T1 hypointensity may represent axonal loss, gliosis, white matter atrophy, & therefore motor disability

Cervical cord T1 relaxation time may be influenced by tissue damage upstream (i.e., cerebral damage)

Well-circumscribed T2 hyperintense lesions (complete demyelination) vs. ill-defined (partial demyelination)

Wedge-shaped lesions with apex directed centrally

Revised diagnostic criteria (99% sensitive, 90% specific)

Myelitis: Longitudinally extensive cord lesion, 3 or more segments in length

Optic neuritis

Onset brain MR nondiagnostic for MS

Seropositivity for neuromyelitis optica immunoglobin G

T2 hyperintense lesion with mild cord expansion

No significant enhancement

Mild T1 hyperintensity due to petechial hemorrhage

Etiologies: Collagen vascular disease, infectious/post-infectious, post-vaccination, post-irradiation, AVM, paraneoplastic

Smooth cord expansion < T2 signal abnormality

T2 hyperintensity more than 2 vertebral segments in length

Central gray matter surrounded by edema, “central dot sign”

Acute contusion: T1 iso-/hypointense, T2 hyperintense with cord swelling

Hemorrhage T1 hyperintense with metHB, blooming on GRE sequences

± Traumatic disc herniation, osseous or vascular injury

T2 hyperintense, T1 iso-/slightly hypointense

Polar & intratumoral cysts (50-90%)

Syrinx

Hemosiderin cap (20-64%)

Central canal widening (20%) & posterior vertebral scalloping

T2 hyperintense, solid portion T1 iso-/hypointense

Usually < 4 segments

Diffuse tumor infiltration, absence of hemorrhage, & intrinsic neoplastic syrinx cavity favor astrocytoma over ependymoma

Concurrent combination of intramedullary cord tumor & nerve sheath tumor is highly suggestive of NF1

Flame-shaped central edema spares the periphery

Low peripheral T2 signal is compatible with venous hypertensive myelopathy

Cord is enlarged & T1 hypointense

Multiple small vascular flow voids are seen on the cord pial surface

± Patchy cord enhancement

Most commonly at level of conus

Small lesions T2 hyperintense/T1 hypointense

Syrinx > 50%, hyperintense to CSF

Lesions > 2.5 cm show flow voids

± Peritumoral edema

Multifocal T1 hypointense/T2 hyperintense lesions with slight cord swelling

Little mass effect or edema

Concomitant brain involvement

T2 hyperintensity involving the gray matter ± adjacent white matter

Increased T2 signal in the adjacent anterior vertebral body or in deep medullary portion near endplate

Cord enlargement in acute phase

More common in thoracic cord because of arterial border zone

Expanded cord with T1 hypointensity & diffuse T2 hyperintensity

Long, contiguous segmental involvement

Acute myelopathy

Enlarged cord with diffuse T2 hyperintensity

Rarely, syrinx or hemorrhagic products (i.e., thyroid, melanoma)

Well-circumscribed < 1.5 cm enhancing lesion

Abscess core appears T1 hypointense/T2 hyperintense with surrounding edema

Idiopathic or hematogenous source in adults; direct extension from dysraphism in children

Axial T2 show “upside-down V-shaped” hyperintensity along dorsal columns

Accumulation of methylmalonic acid thought to cause myelin toxicity

Subacute combined degeneration also occurs in the setting of some types of severe anemia

Neurologic findings may precede the anemia

Treatment with parenteral B12 may improve symptoms, but imaging abnormalities may not completely resolve