S p i n e a n d S p i n a l C o rd

E m e r g e n c i e s : Va s c u l a r
a n d I n f e c t i o u s Ca u s e s
Vincent Y. Wanga, Dean Choua and Cynthia Chinb,*

KEYWORDS
 Spinal cord emergencies  Spine infections
 Spine vascular emergencies

EPIDURAL ABSCESS 60% of patients.1,3,8 Therefore, many patients do

not seek medical treatment with the onset of symp-
Spinal epidural abscess can develop primarily or toms and a delay in diagnosis is not uncommon.4,9
after spinal surgery. Primary spinal epidural In terms of location, epidural abscess can occur
abscess is a rare entity, with an estimated preva- in all 3 regions of the spine (cervical, thoracic, and
lence of 0.2 to 2.0 cases per 10,000 hospital admis- lumbosacral). Of the 3 regions of the spine, the
sions.1 However, its incidence has increased over thoracic and the lumbosacral regions are affected
the last 20 years as a result of better diagnostic more commonly than the cervical spine.1,5,8 There
methods, an aging population, an increase in the are also cases of a spinal epidural abscess
number of patients with medical comorbidities, involving the entire spine.8,10
and an increase in intravenous drug use.1,2 Most The spinal epidural abscess can cause neuro-
cases occur in middle-aged to elderly adults, with logic deficits by either direct compression or by
a predilection for men.1e3 Risk factors include dia- vascular compromise through thrombophlebitis
betes, intravenous drug use, previous invasive or thrombosis.11 Thus, sudden neurologic deterio-
procedures to the spine, superficial infections of ration can occur and prompt diagnosis is impor-
the back, immunocompromised state, and infec- tant. MR imaging is the initial study of choice for
tions at distant sites.1e4 Staphylococcus aureus is identifying a spinal epidural process of any
the most common pathogen and is found in approx- etiology. In the case of an abscess, the diagnosis
imately 70% of cases.1e3,5 Gram-negative rods is often straightforward: isointense or hypointense
were previously reported to be associated with on T1-weighted images and hyperintense on T2-
a significant number of spinal epidural abscesses weighted images.3,8 The collection usually partially
and vertebral osteomyelitis; however, its preva- enhances with gadolinium-based intravenous
lence has been decreasing over the years.1,6 In contrast media (Gad).3,8 The fluid portion of the
rare cases, other pathogens, such as tuberculosis, abscess is typically hyperintense on T2-weighted
fungal, and parasitic agents, can also be associated images.12 The enhancement pattern sometimes
with a spinal epidural abscess.1,7 helps to define the consistency of the collection.
The classic clinical triad of fever, back pain, and Specifically, liquid purulent material is associated
neurologic deficits is found in only a small fraction with a central area of low T1 signal intensity;
of patients.2 Almost all patients have back pain, whereas, a rim of tissue that enhances after
but fever occurs in only about two-thirds of Gad represents granulation tissue.12 Recently,
patients, and neurologic deficits occur in 25% to diffusion-weighted imaging (DWI) has been used
neuroimaging.theclinics.com

a
Department of Neurological Surgery, University of California, 505 Parnassus Avenue, MS112, San Francisco,
CA 94143, USA
b
Section of Neuroradiology, Department of Radiology, University of California, San Francisco, San Francisco,
CA 94143, USA
* Corresponding author.
E-mail address: cynthia.chin@radiology.ucsf.edu

Neuroimag Clin N Am 20 (2010) 639–650

doi:10.1016/j.nic.2010.07.006
1052-5149/10/$ e see front matter Ó 2010 Elsevier Inc. All rights reserved.
640 Wang et al

in the spine; on DWI, the abscess is markedly

hyperintense to the surrounding tissue and hypo-
intense on the apparent diffusion coefficient map
(Fig. 1).13 More than 80% of patients with spinal
epidural abscess have concomitant osteomye-
litis.2,3 Therefore, in patients with a suspected
spinal epidural abscess, it is important to look for
additional findings of osteomyelitis or diskitis.
Patients who are unable to undergo MR imaging
can be studied with CT myelography (CTM), which
has been shown to have similar sensitivity to MR
imaging for detecting an epidural abscess.14 MR
imaging has the advantage of being more specific
in its ability to differentiate the epidural mass from
other pathologies. In addition, it is superior for
evaluating the adjacent paraspinal soft tissues.
Moreover, CTM requires intrathecal injection of
contrast material and therefore has the theoretical
risk of introducing the infectious agents into the
intrathecal space in cases of lumbosacral
abscess. Nevertheless, CTM may be an alternative
diagnostic method for patients who are unable to
undergo an MR imaging examination and for
patients in whom MR imaging may be difficult to
interpret because of previous spinal instrumenta-
tion. Although MR imaging, and to a lesser extent
CTM, is a key diagnostic study to establish the
diagnosis of a spinal epidural abscess, plain radio-
graphs or CT of the spine are often the first diag-
nostic tests that are obtained, especially in
patients who are afebrile without neurologic defi-
cits. Surgical decompression with antibiotic treat-
ment have historically been the mainstay of Fig. 1. Methicillin-resistant Staphylococcus aureus
treatment for spinal epidural abscess.1e5,8 spinal epidural abscess. 58-year-old man with dia-
Recently, nonsurgical treatment has been used betes with progressive weakness. Sagittal fast spin
to treat patients with no neurologic deficits, signif- echo T2 (A) and postgadolinium T1 with fat saturation
icant comorbidities, or complete spinal cord injury (B) sequences through the cervical spine demonstrate
at the affected level below the level of epidural extensive circumferential peripherally enhancing
abscess.2,3 epidural abscess (arrow) with cord compression and
associated cord edema (asterisk). Sagittal diffusion-
weighted imaging (C) demonstrates increased signal,
and apparent diffusion coefficient map (D) demon-
EPIDURAL HEMATOMA strates decreased signal (arrows) relative to cerebro-
spinal fluid (asterisk) compatible with reduced
Spinal epidural hematoma (EDH) can compress diffusion within the epidural abscess.
the spinal cord or nerve roots and result in neuro-
logic deficits. Spinal EDHs occur most commonly
after spinal surgery.15 After discectomy or decom- and coagulopathy (increased international normal-
pression, EDH can be identified in 33% to 100% of ized ratio).
the patients when evaluated by postoperative CT In contrast, spontaneous EDHs of the spine are
or MR imaging.15 However, despite the radio- rare. The incidence of spontaneous spinal epidural
graphic appearance of compression by many of hematomas is estimated to be 0.1/100,000 popu-
these lesions, neurologic symptoms associated lation per year.16 They usually occur in older
with postoperative EDH are extremely rare.15 It is patients (aged 50e80 years) with a slight predom-
estimated that the incidence of symptomatic inance of male patients.16 Limited evidence
EDH after spinal surgery is only 0.1% to 0.2%.15 suggests that the spontaneous spinal EDH is
Risk factors associated with EDH formation caused by bleeding from the valveless venous
include advanced patient age, multilevel surgery, plexus, although some investigators postulate
 Spine Emergencies 641

that arterial rupture may be the cause.16 In most hematoma can have homogenous or heteroge-
cases, there is no clear source of hemorrhage or neous hyperintensity on T2-weighted images.20
a causative event. There have been several case Atypical appearance of the hematoma usually
reports of spinal epidural hematomas occurring involves a shift from isointense to hyperintense
after chiropractic manipulation, epidural anes- on T1-weighted images.20 Importantly, the acute
thesia, and steroid injection.17,18 The incidence of spinal EDH should not enhance with gadolinium-
spinal EDH after chiropractic manipulation is based intravenous contrast media.20 In one series
extremely low, with fewer than 10 cases reported of 19 subjects with a diagnosis of spinal EDH, 2
in the literature.17 The risk of spinal EDH after cases showed Gad enhancement on MR imaging
epidural anesthesia is also low, estimated to be and the intraoperative findings revealed that
about 1:220,000.19 It is thought that coagulopathy neither case was an EDH.20 Most hematomas
increases the risk of spinal EDH in these latter occur in the cervical or the thoracic region
cases.17,18 (Fig. 2).18
The classic clinical presentation of a spinal EDH In the majority of cases, emergent surgical evac-
consists of the sudden onset of back or neck pain. uation of the hematoma is the treatment of choice.
Neurologic symptoms related to the compression Patients with small hematomas and without neuro-
of nerve roots or spinal cord may also occur.20 logic deficit may be managed conservatively.17,20
Many pathologic conditions, including interverte- For patients with neurologic deficits, it is important
bral disc herniation, infection, pathologic fractures to remove the hematoma. Further, because neuro-
associated with tumor, transverse myelitis, and logic improvement has been observed even in
other vascular malformations, may mimic the clin- patients presenting with complete injury, prompt
ical presentation of a spinal EDH. Therefore, recognition, diagnosis, and treatment are essential
prompt evaluation with MR imaging is important for the optimal management of the spinal EDH.20
to establish the diagnosis.
The typical imaging appearance of an acute
ARTERIOVENOUS SHUNTS
spinal EDH is that of a homogenously isointense
to hyperintense mass on T1-weighted images, Arteriovenous shunts and vascular malformations
and hyperintensity on T2-weighted images.20 The in the spinal cord region are classified based on

Fig. 2. Spontaneous epidural hematoma. 3-year-old healthy girl with 4-day history of back pain progressing to
lower extremity weakness and inability to ambulate. Sagittal T1 (A) fast spin echo T2 (B) and postgadolinium
T1 with fat saturation (C) images of the cervical spine demonstrate extensive nonenhancing dorsal epidural
hematoma compressing the spinal cord. A hematocrit level is present within the epidural hematoma (asterisks).
642 Wang et al

their nidus location, vascular supply, and drainage complaints of back pain or radicular pain, followed
pattern. In one of the most commonly used classi- by progressive lower-extremity paresis, and bowel
fications, developed by Oldfield and Doppman, and bladder sphincter dysfunction.22,25,26 Hemor-
the lesions are divided into 4 types:21 rhage is extremely rare.22,26 Histologically, spinal
DAVFs are supplied by a normal dural branch
Type I lesions are the typical dural arteriove- artery and drain into a single, dilated vein.27 This
nous fistula (DAVF), and usually arise near drainage results in retrograde flow into the venous
nerve roots. plexus surrounding the spinal cord. Physiologic
Type II lesions are glomus arteriovenous mal- studies have shown that venous pressure is
formations (AVM), with a mass of dysmor- approximately 75% of systemic arterial pres-
phic arteries and veins without an sure.25 The resultant venous hypertension and
intervening capillary bed. These lesions venous congestion cause a reduction in the
can be partial or entirely intramedullary. arterial-venous pressure gradient, and thus
Type III lesions are juvenile AVMs that are a reduction in tissue perfusion pressure. A reduc-
composed of a network of arteries and tion in tissue perfusion pressure then leads to
veins, without an obvious nidus. These hypoxia, and further vasodilation may occur as
lesions can be extensive and involve the a result of autoregulation.22 Eventually, compen-
spinal cord, spine, and paravertebral tissue. satory mechanisms from autoregulation are ex-
Type IV lesions are perimedullary DAVF. hausted, the spinal cord tissue becomes
Combined, these 4 types of arteriovenous ischemic. Cord edema and progressive loss of
shunts or vascular malformations account for 3% function then develops.
to 16% of all space-occupying lesions of the spinal Although most patients present with progres-
cord, with the Type 1 DAVF being the most sive myelopathy, acute worsening of motor or
common.22 Each of these types are subsequently sphincter function can also occur.24 It is important
discussed. to evaluate patients with an unclear cause of
Spinal vascular malformations/arteriovenous myelopathy, because 50% of untreated patients
shunts can cause neurologic symptoms by 3 with a spinal DAVF can become disabled in 3
mechanisms: years.28 MR imaging is the initial screening test
of choice, and it is important to obtain a whole-
1. These lesions can cause acute neurologic spine MR imaging survey because there can be
symptoms by hemorrhage, and the risk of a discrepancy between the location of the spinal
hemorrhage varies for the 4 types of lesions. DAVF and the spinal level as suggested by clinical
2. Spinal vascular malformations and arteriove- signs and symptoms.28 The most common finding
nous shunts can result in venous hypertension. on MR imaging in patients with DAVF is abnormal
Venous hypertension, in turn, can lead to T2 signal hyperintensity within the cord.22,28 There
reduced perfusion, and thus ischemia. can also be enlargement of the cord, consistent
3. They can cause symptoms by direct mass with swelling from cord edema.29 The T2 signal
effect, resulting in a progressive myelopathy changes can be extensive, extending over 6 to
or radiculopathy. 7 vertebral levels in some cases.30 Occasionally,
prominent, lacelike tortuous and ectatic flow
In one study of 78 subjects with myelopathy of
voids may be seen.22,31 There can also be
unknown cause, 22 subjects had an AVM on angi-
nonspecific enhancement with Gad contrast
ography.23 Importantly, 5 subjects in this series
(Fig. 3).22
had previous MR imaging that was interpreted as
None of the aforementioned imaging findings
normal.23
are specific for DAVF. The current gold standard
for imaging the DAVF is with digital subtraction
Type I: Dural Arterial Venous Fistula
angiography (DSA). Angiography allows a clear
The spinal dural arterial venous fistula is an definition of the anatomy of the DAVF, including
acquired arteriovenous shunt in the dura.22 It is its location, arterial supply, and venous drainage
most commonly located near the exiting nerve pattern.22,24e26 In some cases, the DAVF can
root.22 In some cases, the fistulous vessel may obtain arterial supply from 2 arteries located in
penetrate the dura at a more distant site and adjacent nerve roots.22 One of the most important
have a significant extradural component.24 Spinal angiographic details to assess is the origin of the
DAVFs usually present in adults after the fourth anterior spinal artery. If the anterior spinal artery
or the fifth decade, have a significant male shares a common origin with the supply to the
predominance, and most commonly affect the DAVF, then the DAVF is not amendable to endo-
thoracic spine.22 Patients often present with vague vascular treatment.25
 Spine Emergencies 643

and the fistula was only identified at surgery.33 In

a more recent report, Si-jia and colleagues31 noted
that the spinal DAVF could be readily identified by
MDCT angiography using a 64-row detector. In
their series of 9 subjects, all of the draining veins
were identified, and in 7 of 9 subjects, the feeding
artery was also found.31 Another recent study by
Yamaguchi and colleagues34 evaluated 10
subjects with 16-row detector MDCT angiography
and DSA. Dilated perimedullary veins were found
in all 10 subjects, focal enhancement of nerve
root and intradural draining veins were noted in 8
subjects, and localization of the feeding artery
was correctly depicted in 6 subjects. In 2 subjects,
there were additional feeding arteries from the
contralateral side that were not depicted on the
MDCT angiography but were visualized on
conventional angiography.34 Although these find-
ings are promising in that MDCT angiography
can reveal a spinal DAVF, the temporal and spatial
resolution of MDCT is still inferior to that of DSA.
Fig. 3. Spinal dural arterial venous fistula. 65-year-old Therefore, the anterior or posterior spinal artery
man with progressive lower extremity weakness. cannot be distinguished easily from that of the
Sagittal fast spin echo T2 (A) images of the thoracic
feeding artery.29,31 In addition, the field of view is
cord demonstrate extensive cord edema (asterisk)
often more limited and it is difficult separating the
with flow voids along the dorsal spinal cord (black
arrows). There is associated cord enhancement arterial from venous phase.29 MDCT angiography
demonstrated on sagittal postgadolinium T1 fat satu- also exposes patients to radiation.
rated sequences (B). MR angiography (MRA) has been gaining atten-
tion in the diagnosis of spinal DAVFs. Rapid multi-
phase dynamic MRA with gadolinium and parallel
Although DSA provides high temporal and imaging can achieve better temporal and spatial
spatial resolution imaging information of the resolution than MDCT angiography.29 However,
DAVF, it is not without its drawbacks. DSA is often increase in temporal resolution may come at an
time consuming, as many as 40 injections can be expense of the spatial resolution and signal-to-
needed to catheterize the bilateral intercostal, noise ratio is reduced.30 Using time-resolved
lumbar, and sacral arteries.30 This procedure MRA, Ali and colleagues30 studied 12 subjects
requires a high dose of iodinated contrast and with suspected DAVF based on clinical symptoms
increased radiation exposure. In addition, each and MR imaging findings. In 6 subjects with
catheterization also poses a small risk of vascular a DAVF confirmed by DSA, all of them also demon-
injury and can cause transient neurologic symp- strated arteriovenous shunting on the time-
toms.31 Thus, there is interest in developing nonin- resolved MRA.30 Furthermore, the location of the
vasive imaging technology to optimally evaluate arteriovenous shunting identified on MRA was
the spinal DAVF. Two main technologies, CT angi- within one vertebral level as identified on DSA.30
ography and MR angiography, have shown some Others have used contrast-enhanced MRA to
promising developments. Lai and colleagues32 re- study DAVFs. Using elliptic centric contrast-
ported their experience of 8 subjects with 16-row enhanced MRA, Luetmer and colleagues35 de-
multidetector CT (MDCT) angiography for DAVF. picted DAVFs in 20 out of 22 subjects who had
In all 8 subjects, MDCT angiography correctly DAVFs identified on conventional angiography. In
identified the enlarged radiculomedullary draining 14 subjects, the level of the fistula was within the
vein, the fistula, and the feeding artery.32 Only 1 volume of imaging, and MRA correctly located
subject had an additional feeding artery identified the fistula to within one level of the spine in 13
on the subsequent DSA that was not identified subjects.35 However, MRA does not always
on the MDCT angiography.32 Similarly, Yamaguchi correctly identify the type of lesion. In one case,
and colleagues33 reported the successful identifi- Sharma and Westesson reported that although
cation of 2 out of 3 subjects with a DAVF. In the the MRA showed a convincing type I DAVF, subse-
one case where MDCT angiography failed to iden- quent conventional angiography revealed a type IV
tify the fistula, DSA also failed to identify the DAVF, perimedullary AVF.36
644 Wang et al

Although both MDCT angiography and MRA rebleeding rate if the AVM is not treated; therefore,
show promising results, they are still considered prompt recognition and treatment is warranted.22
to be inferior to conventional angiography; MR imaging is currently the imaging modality of
however, both techniques help demonstrate the choice for the initial evaluation of spinal AVMs. MR
location of the fistula, which may minimize the imaging may show areas of low signal intensity in
number of catheterizations during DSA. Further- the center of the cord (representing either vascular
more, newer techniques will continue to improve flow voids or blood products) and hyperintensity
the temporal and spatial resolution of MDCT and on T2-weighted images.22 Moreover, MR imaging
MRA. These developments may one day enable can show the relationship between the lesion and
these noninvasive techniques to become the the spinal cord and dura, identify recent or remote
primary diagnostic modality for studying spinal hemorrhage and thrombosis, and reveal any para-
DAVFs. vertebral involvement (Fig. 4).22
Because of the potential for neurologic deterio- DSA remains the definitive test for the diagnosis
ration over time, prompt treatment of the spinal and treatment planning of spinal AVMs. The goal
DAVF is advocated. Microsurgery has been the of angiography is to define the normal vasculature
traditional method of treatment. In one meta- around the lesion as well as the diseased vascula-
analysis, Steinmetz and colleagues37 showed ture of the lesion. Features to look for include peri-
a 98% success rate of fistula obliteration with medullary and intramedullary anastomoses, direct
microsurgery. During recent years, endovascular and indirect AVM supply, collateral recruitment,
treatment has also been used to treat spinal associated aneurysms and pseudoaneurysms,
DAVFs. Although early experience demonstrated venous drainage, and normal spinal cord vascular
only limited success, with an overall success rate supply.
of only 46%, recent advances in embolization The goals of treatment include preservation of
material and the possibility of being able to neurologic function and minimization of rebleeding.
perform the treatment during the same setting of Treatment options include surgical excision, endo-
the diagnostic angiogram make endovascular vascular obliteration, or conservative manage-
therapy an option employed as a first line of treat- ment. Spetzler and colleagues40 reported that
ment.25,37,38 Surgical treatment can then be per- 92% of subjects who underwent surgery had
formed if endovascular therapy is unsuccessful complete resection, with 68% of subjects experi-
or contraindicated. In addition, endovascular encing neurologic improvement and 29% of
treatment is not advised for patients with a feeding subjects remaining neurologically unchanged.
artery that shares a common origin with the ante- Others have reported favorable experience with
rior or posterior spinal artery.25 endovascular treatment. For example, Da Costa
and colleagues22 reported that in a series of 47
subjects with spinal AVMs treated with endovascu-
lar obliteration, 77% of subjects had a favorable
Type II: Glomus Arteriovenous Malformation
result, with about half of the subjects achieving
Type II lesions, or glomus AVMs, have a nidus that complete obliteration. However, 22% of subjects
is located completely or partially within the spinal experienced procedure-related complications,
cord.25 These AVMs can be supplied by either with 50% being permanent.22 Conservative
the ventral radiculomedullary or anterior spinal therapy includes physical therapy, pain control,
arteries, or the dorsal radiculopial or posterior and possible anticoagulation in patients with
spinal arteries.22 In 20% to 40% of cases, there thrombosis.22
is an associated arterial or venous aneurysm.25
In 20% of cases, the AVMs are supplied by
Type III: Juvenile Metameric Vascular
multiple shunts.22
Malformation
Compared with the Type I spinal DAVF, the Type
II glomus AVM tends to present in younger age, Type III lesions, also known as juvenile vascular
usually in young adults aged 20 to 30 years.22,25 malformations or metameric vascular malforma-
In 20% of cases, it affects pediatric patients.22 In tions, are large, high-flow lesions with involvement
one series of pediatric subjects with spinal of the paraspinal tissues.25,40 These are
vascular malformations/arteriovenous shunts, uncommon lesions; among the 48 AVMs treated
AVMs were found in 44% of the subjects, repre- surgically by Spetzler and colleagues,40 only 5
senting the most common vascular malformation were metameric vascular malformations. Similarly,
in children.39 Also, unlike the DAVF, AVM most in a series of 72 pediatric subjects with spinal
commonly presents with hemorrhage and sudden vascular malformations/arteriovenous shunts,
onset of neurologic symptoms.22 There is a high only 3 had paravertebral tissue involvement.39 As
 Spine Emergencies 645

Fig. 4. Glomus arteriovenous malformation. 21-year-old man with right leg weakness. Sagittal (A) and axial (B)
fast spin echo T2 sequences of the cervical spine demonstrate cord expansion, intramedullary edema, and flow
voids (arrows) with associated enhancement on postgadolinium sagittal (D) and axial (E) T1 fat saturated images.
Axial gradient echo sequence (C) shows evidence of cord hemorrhage (asterisk).

the name implies, these lesions commonly present Type IV: Perimedullary Arteriovenous Fistula
in the pediatric population. Neurologic deficits
The perimedullary AVF is usually located in the
occur from compression, hemorrhage, or vascular
midline and ventrally in the subarachnoid space.40
steal phenomenon.40 MR imaging remains the
The lesion consists of an abnormal connection
initial diagnostic modality of choice, because it
between the anterior spinal artery and an enlarged
nicely reveals the extent of the lesion in the para-
venous network.25,40 Blood flow through the lesion
vertebral tissue. DSA reveals the flow dynamics
can be rapid, and therefore flow-related acquired
and feeder pattern, which are essential for treat-
lesions, such as aneurysms or ectatic venous mal-
ment planning. A multidisciplinary approach is
formations, can develop.25,40 They most
often required to address these lesions, with
commonly present in young adulthood, but they
a combination of embolization and surgical resec-
can also present in the pediatric population.39,41
tion; however, complete resection and obliteration
The most common presentation is a progressive
is often difficult without incurring significant neuro-
myelopathy, but rupture of an associated
logic morbidity.40
646 Wang et al

aneurysm resulting in hemorrhage can also be the the anatomy and flow dynamics of the arterial
first sign and symptom.41 feeders, fistulas, draining veins, and associated
Perimedullary AVFs have been further subclas- aneurysms.
sified into 3 subtypes. Type I perimedullary AVF Treatment is often advised for patients with peri-
are small, with a single feeder and low flow fistula, medullary AVFs because untreated lesions may
and mild to moderate venous hypertension.25,41 lead to progressive myelopathy and eventually
Type II perimedullary AVFs are larger, supplied paralysis.41 Type I perimedullary AVFs are small
by 1 or 2 spinal medullary arteries, and have and are bested treated with surgery.25,41 For
a more rapid transit time.41 Type III perimedullary Type II lesions with multiple feeders, a combination
AVFs are the most common. These are giant of endovascular therapy and surgery should be
lesions with multiple dilated feeding arteries and used.25,41 For the giant Type III lesions, it is recom-
rapid transiting. The fistula drains into greatly mended that these lesions be first treated endo-
dilated and dysplastic veins.25,41 vascularly , and reserve surgery for patients who
As with all other vascular malformations, MR fail endovascular treatment.25,41
imaging and conventional angiography remain
the primary mode of diagnostics. MR imaging SPINAL CORD INFARCT
may demonstrate T2-hyperintensity within the
spinal cord caused by venous hypertension and Spinal cord infarction is rare in comparison to
edema. Intradural signal voids can often be seen, infarction of brain tissue, comprising only 1% of
which represent dilated vascular structures all strokes.42 It is a disease that typically affects
(Fig. 5).41 More recently, MDCT angiography has older adults.42e44 Most patients experience pain
also been shown to be effective in correctly diag- before the onset of neurologic symptoms.42,43
nosing the perimedullary AVF.31 The gold standard Symptoms usually develop quickly, although
of evaluation, however, is still DSA to best evaluate some patients may experience a transient

Fig. 5. Perimedullary arteriovenous malformation. 13-year-old boy with abrupt onset of back pain and lower
extremity weakness. Sagittal and axial fast spin echo T2 (A, C) and postgadolinium T1 fat saturated (B, D)
sequences of the lumbar spine demonstrate focal hemorrhage within the conus (asterisk) with numerous prom-
inent, dilated enhancing vessels (arrows).
 Spine Emergencies 647

ischemic attack before the actual spinal cord but they are extremely rare in the upper thoracic
infarct.42,43 There are 2 potential pathophysiolog- spine.42,43 The most common pattern involves
ical mechanisms for spinal cord infarction: (1) hy- the anterior spinal artery (unilateral or bilateral).
poperfusion from arterial insufficiency and Other infarct patterns include the posterior spinal
hypotension, and (2) occlusion of a specific arterial artery territory, a central cord infarct that affects
branch (anterior spinal artery or, sometimes, bilateral spinothalamic tracts without any effect
posterior spinal artery).42 on the motor tracts, and a transverse infarct that
The most common risk factors include aortic results in a complete infarct of the level, resulting
disease and atherosclerosis.45,46 Aortic dissec- in bilateral motor function deficits and complete
tions are associated with an overall 4.2% chance sensory deficits.42,43 MR imaging is the imaging
of having paraparesis or paraplegia as a result of tool of choice for evaluation of patients with sus-
spinal cord infarction.47 Furthermore, aortic pected spinal cord infarct. On sagittal T2-
surgery also carries a significant risk of spinal weighted images, a pencil-like hyperintensity can
cord ischemia, ranging from 1% in the upper and be seen in most patients.44 Cord enlargement
lower levels of the aorta to 10% in the midsection caused by swelling may also be seen.44 In patients
of the aorta, corresponding to the watershed area with an anterior spinal artery infarct, the owl’s sign
of the spinal cord.48 Others have proposed (T2 signal hyperintensity within anterior horns bilat-
a mechanical cause, as disk protrusions, foraminal erally) may be identified (Fig. 6).49 Another imaging
fibrosis, and other degenerative spinal disease finding pointing to a cord infarct as the cause for
may put mechanical stress on a radicular artery.42 an intramedullary signal abnormality is the pres-
It is unclear whether degenerative spinal condi- ence of an adjacent vertebral body infarct.42,43
tions, such as disk protrusions, can directly cause Recently, diffusion weighted imaging has been
radicular artery thrombosis/occlusion, because used to evaluate spinal cord infarction.44 Similar
the prevalence of degenerative spine disease is to ischemic infarction of the brain, acute spinal
high; whereas, spinal cord infarction is so rare. cord infarction also shows restricted diffusion
Degenerative spinal changes may potentially with marked hyperintensity on the DWI sequence
predispose patients to a spinal infarct, but other and a reduction in the apparent diffusion coeffi-
factors likely also contribute, such as a traumatic cient.44 Because DWI changes develop before
event. T2 signal changes, the addition of a diffusion
Spinal cord infarcts occur at about equal sequence may expedite the diagnosis of spinal
frequency in the cervical and thoracolumbar spine, cord infarction (Fig. 7).44 In some cases, DSA is

Fig. 6. Cervical spinal cord infarct and right vertebral artery dissection. 61-year-old woman with right shoulder
weakness progressing to bilateral shoulder and upper extremity weakness. Sagittal (A) and axial (B) fast spin echo
T2 sequences demonstrate mild cord expansion with increased signal within the bilateral anterior horns involving
the anterior spinal artery territory (arrows). There is absence of the normal right vertebral artery flow void
(asterisk).
648 Wang et al

Fig. 7. Spinal cord infarct. 49-year-old man with acute back pain, nausea, and lower extremity weakness. Sagittal
(A) and axial (B) fast spin echo T2 images through the thoracic cord demonstrate increased signal within the bilat-
eral anterior horns involving the anterior spinal artery territory. (C) Sagittal diffusion-weighted imaging demon-
strates reduced diffusion compatible with ischemia (arrows).

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