Ross
83 KiB
83 KiB
title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, ddx, anatomy, cases, breadcrumbs
| title | docid | authors | breadcrumbs | category | cmeTopicId | documentVersionId | imageCount | lastUpdated | pageDescription | pageKeywords | pageTitle | enhancedTitle | type | references | ddx | anatomy | cases | breadcrumbs | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| Pediatric Multiple Sclerosis, Brain | f2592b04-f800-4235-9eea-a43f2bf4adfe |
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Pediatrics | 03b623c3-7d10-4a0f-88ec-e7830afde051 | caa247d6-e650-4954-8d11-33d96c2d0244 | 27 | 02/14/24 | Pediatric Multiple Sclerosis, Brain | Pediatrics, Diagnosis, Pediatric Neuroradiology, Brain, Pathology-Based Diagnoses, Inflammatory and Demyelinating Disease, Pediatric Multiple Sclerosis, Brain | Pediatric Multiple Sclerosis, Brain | STATdx | Pediatric Multiple Sclerosis, Brain | DX | true | true |
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title: "Pediatric Multiple Sclerosis, Brain" docid: "f2592b04-f800-4235-9eea-a43f2bf4adfe" authors:
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- name: "Pediatric Neuroradiology" slug: "pediatric-neuroradiology" treeNodeId: "d0eb8f4a-e769-43dd-896c-8c9c27ce8759"
- name: "Brain" slug: "brain" treeNodeId: "feaaadba-649b-4f0a-9aad-9188a8f9926a"
- name: "Pathology-Based Diagnoses" slug: "pathology-based-diagnoses" treeNodeId: "2d26053f-23a7-4062-bf35-a93775ae1209"
- name: "Inflammatory and Demyelinating Disease" slug: "inflammatory-and-demyelinating-dis-" treeNodeId: "cb319228-da96-4d29-8276-c72388a57656"
- name: "Pediatric Multiple Sclerosis, Brain" slug: "pediatric-multiple-sclerosis-brain" treeNodeId: null category: "Pediatrics" cmeTopicId: "03b623c3-7d10-4a0f-88ec-e7830afde051" documentVersionId: "caa247d6-e650-4954-8d11-33d96c2d0244" imageCount: 27 lastUpdated: "02/14/24" pageDescription: "Pediatric Multiple Sclerosis, Brain" pageKeywords: "Pediatrics, Diagnosis, Pediatric Neuroradiology, Brain, Pathology-Based Diagnoses, Inflammatory and Demyelinating Disease, Pediatric Multiple Sclerosis, Brain" pageTitle: "Pediatric Multiple Sclerosis, Brain | STATdx" enhancedTitle: "Pediatric Multiple Sclerosis, Brain" type: "DX" references: true ddx: true anatomy:
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- "Pediatrics"
- "Diagnosis"
- "Pediatric Neuroradiology"
- "Brain"
- "Pathology-Based Diagnoses"
- "Inflammatory and Demyelinating Disease"
- "Pediatric Multiple Sclerosis, Brain"
KEY FACTS
-
Terminology
- Probable autoimmune-mediated demyelination in which environmental factors act upon genetically susceptible individuals
-
Imaging
- Multiple perpendicular callososeptal T2 hyperintensities characteristic of multiple sclerosis (MS) - Perivenular extension: Dawson fingers
- Bilateral, asymmetric, linear/ovoid FLAIR hyperintensities - > 85% periventricular/perivenular - 50-90% callososeptal interface - May also commonly involve subcortical U fibers, brachium pontis, brainstem, spinal cord
- Transient enhancement during active demyelination - > 90% disappear within 6 months
- Rare: Large, tumefactive enhancing rings
- T1-hypointense lesions suggest worse prognosis - Correlate with disability, atrophy, progressive disease
- Advanced imaging techniques show disease in normal-appearing white matter
-
Top Differential Diagnoses
- Acute disseminated encephalomyelitis
- Neuromyelitis optica
- Autoimmune-mediated vasculitis
- Leukodystrophies and mitochondrial diseases
- Lyme disease
- Susac syndrome
-
Pathology
- Probable autoimmune-mediated demyelination in which environmental factors act upon genetically susceptible individuals
- Pathogenesis requires combination of genetically susceptible individual and specific environmental trigger
-
Clinical Issues
- Estimated 2.5 million people in world have MS
- Pediatric MS defined as onset < 18 years - ≈ 5% of MS patients - < 1% of MS patients have onset < 10 years
- Most common disabling CNS disease of young adults; 1:1,000 in Western world
- Adults: M:F = 1:2; adolescents: M:F = 1:3
-
Diagnostic Checklist
- Requires dissemination in time and space within CNS for diagnosis
- McDonald criteria: Consensus statement for diagnostic criteria; last revised in 2010
TERMINOLOGY
-
Abbreviations
- Multiple sclerosis (MS)
-
Synonyms
- Previously known as early-onset MS (EOMS) or juvenile MS
-
Definitions
- Chronic demyelinating disease characterized by recurrent episodes of CNS demyelination separated in space and time
- Pediatric MS defined as onset < 18 years - ≈ 5% of MS patients - < 1% of MS patients have onset < 10 years
IMAGING
-
General Features
-
Best diagnostic clue
- Multiple perpendicular callososeptal T2 hyperintensities -
Location
- > 85% periventricular/perivenular - 50-90% callososeptal interface - Subcortical U fibers, brachium pontis, brainstem, spinal cord - Infratentorial (< 10% in adults, more common in children) -
Size
- Small (5-10 mm); tumefactive lesions several cm -
Morphology
- Linear, round, or ovoid; beveled, target, lesion-in-lesion appearance - Some children present with large, tumor-like demyelinating lesions [tumefactive demyelinating lesions (TDLs)]
-
-
CT Findings
-
CECT
- Iso-/hypodense ± mild/moderate enhancement - Both solid and ring enhancement patterns
-
-
MR Findings
-
T1WI
- Typically hypo- or isointense - Hypointensity correlates with axonal destruction (black holes) - Complete tissue loss following inflammatory injury - T1-hypointense lesions suggest worse prognosis - Correlated with disability, atrophy, progressive disease - Hyperintense dentate nuclei seen in secondary progressive form -
T2WI
- Hyperintense, linear foci radiating from ventricles - Also prevalent in subcortical U fibers, brachium pontis, brainstem, and spinal cord - Lesions tend to be well demarcated - High cortical disease burden can be predictor of PPMS - Hypointense basal ganglia 10-20% of chronic MS -
FLAIR
- Most sensitive sequence for brain lesions but relatively unhelpful in spinal cord - Earliest finding: Alternating linear hyperintensity along ependyma on sagittal FLAIR - Ependymal dot-dash sign - Bilateral, asymmetric, linear/ovoid hyperintensities - Perivenular extension; Dawson fingers - Along path of deep medullary veins - Hyperintensities become confluent with ↑ severity -
DWI
- Majority of acute plaques: Normal or ↑ diffusivity - Few acute MS plaques may show restricted diffusion - Often at margins of acute plaque - Subacute/chronic plaques: ↑ diffusivity - DTI: Reduced longitudinal diffusivity in areas of axonal injury -
T1WI C+
- Transient enhancement during active demyelination (> 90% disappear within 6 months) - Nodular (68%) or ring (23%) - Semilunar, incomplete, horseshoe-shaped (9%) - Rare: Large, tumefactive enhancing rings -
MRS
- ↓ NAA (NAA/Cr), ↑ choline (Cho/Cr), ↑ myoinositol - MRS abnormalities found in normal-appearing white matter - Only secondary progressive MS shows ↓ NAA in normal-appearing gray matter - May allow early distinction between relapsing-remitting and secondary-progressive -
Perfusion MR (contrast-enhanced T2*): Low rCBV - Can separate tumefactive MS from neoplasm
-
Magnetization transfer (MT) - ↓ MT ratio (MTR) in lesions/normal-appearing white matter
-
Functional connectivity MR (fcMR) - ↓ functional connectivity between right/left hemisphere primary visual and motor cortices
-
3.0 T vs. 1.5 T: 21% ↑ number of contrast-enhancing lesions, 30% ↑ enhancing lesion volume, 10% ↑ total lesion volume
-
-
Imaging Recommendations
-
Best imaging tool
- MR -
Protocol advice
- Contrast-enhanced brain MR with FLAIR - Sagittal thin T2 FLAIR sequence in midline - To identify callosal-septal interface demyelinating lesions - Fat saturation to assess for optic neuritis (ON)
-
DIFFERENTIAL DIAGNOSIS
-
Acute Disseminated Encephalomyelitis
- Viral prodrome, monophasic illness; more common in children
- Can mimic MS; gray matter often involved
- Lesions tend to be larger, more edematous, and often symmetric compared to MS
-
- ON and spinal cord lesions
- Brain lesions look atypical for MS, tend to border midline CSF spaces
-
Autoimmune-Mediated Vasculitis
- Enhancing lesions spare callososeptal interface
- Beaded angiogram appearance
-
Leukodystrophies and Mitochondrial Diseases
- Consider in younger patients and atypical presentations
- Genetic &/or laboratory confirmation
-
- Can be identical to MS (skin rash common)
-
- Classic triad: Encephalopathy, branch retinal artery occlusions, hearing loss
PATHOLOGY
-
General Features
-
Etiology
- Unknown; probably virus &/or autoimmune mediated in genetically susceptible individuals - Proposed environmental triggers for MS include exposure to infectious agents (Epstein-Barr virus in particular), low serum vitamin D levels - Higher MS prevalence in northern latitudes has prompted theories about role of vitamin D metabolites in MS pathogenesis - Activated T cells attack myelinated axons - Cox-2, iNOS may cause excitotoxic death of oligodendrocytes - To date, causation has not been proved for any of proposed pathogenic etiologies -
Genetics
- Multifactorial; ↑ incidence in 1st-order relatives
-
-
Staging, Grading, & Classification
- Major clinical subtypes - Relapsing-remitting (RR) 85% initial presentation - Secondary-progressive (SP), a.k.a. relapsing progressive - By 10 years 50%; by 25 years 90% of RR patients enter SP phase - Primary-progressive (PP), a.k.a. chronic progressive - 5-10% of MS population progressive from start - Progressive-relapsing (PR) - Rare; defined as progressive disease with clear acute relapses ± full recovery - Periods between relapses characterized by continuing disease progression - Radiologically isolated syndrome(RIS) - MR findings satisfy criteria for dissemination in space, but with no attributable MS signs and symptoms - Increasingly recognized in pediatric population - Presumed that some will transition to formal MS diagnosis over time
- MS variants/subtypes - Malignant/Marburg disease: Younger patients, febrile prodrome, clinically fulminant, death in months - Schilder type (diffuse sclerosis): Extensive, confluent, asymmetric demyelination in bilateral supra-/infratentorial parenchyma - Balótype (concentric sclerosis): Large lesions with alternating zones of demyelinated/myelinated white matter
- 2017 revised McDonald criteria for MS diagnosis - Dissemination in space - ≥ 1 T2-hyperintense lesion(s) characteristic of MS - In at least 2 of following 4 areas - Periventricular, juxtacortical, infratentorial, spinal cord - Dissemination in time - Simultaneous presence of gadolinium-enhancing and nonenhancing lesions at any time orby new T2-hyperintense or gadolinium-enhancing lesion on follow-up MR with reference to baseline scan, irrespective of timing of baseline MR - Unlike 2010 McDonald criteria, no distinction between symptomatic and asymptomatic MR lesions is required
-
Gross Pathologic & Surgical Features
- Acute: Poorly delineated, yellowish-white, periventricular plaques
- Chronic: Gray, granular, well-demarcated plaques ± generalized volume loss
-
Microscopic Features
- Perivenous demyelination, oligodendrocyte loss - Active: Foamy macrophages with myelin fragments, lipids; reactive astrocytes + perivascular inflammation; atypical reactive astrocytes, mitoses (mimic tumor) - Chronic: Marked loss of myelin, oligodendrocytes; dense astrogliosis; minimal/no perivascular inflammation
- Axonal transection
- CSF positive for oligoclonal bands
CLINICAL ISSUES
-
Presentation
-
Most common signs/symptoms
- Variable; initially impaired/double vision of acute ON - ≈ 50% with positive MR develop MS - Weakness, numbness, tingling, gait disturbances - ↓ sphincter control, blindness, paralysis, dementia - Cranial nerve palsy; usually multiple, 1-5% isolated (CNV, CNVI most common) - Spinal cord symptoms in 80% -
Children may have similar clinical presentation to adults - Clinically distinct episodes of ON, brainstem or cerebellar syndrome, or transverse myelitis followed by at least partial resolution
-
More likely (than adults) to present with isolated ON, brainstem syndrome, or encephalitic symptoms, such as headache, vomiting, seizure, or altered consciousness
-
-
Demographics
-
Age
- 20-40 years; peak onset: 30 years, 3-5% < 15 years, 9% > 50 years -
Sex
- Adults: M:F = 1:2 - Adolescents: M:F = 1:3 -
Ethnicity
- All groups, but White populations most common - Most often occurs in temperate zones -
Epidemiology
- Estimated 2.5 million people in world have MS - Rare disease; estimated frequency ~ 2.5 per 100,000 children - Most common disabling CNS disease of young adults; 1:1,000 in Western world
-
-
Natural History & Prognosis
- Prognostically, pediatric-onset MS (POMS) portends more inflammatory course and higher relapse rate compared with adult-onset MS (AOMS)
- Relapse recovery is faster and more complete compared to adults, disability progression is slower, and longer time elapses before transitioning to secondary progression
- 34% of patients have initial episode followed by normal or near-normal function
- Unfortunately, given younger age at diagnosis, POMS patients reach comparable level of handicap 10 years earlier than patients with AOMS
- Moreover, POMS can impact children's cognitive function and development - > 50% of MS pediatric patients continue to accrue cognitive deficits within first 5 years after disease onset
-
80% with probable MS, positive MR progress to clinically definite MS
- Majority: Protracted course with progression of deficits
- Late: Severe disability, cognitive impairment
-
Treatment
- Immunomodulators &/or immunosuppressants - Emerging trend toward earlier use of disease modifying therapies to achieve prompt immunomodulatory disease control
- Newer, more specific and effective treatments rapidly entering clinical realm
DIAGNOSTIC CHECKLIST
-
Image Interpretation Pearls
- 95% with clinically definite MS have positive MR findings
4f9b413c-409d-4c27-ad17-6de8aa9ba6d3
References
Selected References
- 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
- Kornbluh AB et al: Pediatric multiple sclerosis. Semin Pediatr Neurol. 46:101054, 2023
- 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
- Teleanu RI et al: The state of the art of pediatric multiple sclerosis. Int J Mol Sci. 24(9), 2023
- De Meo E et al: Dynamic gray matter volume changes in pediatric multiple sclerosis: a 3.5 year MRI study. Neurology. 92(15):e1709-23, 2019
- Makhani N et al: Oligoclonal bands increase the specificity of MRI criteria to predict multiple sclerosis in children with radiologically isolated syndrome. Mult Scler J Exp Transl Clin. 5(1):2055217319836664, 2019
- Fadda G et al: MRI and laboratory features and the performance of international criteria in the diagnosis of multiple sclerosis in children and adolescents: a prospective cohort study. Lancet Child Adolesc Health. 2(3):191-204, 2018
- Otallah S et al: Pediatric multiple sclerosis: an update. Curr Neurol Neurosci Rep. 18(11):76, 2018
- Ruet A: Update on pediatric-onset multiple sclerosis. Rev Neurol (Paris). 174(6):398-407, 2018
- Thompson AJ et al: Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 17(2):162-73, 2018
- Yeshokumar AK et al: Pediatric multiple sclerosis. Curr Opin Neurol. 30(3):216-21, 2017
- Waldman A et al: Pediatric multiple sclerosis: clinical features and outcome. Neurology. 87(9 Suppl 2):S74-81, 2016
- Roosendaal SD et al: Imaging phenotypes in multiple sclerosis. Neuroimaging Clin N Am. 25(1):83-96, 2015
- Aliaga ES et al: MRI mimics of multiple sclerosis. Handb Clin Neurol. 122:291-316, 2014
- Ciccarelli O et al: Pathogenesis of multiple sclerosis: insights from molecular and metabolic imaging. Lancet Neurol. 13(8):807-22, 2014
- Fernandez O et al: Biomarkers in multiple sclerosis: an update for 2014. Rev Neurol. 58(12):553-70, 2014
- Hardy TA et al: Baló's concentric sclerosis. Lancet Neurol. 13(7):740-6, 2014
- Miller TR et al: Advances in multiple sclerosis and its variants: conventional and newer imaging techniques. Radiol Clin North Am. 52(2):321-36, 2014
- Steenwijk MD et al: What explains gray matter atrophy in long-standing multiple sclerosis? Radiology. 272(3):832-42, 2014
- Klawiter EC: Current and new directions in MRI in multiple sclerosis. Continuum (Minneap Minn). 19(4 Multiple Sclerosis):1058-73, 2013
- Filippi M et al: MR imaging of multiple sclerosis. Radiology. 259(3):659-81, 2011
- Polman CH et al: Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 69(2):292-302, 2011
- Calabrese M et al: Cortical lesions in primary progressive multiple sclerosis: a 2-year longitudinal MR study. Neurology. 72(15):1330-6, 2009
- Filippi M et al: Conventional MRI in multiple sclerosis. J Neuroimaging. 17 Suppl 1:3S-9S, 2007
- Janardhan V et al: Multiple sclerosis: hyperintense lesions in the brain on nonenhanced T1-weighted MR images evidenced as areas of T1 shortening. Radiology. 244(3):823-31, 2007
- Traboulsee AL et al: The role of MRI in the diagnosis of multiple sclerosis. Adv Neurol. 98:125-46, 2006
Differential diagnosis
Abnormal Shape/Configuration of Corpus Callosum
DDX:238ca32d-6bc6-4f5a-81b1-6601dd605856
Complex Cranial Nerve IX-XII Neuropathy
DDX:2b17f148-bf71-4b13-8373-d3c65459dd67
Enhancing Cranial Nerve(s)
DDX:6471fb1c-d46d-47cd-8322-1671e82335c3
Hemifacial Spasm
DDX:1b390143-1212-4447-beb3-ed9e85ef34e4
Homonymous Hemianopsia
DDX:1cdca8f4-95f8-4d19-b28a-19a433d1a624
Oculomotor, Trochlear, or Abducens Neuropathy
DDX:58b32fb2-78a3-48c1-9aaf-5222667fe59f
Peripheral Facial Nerve Paralysis
DDX:4da52ac4-c03c-4711-ae7e-bb4f2f7c5ab8
Ring-Enhancing Lesions
DDX:3463ac7a-c216-4fbd-aa73-03166a6ebc52
Signal/Attenuation Abnormalities of Corpus Callosum
DDX:578bd09b-da74-43a2-b068-2d4854a61254
Trigeminal Neuralgia
DDX:294f4a67-30d6-4488-bd1a-931d1f8c7609
Trigeminal Neuropathy
DDX:6d668284-4c8e-4a14-90b6-c7abf86065e6
Vocal Cord Paralysis (Left)
DDX:50022134-773c-4771-b07d-4d64c6c2dbe5
Vocal Cord Paralysis (Right)
DDX:b8a07cab-5427-4efe-b55d-2460fec053db
Anatomy
White Matter Tracts
Brain/ANATOMY:846101a2-e892-4c70-9a32-c9fa887d073a
Language Overview
Brain/ANATOMY:40f2ed79-0d31-4943-aaa2-7c3244a7e87b
Cranial Nerves Overview
Brain/ANATOMY:1edc42e3-5c31-42b9-b8b8-44cc3bd38432
Olfactory Nerve (CNI)
Brain/ANATOMY:c4a6920b-a112-4a51-921f-60d2f0a479ef
Optic Nerve (CNII)
Brain/ANATOMY:54712d62-1940-4028-8161-4cfd3c4dbb20
Oculomotor Nerve (CNIII)
Brain/ANATOMY:495aba11-106f-439d-8516-6a445b085919
Trochlear Nerve (CNIV)
Brain/ANATOMY:cc69e654-b9cd-465b-8437-fba44f3c034b
Trigeminal Nerve (CNV)
Brain/ANATOMY:06e99da6-48fc-45f4-a571-97d12a15f365
Abducens Nerve (CNVI)
Brain/ANATOMY:655e63da-d744-4267-9d90-07f52493bbc0
Facial Nerve (CNVII)
Brain/ANATOMY:2f4818dd-6438-405b-8561-5cbbb9c91562
Vestibulocochlear Nerve (CNVIII)
Brain/ANATOMY:498e844d-faca-4c6a-bff1-9c6ad4993e62
Glossopharyngeal Nerve (CNIX)
Brain/ANATOMY:172680f5-d290-4a02-b07e-63c1da75e148
Vagus Nerve (CNX)
Brain/ANATOMY:68b6ede4-c797-4d55-8d29-aed3df441741
Accessory Nerve (CNXI)
Brain/ANATOMY:9d50453e-c26a-46a3-826e-265736e43174
CNXII (Hypoglossal Nerve)
Head and Neck/ANATOMY:f734d678-561c-47fd-afb5-dab6afacc1a8
Optic Nerve/Sheath Complex
Head and Neck/ANATOMY:fdb933e1-ce0c-4f99-9ddb-cbe5f3b0f015
Cranial Nerves Overview
Head and Neck/ANATOMY:170ad135-ca16-497a-80de-5a24b9ca2f47
CNI (Olfactory Nerve)
Head and Neck/ANATOMY:54c329dd-8363-4b61-9af3-bf78909ea790
CNII (Optic Nerve)
Head and Neck/ANATOMY:1b5322bb-bdca-4605-9ab5-43598b5c322f
CNIII (Oculomotor Nerve)
Head and Neck/ANATOMY:ad21daaf-1f28-4f9c-bc74-3d0142c167ab
CNIV (Trochlear Nerve)
Head and Neck/ANATOMY:52486223-9cb5-43f5-b9af-c46431ae6637
CNV (Trigeminal Nerve)
Head and Neck/ANATOMY:9db87cfa-58ff-45fd-a7fd-fe8c73eb9770
CNVI (Abducens Nerve)
Head and Neck/ANATOMY:923d7c4a-93a3-42ba-b8db-c7b15348e473
CNVII (Facial Nerve)
Head and Neck/ANATOMY:98cb2d45-e64c-4295-9662-3470cd46513a
CNVIII (Vestibulocochlear Nerve)
Head and Neck/ANATOMY:e9917c41-94c9-46aa-b9d8-b196c375d35b
CNIX (Glossopharyngeal Nerve)
Head and Neck/ANATOMY:2e74a767-3f28-49be-a50f-1dbcc10ce90f
CNX (Vagus Nerve)
Head and Neck/ANATOMY:83868689-c995-4608-bed3-f59664cbd586
Brain
Ultrasound/ANATOMY:080771c2-02f3-408d-ad70-04a80d849500
Hypoglossal Nerve (CNXII)
Brain/ANATOMY:71012f02-fab7-42ed-bc60-e584dc229ccb
CNXI (Accessory Nerve)
Head and Neck/ANATOMY:18e60151-70bc-40a1-9b4f-4b86f8fd65c2
Cases
- {'cases': [{'authors': [{'key': 'bee1f359-33fb-4cba-9e6b-ed1ca1842439', 'value': 'Jeffrey S. Ross, MD'}], 'caseVersionId': 'a9ec521a-8d2e-4d27-9e87-79eaf424d678', 'description': 'Classic appearance of Devic disease, involving the optic nerves and spinal cord, with no brain parenchymal abnormalities.\n\nBrain examination (#1-4) shows normal FLAIR (#1), and markedly enhancing right optic nerve and chiasm (arrows, #3, 4). There is also abnormal T2 hyperintensity in the left optic nerve on the STIR image (open arrow, #2).\n\nEvaluation of the spinal cord (#5-10) shows a long segment of cord enlargement with T2 hyperintensity, and ill-defined enhancement (arrows).', 'history': 'Myelopathic and blind in both eyes.', 'imagePoolId': '98716ff1-9b49-4826-be9e-8d2b4073814e', 'name': 'Devic Disease (neuromyelitis optica)', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'de2e7c22-1bbb-4ca4-94ea-5a530e24b723', 'description': 'Axial T1WI (#1) with close-up view cropped and adjusted to emphasize the subtle signal abnormalities in this case (#2) show multiple hypointense lesions in the deep cerebral and periventricular white matter. Note slight, hazy "rings" of subtle T1 shortening surrounding many of the lesions (arrows). These lesions are sometimes termed "lesions within a lesion" or "ghostlike rings" of T1 shortening, presumably due to coagulative necrosis in the periphery of chronic MS plaques. The T2WI (#3) and FLAIR scans (#4-7) in this patient show the classic periventricular lesions of MS.', 'history': 'Known MS.', 'imagePoolId': '454e8800-33fe-41df-9e79-25cbb3d8e068', 'name': '3T', 'teachingPoint': None, 'demographics': '39 Years old male'}, {'authors': [{'key': '7cc3ba75-2642-4233-b9f6-0ce69ffe28f3', 'value': 'Sheri L. Harder, MD, FRCPC'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '7de44e74-cd6f-4f8b-9658-e92b7eca7903', 'description': "This is a typical MR case of severe multiple sclerosis. \nAxial T2 MR images (Figs. 1-3) demonstrate very hypointense bilateral basal ganglia (
, Figs. 2-3) atrophy (evidenced by ventricular prominence), and confluent periventricular/subcortical hyperintense plaques 
in keeping with severe multiple sclerosis.", 'history': None, 'imagePoolId': 'c9f6813d-c72f-401f-887c-0c914467d34b', 'name': 'Severe', 'teachingPoint': None, 'demographics': '42 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '019e8634-5336-4c86-b8e5-1668535b67f8', 'description': 'Axial T2WI with fat saturation (#1) shows swelling and hyperintensity of the left optic nerve (open arrow). Note protrusion of the swollen optic nerve head in the posterior segment (curved arrow). Axial (#2) and coronal (#3) scans performed after contrast administration show intense enhancement of the enlarged left optic nerve (open arrows). Mild enhancement of the right optic nerve is present (arrow). \n\nComment: The majority of patients with optic neuritis eventually develop frank multiple sclerosis.', 'history': 'Young woman with first episode of optic neuritis. Funduscopic examination disclosed a swollen, elevated optic nerve head with blurred margins.', 'imagePoolId': '083ccf16-2fdb-4ae6-88a8-255ca6366036', 'name': 'Optic Neuritis', 'teachingPoint': None}, {'authors': [{'key': '83f867a5-a183-4396-82ea-384015da4d2f', 'value': 'Gregory L. Katzman, MD, MBA'}], 'caseVersionId': '0f768485-6b53-4896-a247-ecfa60c89422', 'description': 'Classic MS within both infra- and supratentorial brain.\n\nNumerous MS T2 hyperintense plaques (only a few annotated by arrows) are seen throughout the infra- and supratentorium. A few show a classic perpendicular orientation at the periventricular interface (open arrows). Several demonstrate contrast-enhancement (curved arrows). Note lesions are more conspicuous on FLAIR than T2.', 'history': None, 'imagePoolId': '3e8a21e3-3148-45ff-ab88-72af75fbb13e', 'name': 'Classic', 'teachingPoint': None}, {'authors': [{'key': '83f867a5-a183-4396-82ea-384015da4d2f', 'value': 'Gregory L. Katzman, MD, MBA'}], 'caseVersionId': '5a4b8198-a988-494f-85eb-861a1321481c', 'description': "Figures 1-4 represent typical 3 tesla MR imaging, which exquisitely shows nonenhancing, perivenular, MS lesions oriented perpendicular to the callosomarginal interface .", 'history': None, 'imagePoolId': '880ed8f1-e963-46d6-96d6-344d27ca4f1f', 'name': 'Classic, 3T', 'teachingPoint': '3 tesla has the capability to better image the anatomic relationship of MS plaques.'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'c5bb2f4d-9f63-4ba6-903d-69152d897168', 'description': "Sagittal T1WI (#1) shows multiple hypointense lesions in the deep white matter perpendicular to the lateral ventricle (arrows). Note moderate ventricular and sulcal enlargement for patient's age. Axial T2WIs (#2-4) show round/ovoid lesions in pons, periventricular and deep white matter (arrows). The ovoid configuration along white matter veins (open arrow, #4) represents typical perivenous demyelination or "Dawson fingers." Lesions do not suppress on FLAIR (#5,6).", 'history': 'Longstanding diagnosis of multiple sclerosis.', 'imagePoolId': '908a1f3e-65ff-4730-a2c3-6dd959797e8c', 'name': 'Perivenous demyelination, Dawson fingers', 'teachingPoint': None, 'demographics': '47 Years old female'}], 'caseType': 'typical', 'name': 'TYPICAL'} - {'cases': [{'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}], 'caseVersionId': '6485c987-8966-40d8-82b9-f2b6efcb5519', 'description': "Variant MR case of multiple sclerosis where midbrain, pontine and medullary plaques are prevalent. Axial and sagittal FLAIR images (Figs. 1-8) show extensive suprasellar white matter high-signal lesions typical of severe multiple sclerosis in association with midbrain (, Fig. 4), pontine (
, Figs. 2-3, 6), and medullary (F , Figs. 1, 7) plaques. Axial T2 MR images (Figs. 9-12) even more clearly delineate the midbrain (, Fig. 12), pontine (, Figs. 10-12), and medullary (, Fig. 9) plaques.", 'history': 'Patient presents with known multiple sclerosis with recent onset of multiple brainstem associated symptoms.', 'imagePoolId': '17600538-654b-44fe-83d3-71a36871a3ab', 'name': 'Pontine and medullary plaques', 'teachingPoint': None, 'demographics': '26 Years old female'}, {'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}], 'caseVersionId': '71128702-fdcf-40c1-9c2a-fa8f81b00236', 'description': "This is a variant case of MS with both supratentorial and posterior fossa white matter lesions.\n\nAxial T2 MR images (Figs. 1-2) reveal a prominent MS plaque in the lateral pons in the region of the root exit zone of the facial nerve. Axial (Fig. 3) and sagittal (Fig. 4) FLAIR images in this area also show this hyperintense lesion . The typical corpus callosum plaque (, Fig. 5) and supratentorial white matter plaque (, Fig. 6) help confirm the imaging diagnosis of MS.", 'history': 'Patient presents with intermittent paresthesias and headache over a 2-year period. Facial spasms were reported in the 6 months before MR imaging completed.', 'imagePoolId': '8c7dcb70-b7e4-45bf-835f-b9249d50da5f', 'name': 'Pontine plaque', 'teachingPoint': 'Patients with multiple sclerosis (MS) rarely present with hemifacial spasm. Even when they, do < 1/2 the time a pontine plaque is visible.', 'demographics': '36 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}, {'key': '8d0c0f3b-13c2-45ac-8116-3725810235ec', 'value': 'Gary L. Hedlund, DO'}], 'caseVersionId': '61481d0e-8c44-4a25-aebb-9e79dd861ed8', 'description': 'Sagittal (#1) and axial (#2) T1WIs show a hypodense mass in the left posterior frontal/anterior parietal area (arrows). PD (#3), T2WIs (#4, 5) and FLAIR (#6) show the mass is hyperintense (arrows). The lesion is well-circumscribed and shows no surrounding edema. On the coronal FLAIR (#6) the lesion shows a peripheral crescent of very hyperintense signal (open arrow). Sagittal (#7), axial (#8, 9) and coronal (#10) T1C+ scans show an incomplete "horseshoe" area of peripheral enhancement (arrows). The nonenhancing part of the mass is adjacent to the cortex.\n\nThis finding is classic for "tumefactive" demyelinating disease, most commonly MS. Frozen section of tissue removed at biopsy was initially read as low grade astrocytoma but subsequent histologic examination disclosed tumefactive demyelination.\n\nMS is unusual in pediatric cases but this is a classic imaging presentation of a solitary "tumefactive" focus of demyelination.', 'history': '10 day history of right foot weakness. ', 'imagePoolId': '3d995088-1e68-4ec3-931f-a10016aeaaba', 'name': 'classic tumefactive', 'teachingPoint': None, 'demographics': '12 Years old female'}, {'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}], 'caseVersionId': '9de83fe1-bca7-4bfe-9603-7b69db3df097', 'description': "This is a variant MR case of multiples sclerosis that involves the medulla of the brainstem.\n\nSagittal and axial FLAIR images (Figs. 1-2) show a large dorsal medullary plaque that extends somewhat asymmetrically into the left medullary parenchyma. On axial T2 images (Figs. 3-4) the large plaque is visible (, Fig. 3) as are multiple more inferior and right-sided plaques (, Fig. 4).", 'history': 'Patient presents with history of multiple sclerosis and recent onset of right body numbness and hoarseness.', 'imagePoolId': '62a5e4f3-a927-4530-acc0-2682a7b341d1', 'name': 'Medullary plaques', 'teachingPoint': None, 'demographics': '37 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '3fe0582d-9996-41e9-9319-47b2a7a69f18', 'description': 'Axial T1WI (#1) shows a cystic-appearing mass in the right parietal lobe (open arrow). The lesion (open arrows) is very hyperintense on T2WI (#2) and does not suppress on FLAIR (#3). Note additional white matter lesions in the corpus callosum and frontal lobe (arrows). Axial T1C+ scan (#4) shows a thin rim of enhancement around the lesion (open arrow) and a very subtle enhancing lesion in the corpus callosum (arrow). The coronal T1C+ scan (#5) shows a classic incomplete rim ("horseshoe") of enhancement. The lesion does not restrict on DWI (#6) and is hyperintense on ADC (#7).\n\nClassic multiple sclerosis with a large "tumefactive" demyelinating lesions as well as a few scattered white matter foci near the ventricles and corpus callosum.', 'history': 'Clinically suspicious for MS.', 'imagePoolId': 'c39d220a-c6f3-4b6b-9f62-9da32c86c428', 'name': 'Ring-enhancing', 'teachingPoint': None, 'demographics': '23 Years old female'}, {'authors': [{'key': '40294e37-1dd3-4403-961c-b944b04e62bd', 'value': 'Richard Hewlett, FRCPath'}], 'caseVersionId': 'b9aa851f-7563-4650-8f74-3bdf0d653a87', 'description': 'Variant case of a large solitary demyelinative lesion with brain swelling, in a patient in the sixth decade.\n\nMR images (#1-5) show a near-round mass lesion in the R centrum, with a thin, conspicuous isointense rim on the T2WI (open arrow, #1). This image distinguishes the different external (parenchymal edema) and internal signal (lesion) hyperintensities. The lesion exhibits homogeneous, although discontinuous enhancement after contrast administration (#3, 5); note, moderate suppression of homogeneous lesion contents on the FLAIR sequence (#2). \nFindings considered most suggestive of tumefactive demyelinating disease.\n\nMicroscopy: Intraoperative cytology (#6, H&E x400) shows foamy macrophages (arrow) within a meshwork of axons. Paraffin processed tissue shows complete loss of myelin sheaths with residual myelin debris in macrophages (open arrows, #7, H&E-LB x400), macrophages (#8, CD68 x400), and axons widely separated by inflammatory cells (#9, Neurofilament x400). Morphologic findings consistent with inflammatory demyelination, presumably idiopathic.\n\nComment: Despite the radiologic diagnosis, the patient was subjected to stereotactic biopsy on the suspicion of glioma, yielding a single core of clearly discolored, softened tissue, part of which was squashed for cytologic examination in theater, the rest of the sample being fixed in formalin (UCT frame, needle bore 3 mm). Intra-operative cytology showing hordes of large round cells was initially diagnosed as being likely to represent oligodendroglioma, but intact axons with adherent macrophages most suggestive of demyelination. Histologic proof of macrophages with immunohistochemical (anti-NF antibody) demonstration of axonal conspicuity with interspersed inflammatory infiltrate confirms the diagnosis, and distinguishes demyelination from ischemic injury. \nSolitary demyelinative lesions with associated brain swelling are understandably suspected of being neoplastic, especially on CT, and when appropriate to age. MR features, particularly the pattern of contrast uptake, are now considered characteristic in their way, and are particularly important in the context of pediatric disease. Examination of autopsy material suggests that vascular proliferation/leakage evolves on the lesion periphery, consistent with enhancement, whilst the greatly widened interstitial space forming the demyelinated core is reflected as perturbed water on the FLAIR sequence.', 'history': 'Previously well, normotensive woman. Presented acutely (days) with onset of severe headache followed by L hemiparesis. Apart from weakness, the neurological examination was normal, including funduscopy.', 'imagePoolId': '3d48b4c6-3ebe-48e6-a44b-b7748c6c457a', 'name': 'Solitary, tumefactive', 'teachingPoint': None, 'demographics': '46 Years old female'}, {'authors': [{'key': '7cc3ba75-2642-4233-b9f6-0ce69ffe28f3', 'value': 'Sheri L. Harder, MD, FRCPC'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'fd0cac8a-dcb8-4f24-b400-d8f125491f7a', 'description': 'Variant CT, MRI and MRS case of tumefactive multiple sclerosis.\n\nAxial NECT (#1) demonstrates extensive right parieto-occipital white matter edema (arrow). Axial FLAIR MR images (#2-5) also demonstrate marked white matter edema (arrow) with extension into the corpus callosum. There is a central hypointense mass (curved arrow) which causes mass effect on the adjacent lateral ventricle and effaces the regional sulci. Axial (#6) and coronal (#7) T1 C+ MR images demonstrate ill-defined enhancement at the margin of the white matter edema (open arrows). Long TE MRS (#8) reveals elevated choline (arrow), decreased NAA (open arrow), and a lactate doublet (curved arrow). These MRS findings could be consistent with acute demyelination and probably reflect a combination of membrane disruption, neuronal loss or dysfunction and inflammation.\n\nComment: Although MR spectroscopy can be helpful in evaluation, the MRS findings in multiple sclerosis are not specific. The spectral pattern of demyelination and low grade neoplasms can be similar, and should therefore be interpreted cautiously.', 'history': None, 'imagePoolId': 'be36e86d-23a4-498a-b614-f6b91c73cb95', 'name': 'Tumefactive, Balo type', 'teachingPoint': None, 'demographics': '8 Years old female'}, {'authors': [{'key': 'bee1f359-33fb-4cba-9e6b-ed1ca1842439', 'value': 'Jeffrey S. Ross, MD'}], 'caseVersionId': '37f29d50-e59d-4bd3-893c-6b86eb49257a', 'description': 'Classic pattern of tumefactive demyelination disease, with partial ring enhancement.\n\nMR study (#1-7) shows large T2 hyperintense lesion in right frontal lobe with mild mass effect, and diffusion restriction along the periphery. Following contrast, there is intense enhancement of a portion of the periphery of the lesion. \n\nComment: This pattern of enhancement makes the diagnosis of demyelinating disease highly likely. Tumor and abscess would all show a complete ring of enhancement.', 'history': 'Presented with weakness. Followup study 2 months later showed marked resolution of the lesion.', 'imagePoolId': '920fd052-87a5-41d5-840e-4a78e3d07715', 'name': 'Tumefactive', 'teachingPoint': None, 'demographics': '65 Years old female'}, {'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}], 'caseVersionId': 'fb51616f-a24f-4509-9cbb-f03109749515', 'description': 'Variant MR case of multiple sclerosis (MS) involving both supratentorial white matter and pons-medulla. Lateral pontine plaque is seen associated with enhancing preganglionic segment of the trigeminal nerve.\n\nAxial T2 MR images (#1-4) best delineate the large left lateral pontine MS plaque (curved arrow) with involvement of the root entry zone of CN5 (open arrow, #4). The left middle cerebellar peduncle (open arrow, #2) and bilateral inferior cerebellar peduncles (open arrows, #1) are also affected. Sagittal FLAIR image (#5) shows both the typical supratentorial white matter plaques and the lateral pontine lesion (curved arrow) pointing into the root entry zone (open arrow) and preganglionic segment CN5 (arrow). \n\nEnhance axial (#6-7) and coronal (#8-10) T1 MR images reveal an enhancing preganglionic segment of CN5 on the left (arrow). Interestingly, the root entry zone area of CN5 on the left does not enhance (open arrow) nor does the lateral pontine MS plaque (curved arrow).', 'history': 'Patient presents with previous history of multiple sclerosis and new onset of left trigeminal neuropathy.', 'imagePoolId': '5ce11fd3-2fe9-4356-ab61-259c2a213f78', 'name': 'Pons, medulla plaques; CN5 involvement', 'teachingPoint': None, 'demographics': '48 Years old female'}, {'authors': [{'key': '83f867a5-a183-4396-82ea-384015da4d2f', 'value': 'Gregory L. Katzman, MD, MBA'}], 'caseVersionId': 'd99b0dc5-cbd0-42ce-805c-c629eda08e60', 'description': 'Variant tumefactive MS plaque; biopsy proven.\n\nSagittal T1 imaging reveals a mass-like lesion which is hypointense (image 1, arrows). Axial MRI shows corresponding FLAIR hyperintensity (image 2, open arrows) and irregular, thick, partial ring-enhancement (images 3 & 4, arrows) about this mass-like lesion in a patient not previously diagnosed with MS. Note the lesion crosses the splenium (images 2 & 4, curved arrows).', 'history': 'No prior history of MS. Biopsy confirmed this as a tumefactive MS lesion.', 'imagePoolId': '64fdb676-adb6-4c62-8a45-87bbd2940cd9', 'name': 'Tumefactive', 'teachingPoint': None}], 'caseType': 'variant', 'name': 'VARIANT'}
Images
Selected Images
Sagittal graphic illustrates multiple sclerosis (MS) plaques involving the corpus callosum, pons, and spinal cord. Note the characteristic perpendicular orientation of the lesions 
at the callososeptal interface along penetrating venules.
Sagittal graphic illustrates multiple sclerosis (MS) plaques involving the corpus callosum, pons, and spinal cord. Note the characteristic perpendicular orientation of the lesions at the callososeptal interface along penetrating venules.
Sagittal T1 MR in a 14-year-old presenting with gait instability and facial numbness demonstrates T1-hypointense corpus callosum lesions 
that represent "black holes" of chronic demyelination. This was the initial clinical MS presentation for this patient.
Axial FLAIR MR in the same patient reveals larger lesions in the right frontal lobe and left periventricular white matter. Note surrounding edema in these more acute lesions.
Axial T1 C+ FS MR in the same patient reveals the characteristic heterogeneous enhancement pattern for a demyelinating process in these more recent lesions , meeting McDonald criteria for dissemination in space and time.
Axial FLAIR MR in a teen patient with acute extremity sensory changes and visual disturbance shows a focal periventricular T2-hyperintense lesion . Imaging also showed additional periventricular and callosal-septal lesions (not shown).
Axial T1 C+ FS MR in the same patient confirms abnormal peripheral lesion enhancement with an incomplete ring pattern .
Sagittal T2 MR in a teenager presenting with acute ataxia demonstrates numerous hyperintense corpus callosum lesions extending to the callosal-septal interface as well as brainstem, cervicomedullary 
, and cord lesions 
.
Axial T1 C+ MR in the same patient confirms ring- and solid-enhancing demyelinating lesions, including a characteristic perpendicular periventricular lesion .
Axial FLAIR MR in a teen patient with acute left body weakness and sensory disturbance shows a tumefactive lesion with surrounding T2 hyperintensity extending into the corpus callosum. Differential considerations include neoplasm and abscess in addition to demyelinating disease.
Coronal T1 C+ MR in the same patient reveals an incomplete ring of enhancement surrounding the mildly hypointense lesion , permitting a diagnosis of tumefactive MS.
Additional Images
Sagittal FLAIR MR in a patient with chronic MS demonstrates diffuse thinning of the corpus callosum with extensive abnormal T2 hyperintensity along the callosal-septal interface, reflecting chronic demyelinating disease.
Axial FLAIR MR in the same patient reveals extensive bilateral white matter demyelinating lesions, predominately periventricular but also within more peripheral white matter. Mild diffuse white matter volume loss with passive ventricular enlargement is present.
Axial T1 MR in the same patient reveals fairly extensive hypointensity within the demyelinating lesions, implying chronic disease with white matter axonal destruction (black holes).
Axial SWI demonstrates the characteristic perivenular location of a demyelinating plaque 
with the medullary vein 
coursing through it.
Sagittal T1 C+ MR shows a large, hypointense mass with a peripheral crescent of incomplete or open ring enhancement . This enhancement pattern is classic for a tumefactive demyelinating disease, most commonly MS.
Axial T1 C+ MR in a young male patient with rapid onset of visual disturbance demonstrates large enhancing demyelinating lesions in the deep and periventricular white matter. Marburg disease is an acute fulminant MS variant.
Axial T1 C+ MR demonstrates concentric laminated "onion bulb" enhancement characteristic of acute Baló concentric sclerosis. Baló concentric sclerosis is a rare, aggressive MS variant characterized by acute onset and rapid deterioration.
Sagittal FLAIR MR shows MS plaques with typical perpendicular orientation at the callososeptal interface along penetrating venules (Dawson fingers) as well as involving subcortical white matter.
Sagittal FLAIR MR shows MS plaques with a hyperintense rim and central hypointensity (latter also hypointense on T1WI; not shown). Note the characteristic posterior fossa lesion .
Axial T1 C+ MR demonstrates nodular enhancing MS plaques. Note the common periventricular location with perpendicular orientation as well as involvement of subcortical white matter.
Axial T1 C+ MR shows irregular, thick partial ring enhancement around a mass-like lesion in a patient not previously diagnosed with MS. This was biopsy-proven tumefactive MS. (Courtesy M. Mirfakharee, MD.)
Sagittal FLAIR MR shows callososeptal hyperintensities radiating from the lateral ventricles with a typical perpendicular orientation, characteristic of MS.
Axial FLAIR MR 3T shows multiple nonenhancing, periventricular, hyperintense MS lesions oriented perpendicular to the callosomarginal interface. These lesions are perivenular along the path of the deep medullary veins and represent Dawson fingers. Confluent lesions are also seen along the right periventricular margin.
Axial FLAIR MR shows confluent periventricular white matter hyperintensity typical of advanced, longstanding MS with loss of discrete, linear, periventricular lesions.
Sagittal T1 MR shows multiple hypointense lesions ("black holes") in the deep white matter related to axonal destruction. Note the associated moderate ventricular and sulcal enlargement.
Coronal T1 C+ MR shows a hypointense mass in the left posterior frontal region with a peripheral crescent of incomplete or "horseshoe" enhancement . This enhancement pattern is classic for tumefactive demyelinating disease, most commonly MS.
Axial T1 C+ FS MR shows bright enhancement of the optic nerves similar to the extraocular muscles in a patient with MS with acute bilateral optic neuritis.