eEdE#: 243C
Imaging Spectrum of
Spinal Intramedullary
Lesions
Sagar M Patel DO
Alicia Huang MD
Francisco Delara MD
Daniel R Lefton MD
Mount Sinai St. Luke’s - Roosevelt Hospital Center
Icahn School of Medicine
1000 Tenth Avenue, New York, NY 10019, USA
DISCLOSURE STATEMENT
No authors have any significant relationships, financial or
otherwise, to disclose.
INTRODUCTION/PURPOSE
 Pathological processes of the spinal cord can produce distinct
clinical syndromes yet frequently have both clinical and imaging
overlap.
 A spectrum of diagnostic considerations that may affect the
spinal cord includes developmental anomalies, inflammatory
and infectious processes, degenerative conditions, vascular
disease, as well as benign and malignant neoplasms.
 The purpose of this exhibit is to describe relevant anatomy
important for interpretation as well as present typical and
atypical imaging findings of various pathological entities.
METHOD
 An overview of the normal anatomy of the spine with
compartmental classification will initially be provided with
diagrammatic representation of cross sectional anatomy of
the cord and its blood supply.
 A spectrum of intramedullary lesions will be discussed
through a pictorial essay.
DISCUSSION
1.
2.
Anatomy
3.
Neoplasms
A. Glial Neoplasms
I. Ependymoma
II. Astrocytoma
i. Juvenile Pilocytic
4.
Astrocytoma
ii. Anaplastic Astrocytoma
iii.Glioblastoma Multiforme
III. Ganglioglioma
IV. Subependymoma
B. Non-glial Neoplasms
I. Hemangioblastoma
II. Intramedullary Metastasis 5.
III. Solitary fibrous tumor
IV. Spinal cord lipoma
Vascular
A. Cavernous malformation
B. Spinal dural arteriovenous fistula
C. Arterial venous malformation
D. Spinal cord ischemia/infarction
Inflammatory/Infection
A.
B.
C.
D.
E.
F.
Multiple Sclerosis
Neuromyelitis Optica
Lupus Myelitis
Granulomatous Angiitis
Neurosarcoid
Tuberculosis
Trauma/Degenerative
A. Spinal cord contusion
SPINAL CORD ANATOMY
Compartments of the spinal cord
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Extradural
 Epidural space, vertebral bodies,
neural arches, intervertebral discs,
paraspinous muscles
Intradural
 Subarachnoid space, spinal cord
ligaments, nerve roots, cauda
equina, filum terminale
Intramedullary
 spinal cord, pia
Arterial supply of the spinal cord
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Anterior spinal artery
 Originates from the intradural vertebral arteries,
supplying anterior 2/3 of the cord.
Posterior spinal arteries
 Originates from the posterior rami of the vertebral
arteries, supplying posterior 1/3 of the cord.
Aorta Segmental artery dorsal artery radicular
artery
Artery of Adamkiewicz – dominant thoracic anterior
radicular artery (medullary feeder), arises from
intercostal branches of thoracic aorta, typically left T9
level.
Largest radiculomedullary artery of the cervical spinal
cord is supplied by the artery of Lazorthes, typically at
the C5 or C6 segment.
“Watershed” of the cord is the central gray matter
NEOPLASMS
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Spinal intramedullary neoplasms account for about 4%–10% of all central nervous system (CNS)
tumors and about 2%–4% of CNS glial tumors.
Account for 20% of all intraspinal tumors in adults and 35% of all intraspinal tumors in children.
Intramedullary spinal neoplasms are more common in patients with NF-1 (astrocytomas), NF-2
(ependymomas), and VHL (hemangioblastomas).
70% of tumors are associated with cysts. Two types of recognized cysts:
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Intratumoral cysts:
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Contained within the tumor itself
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Typically demonstrate peripheral enhancement
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Most commonly occurs in ganglioglioma (46%), ependymoma (22%), astrocytoma
(21%), and hemangioblastoma (2-4%)
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Non-tumoral cysts:
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Occurs at the rostral or caudal aspect of the tumor
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Occurs due to dilatation of the central canal
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Does not enhance
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Present in 60% of all intramedullary spinal tumors
Syrinx occurs in approximately 50% of all intramedullary tumors but is most frequently
associated with hemangioblastomas.
In contrast to intracranial neoplasms, the vast majority of spinal cord neoplasms, including even
low-grade forms, enhance after the administration of contrast material to some degree.
Enhanced areas probably represent more active portions of the tumors and may indicate
potential sites for biopsy if resection is not feasible.
EPENDYOMOMA
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Most common intramedullary neoplasm in adults,
comprising 60% of all glial spinal cord tumors.
Second most common intramedullary neoplasm in
the pediatric population, representing 30% of
pediatric intramedullary spinal neoplasms.
Classified as WHO Grade I or II neoplasm.
Most commonly occurs in the cervical region (4467%).
Characterized by slow growth and tends to
compress rather than infiltrate adjacent spinal cord
neural tissue.
Well circumscribed lesion that almost always has a
cleave plane, which facilitates microsurgical
resection (treatment of choice).
Symmetric cord expansion as it arises from the
ependymal cells of the central canal within the
spinal cord.
Rostral and caudal non-tumoral polar cysts are
common (Intratumoral cysts are less common).
Intratumoral hemorrhage, cystic degeneration, and
hemosiderin cap is common. Unlike intracranial
ependymomas, calcifications are uncommon.
Multiple ependymomas can be seen in the setting
of NF-2 (MISME Syndrome – Meningioma,
Schwannoma, and Ependymoma).
Sagittal T2WI with hemosiderin
capping of an ependymoma.
Sagittal post-contrast T1WI,
sagittal T2WI, and axial C+
T1WI demonstrates focal
expansion of the cervical spinal
cord with a centrally enhancing
mass.
Sagittal post-contrast T1WI of
the cervical spine
demonstrates multiple
ependymomas in the setting of
NF-2 (MISME Syndrome).
ASTROCYTOMA
Characterized as:
1.
WHO Grade I – Juvenile Pilocytic Astrocytoma
2.
WHO Grade II – Fibrillary Astrocytoma
3.
WHO Grade III – Anaplastic Astryocytoma
4.
WHO Grade IV – Glioblastoma Multiforme (GBM)
Population

Most common in children, 2nd most common tumor
in adults.
Location
Ependymoma
Astrocytoma
Adult
Pediatric
Central
Eccentric
Wellcircumscribed
Ill-defined

Comprises approximately 40% of spinal tumors.
Morphologic
Appearance
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Generally large, diffuse fusiform enlargement
without obvious (infiltrative) margins.
Hemosiderin
Cap
Common
Rare
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Patchy ill-defined enhancement.
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Can involve the full diameter of the cord but are
more eccentric in location compared to
ependymomas.
Enhancement
Intense,
homogeneous
Patchy,
irregular
Common
Common
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Both polar and intratumoral cysts are common.
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Leptomeningeal spread in seen in 60% of
intramedullary GBM.

Amount and degree of pleomorphism is correlated
with the biologic behavior of these tumors.
Cysts
JUVENILE PILOCYTIC ASTROCYTOMA
Sagittal T2WI and post-contrast T1WI of the
thoracic spine demonstrates a long segment
heterogeneously enhancing mass with rostral
and caudal syrinx formation. Thin, linear glial
bands are noted within the syrinx.
Sagittal T2WI and post-contrast T1WI demonstrate
a focal enhancing heterogeneous hyperintense
mass in the ventral cervical spinal cord. Confluent
pial enhancement of the spinal cord is observed
consistent with subarachnoid dissemination of
disease.
ANAPLASTIC ASTROCYTOMA
Intramedullary anaplastic astrocytoma. Sagittal T2WI, sagittal post-contrast
T1WI, and axial T2WI demonstrate fusiform enlargement of the distal thoracic
spinal cord with mild increased T2 signal. No significant intramedullary
enhancement is observed. Engorgement of the venous arcade around the
conus is present.
GLIOBLASTOMA MULTIFORME
Intramedullary Gliobastoma Multiforme. Sagittal T2WI, sagittal post-contrast T1WI,
axial T2WI and axial post-contrast T1WI, demonstrates fusiform expansion of the
central thoracic spinal cord with abnormal heterogeneous T2 signal. Post-contrast
images demonstrate peripheral enhancement with irregular margins.
GANGLIOGLIOMA
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Most frequent in children and young adults.
Most commonly occurs in the cervical cord
however, holocord involvement is common.
Classified as WHO Grade I or II neoplasm.
Second most common intramedullary tumor in
children after astrocytoma.
Consists of large mature neurons, ganglion cells,
and neoplastic glial cells.
Eccentric in location and commonly contains
polar and intratumoral cysts.
Patchy enhancement is the most common
pattern, but enhancement of the pial surface is
also common. Approximately 15% of these
lesions show no enhancement.
Characteristically involves eight or more vertebral
segments.
Mixed signal intensity on T1 weighted images is
common.
Sagittal post-contrast T1WI and sagittal T2WI
demonstrates marked widening of the
cervicothoracic spinal canal with a long segment
enhancing heterogenous intramedullary mass with
rostral and caudal polar cysts.
SUBEPENDYMOMA
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Uncommon entity occurring mostly in adult
males with less than 50 cases reported in the
literature.
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Believed to arise from tancytes cells that bridge
the pial and ependymal layers.
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Usually manifests with fusiform dilatation of the
spinal cord with well-defined borders.

Unlike ependymomas, they are eccentrically
located and often have bands of normal spinal
cord tissue traversing the tumor.
Sagittal T2WI, post-contrast T1WI, and axial
T2WI demonstrate a T1 isointense, T2
hyperintense intramedullary lobulated tumor
with eccentric cord expansion in the mid
thoracic spine.
HEMANGIOBLASTOMA
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Third most common intramedullary spinal
neoplasm – 1 to 7%.
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Subpial, highly vascular, capillary rich low grade
neoplasm.
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Multiple lesions indicate the manifestation of VHL
syndrome (75% sporadic; 25% associated with
VHL).
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Typically posterior in location.
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25% are solid but can present with classic “cystic
mass with an enhancing mural nodule”
appearance.
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There is marked enhancement of the solid
component. The cystic component does not
enhance.
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Intratumoral arterial flow voids as well as posterior
draining veins can be seen.
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Extensive surrounding edema.
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Commonly associated with cysts and syrinx.
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Spinal angiography demonstrates feeding arteries,
tumor blush, and draining veins.
Sagittal post-contrast T1WI and T2WI demonstrate an
intensely enhancing mass in the dorsal cervical cord
with peritumoral syrinx formation consistent with a
hemangioblastoma.
Sagittal post-contrast T1WI and angiographic image
demonstrate an avidly enhancing hemangioblastoma
with rostral flow voids with corresponding feeding
arteries and draining vein.
INTRAMEDULLARY SPINAL METASTASIS
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Accounts for 3-5% of cases of myelopathy in
patients diagnosed with cancer.
Results from tumor growth along the VirchowRobin spaces and through hematogenous
dissemination.
Mild cord expansion over several segments
with homogeneous enhancement.
Typically presents with surrounding edema,
usually disproportionately increased for the
size of the lesion.
Most common intramedullary spinal
metastasis (in order of frequency):
 Lung
 Breast
 Melanoma
 Colorectal
 Renal
 Gastric
Sagittal T2WI, sagittal post-contrast T1WI, axial T2WI,
and axial post-contrast T1WI demonstrate symmetric
cord expansion with an avidly enhancing lesion in the
distal spinal cord with surrounding edema and mild
syrinx formation. Findings were consistent with an
intramedullary melanotic metastasis.
SOLITARY FIBROUS TUMOR
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Spindle-cell neoplasm of probable
mesenchymal origin.
Most commonly arises from the pleura,
however extrapleural CNS solitary fibrous
tumors can be seen originating from the
dura, spinal cord parenchyma, and nerve
roots.
MR findings include:
 T1 isointense/hypointense
 T2 hypointense
 T1 post-contrast: avid and
homogenous enhancement
T2 hypointensity is caused by
hypocellularity and abundant collagen
stroma that helps distinguish from other
spinal cord neoplasms.
Peritumoral edema is commonly seen.
Differential diagnostic considerations
include meningioma and schwannoma.
Sagittal T2WI, coronal post-contrast T1WI, axial T2WI, and axial
post-contrast T1WI demonstrate a well-circumscribed eccentric
intramedullary focal mass lesion with low T2 signal, mild
peritumoral cord edema, and homogenous enhancement in the
upper thoracic cord. Histopathologic correlation status post
resection confirmed the diagnosis of solitary fibrous tumor.
SPINAL CORD LIPOMA
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More commonly identified in the first three
decades of life.
Most commonly located in the thoracic spine.
If the spinal cord lipoma is located in the
lumbar region, it is usually associated with
myelodysplasia or tethered cord.
Should be followed in neonates as they can
grow significantly during infancy.
MRI characteristics:
 T1WI high signal
 T2WI lower signal
 Dark on fat suppression
Fat-like lesions Ddx
Epidural lipomatosis*
Melanoma
Neurenteric cysts
Pantopaque*
Ruptured dermoid*
Subacute hemorrhage
Teratoma*
*suppresses with fat sat
Two sagittal T1WI and sagittal T2WI demonstrate
a lobulated, multi-segment dorsal cervical spinal
cord lesion with hyperintense T1 signal and mild
hyperintense T2 signal, consistent with an
intramedullary lipoma.
CAVERNOUS MALFORMATION
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Angiogenically immature vascular lesion
with lobulated, thin, sinusoidal vascular
channels and no interspersed neural
tissue.
Usually presents in patients aged 30-50.
Predilection toward females by a ratio of
4:1.
Can cause hematomyelia and BrownSequard syndrome.
Minimal cord expansion and edema unless
there has been recent hemorrhage.
MRI is the study of choice for evaluation:
 Heterogeneous signal intensity on
T1WI and T2WI from methemoglobin.
 Varying age of blood products give
typical “popcorn appearance.”
 Low signal intensity rim on T2WI and
hypointense “blooming” on gradient
echo sequence due to hemosiderin.
Angiography is typically negative.
Axial T2WI demonstrate mild cord expansion secondary to an
eccentric hyperintense lesion with a thin hypointense hemosiderin
peripheral rim. Axial pre-contrast T1WI demonstrates
heterogeneous blood products.
Sagittal T1WI and sagittal T2WI demonstrates a predominately
hyperintense heterogeneous mass at the cervicomedullary junction
with a thin peripheral hypointense hemosiderin rim. A formation of
a caudal syrinx (hematomyelia) is noted.
ARTERIOVENOUS FISTULA/MALFORMATIONS
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There are four types of spinal AV
malformations
Type I Spinal Dural AV Fistula:
 Most common and usually affects a single
radicular feeder.
 Usually located at the nerve root sleeve.
 Foix-Alajuoanine refers to the syndrome
when myelopathy is present.
 Symptoms are typically insidious in onset
with lower extremity weakness and/or
sensory changes.
 Can cause venous hypertension of the cord.
Type II Intramedullary Spinal Cord AV
Malformation:

 Typically presents in the 3rd decade with a
M:F ratio of 1:1.1.
 Typically located in the cervical or thoracic
region.
 There are multiple arterial feeders from both 
the anterior and posterior arteries.
 Hemorrhage may occur and cause acute
symptoms.
 Nidus is located within the spinal cord.
 Commonly associated with spinal artery
aneurysms.
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IMAGING: recommend contrast enhanced
MRI; consider spinal angiography +/embolization.
 T1WI – heterogeneous from blood
products
 T2WI – cord hyperintensity from
edema, gliosis or ischemia
 STIR – flow voids and edema in cord
 T2* GRE – more sensitive to blood
products of AVM hemorrhage
 Variable enhancement of nidus, cord,
and vessels
 MRA – dynamic enhanced MRA can define
the feeding artery and vein
Type III Juvenile AV Malformation:
 Has intramedullary, extramedullary and
extraspinal components.
 Occurs early in life and has a poor prognosis.
Type IV Spinal Cord AV Fistula:
 Located intradurally but along the ventral or
lateral surface of the cord.
 Varied presentation: myelopathy or
hemorrhage including subarachnoid
hemorrhage.
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DURAL ARTERIOVENOUS FISTULA
Axial and sagittal T2WI of the thoracic
spine demonstrates spinal cord
edema and/or gliosis secondary to
venous hypertension. Sagittal postcontrast T1WI demonstrates
abnormally prominent enhancing
vascularity along the surface of the
spinal cord secondary to venous
engorgement.
ARTERIOVENOUS MALFORMATION
Axial and sagittal T2WI (left two
images) and T1WI (right two images)
of the cervical spine demonstrate a
heterogeneously T1 and T2 low signal
intensity mass within the posterior
aspect of the spinal cord at the levels
of C4-C6. Low T1and T2 signal
represent flow voids. The spinal cord
demonstrates mild T2 hyperintensity
compatible with edema and/or gliosis.
SPINAL CORD INFARCT
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Spinal cord infarcts have a predilection for
upper thoracic or thoracolumbar regions
due to the limited blood supply (watershed
region).
Up to 50% of cases have no known
etiology.
Majority of known causes are related to
aortic pathology (atherosclerotic disease).
Other causes include septicemia, systemic
hypotension, fibrocartilaginous embolism,
and iatrogenic etiology.
Patients typically present with abrupt
onset of symptoms with rapid progression.
The dominant blood supply to conus:
Artery of Ademkiewicz
 Infarction of this vessel leads to
impairment in bowel and bladder
function.
Infarcts present with mild cord
enlargement and well demarcated region
of abnormal signal. Cord atrophy can be
seen in chronic infarcts.
Hemorrhagic transformation is rare.
MRI findings:
 T2WI hyperintense central gray
matter
 Restricted diffusion
Sagittal T2WI and sagittal post-contrast T1WI as well as two axial T2
WI demonstrate mild cord expansion and sharply demarcated region
of increased T2 signal involving the distal thoracic spinal cord
extending from T9 through the conus. The cord signal abnormality
predominantly involves the anterior and midline of the distal spinal
cord and is sharply demarcated from the uninvolved posterior thoracic
spinal cord. There is no associated enhancement of the cord. Given
the reported history of acute onset of symptomatology, these findings
are consistent for ischemia of the cord, i.e. cord infarction.
MULTIPLE SCLEROSIS
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Multiphasic primary demyelinating disease of the CNS
with multiple lesions disseminated over time and space.
Peak onset: 20-40 years of age; F>M 1.7:1.
Majority of patients have associated intracranial lesions
(5-24% of cases are confined to the spinal cord).
60% of spinal lesions are located in the cervical region.
Lesions are peripherally located (most commonly at the
dorsolateral aspect of the cord), oval, and asymmetric.
They are usually less than 2 vertebral segments in
length and less than half the cross-sectional area of the
spinal cord.
Wedge-shaped lesions are seen on axial images, with
apex directed centrally.
Lesions do not respect gray-white boundary.
Cord enlargement is uncommon.
There can be myelomalacia (parenchymal loss)
overtime.
MS can cause transverse myelitis.
MRI Findings:
 Presents as T2 hyperintense, T1 isointense lesions.
 Enhancement is seen in acute demyelination.
 Enhancement can last 1-2 months but does not
reflect disease progression.
Axial and sagittal T2WI as well as axial and sagittal
post-contrast T1WI demonstrate abnormal signal
affecting the mid thoracic spinal cord,
predominantly the dorsal columns, with associated
patchy ill-defined enhancement. Findings are
consistent with an active plaque of multiple
sclerosis.
LUPUS MYELITIS
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In patients with an established diagnosis of
systemic lupus erythematosus, transverse
myelitis can usually be presumed to be caused
by the underlying disease.
Etiology is proposed to be secondary to vacuolar
degeneration from an autoimmune process or
ischemia.
Mid to low thoracic spine is the most common
site of involvement.
MR findings include high signal on T2WI and
low/isointense signal of T1WI.
Enhancement is seen in 50% of the cases.
Lack of enhancement does not exclude active
disease however may reflect disease remission
during periods of clinical improvement or
secondary to the stabilizing effect of high dose
steroids.
Axial T2WI and sagittal T2WI demonstrate mild cord
expansion with central abnormal T2 signal. Given
patients history of SLE, findings are consistent with
lupus myelitis.
NEUROMYELITIS OPTICA
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Autoimmune inflammatory disorder involving
myelin of neurons of the optic nerves and spinal
cord, without brain parenchymal involvement.
Longitudinally extensive (>3 vertebral segments)
abnormal signal in the spinal cord with
thickening/enhancement of the optic nerve.
NMO-IgG seropositivity.
On first acute presentation, neuromyelitis optica
cannot be differentiated from acute disseminated
encephalomyelits in patients with simultaneous
optic neuritis and myelitis.
Other concomitant or associated disease:
 Prior viral infection
 ANA positive (10%)
 Autoimmune thyroiditis (9%)
 Myasthenia gravis (2%)
 Sjogren syndrome
Sagittal FLAIR WI, axial T2WI, and sagittal T2WI
demonstrate increased thickening and abnormal
signal intensity within the optic chiasm as well as longsegment confluent patchy signal within the central
thoracic spinal cord, findings which are consistent with
neuromyelitis optica.
GRANULOMATOUS ANGIITIS OF THE CNS
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Uncommon necrotizing vasculitis in adults of unknown
cause restricted to vessels of the CNS.
In the spectrum of Primary Arteritis of the CNS, which also
includes benign angiopathy of the CNS and reversible
vasoconstrictive syndrome.
Diagnosis of exclusion.
No evidence of systemic vasculitis.
Irregularities, stenoses, and vascular occlusions in atypical
pattern for atherosclerotic disease.
Ddx: Intracranial atherosclerotic vascular disease, arterial
vasospasm, drug abuse, moyamoya, viral infection (such
as CMV or Herpes), and systemic CNS vasculitis.
Spine: Axial and sagittal T2WI and post-contrast
T1WI demonstrate abnormal T2 intramedullary signal
without cord expansion in the lower thoracic spinal
cord with mild patchy enhancement. There is
enhancement of the ventral and dorsal nerve rootlets
at the level of the distal thoracic cord, conus
medullaris, and cauda equina.
Brain: Axial T2WI and post-contrast T1WI
demonstrate serpentine, mildly nodular enhancement
in a medullary pattern within both frontotemporal and
subinsular regions, which is associated with T2 signal
abnormality within the adjacent brain parenchyma.
There is no appreciable mass effect related to the
confluent zones of T2 signal abnormality. Enhancing
soft tissue is seen within the subarachnoid space
within the frontal and temporal lobe regions.
NEUROSARCOID
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Non-caseating granulomatous disease of the spine.
6-8% of patients with neurosarcoid have spinal cord
lesions.
Most commonly cervical and upper thoracic in location.
Tumor nodules can present on the leptomeningeal
surface, as a discrete mass, or as diffuse inflammation.
Central intramedullary lesions are from infiltration of
the Virchow – Robin spaces.
Presents with fusiform cord enlargement, enhancing
intramedullary masses, and focal or diffuse T2
hyperintense lesions.
Combination of leptomeningeal (smooth or nodular)
and peripheral intramedullary mass-like enhancement
are highly suggestive of spinal sarcoidosis.
Rarely can have calcifications or cysts.
Improves with steroid therapy.
Four stages of intraspinal sarcoidosis:
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Early Inflammation – linear leptomeningeal enhancement.
Centripetal spread of leptomeningeal inflammatory process
through perivascular spaces – parenchymal enhancement
and swelling.
Less prominent swelling with focal or multiple
enhancement.
Resolution of inflammatory process with normal size or
atrophy of the cord and no enhancement.
Sagittal T2WI, sagittal post-contrast T1WI, and
coronal post-contrast T1WI demonstrate abnormal
enlargement and signal in the spinal cord with
enhancing intramedullary lesions as well as scattered
nodular leptomeningeal enhancement, consistent with
inflammation and noncaseating granulomas in the
setting of sarcoidosis.
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TUBERCULOSIS
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Granulomatous disease caused by Mycobacterium
tuberculosis.
Intramedullary tuberculosis is a rare form of spinal
tuberculosis, even in tuberculosis endemic regions.
Most commonly affects the osseous vertebral
elements.
Secondary to hematogenous spread from another
focus of tubercular infection in the body, usually
pulmonary and nodal disease.
Occurs predominantly in young patients.
Cinical presentation ranges from back pain to
paraparesis and bowel/ bladder dysfunction with or
without low grade fever.
Clinical picture of compressive myelopathy usually
warrants MRI evaluation in these patients.
Can present with myelitis without identifiable
granulomas on the precontrast scan.
Appears as a diffuse ill-defined hyperintensity on
T2WI and hypointensity on T1WI.
Post-contrast T1WI usually demonstrates nodular or
ring enhancing lesions.
Sagittal T2WI and post-contrast T1WI demonstrates a
long segment ill-defined regional of abnormal T2 signal
with multiple underlying contiguous enhancing solid
nodular lesions within the posterior cervical spinal
cord.
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SPINAL CORD CONTUSION
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Spinal cord contusion in adults are typically located
at C4-C6 and associated with a fracture or
subluxation in young adults. Degenerative disease
predisposes the elderly population to spinal cord
injury.
Spinal cord edema without radiographic abnormality
can be seen in children less than eight years old due
to ligamentous laxity.
Incidence in the setting of trauma is 3.7%.
Good neurological prognosis if no hemorrhage is
present.
Poor prognostic factors: hematoma, C4-C6
injuries,greater than 50 years of age.
Usually occult on CT.
MRI findings:
 T1WI: acute: isointense/hypointense with cord
swelling, hyperintense after 3 days if there is a
hematoma; chronic: atrophy +/- cyst,
syringomyelia.
 T2WI: acute: hyperintense from edema that
worsens over a few days, then plateaus; chronic:
atrophy, hyperintense gliosis, +/- cyst,
syringomyelia, hypointensity from hemosiderin if
there is a chronic hematoma.
 Sagittal STIR *key sequence: cord edema,
ligamentous injury.
 T2*: hypointense if there is hemorrhage.
 DWI: restricted diffusion can show early
ischemic changes.
 MRA/CTA can be obtained to evaluate for
vascular injury.
Sagittal T2WI and STIRWI demonstrates
focal short segment cord abnormal signal
signal at the level of C4-C5, consistent with
cord contusion. There is associated disc
herniation at these levels and edema in the
posterior elements, suggestive of
ligamentous injury.
CONCLUSION
 After review of this educational exhibit, the reader will have
an informed understanding of the normal anatomy of the
spinal cord and characteristic imaging findings of various
intramedullary spinal pathologies.
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