R lavayssiere mri and multiple sclerosis in clinical practice jfim hanoi 2015
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mri and multiple sclerosis in clinical practice
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R lavayssiere mri and multiple sclerosis in clinical practice jfim hanoi 2015
- 1. MRI & Multiple Sclerosis in clinical practice Robert Lavayssière Hanoi, Nov 2015
- 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 M > W in PP form 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 • Many systems, many sequences • 1,5 vs 3T: 3D +++ • Know your system: tricks and traps
- 6. 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
- 8. Safety / (Nephrogenic Systemic Fibrosis) GFR > 60 mL/ mn GFR 30-59 mL/ mn GFR < 30 mL/ mn High-risk: Omniscan, OptiMark, Magnevist OK Warning Contra- indicated Medium risk: MultiHance, Ablavar, Primovist OK OK Should be avoided Low-risk: Dotarem, Gadovist, ProHance OK OK Warning
- 9. Evidence of Tissular Gd deposition 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
- 10. GBCAs and Gd Deposition Ü What we know Ü Linear GBCAs induce T1 hypersignals in brain. Macrocyclic GBCAs do not Ü This effect results from gadolinium deposition. It may last for months Ü It is dose dependent but not strictly limited to multiple (≥ 6) injections Ü It does not require a blood brain barrier disruption nor renal dysfunction Ü Long-term retention has also been observed in patients‘s bones and skin Ü Linear and macrocyclic GBCAs display different tissular kinetic profiles Ü What we do not know Ü Has gadolinium deposition any consequence on brain function or integrity? Ü Are there some more at-risk patients? Ü How long should we wait until symptoms occur? Should we wait and see?
- 11. New sequence Ü DDIR Ü DWI
- 12. 3D DIR DIR = Double inversion recupera4on Ü TI: 450 to 625 ms : SB Ü TI: 2600 ms : LCS Ü Resolu4on 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* / Imagerie de susceptibilité 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
- 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
- 40. Pseudo tumour Chol/NAA<2 Long TE JFR 2010 Chol NAA Lactate
- 41. 2 weeks later BALO J. Balo 1928
- 42. 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
- 43. 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
- 44. 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)
- 45. 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
- 46. 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 ???