---
title: "Pediatric Multiple Sclerosis, Spine"
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pageDescription: "Pediatric Multiple Sclerosis, Spine"
pageKeywords: "Pediatrics, Diagnosis, Pediatric Neuroradiology, Spine, Infection and Inflammatory Disorders, Inflammatory and Autoimmune Disorders, Pediatric Multiple Sclerosis, Spine"
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---
# KEY FACTS
- ## Terminology
- Primary demyelinating disease of CNS with multiple lesions disseminated over time & space
- Concomitant intracranial lesions in periventricular, subcallosal, brainstem, or cerebellar white matter
- ## Imaging
- Isolated spinal cord disease (10-20%)
- Cervical segment is most commonly affected
- Dorsolateral aspect of cord
- < 1/2 of cross-sectional area of spinal cord
- < 2 vertebral segments in length
- Sagittal & axial T1WI/T2WI sequences with gadolinium
- Lesions typically oval, peripheral, & asymmetric
- Discrete vs. vague hyperintense lesions
- Enhancement lasts 1-2 months but does not reflect disease progression
- ## Top Differential Diagnoses
- Acute disseminated encephalomyelitis
- Neuromyelitis optica spectrum disorders
- Myelin oligodendrocyte glycoprotein antibody disorder
- Idiopathic transverse myelitis
- Intramedullary neoplasm
- Spinal cord infarct
- ## Pathology
- Autoimmune, cell-mediated inflammatory process focused on CNS myelin
- ## Clinical Issues
- Peak onset: 20-40 years
- Adult females more susceptible than males (1.7:1)
- Multiple clinical presentations
- Relapsing remitting (RR)
- Secondary progressive (SP)
- Primary progressive (PP)
- Progressive relapsing (PR)
- ## Diagnostic Checklist
- Imaging findings must be correlated with clinical & laboratory features to confirm diagnosis
# TERMINOLOGY
- ## Abbreviations
- Spinal cord multiple sclerosis (MS)
- ## Definitions
- Primary demyelinating disease of CNS with multiple lesions disseminated over time & space
# IMAGING
- ## General Features
- ### Best diagnostic clue
- Concomitant T2-hyperintense lesions in ≥ 2 of 4 areas of CNS: Periventricular, cortical or juxtacortical, infratentorial, & spinal cord
- ### Location
- Lesions solitary or multifocal
- Isolated spinal cord disease in 10-20%
- Cervical segment is most commonly affected (2/3 of cord lesions)
- Lesions frequently in dorsolateral cord
- Does not respect gray-white boundary
- ### Size
- < 1/2 of cross-sectional area of spinal cord
- < 2 vertebral segments in length
- ### Morphology
- Wedge-shaped on axial MR
- Apex directed centrally
- ## MR Findings
- ### T1WI
- Iso- to hypointense lesions
- In cord (unlike brain), rarely visible as hypointense
- 30% of brain lesions are dark, "black holes"
- Normal or mild focal cord expansion
- Cord edema
- Resolves after 6-8 weeks
- ### T2WI
- Discrete or ill-defined hyperintense lesions
- May be related to extent of demyelination
- Lesions ↑ in size due to edema associated with inflammatory infiltrates → reach max size at 4 weeks
- Slow ↓ in size over 6-8 weeks as edema resolves ± remyelination
- Lesions typically oval, peripheral, & asymmetric
- ### PD/intermediate
- Hyperintense lesions
- ### STIR
- Improved lesion detection, more artifact
- ### FLAIR
- Lower lesion sensitivity compared to STIR
- ### DWI
- ↑ mean diffusivity, ↓ fractional anisotropy in plaques & areas without T2 abnormality
- ### T1WI C+
- Variable
- Homogeneous, nodular, or ring enhancement during acute or subacute phase
- Enhancement lasts 1-2 months
- Does not reflect disease progression
- No enhancement during chronic phase
- ### MRS
- ↓ N-acetylaspartate level
- ↑ choline levels, even in normal-appearing white matter
- Cord atrophy
- Usually in late stage
- May be seen in early disease course
- Useful for monitoring disease progression & therapeutic efficacy
- Correlates with clinical disability
- fMRI
- Tactile-associated cervical cord fMRI activity ↑ in relapse-onset MS patients
- Overactivation more prominent in patients with more severe locomotor disability
- Suggests abnormality of cord functional properties may be among factors associated with clinical status of MS patient
- ## Nonvascular Interventions
- ### Myelography
- Nonspecific mild cord expansion
- ## Other Modality Findings
- Magnetization transfer (MT) imaging
- ↓ MT ratio in spinal cord
- Better correlation with disability & axonal loss
- ↓ MT ratios in enhancement patterns in which myelin known to be ↓ histopathologically
- ## Imaging Recommendations
- ### Best imaging tool
- T1WI/T2WI spinal cord MR in sagittal & axial planes with gadolinium
# DIFFERENTIAL DIAGNOSIS
- [Acute Disseminated Encephalomyelitis](/document/adem-spine/d2226d10-f582-4cdf-8f32-71718e6c494d)
- Para-/postinfectious immune-mediated inflammatory disorder of spinal cord white matter
- Frequently preceding infection 4-12 days before onset
- Usually monophasic
- [Syringohydromyelia](/document/syringomyelia/fb362df4-5033-4f7c-9f4d-01d701ebab84)
- Central cystic lesion
- CSF intensity on all sequences
- No abnormal enhancement
- [Neuromyelitis Optica Spectrum Disorders](/document/neuromyelitis-optica/11d42d8d-e7bb-4ecf-85ce-d96f0afeb076)
- Autoimmune inflammatory disorder involving myelin of neurons of optic nerves & spinal cord
- Longitudinally extensive cord T2 hyperintensity + optic nerve enhancement
- T2 abnormality involves entire cross section of cord
- Limited brain involvement
- ## Myelin Oligodendrocyte Glycoprotein Antibody Disease
- Autoimmune inflammatory disorder involving neuronal myelin of brain, optic nerves, &/or spinal cord
- Often longitudinally extensive
- Predilection for conus
- [Idiopathic Transverse Myelitis](/document/idiopathic-acute-transverse-myelit-/6e82fa47-19b7-45ac-b195-3c21687fa648)
- Longitudinally extensive, > 2/3 of cord cross-sectional area
- Lesion centrally located, variable enhancement
- No associated intracranial lesions
- Diagnosis of exclusion
- [Intramedullary Neoplasm](/document/spinal-cord-astrocytoma/43d5efa2-7a6d-4972-bfc6-c300cc31f9af)
- Cord expansion, peritumoral edema, cystic ± hemorrhagic components
- Entire cross section of spinal cord
- Diffuse or partial enhancement
- [Spinal Cord Infarction](/document/spinal-cord-infarction/5afcaea7-09a0-49b7-8f23-f93734d627fb)
- Sudden onset of symptoms
- Positive diffusion restriction
- Posterior columns typically spared in anterior spinal infarct
# PATHOLOGY
- ## General Features
- ### Etiology
- Autoimmune, cell-mediated inflammatory process focused on CNS myelin
- Infectious agents may play primary or secondary role
- Humoral mechanism: Cross reactivity between infectious & self-epitopes
- May be association between MS & altered venous return due to multiple extracranial venous strictures
- Hampered cerebrospinal venous drainage in patients with MS determines complex hemodynamic picture → chronic cerebrospinal venous insufficiency (CCSVI)
- Multiple substitute circles with very high incidence of reflux in both intra-/extracranial venous segments
- Loss of postural regulation of cerebral venous outflow
- Primary progressive (PP) course related to CCSVI pattern differs significantly from relapsing remitting (RR) & secondary progressive (SP) → location of venous obstruction plays role in clinical course
- Obstruction at several levels of azygous vein & of lumbar plexuses
- → venous blood of cord can be drained only in upward direction & is shunted toward venous plexuses inside spine
- ↑ cerebral blood flow/volume & ↓ mean transit time (compared with baseline values before relapse) precede development of plaques
- Susceptibility-weighted imaging → venous blood in cerebral veins of patients with MS is less deoxygenated compared with healthy controls
- Previously, these findings interpreted as sign of local flow disturbances mediated by inflammatory & neurodegenerative processes
- However, may be attributable to recent findings of significant stenoses in extracranial veins draining brain & spinal cord
- ### Genetics
- May be inherited as complex multifactorial disorder resulting from interaction of genetic & environmental factors
- Estimated risk to siblings of proband ~ 3.0-5.0%, ↑ to 29.5% if 1 or both parents have MS
- Risk to offspring of person with MS is 2.0-3.0% & higher if both parents have MS
- ### Associated abnormalities
- 90% incidence of associated intracranial lesions
- Neurofibromatosis type 1
- Different serum thyroid hormone & complement C3, C4, & CH50 levels in neuromyelitis optica vs. MS
- Thyroid hormones may play different role in modulating complement activation in MS & neuromyelitis optica
- Focal regions of demyelination of varying size & age scattered throughout CNS white matter
- ## Staging, Grading, & Classification
- McDonald criteria (2001, revised in 2005 & 2017) widely used for adult MS diagnosis
- Has also been shown to be useful for pediatric MS diagnosis
- Relies on lesion dissemination in both time & space
- Dissemination in space
- Demonstrated by ≥ 1 T2-hyperintense lesions that are characteristic of MS in ≥ 2 of 4 areas of CNS
- Periventricular, cortical or juxtacortical, infratentorial brain regions, & spinal cord
- Dissemination in time
- Simultaneous presence of gadolinium-enhancing & nonenhancing lesions at any time
- New T2-hyperintense or gadolinium-enhancing lesion on follow-up MR with reference to baseline scan, irrespective of timing of baseline MR
- ## Microscopic Features
- Discrete lesions of myelin destruction
- Active lesions with macrophages & lymphocytes
- Chronic lesions with gliosis & cavitation
- Perivascular cuffs of lymphocytes & mononuclear cells
- Involvement of dorsal horns common
# CLINICAL ISSUES
- ## Presentation
- ### Most common signs/symptoms
- Cord lesions asymptomatic
- Paresthesia
- ### Other signs/symptoms
- Muscle weakness, hyperreflexia, gait disturbance
- Bladder/bowel dysfunction
- Surveillance includes periodic neurologic examination to track disease progression & periodic brain & spinal cord MRs to monitor disease activity
- Additional examination techniques → ambulation index, 25-foot timed walk, & 25-foot walk combined with 9-hole peg test & paced serial auditory addition test
- ## Demographics
- ### Age
- Peak onset: 20-40 years
- Onset < 18 years in 3-5% of MS cases
- ### Sex
- Women more susceptible than men (1.7:1)
- Men more likely to have progressive relapsing (PR) & SP MS
- Women more likely to have RR MS
- Both sexes equally affected in PP MS
- ### Ethnicity
- Western Europeans have higher risk
- ### Epidemiology
- ↑ prevalence farther north from equator
- 30-80 per 100,000 in northern USA & Europe
- 6-14 per 100,000 in southern USA & Europe
- 1 per 100,000 in equatorial regions
- ## Natural History & Prognosis
- Benign: 20%
- Complete recovery after 1-2 attacks
- Some may experience progressive MS after 10-15 years
- RR: 25%
- Distinct periods of new or worsening symptoms alternating with complete or partial recovery
- 90% will evolve into progressive MS after 25 years
- SP: 40%
- From RR MS
- Worsening deficits & disabilities
- Incomplete & infrequent remission
- PP: 12%
- Steady progression of symptoms
- Motor dysfunction common
- Primary cord involvement; no distinct attacks
- PR: 3%
- Similar to PP MS
- Distinct periods of exacerbation but without recovery
- High mortality rate
- ## Treatment
- Multiple approved medications include interferon, chemotherapy agents, monoclonal antibodies
- Several preparations available of interferon β (interferon β-1b, interferon β-1a)
- Inhibition of immune cells
- Glatiramer acetate
- Synthetic protein similar to myelin protein
- Serves as substrate for T cells
- Mitoxantrone (chemotherapeutic agent)
- Suppression of T lymphocytes & B lymphocytes
- Monoclonal antibodies
- Natalizumab, alemtuzumab, daclizumab, ocrelizumab
- Small-molecule oral agents
- Fingolimod, dimethyl fumarate, teriflunomide
- Supportive therapy
- Symptomatic treatment of pain, muscle spasms, fatigue, depression, sexual/bladder/bowel dysfunction
- Anticholinergics, smooth muscle relaxants
- Physical therapy
# DIAGNOSTIC CHECKLIST
- ## Consider
- Multiplanar spine contrast MR ± contrast, including STIR MR
- Brain MR, including high-resolution fast spin-echo T2 through corpus callosum
- Gray matter atrophy correlates with disability
- Periventricular, subcallosal, brainstem, or cerebellar white matter lesions suggest MS
- ## Image Interpretation Pearls
- Imaging findings must be correlated with clinical & laboratory features to confirm diagnosis
- Acute MS can mimic cord neoplasm
ec82b351-fbdc-43cf-8899-7d0ffed659d4
## References
# Selected References
1. [Bower A et al: Radiologically isolated syndrome and the multiple sclerosis prodrome in pediatrics: early features of the spectrum of demyelination. Semin Pediatr Neurol. 46:101053, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37451751%5Bpmid%5D)
1. [Malani Shukla N et al: Demographic features and clinical course of patients with pediatric-onset multiple sclerosis on newer disease-modifying treatments. Pediatr Neurol. 145:125-31, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37348193%5Bpmid%5D)
1. [Fadda G et al: Comparison of spinal cord magnetic resonance imaging features among children with acquired demyelinating syndromes. JAMA Netw Open. 4(10):e2128871, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34643718%5Bpmid%5D)
1. [Ciccarelli O et al: Spinal cord involvement in multiple sclerosis and neuromyelitis optica spectrum disorders. Lancet Neurol. 18(2):185-97, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30663608%5Bpmid%5D)
1. [Thompson AJ et al: Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 17(2):162-73, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29275977%5Bpmid%5D)
1. [Bigi S et al: Outcomes after early administration of plasma exchange in pediatric central nervous system inflammatory demyelination. J Child Neurol. 30(7):874-80, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25246301%5Bpmid%5D)
1. [Kearney H et al: Spinal cord grey matter abnormalities are associated with secondary progression and physical disability in multiple sclerosis. J Neurol Neurosurg Psychiatry. 86(6):608-14, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25097217%5Bpmid%5D)
1. [Riederer I et al: Double inversion recovery sequence of the cervical spinal cord in multiple sclerosis and related inflammatory diseases. AJNR Am J Neuroradiol. 36(1):219-25, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25169924%5Bpmid%5D)
1. [Russi AE et al: The meninges: new therapeutic targets for multiple sclerosis. Transl Res. 165(2):255-69, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25241937%5Bpmid%5D)
1. [De Stefano N et al: Spinal cord imaging in multiple sclerosis: filling the gap with the brain. Neurology. 83(15):1306-7, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25186859%5Bpmid%5D)
1. [Makary MS et al: Tumefactive demyelinating disease with isolated spinal cord involvement. Acta Radiol Short Rep. 3(5):2047981614539324, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25298871%5Bpmid%5D)
1. [Schlaeger R et al: Spinal cord gray matter atrophy correlates with multiple sclerosis disability. Ann Neurol. 76(4):568-80, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25087920%5Bpmid%5D)
1. [Toosy AT et al: Voxel-based cervical spinal cord mapping of diffusion abnormalities in MS-related myelitis. Neurology. 83(15):1321-5, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25186861%5Bpmid%5D)
1. [Simka M et al: Reinterpreting the magnetic resonance signs of hemodynamic impairment in the brains of multiple sclerosis patients from the perspective of a recent discovery of outflow block in the extracranial veins. J Neurosci Res. 88(9):1841-5, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20127806%5Bpmid%5D)
1. [Tallantyre EC et al: Clinico-pathological evidence that axonal loss underlies disability in progressive multiple sclerosis. Mult Scler. 16(4):406-11, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20215480%5Bpmid%5D)
1. [Valsasina P et al: Cervical cord functional MRI changes in relapse-onset MS patients. J Neurol Neurosurg Psychiatry. 81(4):405-8, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=19965858%5Bpmid%5D)
1. [Zamboni P et al: Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis. J Neurol Neurosurg Psychiatry. 80(4):392-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19060024%5Bpmid%5D)
1. [Zhang B et al: Correlation between serum thyroxine and complements in patients with multiple sclerosis and neuromyelitis optica. Neuro Endocrinol Lett. 29(2):256-60, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18404143%5Bpmid%5D)
1. [Yukawa Y et al: MR T2 image classification in cervical compression myelopathy: predictor of surgical outcomes. Spine (Phila Pa 1976). 32(15):1675-8; discussion 1679, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17621217%5Bpmid%5D)
1. [Stüve O, Oksenberg J. Multiple sclerosis overview. 1993-, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=20301492%5Bpmid%5D)
1. [International Working Group for Treatment Optimization in MS: Treatment optimization in multiple sclerosis: report of an international consensus meeting. Eur J Neurol. 11(1):43-7, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14692887%5Bpmid%5D)
1. [Pretorius PM et al: The role of MRI in the diagnosis of MS. Clin Radiol. 58(6):434-48, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12788312%5Bpmid%5D)
1. [Filippi M et al: Overview of diffusion-weighted magnetic resonance studies in multiple sclerosis. J Neurol Sci. 186 Suppl 1:S37-43, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11334988%5Bpmid%5D)
1. [Institute of Medicine (US) Committee on Multiple Sclerosis: current status and strategies for the future et al: 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=25057543%5Bpmid%5D)
1. [Poser CM et al: Diagnostic criteria for multiple sclerosis. Clin Neurol Neurosurg. 103(1):1-11, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11311469%5Bpmid%5D)
1. [Steiner I et al: Infection and the etiology and pathogenesis of multiple sclerosis. Curr Neurol Neurosci Rep. 1(3):271-6, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11898529%5Bpmid%5D)
1. [Bastianello S et al: MRI of spinal cord in MS. J Neurovirol. 6 Suppl 2:S130-3, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10871800%5Bpmid%5D)
1. [Hickman SJ et al: Imaging of the spine in multiple sclerosis. Neuroimaging Clin N Am. 10(4):689-704 ,viii, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=11359719%5Bpmid%5D)
1. [Simon JH: Brain and spinal cord atrophy in multiple sclerosis. Neuroimaging Clin N Am. 10(4):753-70 ,ix, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=11359723%5Bpmid%5D)
1. [Simon JH: The contribution of spinal cord MRI to the diagnosis and differential diagnosis of multiple sclerosis. J Neurol Sci. 172 Suppl 1:S32-5, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10606803%5Bpmid%5D)
1. [van Waesberghe JH et al: Magnetization transfer imaging of the spinal cord and the optic nerve in patients with multiple sclerosis. Neurology. 53(5 Suppl 3):S46-8, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10496211%5Bpmid%5D)
1. [McFarland HF: The lesion in multiple sclerosis: clinical, pathological, and magnetic resonance imaging considerations. J Neurol Neurosurg Psychiatry. 64 Suppl 1:S26-30, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9647281%5Bpmid%5D)
1. [Campi A et al: Acute transverse myelopathy: spinal and cranial MR study with clinical follow-up. AJNR Am J Neuroradiol. 16(1):115-23, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7900579%5Bpmid%5D)
1. [Miller DH: Magnetic resonance imaging and spectroscopy in multiple sclerosis. Curr Opin Neurol. 8(3):210-5, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7551120%5Bpmid%5D)
1. [Tartaglino LM et al: Multiple sclerosis in the spinal cord: MR appearance and correlation with clinical parameters. Radiology. 195(3):725-32, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7754002%5Bpmid%5D)
1. [Jeffery DR et al: Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. Arch Neurol. 50(5):532-5, 1993](http://www.ncbi.nlm.nih.gov/pubmed/?term=8489410%5Bpmid%5D)
1. [Thomas DJ et al: Magnetic resonance imaging of spinal cord in multiple sclerosis by fluid-attenuated inversion recovery. Lancet. 341(8845):593-4, 1993](http://www.ncbi.nlm.nih.gov/pubmed/?term=8094830%5Bpmid%5D)
1. [Maravilla KR et al: Magnetic resonance demonstration of multiple sclerosis plaques in the cervical cord. AJR Am J Roentgenol. 144(2):381-5, 1985](http://www.ncbi.nlm.nih.gov/pubmed/?term=3871287%5Bpmid%5D)
## Images
### Selected Images

*Sagittal graphic depicts multiple sclerosis (MS) demyelinating plaques within the cervical spinal cord. Lesions are focal and < 2 vertebral bodies in length, typical of MS.*

*Sagittal graphic depicts multiple sclerosis (MS) demyelinating plaques within the cervical spinal cord. Lesions are focal and < 2 vertebral bodies in length, typical of MS.*

*Sagittal T2WI MR (left) demonstrates a solitary active MS plaque
at the C6-C7 level with focal T2 hyperintensity but without significant cord enlargement. Sagittal T1WI C+ FS MR (right) confirms ring enhancement of the focal lesion, consistent with an active MS plaque.*

*Sagittal T2WI (left), PD (middle), and STIR (right) MR images show multiple short-segment MS plaques within the thoracic spinal cord
. Note the relatively improved conspicuity of the plaques on PD and STIR relative to the routine T2 sequence.*

*Sagittal STIR (left), T2WI (middle), and T1WI C+ FS (right) MR images of the thoracic spine show multiple short-segment foci of T2 hyperintensity
in a different patient with MS. Multiple lesions
show solid enhancement.*
### Additional Images

*Sagittal T2WI MR in a patient with MS and characteristic brain lesions (not shown) reveals a focal lesion
centered at C7 with minimal if any cord enlargement.*

*Axial T2WI MR in the same patient reveals a lesion in the left hemicord that is focal and does not involve the entire cord diameter, features favoring MS.*

*Sagittal T2WI (left) and T1WI C+ FS (right) MR images show several T2-hyperintense foci in the cervical cord in this patient with MS. Two of the lesions enhance, reflecting active demyelination
.*

*Sagittal T2WI (left) and T1WI C+ (right) MR images show active enhancing plaque at the C2 level with both focal, well-defined (enhancing) T2 focus
and a small amount of surrounding nonenhancing edema
.*

*Sagittal T2WI MR of the cervical cord shows a more discrete demyelinating focus at C3-C4.*

*Axial T2WI MR of the cervical cord in a different patient shows a poorly defined, wedge-shaped, mildly hyperintense plaque within the right lateral aspect of the cord.*

*Axial T1WI C+ MR with fat suppression of the cervical cord in a different patient shows right peripheral nodular enhancement.*

*Sagittal T2WI MR of the cervical cord shows an ill-defined, hyperintense intramedullary lesion at C5-C6.*

*Sagittal T2WI MR of the cervical spinal cord demonstrates multiple T2-hyperintense foci
, some well defined and others ill defined. The multiplicity of lesions and lack of edema or significant cord expansion is typical for demyelinating disease.*

*Sagittal T1WI C+ MR shows multiple enhancing demyelinating lesions within the cervical spinal cord. Enhancement varies from focal
to ill defined
. The enhancement pattern changes with evolution of inflammation.*

*T1WI C+ MR (sagittal on top, axial on bottom) illustrates an incomplete rim-enhancing lesion
in the dorsal cervical cord at the C3-C4 level. A 2nd small enhancing focus is noted in the ventral cord at the C6 level
.*

*Sagittal PD FSE MR of the cervical spinal cord demonstrates characteristic ovoid hyperintense intramedullary demyelinating lesions
without significant cord expansion.*

*Axial T1WI C+ MR of the cervical spinal cord depicts focal ring enhancement
within an active MS demyelinating lesion.*

*Sagittal STIR MR shows a focal hyperintense demyelinating plaque
within the thoracic cord without significant cord expansion. STIR MR is more sensitive for lesion depiction than T2WI MR at the price of more artifacts.*

*Sagittal high-resolution GRE MR of the thoracic cord shows multiple areas of ↑ signal
in this patient with MS. All lesions are ≤ 2 vertebral bodies in length, typical for MS.*