1) MRI is an important tool for diagnosing and monitoring multiple sclerosis, but clinical information is also needed. 2) Key MRI findings in MS include ovoid lesions perpendicular to ventricles in the white matter, corpus callosum lesions, and asymptomatic medullary lesions. 3) Differential diagnoses require considering other conditions that could cause similar MRI abnormalities such as infections or other inflammatory diseases.

1. MRI & Multiple Sclerosis
in clinical practice
Robert Lavayssière
Sarcelles - France
1st Italian-French Update Imaging – IFUPI
Advanced Multiparametric Imaging - How to use in daily practice
IFUPI – MILAN 2018 march 23-24 www.jfim.org

2. Summary
Ü Clinical approach
Ü Acquisition protocols
Ü Basic signs
Ü Refinements
Ü Differential diagnosis
Ü Take home

3. Epidemiology
• Northern Europe & North America > other regions
• Europe: Prevalence: 83/10 000, Incidence: 4,3/100 000
• Sex Ratio: 2W/1M

4. Clinical aspects
Ü 2 main forms
Ü Relapsing Remitting RR: 58 %
Ü Symptoms > 24 h
Ü Interval > 1 month
Ü Complete or partial restoration
Ü Secondary Progressive SP: 27 %
Ü Progressive handicap
Ü Progression over 6 months
Ü Other forms
Ü Primary Progressive PP: 15 %
Ü Progressive Relapsing: PR
Handicap scale EDSS
RR & SP: earlier beginning 29 vs 40 y
Partnership between clinicians,
neurologist and/or ophtalmologist,
and radiologist

5. Imaging Protocols: brain
Ü T1 2D or 3D before injection (black
holes, baseline before IV)
Ü Axial Flair 2D or 3D
Ü Sagittal: Flair, T2, STIR
Ü Axial T2 thin slices on Posterior Fossa
Ü T1 3D SE post IV Delay between Gd
CA injection and acquisition: 10 minutes
Ü Optional: Magnetization
Transfer post-IV, Diffusion,
Spectroscopy, SWI
Ü Tractography, fMRI…
• Many systems, many sequences
• 1,5 vs 3T: 3D +++
• Know your system: tricks and traps

6. Synthetic MRI…

7. New reading tools
Stéphane Cantin
Clinique du Mail
19, avenue Marie Reynoard
38100 Grenoble
France
stephane.cantin@groupe-du-mail.com

8. Imaging Protocols: medulla
Ü Inaugural
Ü T2 sagittal large FOV no FS
Ü STIR sagittal small FOV
Ü T1/T1 IV small FOV
Ü T2* axial
Ü T1 axial post IV
Ü Known MS
Ü STIR sagittal small FOV
Ü T1 sagittal small FOV
Ü T1 sagittal small FOV post
IV, if needed
Ü T2* axial

10. The Gadolinium question…
Gadolinium deposits in
the brains of patients
without renal disease:
- Xia et al. 2010
- McDonald et al. 2015
- Kanda et al. 2015
Gadolinium deposits in the
eyes of NSF patients
- Barker-Griffith et al. 2010
Gadolinium deposits in the
skin of NSF patients
- Thakral & Abraham 2009
- Birka et al. 2015
Gadolinium deposits in the
liver, lung, kidney, heart of
NSF patients :
- Sanyal et al. 2011
- Swaminathan et al. 2008
Gadolinium deposits in
the femoral bones of
patients after hip surgery:
- White et al. 2006
- Darrah et al. 2009
- Goto et al. 2015

11. New (or rediscovered) sequence
Ü DDIR
Ü DWI

12. 3D DIR
DIR = Double inversion
recuperation
Ü TI: 450 to 625 ms : SB
Ü TI: 2600 ms : LCS
Ü Resolution 1 mm (3D, 3T)

13. Double inversion recuperation DIR
• Fat and water nulling
• Better visualization of
cortical/sub-cortical lesions
• Low S/N
• Some artifacts
DIR
FLAIR

14. T2* /susceptibility imaging
SWI et veinules
SWI et veinules

15. MS imaged

16. Plaques ?
Inflammation Demyelinization Gliosis Axonal loss
T2 High signal High signal High signal High signal
T1 Low signal Low signal
Gd + ? Gd -

17. MS or not?
Ü High signal intensity zone: NOT specific !
Ü Probably MS
Ü Ovoïd (not “nodular/round”)
Ü Corpus callosum lesion (sagittal +++)
Ü Perpendicular to ventricles
Ü Dawson’s digitation
Ü (Asymptomatic) medullar lesion (s)
Ü Not MS (importance of clinical information and biology)
Ü Contrast enhancement lasting > 3 months
Ü Mass effect
Ü Meningeal enhancement

18. High signal intensity zone in MS
Ü Shape
Ü Ovoid
Ü Perpendicular to ventricles
Ü Variable in size, mm to cms
Ü Halo = oedema
Ü Confluence
Ü Topography
Ü Periventricular: lateral, temporal
Ü Sub-cortical: U fibres
Ü Optic nerve (STIR,T2 HR)
Ü Infra-tentorial:
Ü middle cerebellar peduncle
Ü V4 floor
Ü Pons

21. 27 YO F
Non specific symptoms
Referred by GP for LL weakness
Pulmonary embolism post delivery
Birth control : pill

23. 30
YO
Female
Lower
Limb
Weakness
3D 1mm thickness

24. RR MS3D 1mm reconstructed
MT

25. Cortical and sub cortical: DIR>FLAIR
Nelson et al. Am J Neuroradiol 2007

27. Enhancement
Ü “Biomarker”: active inflammation
Ü Early sign, tends to decrease
Ü BBB lesion
Ü Short time span < 3 months,
between 3 w to 1 month
Ü Parallel to size of lesion (s)
Ü (No need to inject higher dose) Annular
C shape
Nodular

28. HR MR veinographie (SWI)
Venula
Plaque
Dawson J. Trans Roy Soc
Edinb 1916
Ormerod et al. Brain. 1987
Peri veinous: Dawson’s fingers

29. FLAIR/DWI

30. Low signal
Ü Acute: oedema. Regression ?
Ü Chronic: “black holes”
Ü Destruction/atrophy
Ü Large plaques
Ü Associated with enhancing and
non enhancing plaques
Ü May be associated, up to 50 %, with
Ü lipid deposits in macrophages :
high signal rings
Ü iron deposits: T2*/SWI signal loss

31. Traps and Tricks
Fosse postérieure : 2D VS 3D
2D FLAIR HR 3D FLAIR
T2 HR
FLAIR 2D vs 3D : 2D better detection,
but more flow artifacts = 3D : PF +++
Posterior fossa,
optic nerve:
thin slices, T2 HR

32. Traps and Tricks
3D T1 SE Better sensitivityFewer or no flow artifact
From Hodel & al

33. 2D Vs 3D FLAIR
3D T1 EG 3D DIR 1/5 3D FLAIR 1/5 2D FLAIR 4

34. Spectroscopy
Acute
Ü Inflammation, demyelinization,
neuronal disturbance
Ü Choline, lactate, lipids, myo-inositol
increase
Ü NAA, creatin decrease
Ü May precede plaque apparition on
MRi
Chronic
Ü Gliosis, neuronal loss
Ü (Sub)Normal spectrum, myo-inositol increase
Ü Neuronal loss: NAA decrease in “black
holes”

35. Medulla
Ü 80 % of RR have medullar
lesion (s) at early phase !
Ü Medullar lesion in 75 to 92 %
of MSs vs 6% in non MS WM
disease.
Ü Look for brain lesion and
vice versa
Ü Cervical: 50 %
Ü Postero-lateral, including gray
matter: not centered !
Ü Size: limited +++
Ü 2 vertebral height (sag) <
Ü Half medulla(axial) <
Ü Often multiple.
Ü High SI on T2, Iso on T1. Gd+ ?
Ü Medulla: normal, swollen,
atrophy…

36. 27 YO F Left LL anesthesia

37. Sequelae

38. Not so usual

39. Optic neuritis
STIR

40. Pseudo tumour
Chol/NAA<2
Long TE
JFR 2010
Chol
NAA
Lactate

41. 2 weeks later
BALO
J. Balo
1928

42. 2nd line treatment
Ü Pre Tt requirements : ≥ 1 Gd +
lesion or ≥ 9 T2 lesions
Ü Follow-up Tisabri (Natalizumab)
Ü Annual JCV* serology -, 3 to 6
months JCV +
Ü MRI evolution ?
Ü Tysabri : sub-clinical LEMP ???
(mortality = about 25 to 30 %)
Ü Gilenya (fingolimod): viral
encephalitis (some case report)
(* Polyomavirus)

43. Radiologically Isolated Symptoms (RIS)
Ü Incidental discovery suggesting
demyelinationg disease fulfilling
Barkhof criteria, in patients without
symptoms: high risk ?
Ü First step: review of brain and spinal
MRI studies…
Ü Second step: control MRI at 3 months:
dissemination? VEP and CSF

44. Jan 2017 Jan 2018
Jan 2017 Jan 2018
RIS ?

45. Jan 2017
Jan 2018

46. Other diagnosis: not MS ???
Importance of clinical input
Ü Age/sex
Ü Type of onset
Ü Associated signs
Ü Infectious
Ü Biology
Multiple diagnosis
Unusual MRI signs for MS ???
Inflammatory/infectious +++
Ü HIV
Ü Neuro-Behcet
Ü Neuro-Sarcoïdis
Ü Lyme disease
Ü Gougerot-Sjögren
Ü Syphilis

47. Clinical and Imaging Integration
Ü Barkhof
Ü ≥ 9 T2 HI lesions or 1Gd +
Ü 1 sub-cortical
Ü ≥ 3 peri-ventricular lesions
Ü 1 infra-tentorial lesion
80 % patients evolve toward MS
Ü Mac Donald (revised)
Ü Spatial spread: ≥ 1 T2 HI lesion in at least 2
out of 4 localization (periventricular,
juxtacortical, infra-tentorial, medulla)
Ü Temporal spreading:
Ü New T2 HI lesion and/or Gd+ at follow
up
Ü Simultaneous Gd - and Gd + lesions at
the same time
Ü Low reproductibility (Korteweg 2007)
Spreading ?
Temporal Spatial
Clinical
(RR/SP)
and/or MRI
Clinical
(new symptoms)
and/or MRI
MRI and MS
Ü MS suspected
Ü Confirm: CDMS
Ü Other diagnosis…
Ü MS not suspected: MS diagnosis
suggested
Ü Follow-up, research

48. Clinical value ? Follow up
Ü No correlation between
handicap and number of lesions
& evolution of EDSS
Ü No MRI difference between RR
and SP
Ü Initial prognosis ?
Ü Worse if multifocal
Ü Optic Neuritis : better
Ü Transverse myelitis do not evolve
toward MS in most cases
Ü Predictive value G+:
Ü Relapse rate: nb G+ initially
Ü No correlation between nb
G+ and EDSS score 12/24
months
Ü Poor prognosis/early Tt
Ü Inflammatory/heavy lesion
weight
Ü Sequela after first strike
Ü Severity of the strike
Ü UnderTt ß Interferon:
probability of failure % nb of
new lesions within one year

49. In the wake of AI…

50. Where are we, really ?
Machine learning…

51. Next step : automated report

52. Routine tools ?
Longitudinal Brain Imaging (LoBI, Philips) Quantibrain (GE)
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53. Conclusion
Ü All that shines is not MS J
Ü Integration of clinical (and biological)
background with “compatible images”.
Ü Handle with care: beware of words…
Ü Follow-up: treatment ???
Ü Look after new tools (AI, Huge Data)