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 CenterIcahn School of Medicine

1000 Tenth Avenue, New York, NY 10019, USA

eEdE#: 243C

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. Anatomy

2. Neoplasms

A. Glial Neoplasms

I. Ependymoma

II. Astrocytoma

i. Juvenile Pilocytic Astrocytoma

ii. Anaplastic Astrocytoma

iii.Glioblastoma Multiforme

III. Ganglioglioma

IV. Subependymoma

B. Non-glial Neoplasms

I. Hemangioblastoma

II. Intramedullary Metastasis

III. Solitary fibrous tumor

IV. Spinal cord lipoma

3. Vascular

A. Cavernous malformation

B. Spinal dural arteriovenous fistula

C. Arterial venous malformation

D. Spinal cord ischemia/infarction

4. Inflammatory/Infection

A. Multiple Sclerosis

B. Neuromyelitis Optica

C. Lupus Myelitis

D. Granulomatous Angiitis

E. Neurosarcoid

F. Tuberculosis

5. Trauma/Degenerative

A. Spinal cord contusion

SPINAL CORD ANATOMY

Compartments of the spinal cord 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 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 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:

Intratumoral cysts:

Contained within the tumor itself

Typically demonstrate peripheral enhancement

Most commonly occurs in ganglioglioma (46%), ependymoma (22%), astrocytoma

(21%), and hemangioblastoma (2-4%)

Non-tumoral cysts:

Occurs at the rostral or caudal aspect of the tumor

Occurs due to dilatation of the central canal

Does not enhance

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 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 (44-

67%).

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).

ASTROCYTOMACharacterized 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)

Most common in children, 2nd most common tumor

in adults.

Comprises approximately 40% of spinal tumors.

Generally large, diffuse fusiform enlargement

without obvious (infiltrative) margins.

Patchy ill-defined enhancement.

Can involve the full diameter of the cord but are

more eccentric in location compared to

ependymomas.

Both polar and intratumoral cysts are common.

Leptomeningeal spread in seen in 60% of

intramedullary GBM.

Amount and degree of pleomorphism is correlated

with the biologic behavior of these tumors.

Ependymoma

Astrocytoma

Population Adult Pediatric

Location Central Eccentric

Morphologic Appearance

Well-circumscribed

Ill-defined

Hemosiderin Cap

Common Rare

Enhancement

Intense, homogeneous

Patchy, irregular

Cysts Common Common

JUVENILE PILOCYTIC ASTROCYTOMA

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.

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.

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

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

Uncommon entity occurring mostly in adult

males with less than 50 cases reported in the

literature.

Believed to arise from tancytes cells that

bridge the pial and ependymal layers.

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

Third most common intramedullary spinal

neoplasm – 1 to 7%.

Subpial, highly vascular, capillary rich low grade

neoplasm.

Multiple lesions indicate the manifestation of VHL

syndrome (75% sporadic; 25% associated with

VHL).

Typically posterior in location.

25% are solid but can present with classic “cystic

mass with an enhancing mural nodule”

appearance.

There is marked enhancement of the solid

component. The cystic component does not

enhance.

Intratumoral arterial flow voids as well as posterior

draining veins can be seen.

Extensive surrounding edema.

Commonly associated with cysts and syrinx.

Spinal angiography demonstrates feeding arteries,

tumor blush, and draining veins.Sagittal post-contrast T1WI and angiographic image demonstrate an avidly enhancing hemangioblastoma with rostral flow voids with corresponding feeding arteries and draining vein.

Sagittal post-contrast T1WI and T2WI demonstrate an intensely enhancing mass in the dorsal cervical cord with peritumoral syrinx formation consistent with a hemangioblastoma.

INTRAMEDULLARY SPINAL METASTASIS

Accounts for 3-5% of cases of myelopathy in

patients diagnosed with cancer. Results from tumor growth along the Virchow-

Robin 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

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

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 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 Brown-

Sequard 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 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.

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. 20

DURAL ARTERIOVENOUS FISTULA

Axial and sagittal T2WI of the thoracic spine demonstrates spinal cord edema and/or gliosis secondary to venous hypertension. Sagittal post-contrast 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 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 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 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

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 long-segment confluent patchy signal within the central thoracic spinal cord, findings which are consistent with neuromyelitis optica.

GRANULOMATOUS ANGIITIS OF THE CNS 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 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:

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.

28

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.

TUBERCULOSIS

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.

29

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.

SPINAL CORD CONTUSION 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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