Introduction
Spinal cord arteriovenous malformations have been classified into four subtypes including
Type I, spinal dural arteriovenous fistulas (SDAVFs); Type II, intramedullary glomus
malformations; Type III, extensive juvenile malformations; and Type IV, intradural
perimedullary arteriovenous fistulas (AVFs). Type IV spinal cord arteriovenous malformations
have been further divided into three subtypes including Type IVa, small or low-flow
AVF supplied by single arterial branch of the anterior spinal artery (ASA); Type IVb,
intermediated-sized fistula supplied by multiple arterial feeders; and Type IVc, giant
high-flow fistula fed by several feeding vessels of the ASA and posterior spinal artery.[[1 ]],[[2 ]]
SDAVFs are the most common type of spinal vascular malformations.[[3 ]] These fistulas, also known as intradural dorsal AVFs, are the arteriovenous shunts
supplied by radiculomeningeal arteries draining into the radicular veins arterializing
the coronal venous plexus around the spinal cord, usually under low pressure, resulting
in venous congestion.[[4 ]],[[5 ]],[[6 ]] These fistulas affect primarily the lower thoracic and upper lumbar spine and are
located within the dorsal surface of the dural root sleeve in the intervertebral foramen.[[7 ]],[[8 ]] SDAVFs at the level of lower lumbar (L3–L5) or sacral region are uncommon.[[9 ]] The patients harboring SDAVFs, typically middle-aged men, commonly manifest with
progressive myelopathy induced by chronic venous hypertension.[[10 ]] Hemorrhage from SDAVFs is usually rare and may occur as subarachnoid hemorrhage
or intramedullary hemorrhage.[[11 ]] The characteristic findings on T2-weighted sequences in magnetic resonance imaging
(MRI) are a combination of spinal cord edema and perimedullary flow voids.[[12 ]] SDAVFs are often initially misdiagnosed because of its insidious onset.[[13 ]]
The pathogenesis of SDAVFs remains unclear. However, the symptoms of these fistulas
usually appear in adulthood, probably considering as acquired origin.[[9 ]] Most of SDAVFs are spontaneous. Some studies reported SDAVFs associated with trauma
or previous operation.[[14 ]],[[15 ]],[[16 ]],[[17 ]],[[18 ]] The authors described two cases of SDAVFs coexisting with disc herniation and spinal
canal stenosis at the same level, highly suspected of a pathophysiological link. The
mechanism of the formation of these fistulas in this situation was discussed.
Case Reports
Case 1
A 46-year-old male was admitted to our institute due to a history of progressive paraparesis
for 2 weeks. Eight months earlier, he experienced severe left buttock pain radiating
to left leg for 2 weeks. He was admitted to other private hospital and underwent discectomy
L5-S1. Five months later, he suffered from right leg pain and urinary retention. He
went back to the same private hospital and underwent revised surgery with spinal fusion
L5-S1. Two weeks before hospitalization, he developed progressive paraparesis and
constipation. He was unable to walk more than about 100 m. The patient went to another
private hospital and was transferred to Prasat Neurological Institute for further
investigation and proper treatment after performing MRI of the lumbosacral and thoracic
spine. The neurological examination revealed the evidence of spastic paraparesis (muscle
strength 3/5) and the lack of pinprick sensation below T10 level, impairment of proprioception,
hyperreflexia, and presence of Babinski's sign in the lower extremities. The previous
series of MRI of the lumbosacral and thoracic spine were retrospectively reviewed
and revealed spinal canal stenosis and bilateral lateral recesses stenosis at L5-S1
level due to moderate diffuse annular disc bulging with moderate enlargement of facet
joints and thickening of the ligamentum flavum [[Figure 1 ]]. There was an abnormal hyperintense T2 signal with patchy enhancement representing
spinal cord congestion extending from the conus medullaris to the level of T4 with
subtle perimedullary flow voids along ventral and dorsal cord surfaces [[Figure 2 ]] and [[Figure 3 ]]a. Magnetic resonance (MR) myelography also showed “worm-like” appearance of the
area from thoracic level to the conus medullaris [[Figure 3 ]]b. MR angiography (MRA) of the thoracolumbar spine demonstrated early opacification
of perimedullary venous plexus along anterior and posterior surfaces of spinal cord
[[Figure 3 ]]c. Furthermore, there was a curvilinear flow void, probably the dilated vein of
the filum terminale, running from lower lumbar level to the conus medullaris [[Figure 2 ]]. Spinal angiography demonstrated SDAVF at the level of L5-S1, probably located
on the left S1 nerve root sleeve, which is supplied by the left lateral sacral artery
(LSA) originating from the internal iliac artery with venous drainage through the
dilated radicular vein into the dilated vein of the filum terminale [[Figure 4 ]]a and [[Figure 4 ]]b. The artery of Adamkiewicz arose from the left L2 lumbar artery and left T9 intercostal
artery. Transarterial embolization with N-butyl-cyanoacrylate (NBCA) through the left
LSA was successfully performed with NBCA filling across the fistula into the proximal
draining vein [[Figure 4 ]]c. The patient had gradually improved until being the ability to walk independently
3 months later. His bowel and bladder controls had completely regained. Six months
after the embolization, follow-up MRI of the thoracolumbar spine also confirmed completely
regression of spinal cord congestion [[Figure 5 ]].
Figure 1: (a) Sagittal T2-weighted image of the lumbosacral spine and (b) axial T2-weighted
image of the L5-S1 level demonstrate spinal canal stenosis and bilateral lateral recesses
stenosis due to moderate diffuse annular disc bulging with moderate enlargement of
facet joints and thickening of the ligamentum flavum
Figure 2: The series of sagittal T2-weighted magnetic resonance images of the lumbosacral spine,
obtained (a) before surgery, (b) after discectomy; and (c) after spinal fusion, reveal
abnormal hyperintense T2 signal representing spinal cord congestion extending from
the conus medullaris to the lower thoracic. There was a curvilinear intradural flow
void (arrowheads), probably the dilated vein of the filum terminale, running from
the lower lumbar area to the conus medullaris
Figure 3: (a) Sagittal T2-weighted image of the thoracic spine shows spinal cord congestion
extending from the conus medullaris to the level of T4 with subtle perimedullary flow
voids along ventral and dorsal cord surfaces. (b) Coronal magnetic resonance myelography
of the lumbosacral spine demonstrates "worm -like" appearance, representing a contiguous
dilated and tortuous medullary vein from the conus medullaris to thoracic level. There
is a dilated intradural vessel (black arrowheads) located in rather midline, probably
the vein of the filum terminale. (c) Sagittal source image of contrast-enhanced spinal
magnetic resonance angiography of the thoracolumbar spine reveals early opacification
of perimedullary venous plexus (white arrowheads) along anterior and posterior surfaces
of spinal cord
Figure 4: (a) Anteroposterior view of the left internal iliac artery angiography shows spinal
dural arteriovenous fistula arrowheads, which is supplied by the left lateral sacral
artery with cranial drainage into the dilated vein of the filum terminale. (b) Anteroposterior
view of the left lateral sacral artery clearly demonstrates the fistula (arrowhead)
at the level of L5-S1, probably located on the left S1 nerve root sleeve. (c) Anteroposterior
view of nonsubtracted angiographic image reveals the glue cast (arrow) filling into
the proximal draining vein
Figure 5: Sagittal T2-weighted image of the (a) lumbosacral and (b) thoracic spine, obtained
six months after endovascular treatment, confirm the complete resolution of spinal
cord congestion
Case 2
A 51-year-old male, with a medical history of hypertension and diabetes mellitus,
was admitted to the local hospital due to intermittent acute exacerbation of myelopathy
for 3 months. One year earlier, he had developed gait disturbance and difficulty in
balancing. There was no history of trauma. Nine months later, the patient had acute
onset of paraparesis after waking up in the morning. He collapsed on the ground and
could not stand up for a while. After 30 min, he could raise his legs and walk as
baseline. He complained of minimal back pain and denied numbness. Two months before
hospitalization, he could not stand up after having dinner in the evening. After 30
min later, his symptoms improved. He had occasionally numbness on his left leg. After
this event, he had a limitation on ambulation and was unable to walk more than about
50–100 m without stopping to rest. No bowel or bladder involvement was complained.
Three weeks before admission, the patient had the same symptoms and rest for about
30 min then improved. MRI of whole spine was performed and was interpreted of a long
segment T2 hyperintense cord lesion extending from the level of T4 to the conus medullaris.
Lumbar puncture was performed due to the putative diagnosis of transverse myelitis.
Cerebrospinal fluid pressure, cell count, and chemistries were within normal limits.
The patient was transferred to Prasat Neurological Institute for definite diagnosis
and proper management. The physical examination revealed bilateral lower extremity
weakness (muscle strength 4/5) without paresthesia. Hyperreflexia was noted in the
lower extremities. Babinski's sign was also positive. By counting vertebrae from whole
spine screening, there was a degenerative bulging disc at the level of L4–L5 with
spinal canal stenosis and compression of bilateral L5 traversing roots [[Figure 6 ]]. MRI of the thoracolumbar spine showed the spinal cord congestion at the level
of T4 to the conus medullaris with subtle perimedullary flow voids along ventral and
dorsal cord surfaces [[Figure 7 ]]a and [[Figure 7 ]]b. Furthermore, there was a curvilinear intradural flow void on T2-weighted image,
identified below the conus medullaris. Contrast-enhanced MRA of the thoracolumbar
spine demonstrated an enlarged intradural vessel in the midline location extending
from the lower lumbar level to the conus medullaris, probably the vein of the filum
terminale [[Figure 7 ]]c, corresponding with the curvilinear flow void on MRI. Spinal angiography demonstrated
SDAVF at the level of L4–L5, probably located on the right L5 nerve root sleeve, which
is supplied by the right iliolumbar artery originating from the internal iliac artery
with cranial drainage into the dilated vein of the filum terminale. The artery of
Adamkiewicz arose from the right T8 intercostal artery. Endovascular treatment with
NBCA through the right iliolumbar artery was successfully performed to fill in the
arterial feeder and fistulous site but fail to reach the proximal vein [[Figure 8 ]]c. Postembolization angiography of the internal iliac and iliolumbar arteries revealed
complete obliteration of the fistula. The patient had gradually improved and was sent
back to the local hospital for further physiotherapy. Four months later, he returned
and was readmitted to our institution with gait disturbance with the deterioration
of clinical symptoms. Follow-up MRI and MRA of the lumbosacral spine revealed unchanged
long segment of spinal cord congestion with the presence of SDAVF at the same level.
One week later, the patient underwent decompressive laminectomy with obliteration
of the intradural draining vein. The patient had significantly improved until being
the ability to walk independently 2 weeks later. Spinal angiography, obtained 2 weeks
after surgery, confirmed complete obliteration of the fistula [[Figure 9 ]]. MRI of the thoracolumbar spine, obtained 4 months after surgery, confirmed the
resolution of spinal cord congestion [[Figure 10 ]].{Figure 10}
Figure 6: (a) Sagittal T2-weighted image of the lumbosacral spine and (b) axial T2-weighted
image of the L4-5 level (counting vertebral bodies from unshown whole spine screening)
demonstrate spinal canal stenosis due to moderate broad base posterior bulging disc
compressing bilateral L5 traversing roots
Figure 7: Sagittal T2-weighted images of the (a) lumbosacral and (b) thoracic spine show spinal
congestion extending from the conus medullaris to the level of T4 with subtle perimedullary
flow voids along ventral and dorsal cord surfaces. There is a curvilinear flow void
(arrowheads), identified below the conus medullaris. (c) Contrast-enhanced magnetic
resonance angiography of the thoracolumbar spine demonstrates an enlarged intradural
vessel (arrowheads) in the midline location extending from the lower lumbar level
to the conus medullaris, probably the vein of the filum terminale, corresponding with
the curvilinear flow void
Figure 8: Anteroposterior view of the right iliolumbar artery (a) before and (b) after superselective
angiography show spinal dural arteriovenous fistula (arrowheads), probably located
along the right L5 nerve root sleeve, with cranial drainage into the dilated vein
of the filum terminale. (c) During endovascular treatment, the glue cast fills in
the distal feeder and fistulous site
Figure 9: (a) Anteroposterior view of the right iliolumbar artery angiography, obtained 2 weeks
after surgery, confirms complete obliteration of the fistula. (b) Nonsubtracted angiographic
image shows small silver vessel clips (arrowhead) using during the operation
Figure 10: Sagittal T2-weighted images of the (a) lumbosacral and (b) thoracic spine, obtained
4 months after surgery, confirm the resolution of spinal cord congestion
Discussion
Delayed or missed diagnosis of SDAVFs frequently leads to unnecessary pharmacologic
and/or surgical treatments and results in high rates of additional morbidity, often
being irreversible despite successful obliteration of the fistula.[[19 ]],[[20 ]] A long period of venous hypertension can result in irreversible injury to spinal
neurons.[[21 ]] Based on the analysis of the patients harboring SDAVFs by Qi et al.,[[13 ]] 13 patients (25%) of all the 52 patients were mistakenly diagnosed as disc herniation
or lumbar spinal stenosis.
Initial symptoms of SDAVFs are often nonspecific symptoms including gait difficulties,
sensory disturbances, and/or radicular pain.[[3 ]] Patient with SDAVF associated a herniated nucleus pulposus, and spinal canal stenosis
may initially present with back pain and/or radiculopathy and was initially misdiagnosed
of SDAVF.[[22 ]],[[23 ]] Similarly, our first case had initial symptoms that mimic discogenic radiculopathy
correlating to disc herniation and spinal canal stenosis on MRI, leading to discectomy
and spinal fusion with subsequent worsening symptoms. According to a large series
of 326 patients with SDAVFs by Donghai et al.,[[9 ]] degenerative disc disease and myelitis were the most common misdiagnoses, and the
patients were often treated incorrectly. Our second case was also misdiagnosed of
myelitis due to nonspecific clinical features of intermittent acute episodes of weakness.
Acute worsening of symptoms is uncommon and may occur after exercise or relate to
changes in posture, probably due to an increase in venous pressure resulting from
an increase in arterial pressure during physical activity.[[3 ]]
MRI findings, including spinal cord edema or perimedullary flow voids, are important
in the confirmation of the diagnosis of SDAVFs.[[12 ]] Therefore, careful screening of MRI for conus medullaris signal or vascular flow
voids is needed to avoid misdiagnosis. On myelography or MR myelography, severe spinal
stenosis may display engorged and tortuous flow voids, which are possible redundant
nerves and vessels, just proximal to the level of stenosis. Misinterpretation of these
findings may lead to underdiagnose SDAVF, resulting in deleterious consequence. In
our first case, MR myelography could identify contiguous dilated and tortuous medullary
veins. Contrast-enhanced MRA may be helpful in identifying serpentine perimedullary
structures and the possible arterial feeders of SDAVFs. However, spinal angiography
remains the gold standard for the diagnosis.[[3 ]]
Based on the vascular anatomy of the cauda equina reviewed by Namba,[[24 ]] the iliolumbar artery is usually the first branch of the internal iliac artery
and gives rise to a lumbar branch that travels to the intervertebral foramen between
the L5 and S1 vertebrae. Our second case, the fistula was located at the right L5
nerve root sleeve and supplied by the right iliolumbar artery. LSA, also the branch
of the internal iliac artery, lies on the anterior surface of the sacral, medial to
the sacral foramen. This artery gives rise to five pairs of the medial and lateral
branches. The medial branches form a network of vessels and anastomose with the middle
sacral artery. The lateral branches reach the anterior sacral foramen and supply the
structures within the sacral canal. Our first case, the sacral DAVFs located at the
left S1 root sleeve and supplied by the left LSA.
Brinjikji et al.[[25 ]] studied and reviewed spinal dural and epidural AVFs and found that dural and epidural
AVFs with intradural venous drainage at lower lumbar and sacral level usually drain
through the vein of the filum terminale, the only intradural venous structure below
the L2 vertebral body. The presence of a dilated vein of the filum terminale, identified
as a curvilinear flow void on T2-weighted images, could be an imaging marker for lower
lumbar and sacral fistulas. This finding can be used to facilitate to reduce radiation
exposure and contrast dose. Fortunately, MRI of the lumbosacral spine in both our
cases could be detected curvilinear flow voids even through perimedullary flow voids
could barely be seen.
We reviewed the published case reports and series which have enough clinical description
and clearly demonstrated figures of SDAVFs associated with lumbosacral disc herniation
and/or spinal canal stenosis. The collected data in this review include demographic
data (i.e., gender and age of patient), symptoms and signs, level of disc herniation
and/or spinal canal stenosis, previous history of spinal surgery, location and artery
supply of the fistulas, treatment, and neurological outcome of the patients [[Table 1 ]].[[8 ]],[[16 ]],[[17 ]],[[18 ]],[[19 ]],[[20 ]],[[22 ]],[[23 ]],[[26 ]] From the literature review, there were 11 cases including our two cases. All patients
were male with a median age of 54 years, range 27–79 years. The symptoms and signs
of the fistulas included chronic low back pain, sciatica pain, claudication, paresthesia,
gait disturbance, progressive paraparesis, and/or bowel and bladder dysfunction. Eight
(72.7%) patients underwent previous spine surgery. Most SDAVFs were located around
or at the level of disc herniation, spinal stenosis, and/or spondylolisthesis, range
L1-S1. All fistulas were supplied by lumbar artery, iliolumbar artery, and/or LSA.
Surgical treatment was performed in three patients, endovascular treatment in three,
and combination of surgical and endovascular treatments in four. Most patients resulted
in good neurological outcome. Five of 11 patients, including our first case, had delayed
or missed diagnosis of SDAVFs.[[19 ]],[[20 ]],[[22 ]],[[23 ]]
Table 1: Literature review of spinal dural arteriovenous fistulas associated with lumbosacral
disc herniation and/or spinal canal stenosis
The exact mechanism of the development of SDAVFs remains unclear. Acquired SDAVFs
have been reported to develop secondarily to trauma. Kang et al.[[14 ]] reported a 60-year-old female with the SDAVF located at the same level of a fracture
L1 vertebral body. They found that all the feeding arteries, including right L1 radicular
and T12 intercostal arteries, linked to the affected area and speculated that the
SDAVF may result from the damage of the spinal radicular artery by fracture. Vankan
et al.[[15 ]] also reported the possibility of a SDAVF at the level of C1 occurring following
an upper cervical spine fracture in a young male. It is likely that this traumatic
fracture caused microtears of the arterial wall of the affected radiculomeningeal
artery and produced an AVF. In addition, they speculated that establishing an abnormal
shunt may cause by thrombosis of the perimedullary veins. Recently, Kanematsu et al.[[27 ]] described a middle-aged male with an acquired cervical DAVF as a late complication
after cervical anterior fusion. The radiologic findings, obtained 2 years before the
initial operation, clearly showed no evidence of SDAVF. They also reviewed all previously
published cases of secondary SDAVF following spinal surgery and found that some spinal
epidural AVFs with or without intradural venous drainage have been recognized after
lumbar surgeries.
Some reports have described a SDAVF secondary to some trauma from previous surgery.
Since 1985, Burguet et al.[[16 ]] reported a young male with SDAVF at the right S1 nerve root, occurred 2 years after
discectomy L5-S1. The strongly increased perimedullary venous pressure in the absence
of any normal epidural venous drainage is considered the main pathogenesis of clinical
symptoms. They speculated that the possibility of an acquired origin of this fistula
may relate to the previous discectomy, damaging epidural veins, resulting in inefficient
venous drainage. Several years later, Yoshino et al.[[17 ]] presented the radiographic evidence of formation of the SDAVF occurring at the
same level of previous lumbar discectomy combined with spinal fusion. The investigation,
obtained 7 years prior lumbar surgery, clearly showed no abnormal intradural vascular
anomaly. They speculated that these operations might have induced thrombosis in the
radicular vein or impairment of venous return. Asakuno et al.[[18 ]] also reported a 60-year-old male with a SDAVF, developed at the site S1 nerve root
sleeve damage as a result of lumbar disc extrusion. They demonstrated that MRI obtained
before the discectomy showed no abnormalities. However, he had started to experience
dysesthesia in both legs and progressive gait and urinary disturbances 1 year after
the discectomy. MRI, obtained 2.5 years following the discectomy, revealed venous
congestion extending from the conus medullaris to the level of T6. This SDAVF was
supplied by the LSA. During surgical treatment for obliteration of the SDAVF, intraoperative
findings demonstrated a thick fibrous scar tissue covering around an area of the fistula
at the site of the previous discectomy. They speculated that an injury to the nerve
root sleeve may result in the formation of this fistula.
In our literature review, seven patients, including our two cases, had preexistent
fistulas coexisting with degenerative lumbosacral spondylosis.[[8 ]],[[19 ]],[[22 ]],[[23 ]],[[26 ]] Stevens et al.[[22 ]] reported a middle-aged male with a preexistent, asymptomatic SDAVF that became
acutely symptomatic after lumbar discectomy. MRI of the lumbosacral spine obtained
before the surgery clearly demonstrated increased signal intensity within the conus
medullaris and perimedullary flow voids. Nishimura et al.[[8 ]] described an elderly male with isthmic spondylolisthesis with severe canal stenosis
that may give rise to the secondary SDAVF at the same level. They speculated that
a SDAVF formation may develop as a consequence of any sort of trauma or inflammation
associated with segmental instability inducing direct nerve root injury or impairment
of venous return. Furthermore, they suggested that both the spinal dural AVF and the
underlying pathology should be considered the concomitant treatment. Verma et al.[[23 ]] reported a middle-aged male presented with chronic low back pain and new-onset
left radiculopathy of L2. The patient underwent a left-sided L1–L2 neuroforaminal
decompression and discectomy owing to a large disc extrusion causing severe compression
of the left L2 nerve root. Ten weeks after the operation, he suffered from recurrent
symptoms and obtained follow-up MRI of the lumbar spine, suggesting a new disc extrusion.
Due to previous extensive bleeding during previous surgery, there was concern for
a vascular etiology. Therefore, spinal angiography was performed and demonstrated
SDVAF at the level of L1-2, successfully treated by microsurgical resection with good
results. Brinjikji et al.[[19 ]] clearly demonstrated SDAVF, supplied by L2 radiculomeningeal artery, associated
with severe spinal stenosis L1-5 in a 68-year-old male. Alvarado et al.[[26 ]] reported sacral DAVF in a 69-year-old male presenting with long-standing low back
pain and acute exacerbation of myelopathy 2 years before presentation. MRI of the
lumbosacral spine clearly demonstrated severe spinal canal stenosis L3-5.
Previously, we published and reviewed the studies about acquired FTAVFs in association
with degenerative lumbosacral spinal canal stenosis.[[28 ]],[[29 ]] We found that the FTAVFs were located around or at the level of spinal canal stenosis
and speculated that severe spinal canal stenosis may induce local injury or inflammation
to the filum terminale and produce fistulous formation. In addition, the formation
of the fistula may be induced from blocked or impaired venous drainage owing to severe
spinal canal stenosis. Similarly, it seems plausible that disc herniation and spinal
stenosis, occurring at the same level of the fistula, are environmental factors leading
to local injury to affected nerve root sleeve and/or impairment of venous outflow,
resulting in the formation of SDAVF in the present study.
SDAVFs can be treated by surgery, endovascular treatment, or combined approach depends
on institutions preference.[[4 ]],[[5 ]],[[13 ]],[[18 ]],[[26 ]] The goal of treatment of SDAVF is to obliterate the fistula, including the proximal
portion of the draining vein, without excision of the dilated venous plexus.[[6 ]] Endovascular treatment has a chance of recanalization or recurrence of the fistula
more than surgery.[[10 ]],[[13 ]],[[30 ]] Despite more invasive technique, surgical interruption of the intradural proximal
draining vein is a promising method for the treatment of the SDAVFS without recurrence.[[10 ]] A favorable result could be achieved by surgical treatment before endovascular
treatment, especially in patients with poor functional status or micturition dysregulation
at diagnosis.[[21 ]]
The potential for functional outcome was poor despite successful obliteration of the
fistula and prolonged rehabilitation treatment in late diagnosis of SDAVF. Therefore,
early diagnosis of SDAVF and promptly intervention treatment may result in better
prognosis.[[20 ]] SDAVFs associated with lumbosacral disc herniation and/or spinal canal stenosis
should be suspected when the patients develop progressive myelopathy and/or bowel/bladder
dysfunction. MRI scans should be inspected carefully for the evidence of the fistula,
including increased T2 hyperintensity in spinal cord from the conus medullaris extending
up to thoracic level, abnormal curvilinear intradural flow void, and/or perimedullary
flow voids. Spinal MRA and/or angiography may be required to confirm this possibility.
Conclusion
SDAVFs are widely accepted to be an acquired in origin due to symptomatic onset in
adulthood. The exact etiology of SDAVFs remains unclear. SDAVFs at the level of lower
lumbar or sacral region are rare. It has been reported that some trauma from the previous
surgery resulted in the development of these diseases. Our two case reports may provide
additional evidence supporting an acquired etiology of SDAVFs, probably secondary
to lumbosacral disc herniation and spinal canal stenosis. From our review, the level
of SDAVFs in most patients is correlated with the level of disc herniation, spondylolisthesis,
and/or spinal canal stenosis. It seems plausible that disc herniation and spinal stenosis
are environmental factors leading to local injury to affected nerve root sleeve and/or
impairment of venous outflow, resulting in the formation of SDAVF. It should be aware
of SDAVF when the patients have disc herniation and/or spinal stenosis.
Consent
The patients have given consent to be enrolled and have their data published.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms.
In the form, the patients have given their consent for their images and other clinical
information to be reported in the journal. The patients understood that name and initials
will not be published, and due efforts will be made to conceal identity, but anonymity
cannot be guaranteed.
