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1201

Neurologic/Head and Neck Imaging

Incomplete Cord Syndromes:
Clinical and Imaging Review
Vamsi K. Kunam, MD
Vinodkumar Velayudhan, DO The ability to localize the three spinal tracts (corticospinal tract,
Zeshan A. Chaudhry, MBBS spinothalamic tract, and dorsal [posterior] columns) involved in
Matthew Bobinski, MD, PhD incomplete spinal cord syndromes at cross-sectional imaging and
Wendy R. K. Smoker, MD knowledge of the classic clinical manifestations of the various syn-
Deborah L. Reede, MD dromes enable optimized imaging evaluation and provide clinicians
with information that aids in diagnosis and treatment. The requisite
Abbreviations: ASA = anterior spinal artery, knowledge for localizing these tracts is outlined. The authors review
CCS = central cord syndrome, CES = cauda the spinal cord anatomy, blood supply, and course of these tracts
equina syndrome, CMS = conus medullaris syn-
drome, CST = corticospinal tract, DCS = dorsal and describe the various associated syndromes: specifically, dorsal
cord syndrome, IMSCT = intramedullary spinal cord, ventral cord, central cord, Brown-Séquard, conus medul-
cord tumor, ISCS = incomplete spinal cord syn-
drome, LMN = lower motor neuron, PSA = pos- laris, and cauda equina syndromes. In addition, they describe the
terior spinal artery, STT = spinothalamic tract, anatomic basis for the clinical manifestation of each syndrome and
UMN = upper motor neuron, VCS = ventral
cord syndrome
the relevant imaging features of the classic causes of these enti-
ties. Knowledge of the anatomy and clinical findings of the spinal
RadioGraphics 2018; 38:1201–1222
cord is essential for examining and treating patients with cord
https://doi.org/10.1148/rg.2018170178 abnormalities.
Content Codes: ©
RSNA, 2018 • radiographics.rsna.org
From the Department of Radiology, SUNY
Downstate Medical Center, University Hospi-
tal of Brooklyn, 450 Clarkson Ave, Brooklyn,
NY 11203 (V.K.K., V.V., Z.A.C., D.L.R.); De-
partment of Radiology, University of Califor-
nia Davis Health System, Sacramento, Calif Introduction
(M.B.); and Department of Radiology, Univer- The spinal cord serves as a highway for information to travel be-
sity of Iowa Hospital and Clinics, Iowa City,
Iowa (W.R.K.S.). Recipient of a Certificate tween the brain and peripheral nervous system. The information is
of Merit award for an education exhibit at the transmitted by way of highly specialized afferent (traveling toward
2016 RSNA Annual Meeting. Received August
11, 2017; revision requested October 13 and
the cord and relaying sensory information) and efferent (predomi-
received December 11; accepted December 20. nantly motor, traveling away from the cord) pathways, relay neu-
For this journal-based SA-CME activity, the au- rons, and interconnections. Interruption of these pathways results
thors, editor, and reviewers have disclosed no rel-
evant relationships. Address correspondence in development of spinal cord syndromes, which are classified
to V.K.K. (e-mail: [email protected]). neurologically as complete or incomplete. Each of these syndromes
©
RSNA, 2018 has a variety of causes and clinical manifestations.
Complete cord syndrome is caused by lesions involving a whole
SA-CME Learning Objectives spinal cord segment and will cause complete motor, sensory, and
autonomic dysfunction below the level of the lesion (1,2). It has
After completing this journal-based SA-CME
activity, participants will be able to: the worst prognosis for recovery and is due to entities such as cord
■■Describe the anatomy and function of
transection secondary to trauma, severe tumor compression of the
the major neuronal pathways involved in cord, epidural abscess, and acute inflammatory processes such as
incomplete cord syndromes. transverse myelitis.
■■LocalizeISCS lesions in the spinal Incomplete spinal cord syndrome (ISCS) occurs when lesions
cord according to the associated clinical involve specific structural and/or functional anatomic regions of
findings.
the cord, with some preservation of sensory and/or motor function
■■Cite examples of common diseases as-
sociated with each of the six incomplete
below the lesion. There are six basic types of ISCS based on clinical
cord syndromes described in this review. findings: (a) central cord syndrome (CCS), (b) Brown-Séquard
See rsna.org/learning-center-rg. syndrome, (c) ventral (anterior) cord syndrome (VCS), (d) dorsal
(posterior) cord syndrome (DCS), (e) cauda equina syndrome
(CES), and (f) conus medullaris syndrome (CMS) (1,3). Table 1
summarizes these syndromes, including tracts involved, location of
involved lesions, common causes, and typical clinical manifestations.
1202 July-August 2018 radiographics.rsna.org

median fissure anteriorly and a shallower dorsal

Teaching Points median sulcus and septum posteriorly (6).
■■ Damage to neurons in the motor cortex and CST causes
Dorsal nerve roots enter the cord on the pos-
UMN deficits. Injury to neurons in the ventral horns and pe-
ripheral nerves results in lower motor neuron (LMN) deficits. terior cord surface through dorsolateral sulci.
■■ Axons in the CST and STT have a similar laminar somatotopic
Ventral nerve roots emerge from the anterior
arrangement. Axons from the cervical and thoracic segments, cord surface through the ventrolateral sulci
which innervate the upper extremities and thorax, are located (Fig 1) (6). The cord surface topography is best
medially, and axons from the lumbar and sacral segments, demonstrated on axial T2-weighted magnetic
which innervate the abdomen and lower extremities, are po- resonance (MR) images (Fig 1b)—especially
sitioned laterally.
those obtained with heavily T2-weighted gradi-
■■ The second-order neurons in the dorsal horn carrying pain
ent-echo sequences (eg, fast imaging employing
and temperature sensation cross at the anterior spinal com-
missure and ascend as the STT in the contralateral anterolat- steady-state acquisition, constructive interfer-
eral white matter. Among the tracts described, the STT is the ence in steady state, balanced fast field echo,
only one that decussates at the level of the spinal cord. and driven equilibrium)—and computed tomo-
■■ CCS is the most common ISCS. It occurs secondary to injury graphic (CT) myelograms.
or lesions around the central canal. Trauma is the most com- In contrast to the gray matter in the brain, the
mon cause of CCS. gray matter in the spinal cord is located centrally
■■ The primary difference between CMS and CES is in the type and surrounded by white matter columns. The
of motor deficit. CMS causes mixed UMN and LMN deficits,
gray matter appears as an H- or butterfly-shaped
while CES causes a purely LMN deficit.
region in the center of the cord that is relatively
hypointense on T1-weighted MR images and hy-
perintense on T2-weighted and other fluid-sensi-
Knowledge of the spinal cord anatomy and the tive MR images. The peripherally located ascend-
ability to recognize the typical clinical findings of ing and descending white matter columns appear
common spinal cord syndromes are essential for hyperintense to gray matter on T1-weighted
patient examination and treatment. Imaging plays MR images. The central gray matter has ven-
a pivotal role in localizing disease and determin- tral and dorsal extensions (ie, horns) along the
ing the cause, treatment, and prognosis. Herein, entire length of the cord, with small lateral horns
we review the relevant anatomy of three impor- extending from approximately the T1-L1 spinal
tant white matter tracts—corticospinal tract segments (Fig 1a) (6). Dorsal horns are primar-
(CST), spinothalamic tract (STT), and dorsal ily involved in sensory processing and receive
(posterior) columns—the understanding of which primary afferent fibers from the dorsal roots of
is crucial for determining the type of ISCS. spinal nerves. Ventral horns contain motor neu-
rons, and lateral horns contain autonomic nuclei
Spinal Cord Anatomy and interneurons (6). The ventral and dorsal gray
The spinal cord, which is contained within the matter commissures form a horizontal line con-
thecal sac, begins below the foramen magnum necting the arms of the “H” around the central
and ends at the tip of the conus medullaris canal. When visible at MR imaging, the central
(between the T12 and L2-3 disk level), typically canal appears as a thin longitudinally oriented,
ending around the L1 or L1-2 disk level (4). The nonenhancing fluid-signal-intensity structure be-
cord has a tubular shape that on a cross section is tween the ventral one-third and dorsal two-thirds
elliptical in the cervical region and round in the of the cervical or thoracic cord or more centrally
thoracic region. The cord is thickest in two areas in the lumbar region (7,8).
that innervate the limbs: a cervical enlargement White matter in the spinal cord consists of
at the C5-T1 spinal level that innervates the three columns or funiculi—the ventral (ante-
upper extremities, and a smaller lumbar enlarge- rior), lateral, and dorsal (posterior) columns—
ment at the T9-L2 spinal level that innervates the which are bundles of nerve axons that make up
lower extremities and pelvis (5). The spinal cord the neural pathways. The ventral columns are
is divided along its length into 31 spinal segments between the ventral median septum and ventral
that give rise to the spinal nerves: eight cervical, nerve roots. The lateral columns are between
12 thoracic, five lumbar, and five sacral seg- the ventrolateral and dorsolateral sulci, where
ments, and one coccygeal segment. A thin band ventral and dorsal nerve roots enter and exit,
of connective tissue, the filum terminalis, extends respectively. The dorsal columns are between the
from the tip of the conus medullaris through the dorsal median sulcus and dorsolateral sulci on
caudal end of the thecal sac and attaches to the each side (6,9). Ascending sensory and descend-
first coccygeal segment (6). ing motor pathways travel in these columns. It
The spinal cord is nearly completely sepa- is important to know the location, function, and
rated into right and left halves by a deep ventral somatotopic organization of three specific spinal
RG  •  Volume 38  Number 4 Kunam et al  1203

Table 1: Summary of ISCS Features

ISCS Type Tracts Involved Lesion Location Common Causes Typical Clinical Manifestations
Central
 Small Anterior commis- Near the central Syringomyelia, intra- Suspended sensory deficit, clas-
 lesion sure where STT canal medullary tumor, hy- sic cape distribution in lesion
fibers cross perextension injury in of cervical cord
cervical spondylosis
 Large Bilateral STT, Large central Syringomyelia, intra- Disproportionate motor (UMN
 lesion CST, dorsal col- lesion medullary tumor, hy- type) and sensory deficits—
umns (variable), perextension injury in greater in upper extremities
autonomic cen- cervical spondylosis than in lower extremities,
ter, and anterior LMN deficit at level of lesion
horn cells (anterior horn cells), variable
loss of proprioception, auto-
nomic dysfunction
Ventral Bilateral STT, Ventral two- Spinal cord infarction, Loss of pain and temperature
CST, and auto- thirds of cord trauma, multiple scle- sensations, weakness, bladder
nomic center rosis, disk herniation dysfunction
Dorsal Predominately Dorsal one-third Vitamin B12 deficiency, Loss of proprioception and
dorsal columns; of cord multiple sclerosis, vibration sensations, sensory
large lesions tabes dorsalis, AIDS* ataxia with positive Romberg
involve bilateral myelopathy, epidural sign, variable weakness, blad-
CST and bilat- metastases der dysfunction
eral autonomic
fibers (to vari-
able degree)
Brown- Unilateral STT, Hemicord lesion Knife or bullet injury, Ipsilateral weakness (UMN
Séquard CST, and dorsal multiple sclerosis, type) and loss of propriocep-
columns transdural migration tion, contralateral loss of pain
of spinal cord and temperature sensations,
small band of LMN and sen-
sory deficits at level of lesion
Conus Distal spinal cord Spinal cord at Disk herniation, trauma, Bladder or rectal dysfunction,
medullaris containing level of T12 tumors saddle anesthesia, parapare-
lumbosacral seg- through L2 sis (mixed UMN and LMN
ments vertebrae types)
Cauda equina Lumbosacral nerve Lesion compress- Disk herniation, arach- Asymmetric multiradicular pain,
roots in spinal ing or involving noiditis, tumor, lum- leg weakness (purely LMN)
canal nerve roots of bar spine stenosis and sensory loss, bladder
cauda equina dysfunction, areflexia
*AIDS = acquired immunodeficiency syndrome.

pathways when examining patients who have area, and sensory cortex. These fibers descend
incomplete cord syndromes: the CST, dorsal through the cerebral white matter, posterior limb
columns, and STT. Knowing the sites at which of the internal capsule, cerebral peduncle, and
these pathways decussate and their location ventral pons. In the medulla, 75%–90% of the
within the cord cross section is key to identify- fibers in the CST decussate in the pyramid and
ing, at imaging, which of them are involved. continue as the lateral CST in the lateral column
(Fig 2). The neurons of the lateral CST synapse
Corticospinal Tract in the ventral horn before exiting the cord. Ten
The CST is a descending motor tract that controls percent of the axons do not decussate but rather
fine movements and the most important mo- continue as the anterior CST, crossing over to the
tor pathway in humans. It consists of axons from opposite side in each spinal cord segment sup-
upper motor neurons (UMNs), more than 50% plying motor neurons in the ventral horn (Fig
of which arise from the primary motor cortex (ie, 1a). Damage to neurons in the motor cortex and
precentral gyrus), with the remainder contributed CST causes UMN deficits. Injury to neurons in
by the premotor cortex, supplementary motor the ventral horns and peripheral nerves results in
1204  July-August 2018 radiographics.rsna.org

Figure 1.  Axial anatomy of the spinal cord. (a) Drawing illustrates a cross section of the thoracic cord, with central
H- or butterfly-shaped gray matter and peripheral white matter. The central gray matter has a dorsal (posterior)
horn (dark blue) involved in sensory processing, a lateral horn (yellow) containing interneurons and autonomic
nuclei, and a ventral (anterior) horn (pink) that contains motor neurons. White matter tracts—specifically the dorsal
columns (DC), lateral CST, and STT—are located at the periphery. Note the somatotropic organization of fibers
in the CST and STT, from medial to lateral: thoracic (T), lumbar (L), and sacral (S) fibers. Ten percent of the CST
fibers do not decussate and continue ipsilaterally as the anterior CST (). Dorsal and ventral nerve roots enter the
spinal cord at the dorsolateral (straight arrow) and ventrolateral (curved arrow) sulci, respectively. (Reprinted, with
permission, from Jill K. Gregory.) (b) Axial T2-weighted fast imaging employing steady-state acquisition MR image
of the cervical cord shows dorsal nerve roots (arrowheads) at the dorsolateral sulci and ventral nerve roots (arrows)
at the ventrolateral sulci.

Figure 2.  Descending (green arrow) CST.

Drawing depicts axons from the primary mo-
tor cortex in the cerebral hemisphere coursing
through the internal capsule (thin black arrows),
midbrain (not shown), ventral pons (not shown),
and medullary pyramids. Ninety percent of the
fibers cross to the opposite side at the pyramidal
decussation (thick black arrow) and continue as
the lateral CST. The somatotopic organization of
fibers in the CST, from medial to lateral, is as fol-
lows: cervical (C, blue), thoracic (T, pink), lumbar
(L, red), and sacral (S, purple) fibers. (Reprinted,
with permission, from Jill K. Gregory.)

lower motor neuron (LMN) deficits. The impor-

tant differences between UMN and LMN deficits
are outlined in Table 2 (10).
Axons in the CST and STT have a similar
laminar somatotopic arrangement. Axons from
the cervical and thoracic segments, which in-
nervate the upper extremities and thorax, are
located medially, and axons from the lumbar
and sacral segments, which innervate the ab-
domen and lower extremities, are positioned
laterally (6).Therefore, disease originating in
the central spinal cord affects the upper ex-
tremities initially, as the lesion grows outward
(Figs 1a, 2) (3,6,10).

Dorsal Columns
Information about proprioception, vibrating sensa-
tion, and fine-touch sensation travels in the dorsal
(posterior) column. This column consists of two
large ascending tracts: the medial fasciculus graci-
lis and lateral fasciculus cuneatus. The fasciculus
RG  •  Volume 38  Number 4 Kunam et al  1205

Table 2: Findings of UMN versus LMN Deficits

Feature UMN Deficit LMN Deficit

Lesion location Above anterior horn cell (ie, motor cor- Anterior horn cell or distal to anterior horn cell
tex, brainstem, spinal cord) (ie, root, plexus, peripheral nerve)
Muscle tone Increased (spastic paresis) Decreased (flaccid paralysis)
Muscle bulk Maintained or mildly atrophic Severely atrophic
Weakness In legs, greater in flexors than in exten- Depends on location: uniform spinal cord weak-
sors; in arms, greater in extensors ness in all muscle groups of the segment;
than in flexors, producing a pyrami- peripheral nerve weakness of specific muscle
dal pattern of weakness groups
Reflexes Increased Areflexia
Babinski sign re- Positive: upgoing plantar response Negative
sponse
Fasciculations No Yes
Source.—Reference 10.

gracilis begins at the distal cord and consists of the axons in the STT also have a somatotopic
fibers carrying sensory input from the lower ex- arrangement (Figs 1a, 4).
tremities and lower trunk—specifically, the medial
sacral and lumbar fibers. The fasciculus cuneatus Spinal Cord Blood Supply
carries sensory input from the upper extremities The spinal cord is supplied by a single anterior
and upper trunk (lateral thoracic and cervical spinal artery (ASA) and paired posterior spinal ar-
fibers) and begins in the thoracic region. Fibers teries (PSAs) (Fig 5a). The ASA is formed by the
from the dorsal column receive input from the fusion of vertebral artery branches, while the PSAs
dorsal root ganglion, ascend on the same side of arise from either the posterior inferior cerebellar
the cord, synapse in their respective nuclei (gracilis artery or vertebral arteries. The ASA runs in the
or cuneatus), and decussate in the medulla. After ventral midline sulcus of the cord, and the PSAs
crossing over, fibers of the dorsal column form the run along the right and left dorsolateral sulci. Both
medial lemniscus, ascend within the brainstem, vessels form a vascular pial plexus that surrounds
synapse in the ventral posterior nucleus of the the cord and is reinforced by medullary branches
thalamus, and terminate in the primary somato- of radicular arteries from the posteroinferior
sensory cortex of the postcentral gyrus (Fig 3). cerebellar, vertebral, deep cervical, intercostal,
Figures 1a and 3 illustrate the somatotopic ar- and lumbar arteries (Fig 5b). The largest radicular
rangement of these fibers. artery usually arises off the left side of the aorta
between the T9 and L2 vertebral levels and is
Spinothalamic Tract called the artery of Adamkiewicz. This artery pro-
The STT carries information about pain, vides the primary blood supply to the lumbar and
temperature, and crude touch. Small-diameter sacral cord segments and commonly demonstrates
unmyelinated axons from the dorsal root gan- a “hairpin” loop before joining the ASA (5).
glion that carry pain, temperature, and crude- The ASA supplies the anterior two-thirds
touch sensation information enter the cord and of the spinal cord, and the PSA supplies the
synapse immediately in the dorsal horn. The posterior one-third. Watershed regions in the
second-order neurons in the dorsal horn car- spinal cord depend on the number of radicular
rying pain and temperature sensation cross at branches and the level of the origin of these ves-
the anterior spinal commissure and ascend as sels. However, they are typically located around
the STT in the contralateral anterolateral white the middle to lower thoracic cord. These regions
matter (3). Among the tracts described, the are susceptible to ischemia during hypoperfu-
STT is the only one that decussates at the level sion states such as that induced by major cardiac
of the spinal cord. The decussating fibers must aortic surgery or shock (11–13).
ascend at least two to three spinal segments
before reaching the opposite side; therefore, Incomplete Cord Syndromes
a lesion affecting the STT causes contralat-
eral loss of pain and temperature sensations, Dorsal Cord Syndrome
beginning a few segments below the level of the A lesion in the posterior one-third of the spinal
lesion (10). Like the nerve fibers in the CST, cord that involves primarily the posterior column
1206 July-August 2018 radiographics.rsna.org

Figure 3.  Ascending (orange arrow)

dorsal column. Drawing depicts axons
of first-order neurons of the dorsal root
ganglion (small straight black arrows)
that carry information about proprio-
ception, vibration, and fine touch
and ascend in the ipsilateral posterior
columns. Medial sacral and lumbar fi-
bers terminate in the nucleus gracilis
(large straight black arrow). Lateral
thoracic and cervical fibers project to
the nucleus cuneatus (arrowhead). Ax-
ons from second-order neurons in the
nucleus gracilis and nucleus cuneatus
decussate in the medulla and travel to
the contralateral ventral posterolateral
nucleus of the thalamus (not shown).
Third-order neurons from the ventral
posterolateral nucleus of the thalamus
terminate in the primary sensory cor-
tex (curved arrow). The somatotopic
organization of fibers in the dorsal
columns, from medial to lateral, is as
follows: sacral (S, purple), lumbar (L,
red), thoracic (T, pink), and cervical Figure 4.  Ascending (blue arrow) STT.
(C, blue) fibers. (Reprinted, with per- Drawing depicts axons from first-order
mission, from Jill K. Gregory.) neurons of the dorsal root ganglion (ar-
rowheads) that carry information about
crude touch, pain, and temperature and
synapse immediately into the dorsal horn.
can cause DCS that results in loss of fine-touch,
Axons from second-order neurons of the
vibration, and proprioception sensations (Fig 6). dorsal horn cross over into the anterior
Patients present with sensory ataxia, usually in commissure (small black arrows) at each
association with a history of dizziness, unsteady segment and ascend as the STT into the
anterolateral white matter of the contra-
gait, and frequent falls, especially during activities
lateral cord. The STT terminates in the pri-
in the dark or when the eyes are closed (3,14). mary sensory cortex (large black arrow)
At clinical examination, patients have a posi- via the thalamus (second-order neurons
tive Romberg sign—that is, a loss of balance or not shown). The somatotopic organiza-
tion of fibers in the STT, from medial to
swaying when standing erect with the eyes closed.
lateral, is as follows: cervical (C, blue), tho-
For normal balance, three sensory inputs—ves- racic (T, pink), lumbar (L, red), and sacral
tibular, visual, and proprioception—are required. (S, purple) fibers. (Reprinted, with permis-
Dark environments and activities involving sion, from Jill K. Gregory.)
closed eyes, such as showering, remove visual
input, and a lack of proprioception due to dorsal
column involvement results in a loss of balance. from epidural or intradural extramedullary
Large lesions can also affect the lateral CST and tumors (3,15). Posterior spinal cord infarction
autonomic tracts to the sacral cord. Involvement can manifest in association with unilateral DCS
of these tracts causes weakness and spasticity and is rare, compared with anterior spinal cord
(involving the CST), bowel and bladder inconti- infarction, owing to a rich vascular pial plexus
nence, erectile dysfunction, and orthostatic hypo- and paired posterior spinal cord arteries (16).
tension (involving the autonomic tracts) (3,14). The classic imaging appearance of subacute
The causes of DCS include subacute combined degeneration on axial T2-weighted
combined degeneration due to vitamin B12 MR images is increased signal intensity in the
deficiency, multiple sclerosis, tabes dorsalis, posterior columns, with the configuration of an
cervical spondylotic myelopathy, acquired im- inverted V (Fig 7) (14). Increased signal intensity
munodeficiency syndrome–related myelopathy, in the CST is seen at T2-weighted MR imag-
Friedreich ataxia, and external compression ing in more severe cases (Fig 8). These imaging
RG  •  Volume 38  Number 4 Kunam et al  1207

Figure 5.  Spinal cord blood supply. (a) Drawing

depicts a single ASA and paired PSAs forming a pial
plexus around the spinal cord. The ASA supplies
the anterior two-thirds of the cord (shaded tan),
and PSAs supply the posterior one-third (shaded
dull pink). (b) Drawing depicts the major branches
reinforcing the pial plexus via medullary branches
of radicular arteries. A large radicular artery—the
artery of Adamkiewicz—arises from the left side of
the aorta, commonly between the T9 and L2 ver-
tebral levels, and has a characteristic hairpin bend
before it joins the ASA. The watershed regions
in the cord are typically located in the middle to
lower region (oval) of the thoracic cord. (Reprinted,
with permission, from Jill K. Gregory.)

Figure 6.  DCS. (a) Drawing depicts the cross

section of the spinal cord at the level of the upper
thoracic spinal cord. The patchy shaded area rep-
resents the region involved in DCS. As the lesion
grows, it may affect the CST and autonomic center
in the lateral horn (arrow). The thoracic (T), lumbar
(L), and sacral (S) fibers are illustrated. DC = dorsal
columns. (b) Drawing depicts the areas affected
by the clinical features of DCS involving a lesion at
the T1 spinal level. These features include bilateral
loss of fine-touch, proprioception, and vibration
sensations. (Reprinted, with permission, from Jill K.
Gregory.)
1208 July-August 2018 radiographics.rsna.org

Figure 7.  Subacute combined degeneration

in a 42-year-old man who had been on a vegan
diet for the past 2 years and had a history of fre-
quent falls, most recently while showering. Axial
T2-weighted MR image shows a hyperintense
signal, with the classic inverted V configuration
(arrows), in the dorsal columns.

Figure 8.  Subacute combined degeneration in a 58-year-old man with ataxia and mild weakness in
the upper extremities, which was greater on the right than on the left. (a) Axial T2-weighted MR image
shows increased signal intensity (arrow) in the dorsal columns and subtle increased signal intensity (ar-
rowheads) in the lateral CST. (b) Sagittal T2-weighted MR image shows linear increased signal intensity
(arrows) in the dorsal columns.

changes are reversible with use of vitamin B12 mon causes of spinal cord ischemia in children
therapy. MR imaging can be used to monitor the are hypotension and hypoxemia secondary to
clinical response to treatment (14). Patients with cardiac malformations and trauma. In adults, the
multiple sclerosis who are found to have DCS most common cause of spinal cord infarction is
after presenting have demyelination plaques in stenosis or an embolic phenomenon secondary to
the dorsal cord. With active demyelination, a T2- atherosclerosis. Other causes include aortic dis-
hyperintense signal that is disproportionate to the section, aortic aneurysm, aortic surgery, systemic
lesion size (secondary to edema) (Fig 9a), with hypotension or shock, major thoracic surgery such
variable contrast material enhancement (Fig 9b), as coronary artery bypass graft placement, disk
is seen at MR imaging (15,17). compression of the radicular artery, cocaine abuse,
and sickle cell disease. Venous hypertension or
Ventral Cord Syndrome occlusion secondary to coagulopathies, epidural
Lesions that involve the anterior two-thirds of infection with subsequent epidural venous throm-
the cord and spare the dorsal columns cause bosis, and spinal arteriovenous malformations also
VCS (Fig 10a) (3,18). The most common cause can cause spinal cord ischemia (13,20).
of VCS, also known as ASA syndrome, is spinal Patients present with complete motor de-
cord ischemia or infarction. Other common ficiency below the level of the lesion due to
causes include trauma with disk herniation, cord involvement of the CST and anterior horn cells;
impingement by fracture fragments, and multi- loss of pain, temperature, and crude-touch
ple sclerosis (3,19). Among all of the incomplete sensations (involving the STT); and orthostatic
cord syndromes, VCS is associated with the hypotension, bladder and/or bowel incontinence,
worst prognosis (18). and sexual dysfunction (involving the autonomic
Spinal cord ischemia accounts for 6% of acute center) (Fig 10b). The sensations of fine touch,
myelopathies and has a poor prognosis. Com- proprioception, and vibration are preserved.
RG  •  Volume 38  Number 4 Kunam et al  1209

Figure 9.  Active demyelination in a 35-year-old woman with multiple sclerosis and paresthesia in the
upper extremities. Sagittal T2-weighted (a) and contrast material–enhanced (b) MR images show a hy-
perintense signal and focal enhancement (arrow) in the dorsal cord.

Figure 10.  VCS. (a) Drawing shows a patchy

shaded area, representing the region involved in
VCS, with sparing of the dorsal columns (DC). The
lesion affects the CST, STT, anterior horn motor
neurons (*), and autonomic center (). (b) Draw-
ing depicts the areas affected by the clinical fea-
tures of VCS. These features include motor deficit
involving the CST and loss of pain and temperature
sensations involving the STT. (Reprinted, with per-
mission, from Jill K. Gregory.)

Early motor deficits due to spinal shock include since the STTs ascend at least two to three seg-
flaccidity with absent reflexes, followed by a ments before crossing to the opposite side at the
gradual return of the reflexes and increased tone anterior commissure.
or spasticity. Bilateral sensory deficits start two MR imaging is the imaging modality of
to three segments below the level of the lesion, choice for evaluation of spinal cord ischemia,
1210 July-August 2018 radiographics.rsna.org

Figure 11.  Acute spinal cord ischemia in a 66-year-old man who presented with acute paraplegia 2 days after undergoing coro-
nary artery bypass graft placement. (a, b) Axial diffusion-weighted MR image (a) and corresponding apparent diffusion coefficient
map (b) show restricted diffusion (arrow). (c) Sagittal T2-weighted MR image shows a linear pencil-like hyperintense signal (ar-
rows) in the lower thoracic cord.

Figure 12.  Spinal cord infarction in a 53-year-

old woman with a history of sepsis and severe
hypotension, who presented with paraparesis
and urinary incontinence after recovering from
shock. Axial T2-weighted MR image shows a hy-
perintense signal (arrows) resembling snake eyes
in the anterior spinal cord.

which should include axial and sagittal diffu-

sion-weighted MR imaging examinations. Char-
acteristic MR imaging features of acute spinal
cord ischemia include diffusion restriction in
the ASA territory on diffusion-weighted images
(Fig 11a, 11b) and a pencil-like hyperintense
signal on sagittal T2-weighted images, with or
without cord enlargement (Fig 11c). Axial MR
images show a central T2-hyperintense signal on
either side of the median fissure because there is ligamentum flavum and anterior disk-osteo-
relative sparing of the peripheral and posterior phyte complexes (19,26–28) (Figs 13, 14). In
cords due to collateral vessels from the vascular young patients, the most common mechanism
pial plexus and both PSAs (13,20,21). In some of injury is fracture dislocation or herniation
cases, a central T2-hyperintense signal resem- secondary to hyperflexion injury, with associ-
bling snake eyes is seen in the anterior spinal ated cord compression (Fig 15) (26). Congeni-
cord on either side of the median fissure (Fig tal spinal canal stenosis predisposes individu-
12) (13,21). Although this finding is considered als to CCS (29–31). Other causes of CCS
specific for spinal cord infarction, it can also include intramedullary spinal cord tumors and
appear in association with compression my- syringohydromyelia.
elopathy and various infectious or inflammatory The clinical manifestations of CCS correlate
spinal conditions (13,22–25). with the lesion size. Small lesions in the central
cord region involve the STT, where they cross to
Central Cord Syndrome the contralateral side in the anterior commissure
CCS is the most common ISCS. It occurs sec- (Fig 16a) and cause bilateral segmental loss of
ondary to injury or lesions around the central pain and temperature sensations. Since the de-
canal (18,26,27). Trauma is the most common cussating fibers must ascend at least two to three
cause of CCS. Hyperextension is the classic spinal segments before reaching the opposite
mechanism of injury in elderly patients with side, loss of pain and temperature sensations be-
underlying spinal stenosis secondary to cervi- gins two to three segments below the level of the
cal spondylosis. With this condition, the spinal lesion. Sensations above and below this level are
cord is pinched between a posterior buckled normal, with a band of sensory loss in between
RG  •  Volume 38  Number 4 Kunam et al  1211

Figures 13, 14.  (13) Drawing depicts the hyperextension injury seen in older patients with CCS sec-
ondary to underlying cervical spondylosis. Note the pinching of the spinal cord between the anterior
disk-osteophyte complexes (arrows) and buckled posterior ligamentum flavum (arrowheads). (Reprinted,
with permission, from Jill K. Gregory.) (14) Cervical spondylosis with cervical stenosis in a 73-year-old man
who presented with a burning sensation and weakness in the upper extremities 2 years after a fall. Sagit-
tal T2-weighted MR image shows severe cervical spondylotic changes (arrow), with a disk-osteophyte
complex and buckled ligamentum flavum (white arrowheads). Note the mild increased signal intensity
(black arrowhead) in the cord secondary to myelomalacia.

Figure 15.  Hyperflexion distrac-

tion injury in a 21-year-old man in-
volved in a motor vehicle accident.
(a) Three-dimensional volume-
rendered CT image shows anterior
translation of C5 over C6 (single
arrow), distraction of the posterior
elements with perched facets (ar-
rowhead), and an increased pos-
terior interspinous distance (dou-
ble-headed arrow). (b) Sagittal
T2-weighted MR image obtained
in the immediate postoperative
period shows a hyperintense signal
(white arrows) at the C4-C7 spinal
level (secondary to cord contu-
sion), disruption of the posterior
ligaments (black arrow), and an-
terior fusion changes (arrowhead).
1212 July-August 2018 radiographics.rsna.org

Figure 16.  Small-lesion CCS. (a) Drawing shows a

small patchy shaded area (arrows) that represents a
small lesion involving the SSTs at the anterior com-
missure. The cervical (C), thoracic (T), lumbar (L),
and sacral (S) fiber segments are illustrated. Light
blue line and arrow illustrate the path of the STT
on the right side, crossing over to the opposite side
and ascending in the STT location in the antero-
lateral tract. Dark blue line and arrow illustrate this
path on the left side. (b) Drawing depicts the re-
gion classically affected by the clinical features of
CCS. These features include bilateral suspended
sensory loss of pain and temperature sensations at
the level of the lesion. The affected region manifests
in the classic cape distribution of sensory loss that
is seen with lesions in the cervical cord. (Reprinted,
with permission, from Jill K. Gregory.)

(suspended sensory loss) (Fig 16b). Patients who signal intensity on gradient-echo MR images
have cervical spinal cord lesions caused by either suggests intramedullary hemorrhage. How-
canal stenosis and underlying cervical spondylo- ever, this finding is uncommon in patients with
sis, or syringohydromyelia in the cervical spinal CCS; if present, it portends a poor prognosis
cord present with loss of pain and temperature (27,28,31). Relatively new techniques such as
sensations in the upper thorax, both shoulders, quantitative diffusion-tensor MR imaging and
and upper arms—in a classic “cape” distribution fiber tractography show promise as examina-
(Fig 16b) (3). tions that will enable better delineation of
Large central cord lesions can involve the an- white matter lesions in the spinal cord (32).
terior horn cells, CST, posterior columns, STT, Intramedullary spinal cord tumors (IMSCTs)
and autonomic centers in the lateral horn (Fig can also manifest in association with symptoms
17a). Owing to the somatotopic organization of of CCS. Glial tumors (ependymoma and astro-
fibers in the CST and STT (Fig 17a), sensory cytoma) are the most common IMSCTs (33).
and motor deficits are disproportionately severe Ependymomas, which arise from ependymal cells
in the upper compared with lower extremities lining the central canal, are common in adults and
(3,19) (Fig 17b). LMN motor deficits occur at account for 60% of all glial tumors. These tumors
the level of the lesion owing to involvement of are slow-growing, relatively well-circumscribed
anterior horn cells, whereas UMN deficits oc- expansile lesions that typically occur in the cervical
cur below the level of the lesion owing to CST cord. They demonstrate cord expansion, an isoin-
involvement. Mixed sensory loss with sacral tense to slightly hypointense signal on T1-weighted
sparing occurs below the level of the lesion owing MR images, a hyperintense signal on T2-weighted
to variable involvement of the STT and posterior MR images (Fig 18a), and contrast enhancement
columns (Fig 17b) (3). (Fig 18b, 18c). A T1-hypointense signal can be
MR imaging is the primary imaging mo- seen in tumors with internal hemorrhage. Cysts,
dality for evaluation of acute traumatic CCS. either polar nontumoral cysts (60%) (Fig 18a,
In the acute setting, there is an increased T2 18b) or less frequently intratumoral cysts with an
signal secondary to cord edema (Fig 15b). enhancing wall, are common with ependymomas
Thinning of the cord and myelomalacia are (78%–84% of cases) (34). Twenty percent to 33%
seen with chronic cord injuries (Fig 14). Low of ependymomas have a rim of very low T2 signal
RG  •  Volume 38  Number 4 Kunam et al  1213

Figure 17.  Large-lesion CCS. (a) Draw-

ing shows a patchy shaded area that rep-
resents a large lesion causing CCS. The
dorsal columns (DC), CST, STT, and ventral
horn neurons () at the level of the lesion
are affected. Note the sparing of the sacral
(S) fiber segments (arrows) in the CST and
STT. The cervical (C), thoracic (T), lumbar
(L), and sacral fiber segments are illustrated.
(b) Drawing depicts the areas affected by
the clinical features of large-lesion CCS.
These features include UMN deficit involv-
ing the CST; loss of fine-touch, propriocep-
tion, and vibration sensations involving the
dorsal columns; and loss of crude-touch,
pain, and temperature sensations involving
the STT, with sacral sparing (). (Reprinted,
with permission, from Jill K. Gregory.)

intensity at the pole secondary to hemorrhage— images and high signal intensity on T2-weighted
that is, a tumor cap sign (Fig 18a) (34). images, with flow voids, diffuse cord edema, and
Astrocytoma is the most common IMSCT in intense homogeneously enhancing tumor nodules
children, with ependymoma following as the next (Fig 20) (33,34).
most common (34). In adults, astrocytoma is the Syringohydromyelia is a fluid-filled cavity in
second most common IMSCT (34). The thoracic the spinal cord; it can be classified as primary
cord is the most frequent location for astrocy- or secondary. Primary causes of syringohy-
toma, with the cervical cord being the second dromyelia include basilar invagination, Chiari
most frequent location (34). These slightly ec- malformation (Fig 21), and idiopathic entities.
centric tumors have no surrounding capsule and Trauma, infection, and tumor are secondary
cause diffuse fusiform enlargement of the cord. At causes (35,36).
MR imaging, these lesions are ill defined, with a
T1-isointense to T1-hypointense signal, a T2-hy- Brown-Séquard Syndrome
perintense signal (Fig 19a), and variable enhance- Brown-Séquard syndrome, also known as hemi-
ment (33,34) (Fig 19b). Other IMSCTs, such as cord syndrome, occurs with lesions that af-
ganglioglioma and metastases, also can manifest fect one-half of the spinal cord (Fig 22a) (21).
in association with CCS. Metastases usually have Penetrating trauma, such as knife or bullet injury,
cord edema that is disproportionate in size com- is the most common cause of this syndrome
pared with the lesion, and cysts are less frequently (37,38). Other causes include idiopathic spinal
encountered than are primary tumors (33,34). cord herniation, blunt trauma, cord ischemia,
Hemangioblastoma is the third most com- disk herniation, spinal cord tumors, epidural
mon IMSCT, and it frequently (in 50% of cases) hematoma, intramedullary hemorrhage, and arte-
involves the thoracic cord, followed closely by the riovenous malformations (3,38–42).
cervical cord (in 40% of cases) (34). One-third of At clinical examination, patients with Brown-
patients with hemangioblastoma have von Hip- Séquard syndrome are found to have an ipsilateral
pel–Lindau syndrome (34). These slow-growing, UMN deficit secondary to interruption of the
highly vascular tumors cause cord expansion and CST. Damage to the posterior columns causes
are frequently associated with cystic changes or ipsilateral loss of proprioception and vibration
syringohydromyelia (Fig 20a). At MR imaging, sensations. Injury to the STT results in contra-
they have variable signal intensity on T1-weighted lateral loss of crude-touch, pain, and temperature
1214  July-August 2018 radiographics.rsna.org

Figure 18.  Ependymoma in a 45-year-old man with numbness, tingling, and weakness in both upper extremities, as well as mild
ataxia. (a) Sagittal T2-weighted MR image shows an expansile lesion (thick straight white arrows) with a heterogeneous mild hyper-
intense signal at the C7-T1 spinal level, a focal hypointense signal (black arrow) due to hemorrhage, polar cysts (thin straight white
arrows) at the C4-C6 spinal level, and cord edema (curved arrows). Note the “tumor cap” sign—that is, the hypointense signal (white
arrowhead) along the cranial margin of the lesion. There is a fluid-fluid level (black arrowheads) in the cyst at the C5-C6 level.
(b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile mass (large white arrow), with a focal hypointense
signal (arrowhead) secondary to hemorrhage and polar cysts (small white arrows). (c) Axial contrast-enhanced MR image shows an
intensely enhancing lesion with focal hemorrhage (arrowhead). The lesion nearly replaces the entire cord.

Figure 19.  Findings in a 10-year-old boy with a

grade III astrocytoma who presented with neck
and bilateral shoulder pain, difficulty gripping a
pen, and a change in handwriting. Sagittal T2-
weighted (a) and contrast-enhanced (b) MR
images show an expansile lesion (arrows) with a
homogeneous hyperintense signal and mild dif-
fuse enhancement.

sensations (3,18,19). Contralateral sensory deficit function and total sensory deficit occurs owing to
starts two to three segments below the level of the damage to the anterior horn cells and dorsal horn,
lesion, as STT fibers ascend at least two to three respectively (Fig 22b).
segments before crossing over to the opposite side In the evaluation of penetrating trauma, CT
(Fig 22b). At the level of the lesion, a small band and MR images provide valuable and complemen-
of combined ipsilateral segmental loss of motor tary information. CT best depicts bone injury,
RG  •  Volume 38  Number 4 Kunam et al  1215

Figure 20.  Hemangioblastoma in

a 16-year-old girl with a history of
neck pain. (a) Sagittal T2-weighted
MR image shows an expansile lesion
with a heterogeneous hyperintense
signal (long straight arrows) from the
C4 through C6 level, diffuse edema
(short straight arrows), cystic changes
(curved arrows), and foci of hypoin-
tense signal (arrowhead) due to hem-
orrhage or flow voids. (b) Sagittal
contrast-enhanced MR image shows
an intensely enhancing expansile le-
sion (arrows) and foci of hypointense
signal (arrowhead) due to hemor-
rhage or flow voids.

Figure 21.  Chiari I malformation with

syringohydromyelia in a 7-year-old girl
with recurrent headaches, frequent cuts
to both hands, bilateral upper-extremity
weakness, and mild ataxia. (a) Sagittal
T2-weighted MR image shows pointed
cerebellar tonsils (double-headed arrow)
below the plane of the foramen magnum
(white line) and interrupted syringohy-
dromyelia, which is greater in the cervi-
cal cord (arrow) than in the thoracic cord
(arrowhead). (b) Axial T2-weighted MR
image of the cervical cord shows a large
syrinx (arrow).

ing the extent of injury to the spinal cord, nerve

roots, soft tissues, ligaments, and/or paraspinal
musculature and detecting epidural or subdural
hematomas (Figs 23b, 24). It is also useful in the
evaluation of postoperative complications such as
infection, cerebrospinal fluid leakage, and pseudo-
meningocele (37,43,44) (Fig 24).
Idiopathic spinal cord herniation is a rare
condition that involves the thoracic cord, typically
between the T4 and T7 spinal levels. This condition
can manifest in association with Brown-Séquard
syndrome (45). The cord protrudes ventrally
through an anterior or lateral defect in the dura
(Fig 25a). On MR images, the cord at the level of
the knife or bullet path, and free fracture or bullet herniation has an anterolateral kink and an increase
fragments or air in the spinal canal (Fig 23a). in the dorsal cerebrospinal fluid space (Fig 25). The
MR imaging is the modality of choice for evaluat- cord appears narrowed or deformed, and it may
1216 July-August 2018 radiographics.rsna.org

Figure 22.  Brown-Séquard syndrome. (a) Draw-

ing shows a patchy shaded area representing the
region involved in Brown-Séquard syndrome. The
dorsal columns (DC), CST, STT, ventral horn (*),
and dorsal horn () are affected. (b) Drawing de-
picts the areas affected by the clinical features of
Brown-Séquard syndrome. These features include
ipsilateral spastic paralysis (UMN type involving the
CST); ipsilateral loss of fine-touch, proprioception,
and vibration sensations involving the dorsal col-
umns; and contralateral loss of pain and tempera-
ture sensations involving the STT. The loss of con-
tralateral pain and temperature sensations starts
two to three segments below the level of the motor
deficit because STT fibers ascend two to three seg-
ments before crossing to the opposite side. A small
segmental ipsilateral region of combined LMN defi-
cit and complete sensory deficit (arrow) is present
at the level of the lesion. (Reprinted, with permis-
sion, from Jill K. Gregory.)

Figure 23.  Penetrating injury

with hemicord transection, leading
to Brown-Séquard syndrome, in a
32-year-old woman. (a) Three-
dimensional volume-rendered CT
image shows a knife traversing
the right lamina and hemicord.
(b) Axial T2-weighted MR image
obtained in the immediate postop-
erative period shows asymmetric
increased signal intensity (arrow)
on the right side of the cord, as
compared with the signal intensity
on the left, and a defect (arrow-
heads) in the right lamina.

have increased signal intensity on T2-weighted MR Conus Medullaris Syndrome

images. Increased turbulence in the dorsal cerebro- Injury or lesions involving the tapered distal end of
spinal fluid space may mimic a flow void on T2- the spinal cord (T12 through L2) can lead to CMS.
weighted MR images and help differentiate cord Common causes of this syndrome include disk
herniation from a type III meningeal (intradural herniation in the lower thoracic and upper lumbar
arachnoid) cyst (45). Rarely, arteriovenous mal- spine, trauma resulting in a compression or burst
formations manifest in association with hemicord fracture with retropulsed fragments causing cord
syndrome secondary to cord ischemia from venous compression, intramedullary tumor (metastasis or
hypertension or the steal phenomenon. primary tumor), infection (ie, epidural abscess), spi-
RG  •  Volume 38  Number 4 Kunam et al  1217

Figure 24.  Penetrating injury

with hemicord transection and a
pseudomeningocele in a 23-year-
old man. (a) Axial T2-weighted
MR image shows a hyperintense
signal (arrow) in the right hemi-
cord and a knife tract (arrowheads)
with signal intensity similar to that
of cerebrospinal fluid. (b) Sagittal
T2-weighted MR image shows a
hyperintense signal (arrowhead) in
the cord at the C2 level and a knife
tract (arrow) communicating with
the spinal canal.

Figure 25.  Idiopathic transdural spinal cord herniation in a 38-year-old woman with right
lower-extremity weakness and a chronic nonhealing ulcer of the left foot. (a) Axial T2-weighted
MR image shows herniation of the right hemicord through a focal anterolateral dural defect
(arrow), as well as an increase in the dorsal and left lateral cerebrospinal fluid space (arrow-
heads). (b) Sagittal T2-weighted MR image shows a kinked or S-shaped cord (arrow) at the T6
level, with an associated increase in the dorsal cerebrospinal fluid space (arrowheads).

nal dural arteriovenous fistulas, and cord infarction CMS following trauma. CT is used to evaluate
(18,33,34,46–49). The clinical features of CMS bone injury (Fig 27a), and MR imaging is used
are severe back pain, lower-extremity weakness to assess the cord, disk, and soft tissues (Fig 27b)
(mixed UMN and LMN deficit), saddle anesthesia (18,46,49). Early surgical intervention substan-
or hypoesthesia (Fig 26), early bladder and rectal tially improves the patient’s prognosis.
sphincter dysfunction, and impotence (18,19). Myxopapillary ependymoma, a variant of
The lumbar and sacral nerve roots that form ependymoma arising from the ependymal glia of
the cauda equina also arise from this region. the filum terminale, is the most common neo-
Therefore, the pathologic entities that cause plasm in this region (33,34). These soft, lobulated,
CMS can also affect the cauda equina and result encapsulated mucin-producing tumors are slow
in an overlap in the clinical findings of CMS and growing, are more common in males, appear in
CES. The primary difference between CMS and persons at an earlier age compared with typi-
CES is in the type of motor deficit. CMS causes cal ependymomas, and can cause widening of
mixed UMN and LMN deficits, while CES the spinal canal (33,34). Clinically, these tumors
causes a purely LMN deficit (18). manifest with various combinations of CMS and
Both CT and MR imaging should be used to CES symptoms. At MR imaging, these lesions
examine patients who present with symptoms of demonstrate an isointense signal on T1-weighted
1218 July-August 2018 radiographics.rsna.org

Figure 27.  CMS secondary to burst fracture in a patient who presented

with paraparesis, saddle anesthesia, and urinary incontinence. (a) Sagittal
CT image shows a burst fracture (arrow) at the T12 vertebral level, with
a retropulsed component (arrowhead) in the spinal canal causing severe
canal stenosis. (b) Sagittal T2-weighted MR image shows a compression
fracture at the T12 vertebral level with retropulsion (arrow), and a mild
hyperintense signal (arrowhead) in the conus medullaris due to edema.

progressive myelopathy, with patients presenting

with clinical features of CMS (47,50).
On T2-weighted MR images, the conus medul-
Figure 26.  CMS with a saddle anesthesia
or hypoesthesia pattern. Drawing depicts laris and distal spinal cord show a diffuse ill-defined
the areas affected by the clinical features central hyperintense signal due to edema, a pe-
of this syndrome. These features include ripheral rim of hypointense signal due to chronic
bilateral symmetric sensory deficit in the
buttocks, perineum, and inner thighs. venous hypertension (ie, deoxygenated blood),
With CES, asymmetric loss of sensation in and multiple flow voids along the dorsal surface of
these regions occurs when there is involve- the cord (Fig 30a). Contrast-enhanced spinal MR
ment of the sacral nerve roots. (Reprinted, angiography or CT angiography can be used to
with permission, from Jill K. Gregory.)
localize a shunt, which is commonly located below
the pedicle, and the spinal cord may show variable
enhancement (Fig 30b). Digital subtraction angi-
images, high signal intensity on T2-weighted im- ography enables the confirmation and endovascu-
ages, and intense contrast enhancement (Fig 28). lar management of these lesions (50).
Other IMSCTs that manifest with CMS include
astrocytoma (Fig 29), hemangioblastoma, lipoma, Cauda Equina Syndrome
and metastasis (33,34). Compression of the lower lumbar and sacral nerve
Spinal dural arteriovenous fistulas, or type I roots in the vertebral canal below the level of the
spinal arteriovenous fistulas, are the most com- conus medullaris can cause CES. Although this is
mon vascular malformations of the spinal cord not a true ISCS, it is included in this discussion
and are frequently located in the thoracolumbar because there is substantial overlap between the
region; 80% of them are located between the clinical features of CES and those of CMS. The
T6 and L2 spinal levels (50). These abnormal most common cause of CES is disk herniation
arteriovenous shunts occur at the junction of secondary to degenerative disease (51,52). Other
bridging or radicular veins and the epidural causes include trauma, lumbar spinal stenosis,
venous plexus in the lateral epidural space, close arachnoiditis, and epidural abscess. The neoplas-
to the nerve root, and are fed by radiculomen- tic processes that lead to CES include primary
ingeal arteries. Chronic venous hypertension or tumors such as myxopapillary ependymoma (Fig
congestion of intramedullary veins secondary 28) and astrocytoma involving the cauda equina;
to these shunts results in chronic hypoxia and space-occupying extramedullary intradural tumors
RG  •  Volume 38  Number 4 Kunam et al  1219

Figures 28, 29.  (28) Myxopapillary

ependymoma in a 20-year-old woman
with bilateral lower-extremity weakness,
back pain, and urinary incontinence.
Sagittal contrast-enhanced MR image
shows an intensely enhancing expansile
lesion (arrows) in the region of the co-
nus medullaris and cauda equina, with
mild scalloping of the posterior vertebral
bodies (arrowheads). (29) Juvenile pilo-
cytic astrocytoma in a 5-year-old girl with
difficulty walking, bilateral leg pain, and
urinary and fecal incontinence. Sagittal T2-
weighted MR image shows an expansile
lesion with solid (large arrow) and cystic
(small arrows) components in the conus
medullaris and edema (arrowhead) in the
adjacent cord. This solid component ex-
hibited intense enhancement (not shown).

Figure 30.  Spinal dural arteriovenous fistula in

a 45-year-old man with progressive weakness,
tingling and numbness in the bilateral lower ex-
tremities, and urinary incontinence. (a) Sagittal
T2-weighted MR image shows a central hyper-
intense signal in the conus medullaris and lower
thoracic cord (straight arrows), a peripheral hy-
pointense signal (arrowheads), and flow voids
(curved arrows) along the dorsal surface of the
cord. (b) Sagittal contrast-enhanced MR image
shows tortuous enhancing vessels (arrows) along
the dorsal surface and variable contrast enhance-
ment (arrowheads) of the cord.

such as schwannoma, meningioma, and neuro- tious causes of arachnoiditis can be viral, bacterial,
fibroma; and rarely, extradural tumors such as mycobacterial, fungal, or parasitic (53,54,56,57).
vertebral metastases (51–55). Inflammatory causes of arachnoiditis include
Arachnoiditis is inflammation of the meninges autoimmune diseases such as Guillain-Barré syn-
and subarachnoid space secondary to a broad drome, subarachnoid hemorrhage, recent spinal
group of pathologic entities that include infectious, surgery, and administration of intrathecal agents
inflammatory, or neoplastic processes. The infec- (eg, steroids, anesthetics, contrast media, epidural
1220 July-August 2018 radiographics.rsna.org

Figure 31.  Lumbar spondylosis

with canal stenosis and CES in a
72-year-old man with increasing
bilateral lower-extremity weakness
and right lower-extremity pares-
thesia. (a) Sagittal T2-weighted
MR image shows a multilevel disk
bulge or herniation (arrowheads)
and ligamentum flavum buckling
(thin arrows). The combination
of these findings can lead to an
hourglass appearance of the spinal
canal. Crowded redundant cauda
equina nerve roots (thick arrows)
have a serpiginous appearance.
(b) Axial T2-weighted MR image
shows a “trefoil” configuration
(arrows) of the central canal and
buckling (arrowheads) of the liga-
mentum flavum.

Figure 32.  Type I arachnoiditis in a 32-year-

old man who had a history of meningitis and
presented with back pain, bilateral lower-
extremity weakness, and urinary and fecal
incontinence. Axial T2-weighted MR image
shows central conglomeration (arrow) of the
nerve roots.

anesthetic) (51,52,57). Neoplastic causes include

primary tumors with intrathecal spread, such as
ependymoma, and secondary metastasis or lepto-
meningeal carcinomatosis from breast carcinoma,
lung carcinoma, melanoma, or non-Hodgkin
lymphoma (51,52,55).
Clinically, CES is classified as incomplete
or complete. Incomplete CES manifests with
unilateral or bilateral sciatica, back pain, variable 33). With type III, a large central soft-tissue mass
sensory deficit in the lower extremities, saddle replaces the thecal sac (57,58). Rarely, chronic
anesthesia (at S4 and the S5 nerve roots), and inflammation and fibrosis can progress to arach-
asymmetric unilateral or bilateral LMN-type noiditis ossificans, which involves intradural calci-
motor deficit in the lower extremities, depending fication and clumped nerve roots (Fig 34) (59).
on the level of compression and the nerve roots
involved. Complete CES manifests with urinary Conclusion
and bowel retention or incontinence, in addition An understanding of the spinal cord anatomy and
to the aforementioned clinical features of incom- clinical features of spinal cord syndromes aids in
plete CES (18,51,52). the imaging and localization of cord abnormali-
MR imaging is the imaging modality of choice ties that manifest with classic incomplete cord
for evaluation of CES. Lumbar canal stenosis— syndromes. A summary of the six basic types of
either primary or congenital, or acquired owing ISCS is provided in Table 1.
to degenerative disease and disk herniation—is
best depicted on MR images (Fig 31). Acknowledgment.—The authors thank Jill K. Gregory,
Arachnoiditis is classified into three types on MFA, Certified Medical Illustrator, for creating the drawn il-
the basis of the MR imaging appearance: Type I lustrations included in this article.
arachnoiditis involves central clumping or con-
glomeration of the roots (Fig 32). With type II References
arachnoiditis, the nerve roots are adherent to the 1. Kirshblum SC, Burns SP, Biering-Sorensen F, et al.
International standards for neurological classification
periphery of the thecal sac, creating the “empty of spinal cord injury (revised 2011). J Spinal Cord Med
thecal sac” sign on MR or CT myelograms (Fig 2011;34(6):535–546.
RG  •  Volume 38  Number 4 Kunam et al  1221

Figure 33.  Type II arachnoiditis

in a 40-year-old woman who had
a history of prior spinal surgery and
presented with lower-extremity
weakness (greater on the left than
on the right) and altered sensa-
tion. (a) Sagittal T2-weighted MR
image shows an empty thecal sac
(arrow). (b) Axial T2-weighted MR
image shows an empty thecal sac
(arrow), with peripheral clumping
of the nerve roots (arrowheads).

Figure 34.  Arachnoiditis ossificans in

a 35-year-old woman who had a history
of arachnoiditis after spinal anesthesia,
with increasing weakness in the lower ex-
tremities during the next 2 years. Sagittal
nonenhanced CT image shows clumps of
intradural calcification (arrows) along the
cauda equina.

8. Naidich TP, Delman BN, Tang CY, et al. The normal spinal
cord and meninges. In: Naidich TP, Castillo M, Cha S, et
al, eds. Imaging of the spine. Philadelphia, Pa: Saunders/
Elsevier, 2011; 109–144.
9. Solsberg MD, Lemaire C, Resch L, Potts DG. High-
resolution MR imaging of the cadaveric human spi-
nal cord: normal anatomy. AJNR Am J Neuroradiol
1990;11(1):3–7.
10. Blumenfeld H. Corticospinal tract and other motor path-
ways. In: Neuroanatomy through clinical cases. 2nd ed.
Sunderland, Mass: Sinauer Associates, 2010; 225–271.
11. Gailloud P, Ponti A, Gregg L, Pardo CA, Fasel JH. Focal
compression of the upper left thoracic intersegmental arter-
ies as a potential cause of spinal cord ischemia. AJNR Am J
Neuroradiol 2014;35(6):1226–1231.
12. Shamji MF, Maziak DE, Shamji FM, Ginsberg RJ, Pon R.
Circulation of the spinal cord: an important consideration for
thoracic surgeons. Ann Thorac Surg 2003;76(1):315–321.
2. Waters RL, Adkins RH, Yakura JS. Definition of complete 13. Vargas MI, Gariani J, Sztajzel R, et al. Spinal cord ischemia:
spinal cord injury. Paraplegia 1991;29(9):573–581. practical imaging tips, pearls, and pitfalls. AJNR Am J Neu-
3. Blumenfeld H. Somatosensory pathways. In: Neuroanatomy roradiol 2015;36(5):825–830.
through clinical cases. 2nd ed. Sunderland, Mass: Sinauer 14. Timms SR, Curé JK, Kurent JE. Subacute combined
Associates, 2010; 275–315. degeneration of the spinal cord: MR findings. AJNR Am J
4. Macdonald A, Chatrath P, Spector T, Ellis H. Level of Neuroradiol 1993;14(5):1224–1227.
termination of the spinal cord and the dural sac: a magnetic 15. Pou Serradell A, Roquer González J, Perich Alsina X. Acute
resonance study. Clin Anat 1999;12(3):149–152. posterior cord lesions in multiple sclerosis: an MRI study
5. Nadgir R, Yousem DM. Anatomy and degenerative diseases of the clinical course in 20 cases [in French]. Rev Neurol
of the spine. In: Neuroradiology: the requisites. 4th ed. (Paris) 2000;156(12):1126–1135.
Philadelphia, Pa: Elsevier, 2017; 559–604. 16. Lyerly MJ, Bag AK, Geldmacher DS. Spinal cord vascular
6. Mancall EL. Spinal cord and nerve roots. In: Mancall EL, disease. In: Daroff RB, Jankovic J, Mazziotta JC, Pomeroy
Brock DG, Gray H, eds. Gray’s clinical neuroanatomy: the SL, Bradley WG, eds. Bradley’s neurology in clinical practice.
anatomic basis for clinical neuroscience. Philadelphia, Pa: 7th ed. London, England: Elsevier, 2016; 1007–1014.
Elsevier Saunders, 2011; 117–147. 17. Lycklama G, Thompson A, Filippi M, et al. Spinal-cord MRI
7. Petit-Lacour MC, Lasjaunias P, Iffenecker C, et al. in multiple sclerosis. Lancet Neurol 2003;2(9):555–562.
Visibility of the central canal on MRI. Neuroradiology 18. Snyder LA, Tan L, Gerard C, Fessler RG. Spinal cord
2000;42(10):756–761. trauma. In: Daroff RB, Jankovic J, Mazziotta JC, Pomeroy
1222 July-August 2018 radiographics.rsna.org

SL, Bradley WG, eds. Bradley’s neurology in clinical practice. 39. Barnwell SL, Dowd CF, Davis RL, Edwards MS, Gutin
7th ed. London, England: Elsevier, 2016; 881–902. PH, Wilson CB. Cryptic vascular malformations of the
19. Dobkin BH. Paraplegia and spinal cord syndromes. In: spinal cord: diagnosis by magnetic resonance imaging and
Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, Bradley outcome of surgery. J Neurosurg 1990;72(3):403–407.
WG, eds. Bradley’s neurology in clinical practice. 7th ed. 40. Choi KB, Lee CD, Chung DJ, Lee SH. Cervical disc her-
London, England: Elsevier, 2016; 273–278. niation as a cause of Brown-Séquard syndrome. J Korean
20. Masson C, Pruvo JP, Meder JF, et al. Spinal cord infarc- Neurosurg Soc 2009;46(5):505–510.
tion: clinical and magnetic resonance imaging findings 41. Mathews MS, Peck WW, Brant-Zawadzki M. Brown-
and short term outcome. J Neurol Neurosurg Psychiatry Séquard syndrome secondary to spontaneous bleed from
2004;75(10):1431–1435. postradiation cavernous angiomas. AJNR Am J Neuroradiol
21. Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. 2008;29(10):1989–1990.
Spinal cord infarction: MR imaging and clinical features in 42. Lipper MH, Goldstein JH, Do HM. Brown-Séquard syn-
16 cases. Neuroradiology 2002;44(10):851–857. drome of the cervical spinal cord after chiropractic manipula-
22. Malzberg MS, Rogg JM, Tate CA, Zayas V, Easton JD. tion. AJNR Am J Neuroradiol 1998;19(7):1349–1352.
Poliomyelitis: hyperintensity of the anterior horn cells 43. Kamaoui I, Maaroufi M, Benzagmout M, Sqalli Hous-
on MR images of the spinal cord. AJR Am J Roentgenol saini N, Boujraf S, Tizniti S. MRI findings in spinal
1993;161(4):863–865. cord penetrating injury: three case reports. J Neuroradiol
23. Arita J, Nakae Y, Matsushima H, Maekawa K. Hopkins 2007;34(4):276–279.
syndrome: T2-weighted high intensity of anterior horn on 44. Moyed S, Shanmuganathan K, Mirvis SE, Bethel A, Roth-
spinal MR imaging. Pediatr Neurol 1995;13(3):263–265. man M. MR imaging of penetrating spinal trauma. AJR Am
24. Thomas T, Branson HM. Childhood transverse myelitis and J Roentgenol 1999;173(5):1387–1391.
its mimics. Neuroimaging Clin N Am 2013;23(2):267–278. 45. Parmar H, Park P, Brahma B, Gandhi D. Imaging
25. Chen CY, Chang YC, Huang CC, Lui CC, Lee KW, Huang of idiopathic spinal cord herniation. RadioGraphics
SC. Acute flaccid paralysis in infants and young children with 2008;28(2):511–518.
enterovirus 71 infection: MR imaging findings and clinical 46. Khurana B, Sheehan SE, Sodickson A, Bono CM, Harris
correlates. AJNR Am J Neuroradiol 2001;22(1):200–205. MB. Traumatic thoracolumbar spine injuries: what the
26. Brooks NP. Central cord syndrome. Neurosurg Clin N Am spine surgeon wants to know. RadioGraphics 2013;33(7):
2017;28(1):41–47. 2031–2046.
27. Molliqaj G, Payer M, Schaller K, Tessitore E. Acute 47. Jellema K, Tijssen CC, van Gijn J. Spinal dural arte-
traumatic central cord syndrome: a comprehensive review. riovenous fistulas: a congestive myelopathy that initially
Neurochirurgie 2014;60(1-2):5–11. mimics a peripheral nerve disorder. Brain 2006;129(pt
28. Quencer RM, Bunge RP, Egnor M, et al. Acute traumatic 12):3150–3164.
central cord syndrome: MRI-pathological correlations. 48. Ajiboye RM, Nelson SD, Shamie AN. Rare case of conus
Neuroradiology 1992;34(2):85–94. medullaris syndrome from a metastatic yolk sac tumor origi-
29. Finnoff JT, Mildenberger D, Cassidy CD. Central cord nating from the mediastinum of an adult male: a case report
syndrome in a football player with congenital spinal stenosis: and review of the literature. Int J Spine Surg 2015;9:59.
a case report. Am J Sports Med 2004;32(2):516–521. 49. Harrop JS, Hunt GE Jr, Vaccaro AR. Conus medullaris
30. Rich V, McCaslin E. Central cord syndrome in a high school and cauda equina syndrome as a result of traumatic
wrestler: a case report. J Athl Train 2006;41(3):341–344. injuries: management principles. Neurosurg Focus
31. Harrop JS, Sharan A, Ratliff J. Central cord injury: patho- 2004;16(6):e4.
physiology, management, and outcomes. Spine J 2006;6(6 50. Krings T, Geibprasert S. Spinal dural arteriovenous fistulas.
suppl):198S–206S. AJNR Am J Neuroradiol 2009;30(4):639–648.
32. Shanmuganathan K, Gullapalli RP, Zhuo J, Mirvis SE. Dif- 51. McNamee J, Flynn P, O’Leary S, Love M, Kelly B. Imaging
fusion tensor MR imaging in cervical spine trauma. AJNR in cauda equina syndrome: a pictorial review. Ulster Med
Am J Neuroradiol 2008;29(4):655–659. J 2013;82(2):100–108.
33. Samartzis D, Gillis CC, Shih P, O’Toole JE, Fessler RG. 52. Gitelman A, Hishmeh S, Morelli BN, et al. Cauda
Intramedullary spinal cord tumors. I. Epidemiology, patho- equina syndrome: a comprehensive review. Am J Orthop
physiology, and diagnosis. Global Spine J 2015;5(5):425–435. 2008;37(11):556–562.
34. Koeller KK, Rosenblum RS, Morrison AL. Neoplasms of 53. Sharma A, Goyal M, Mishra NK, Gupta V, Gaikwad SB.
the spinal cord and filum terminale: radiologic-pathologic MR imaging of tubercular spinal arachnoiditis. AJR Am J
correlation. RadioGraphics 2000;20(6):1721–1749. Roentgenol 1997;168(3):807–812.
35. Batnitzky S, Price HI, Gaughan MJ, Hall PV, Rosenthal 54. Cohen DB. Infectious origins of cauda equina syndrome.
SJ. The radiology of syringohydromyelia. RadioGraphics Neurosurg Focus 2004;16(6):e2.
1983;3(4):585–611. 55. Bagley CA, Gokaslan ZL. Cauda equina syndrome caused
36. Smoker WR, Keyes WD, Dunn VD, Menezes AH. MRI by primary and metastatic neoplasms. Neurosurg Focus
versus conventional radiologic examinations in the evalua- 2004;16(6):e3.
tion of the craniovertebral and cervicomedullary junction. 56. Gupta RK, Gupta S, Kumar S, Kohli A, Misra UK, Guj­
RadioGraphics 1986;6(6):953–994. ral RB. MRI in intraspinal tuberculosis. Neuroradiology
37. Jacobsohn M, Semple P, Dunn R, Candy S. Stab injuries 1994;36(1):39–43.
to the spinal cord: a retrospective study on clinical findings 57. Georgy BA, Snow RD, Hesselink JR. MR imaging of spinal
and magnetic resonance imaging changes. Neurosurgery nerve roots: techniques, enhancement patterns, and imaging
2007;61(6):1262–1266; discussion 1266–1267. findings. AJR Am J Roentgenol 1996;166(1):173–179.
38. Miranda P, Gomez P, Alday R, Kaen A, Ramos A. 58. Ross JS, Masaryk TJ, Modic MT, et al. MR imaging of lumbar
Brown-Sequard syndrome after blunt cervical spine arachnoiditis. AJR Am J Roentgenol 1987;149(5):1025–1032.
trauma: clinical and radiological correlations. Eur Spine J 59. Maulucci CM, Ghobrial GM, Oppenlander ME, Flanders
2007;16(8):1165–1170. AE, Vaccaro AR, Harrop JS. Arachnoiditis ossificans: clinical
series and review of the literature. Clin Neurol Neurosurg
2014;124:16–20.

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