood, AVFs are presumed to be acquired (possibly posttraumatic) and not developmental in nature. These lesions are notoriously difficult to diagnose, given their insidious onset and vague symptoms of myelopathy. We present an unusual case of an intradural dorsal AVF (type 1 AVF3,16) presenting in an adult woman in a delayed fashion after scoliosis correction. The diagnosis of AVF in this patient was made only after referral to our center for unknown etiology of her thoracic myelopathy. This is believed to be the first description in the medical literature of an AVF developing post–spinal deformity correction. This phenomenon presents as a diagnostic and therapeutic dilemma. A current literature review of spinal vascular lesions is also presented.

Case Report

The patient was a 74-year-old woman with a history of scoliosis and had undergone decompression and T11–pelvis instrumented fusion for deformity correction at an outside facility 5 years prior to presentation. At the same facility, the patient underwent extension of fusion to T7 for instrumentation loosening the following year (Fig. 1). She presented to our clinic with 6 months of progressive bilateral lower-extremity weakness, numbness, and urinary incontinence, without back pain or radicular symptoms. The symptoms had worsened precipitously over the preceding 6 weeks, such that she presented with an indwelling urinary catheter and was unable to walk independently. She denied symptoms in her upper extremities. No diagnosis was made by the referring physician. On examination, she had full strength in her upper extremities; 3/5 strength in bilateral hip flexion; and 4/5 strength in knee extension, dorsiflexion, and plantar flexion. She had decreased sensation throughout the lower extremities and feet, and she was unable to ambulate due to severely impaired gait. There were no pathologic reflexes.

FIG. 1.
FIG. 1.

Anteroposterior (left) and lateral (right) scoliosis radiographs showing the T7–pelvis fusion construct.

MR images of the entire spine were obtained early in the year the patient presented and again 6 months later. Over this 6-month period, she had developed new extensive thoracic spinal cord edema that was not present on the initial MR image (Fig. 2). There was no evidence of an enhancing lesion. CT myelography showed no stenosis and no new spinal fracture. A region of rod breakage was identified on CT scans and scoliosis radiographs, but no malalignment was seen, and arthrodesis was evident at this level. A lumbar puncture performed at an outside facility showed a normal cell profile, normal protein, and no abnormalities on flow cytometry, and was negative for CSF oligoclonal bands.

FIG. 2.
FIG. 2.

T2-weighted MR images of the midsagittal thoracic spine. Left: Image obtained in January 2018, showing no evidence of spinal cord edema. Right: Image obtained in July 2018, showing extensive edema throughout the thoracic spinal cord.

Given the absence of mass lesion or other causative factor for the cord edema, a vascular malformation was suspected, and a spinal angiogram was obtained. A type 1 spinal dAVF supplied by an inferior branch of the left L1 segmental artery was discovered (Fig. 3).

FIG. 3.
FIG. 3.

Digital subtraction spinal angiogram (left) revealing an inferior branch of the left T12 segmental artery forming a fistulous connection with the coronal venous plexus. Three-dimensional reconstruction (right).

Treatment

One day after the discovery of the dAVF, the patient underwent T12–L1 laminectomies for ligation of the fistula. The laminectomies were through a fusion mass, increasing the complexity of the operation. After dural opening, a large arterialized vessel was seen emanating from the left L1 foramen and connected directly to the dorsal coronal venous complex. Insonation revealed biphasic arterial waves within this abnormal vessel. Intraoperative indocyanine green (ICG) angiography revealed extremely early filling of the venous plexus. The abnormal vessel was then ligated. After ligation, repeat ICG angiography demonstrated normal venous-phase filling of the dorsal venous plexus. The abnormal vessel was then coagulated with bipolar cautery and cut (Fig. 4). Images from intraoperative ICG angiography before and after the abnormal vessel was divided are displayed in Fig. 5. Neuromonitoring remained stable throughout the procedure.

FIG. 4.
FIG. 4.

Intraoperative photographs of the spinal dAVF before (upper) and after (lower) the vessel was cauterized and cut. Note the congested dorsal venous plexus. Figure is available in color online only.

FIG. 5.
FIG. 5.

Intraoperative ICG angiographs of the spinal dAVF obtained before (upper) and after (lower) the vessel was cauterized and cut.

Postoperative Course

The patient was admitted to the neurosurgical ICU postoperatively for 24 hours for close serial neurological assessments, which remained stable compared with her preoperative examination. Her activity was gradually advanced with physical therapy, occupational therapy, and physical medicine and rehabilitation consults. On postoperative day 6, she was discharged to inpatient rehabilitation. At the time of discharge, her lower-extremity strength had begun to improve with 4+/5 strength in bilateral hip flexion, 4/5 in left knee extension, 5/5 in right knee extension, 4/5 in left dorsiflexion, 5/5 in right dorsiflexion, and 5/5 in bilateral plantar flexion.

A new thoracic MR image was obtained at the routine 5-month outpatient follow-up (Fig. 6). The image demonstrated vast improvement in the previously seen edema noted throughout the thoracic spinal cord. The patient had gained the ability to ambulate with the use of a walker, and she described improvement in the numbness and paresthesias in her lower extremities. However, she had persistent bladder dysfunction.

FIG. 6.
FIG. 6.

T2-weighted MR image of the midsagittal thoracic spine obtained at the 5-month follow-up after fistula ligation, demonstrating vast improvement in the patient’s spinal cord edema.

Discussion

The history of spinal vascular lesions published in the medical literature dates to the late 19th century. The earliest description of a spinal arteriovenous malformation (AVM) was published in 1888.8 In subsequent years, these lesions were addressed surgically, first by Krause in 1910,13 when he operated on a spinal dAVF. Elsberg6 successfully operated on an AVM a few years later. The well-described Foix-Alajouanine syndrome, a subacute necrotizing myelopathy, was subsequently published in the mid-1920s.7 The patient we present here developed a similar clinical condition.

A brief review of the venous drainage of the spinal cord can help facilitate understanding of the pathophysiology of spinal dAVF formation (Fig. 7). Venous drainage of the spinal cord begins with intrinsic spinal cord veins and pial veins, which drain superficially into the longitudinal anastomosing veins of the spinal cord, including the anterior median spinal vein, posterior median spinal vein, anterolateral spinal vein, and posterior intermediate spinal vein. Significant variation can exist in the network of superficial anastomosing veins of the spinal cord. These veins tend to follow the anterior and posterior spinal arteries. They drain into the radiculomedullary veins, which also receive venous drainage from the epidural venous plexus. The radiculomedullary veins drain into the segmental (or intervertebral) veins, which continue on to drain into the subcostal veins and azygous and hemiazygous veins.19

FIG. 7.
FIG. 7.

Illustration of normal venous anatomy of the spinal cord. Reprinted from Fundamental Neuroscience for Basic and Clinical Applications, 5th edition, Haines DE and Mihailoff GA (eds), Haines DE: A survey of the cerebrovascular system, pp 122–137.e1, © 2018, with permission from Elsevier. Figure is available in color online only.

Spinal vascular malformations are most frequently classified by anatomical location. The most popular classification identifies 4 types.3,16 Type 1 lesions are dAVFs and occur when a radicular artery forms an abnormal communication with dural veins along the nerve root sleeve. Subsequently, the perimedullary coronal venous plexus becomes arterialized, leading to venous hypertension. Type 2 lesions are referred to as glomus type or intramedullary AVMs. Type 3 lesions are juvenile-type AVMs and incorporate both an extradural and intradural component of the AVM. A type 4 AVM is a perimedullary fistula, and these ventral lesions predominantly receive their arterial flow from anterior spinal artery branches.4,10 Spetzler and colleagues11,20 proposed a modified classification system in the early 2000s to describe these arteriovenous lesions based on anatomical and pathophysiological factors. This classification system categorized spinal dAVFs as extradural, intradural dorsal, or intradural ventral. AVMs were reclassified as extradural-intradural, intramedullary, or conus medullaris AVMs.

Multiple mechanisms have been proposed to explain the development of these arteriovenous shunts.12 These lesions were initially thought to be congenital. However, increasing evidence suggests that spinal dAVFs are acquired lesions that occur due to obstructed venous drainage, resulting in increasing venous outflow through the perimedullary spinal veins and development of a spinal AVF.14,15 This obstruction may be due to fibrosis, thrombosis, or any other cause.9 The pathophysiology of these AVFs is well described and has been studied extensively. The medullary vein carries the arterialized blood in a retrograde fashion into the coronal venous plexus and impairs the local venous outflow draining toward Batson’s epidural venous plexus. This high pressure in the coronal venous plexus leads to engorgement and dilation of these same small veins. This intrathecal venous plexus is valveless, and therefore these high pressures are transmitted further into radial and sulcal veins directly affecting the spinal cord. Venous congestion and venous hypertension ensue, and this leads to reduced arterial perfusion to the cord; myelopathy then ensues from regional spinal cord ischemia.5 In the present case, we suspect a degree of surgical or postsurgical trauma led to the cascade of development of the dAVF. The CT myelogram was reviewed extensively, although it did not identify a clear pedicle breach or an osteotomy level that could be seen as an initial cause.

The case presented here is that of a type 1 AVF or intradural dorsal AVF. Although these lesions are thought to be acquired and not developmental, the etiology and cause are not perfectly understood. These lesions are relatively rare, and only a few published cases have described patients becoming symptomatic from a dAVF following treatment or identification of a degenerative spinal condition. Moreover, in most of these cases, the fistula was located remotely from the operated area. Asakuno et al.1 published in 2002 the case of a patient who developed a myelopathy of the conus region following a lumbar microdiscectomy; the patient was subsequently found to have a dural AVF and improved after treatment. Stevens et al.21 published a report in 2009 of a 53-year-old man who developed a rapidly progressive conus medullaris syndrome from an AVF after undergoing an L4–5 and L5–S1 microdiscectomy for radiculopathy. Nishimura et al.,17 in 2014, described the case of an AVF associated with an isthmic spondylolisthesis of L4–5, but this was not related to prior surgical intervention.

The present case is unique because the dAVF developed in a delayed fashion after thoracolumbar fusion for scoliosis. The vascular lesion was identified in an area that previously had been instrumented. The patient became symptomatic several years after her last operation, and indeed, prior MRI scans did not demonstrate cord edema or flow voids. The patient presented with progressive weakness in her legs, inability to ambulate independently, and urinary retention and incontinence. These symptoms correlated with the new onset of thoracic spinal cord edema. The patient’s spinal cord edema mostly resolved, and her neurological symptoms improved after ligation of the fistula. These observations suggest that her symptoms were caused by the dAVF.

This report further supports the notion of a traumatic or inflammatory mechanism to account for the formation of spinal AVFs. The patient’s initial operation was a T11–ilium fusion. She subsequently developed pseudarthrosis at T11–12 with loosening of instrumentation and junctional kyphosis, which prompted a revision and extension to the midthoracic spine. Her fistula was found to originate from a segmental artery of T12. Although the true causation of the AVF can only be postulated, it is evident that there was a high degree of biomechanical stress at the most proximal levels of the original fusion, adjacent to the site of fistula formation. If the scoliosis correction’s proximal junctional failure was in fact the causative event, this report suggests a potential timeline for the development of a dAVF after a traumatic event. In addition, this case represents an initial diagnostic dilemma, wherein the AVF was not considered an etiology until evaluation at a quaternary referral center. Imaging was additionally difficult to interpret, because instrumentation artifact on MRI precluded adequate visualization of the spinal cord, and CT myelography did not demonstrate the spinal syrinx. Only after clinical suspicion for a dAVF arose was the conventional spinal angiogram performed and the diagnosis made. Therefore, dAVF should be considered in the workup of thoracic myelopathic symptomatology after spinal deformity surgery.

This report represents a unique etiology in the formation of a spinal dAVF. Given the delayed diagnosis in this patient, this case serves as a reminder that in the absence of additional deformity or stenosis on imaging after deformity correction, spinal dAVFs should be considered in patients who develop new-onset myelopathy.

Disclosures

Dr. Oppenlander: consultant for Globus Medical, DePuy Spine, and LifeNet Health.

Author Contributions

Conception and design: Oppenlander. Drafting the article: Elswick, Khalsa, Saadeh. Critically revising the article: all authors. Reviewed submitted version of manuscript: Oppenlander, Elswick. Approved the final version of the manuscript on behalf of all authors: Oppenlander. Study supervision: Oppenlander.

References

  • 1

    Asakuno K, Kim P, Kawamoto T, Ogino M: Dural arteriovenous fistula and progressive conus medullaris syndrome as complications of lumbar discectomy. Case report. J Neurosurg 97 (3 Suppl):375379, 2002

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Bao YH, Ling F: Classification and therapeutic modalities of spinal vascular malformations in 80 patients. Neurosurgery 40:7581, 1997

  • 3

    Di Chiro G, Doppman JL, Ommaya AK: Radiology of spinal cord arteriovenous malformations. Prog Neurol Surg 4:329354, 1971

  • 4

    Djindjian M, Djindjian R, Rey A, Hurth M, Houdart R: Intradural extramedullary spinal arterio-venous malformations fed by the anterior spinal artery. Surg Neurol 8:8593, 1977

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Dumont AS, Oldfield EH: Spinal vascular malformations, in Youmans JR (ed): Neurological Surgery, ed 6. Philadelphia: Elsevier Saunders, 2011, Vol 4, pp 41674202

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Elsberg C: Treatment of Surgical Diseases of Spinal Cord and Its Membranes. Philadelphia: Saunders, 1916

  • 7

    Foix C, Alajouanine T: La myélite nécrotique subaigue. Rev Neurol (Paris) 2:142, 1926

  • 8

    Gaupp J: Hamorrhoiden der pia mater spinalis im gebiet des lendenmarks. Beitr Pathol 2:516518, 1888

  • 9

    Geibprasert S, Pereira V, Krings T, Jiarakongmun P, Toulgoat F, Pongpech S, et al.: Dural arteriovenous shunts: a new classification of craniospinal epidural venous anatomical bases and clinical correlations. Stroke 39:27832794, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 10

    Heros RC, Debrun GM, Ojemann RG, Lasjaunias PL, Naessens PJ: Direct spinal arteriovenous fistula: a new type of spinal AVM. Case report. J Neurosurg 64:134139, 1986

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Kim LJ, Spetzler RF: Classification and surgical management of spinal arteriovenous lesions: arteriovenous fistulae and arteriovenous malformations. Neurosurgery 59 (5 Suppl 3):S195S201, S3–S13, 2006

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Koch C: Spinal dural arteriovenous fistula. Curr Opin Neurol 19:6975, 2006

  • 13

    Krause F: Chirurgie Des Gehirns und Rückenmarks. Berlin: Urban und Schwarzenberg, 1911

  • 14

    Krings T, Geibprasert S: Spinal dural arteriovenous fistulas. AJNR Am J Neuroradiol 30:639648, 2009

  • 15

    Krings T, Mull M, Gilsbach JM, Thron A: Spinal vascular malformations. Eur Radiol 15:267278, 2005

  • 16

    Malis LI: Arteriovenous malformations of the spinal cord, in Youmans JR (ed): Neurological Surgery. A Comprehensive Reference Guide to the Diagnosis and Management of Neurosurgical Problems. Philadelphia: WB Saunders, 1982, pp 18501874

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    Nishimura Y, Natsume A, Ginsberg HJ: Spinal dural arteriovenous fistula associated with L-4 isthmic spondylolisthesis. J Neurosurg Spine 20:670674, 2014

  • 18

    Rangel-Castilla L, Russin JJ, Zaidi HA, Martinez-Del-Campo E, Park MS, Albuquerque FC, et al.: Contemporary management of spinal AVFs and AVMs: lessons learned from 110 cases. Neurosurg Focus 37(3):E14, 2014

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    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 67:795802, 1987

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Spetzler RF, Detwiler PW, Riina HA, Porter RW: Modified classification of spinal cord vascular lesions. J Neurosurg 96 (2 Suppl):145156, 2002

  • 21

    Stevens EA, Powers AK, Morris PP, Wilson JA: Occult dural arteriovenous fistula causing rapidly progressive conus medullaris syndrome and paraplegia after lumbar microdiscectomy. Spine J 9:e8e12, 2009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • Collapse
  • Expand

Figure from Lau et al. (pp 23–30).

  • FIG. 1.

    Anteroposterior (left) and lateral (right) scoliosis radiographs showing the T7–pelvis fusion construct.

  • FIG. 2.

    T2-weighted MR images of the midsagittal thoracic spine. Left: Image obtained in January 2018, showing no evidence of spinal cord edema. Right: Image obtained in July 2018, showing extensive edema throughout the thoracic spinal cord.

  • FIG. 3.

    Digital subtraction spinal angiogram (left) revealing an inferior branch of the left T12 segmental artery forming a fistulous connection with the coronal venous plexus. Three-dimensional reconstruction (right).

  • FIG. 4.

    Intraoperative photographs of the spinal dAVF before (upper) and after (lower) the vessel was cauterized and cut. Note the congested dorsal venous plexus. Figure is available in color online only.

  • FIG. 5.

    Intraoperative ICG angiographs of the spinal dAVF obtained before (upper) and after (lower) the vessel was cauterized and cut.

  • FIG. 6.

    T2-weighted MR image of the midsagittal thoracic spine obtained at the 5-month follow-up after fistula ligation, demonstrating vast improvement in the patient’s spinal cord edema.

  • FIG. 7.

    Illustration of normal venous anatomy of the spinal cord. Reprinted from Fundamental Neuroscience for Basic and Clinical Applications, 5th edition, Haines DE and Mihailoff GA (eds), Haines DE: A survey of the cerebrovascular system, pp 122–137.e1, © 2018, with permission from Elsevier. Figure is available in color online only.

  • 1

    Asakuno K, Kim P, Kawamoto T, Ogino M: Dural arteriovenous fistula and progressive conus medullaris syndrome as complications of lumbar discectomy. Case report. J Neurosurg 97 (3 Suppl):375379, 2002

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Bao YH, Ling F: Classification and therapeutic modalities of spinal vascular malformations in 80 patients. Neurosurgery 40:7581, 1997

  • 3

    Di Chiro G, Doppman JL, Ommaya AK: Radiology of spinal cord arteriovenous malformations. Prog Neurol Surg 4:329354, 1971

  • 4

    Djindjian M, Djindjian R, Rey A, Hurth M, Houdart R: Intradural extramedullary spinal arterio-venous malformations fed by the anterior spinal artery. Surg Neurol 8:8593, 1977

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Dumont AS, Oldfield EH: Spinal vascular malformations, in Youmans JR (ed): Neurological Surgery, ed 6. Philadelphia: Elsevier Saunders, 2011, Vol 4, pp 41674202

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Elsberg C: Treatment of Surgical Diseases of Spinal Cord and Its Membranes. Philadelphia: Saunders, 1916

  • 7

    Foix C, Alajouanine T: La myélite nécrotique subaigue. Rev Neurol (Paris) 2:142, 1926

  • 8

    Gaupp J: Hamorrhoiden der pia mater spinalis im gebiet des lendenmarks. Beitr Pathol 2:516518, 1888

  • 9

    Geibprasert S, Pereira V, Krings T, Jiarakongmun P, Toulgoat F, Pongpech S, et al.: Dural arteriovenous shunts: a new classification of craniospinal epidural venous anatomical bases and clinical correlations. Stroke 39:27832794, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 10

    Heros RC, Debrun GM, Ojemann RG, Lasjaunias PL, Naessens PJ: Direct spinal arteriovenous fistula: a new type of spinal AVM. Case report. J Neurosurg 64:134139, 1986

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Kim LJ, Spetzler RF: Classification and surgical management of spinal arteriovenous lesions: arteriovenous fistulae and arteriovenous malformations. Neurosurgery 59 (5 Suppl 3):S195S201, S3–S13, 2006

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Koch C: Spinal dural arteriovenous fistula. Curr Opin Neurol 19:6975, 2006

  • 13

    Krause F: Chirurgie Des Gehirns und Rückenmarks. Berlin: Urban und Schwarzenberg, 1911

  • 14

    Krings T, Geibprasert S: Spinal dural arteriovenous fistulas. AJNR Am J Neuroradiol 30:639648, 2009

  • 15

    Krings T, Mull M, Gilsbach JM, Thron A: Spinal vascular malformations. Eur Radiol 15:267278, 2005

  • 16

    Malis LI: Arteriovenous malformations of the spinal cord, in Youmans JR (ed): Neurological Surgery. A Comprehensive Reference Guide to the Diagnosis and Management of Neurosurgical Problems. Philadelphia: WB Saunders, 1982, pp 18501874

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    Nishimura Y, Natsume A, Ginsberg HJ: Spinal dural arteriovenous fistula associated with L-4 isthmic spondylolisthesis. J Neurosurg Spine 20:670674, 2014

  • 18

    Rangel-Castilla L, Russin JJ, Zaidi HA, Martinez-Del-Campo E, Park MS, Albuquerque FC, et al.: Contemporary management of spinal AVFs and AVMs: lessons learned from 110 cases. Neurosurg Focus 37(3):E14, 2014

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    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 67:795802, 1987

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    Spetzler RF, Detwiler PW, Riina HA, Porter RW: Modified classification of spinal cord vascular lesions. J Neurosurg 96 (2 Suppl):145156, 2002

  • 21

    Stevens EA, Powers AK, Morris PP, Wilson JA: Occult dural arteriovenous fistula causing rapidly progressive conus medullaris syndrome and paraplegia after lumbar microdiscectomy. Spine J 9:e8e12, 2009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation

Metrics

All Time Past Year Past 30 Days
Abstract Views 1616 88 0
Full Text Views 279 81 22
PDF Downloads 269 56 3
EPUB Downloads 0 0 0