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MRI in MS MS Masterclass, Sheffield, March 2019 Dr David Paling - PowerPoint PPT Presentation

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MRI in MS MS Masterclass, Sheffield, March 2019 Dr David Paling Royal Hallamshire Hospital, Sheffield University of Sheffield Overview Diagnosis (and differential diagnosis of MS) Surveillance (Monitoring patients on treatment) The

  1. MRI in MS MS Masterclass, Sheffield, March 2019 Dr David Paling Royal Hallamshire Hospital, Sheffield University of Sheffield

  2. Overview • Diagnosis (and differential diagnosis of MS) • Surveillance (Monitoring patients on treatment) • The future is here (Measuring brain atrophy and other advanced techniques) • Stamp collecting (weird and wonderful)

  3. Diagnosis

  4. “Odd one in” Which of the following 8 cases is MS? (Scans courtesy of Dr. Ian Turnbull)

  5. 2 1 3 PML 4 5 6 8 7

  6. MS HIV CMV PML Lymphoma Behcet’s CVD Sarcoid IRIS

  7. Diagnosis Symptoms consistent with inflammatory demyelination Exclude another pathology Classify demyelinating disease

  8. Diagnosis 3 week history of left sided clumbsiness and falls ü O/E left hemi ataxia Symptoms consistent with inflammatory demyelination û Exclude another pathology

  9. Diagnosis 12 months ago – subacute left hemisensory disturbance – resolved 8 week history of progressive unsteadiness. ü Symptoms consistent with inflammatory demyelination û Exclude another pathology

  10. Diagnosis 12 month history of progressive walking difficulty O/E spastic paraplegia ü Symptoms consistent with inflammatory demyelination û Exclude another pathology

  11. Diagnosis

  13. Diagnosis Periventricular lesions

  14. Juxtacortical lesions

  15. Diagnosis Callosal lesions and Dawson’s fingers

  16. Diagnosis Callosal lesions and Dawson’s fingers

  17. Diagnosis Mistry e et a al. M Mult Sc Scler 2 2015;22:1289-1296 1296

  18. Posterior fossa and brainstem

  19. Posterior fossa and brainstem

  20. Temporal lobe

  21. Optic nerve

  22. Spinal cord

  23. MS vs vascular lesions Vascular Lesions MS lesions Corpus Callosum + +++ U Fibres + +++ Basal ganglia +++ + Infratentorial + +++ Temporal Lobe + +++ Periventricular + +++ Spinal cord - +++ Optic nerve - +++ Dawsons fingers - +++

  24. Atypical lesions:

  25. Atypical lesions:

  26. Atypical lesions:

  27. Atypical lesions:

  28. Atypical lesions

  29. Surveillance

  30. Treatment Monitoring Case St Study • 29 year old man • Initial symptoms 3 year ago – left optic neuritis • Further symptoms 2 years ago – sensory disturbance both legs • Started on interferon beta-1a 1 year ago • “Stable” • Difficult to characterise difficulties at work needing 8 weeks off in the context of mood disturbance • Mild increase in tone, brisk reflexes, upgoing plantars, reduction in vibration sensation below knees, positive rhombergs test.

  31. What would help you.

  32. Enhancing lesions

  33. Enhancing lesions

  34. Monitoring treatment effect 12 Rio et al. Multiple Sclerosis 2009;15:848 9.8 10 8.3 8 7.1 6.5 6 4.4 4 3.3 2 1.1 1 1 0.5 0 No relapse, Relapse, no Progression with Relapse and new Relapse, progression, new progression, no new MRI lesion MRI lesion progression and lesions new lesions new MRI lesion Odds ratio of further relapses at 3 years Odds ratio of progression at 3 years

  35. Monitoring treatment effect EDSS increase of at least 1 point Confirmed at 6 months at 5 years

  36. MRI only MS or the tip of the iceberg • MRI lesions occur 7-9 times more Relapses frequently than clinical relapses MRI

  37. “MRI only MS” or the whole iceberg? n=17 n=82 SDMT: Symbol Digit Modalities Test

  38. “MRI only MS” 20% of people with GAD lesion had reduction in symbol digits modality test of at least 4 points All in frontoparietal areas. Not recognised by patients Some recognised by carers 1. Pardini et al. Isolated cognitive relapses and informant based evaluation of neuropsychological performance in MS. Poster at ECTRIMS 2015

  39. Surveillance

  40. Surveillance • MRI within the first year can predict longer term response to interferons • Addition of clinical markers can increase reliability • “Subclinical” lesions can have demonstrable and persistent effects upon cognition

  41. Clinical case • 22 year old man – training to be a solicitor • Oct 14 Subacute ascending spinal sensory syndrome with ataxia • March 15 Bilateral leg weakness; uses stick for 6 weeks • Returns to work, sport, walking unlimited • Increased tone , mild weakness, reduction in vibration sensation left leg

  42. Clinical case • Spinal onset and subsequent relapses • Short duration between first and second relapses • Poor recovery after second episode (EDSS 1.5) • Spinal cord and multiple brain lesions including posterior fossa • Contrast enhancing lesions on MRI scan • 25 birthday 50% chance of moderate disability (EDSS 3 or higher) • 27 birthday 1/3 chance walking 100m with stick (or worse)

  43. Reduction in annualised relapse rate 1.6 1.4 1.2 80% 1 0.8 0.6 0.4 0.2 0 Placebo Natalizumab Annualised Relapse Rate Hutchinson M, et al. J Neurol. 2009; 256:405-15

  44. • 3 years of treatment • Personality change. Somnolent Images courtesy of Prof Wattjes

  46. • JC virus • Asymptomatic infection • Persists in quiescent state in kidneys, bone marrow and lymphoid tissue • Immunosuppresion • Mutated pathogenic form of virus

  47. • Symptoms of PML • Subacute (weeks to months) • Cortical features • Dysphasia • Behaviour changes • Visual field defects • Hemipareisis • Seizures

  48. Treatment of PML • Suspend Natalizumab, Plasma Exchange, Steroids 1,2 • Short duration symptoms, localised disease good prognostic factors 3,4 Mortality 30 25 20 15 9 fold 10 5 0 Symptoms Asymptomatic Mortality

  51. With great power comes great responsibility • Presymptomatic MRI phase of PML • If PML picked up at this stage and treated then • mortality is less (1 in 30 vs 1 in 4) • Neurological disability is less • JC Virus index and length of time on treatment can predict risk which can be used to determine frequency of scanning

  53. Grey matter

  54. Atrophy

  55. Atrophy

  56. Atrophy

  57. Diffusion tensor imaging Decreases in fractional anisotropy, and increases in mean and radial diffusivity seen

  58. Sodium MRI

  60. The Future is here • MRI only visualises a proportion of pathology of MS • Techniques exist that can image • Grey matter lesions (DIR, PSIR) • Neuroaxonal loss (Atrophy) • White matter microstructural changes below resolution of imaging voxel (DTI and others) • Neuroaxonal metabolic dysfunction (Sodium imaging and others) • Of these atrophy is closest to clinical use • Issues • Technical – related to scanner and sequence • Patient related – drugs and hydration

  61. Overview • Diagnosis and differential diagnosis of MS • MRI can diagnose MS (even after one relapse) • Predicting the future (disease course) • Early MRI has predictive role – number and location of lesions • Surveillance (Monitoring patients on treatment) • New lesions on beta interferons, particularly in patients that are felt to be relapsing or progressing indicates worse outcome • MRI can detect changes of PML before symptoms – can lead to better outcomes • The future is here (Measuring brain atrophy and other advanced techniques) • We need to work out how to integrate into clinical practise

  63. Case 3 • Cerebellar dysarthria • Nystagmus on lateral gaze + left 6 th nerve palsy • Increased tone in legs • Gd 4 weakness in legs • F/N + heel shin ataxia • Frame to walk

  64. Case 4

  66. Case 3

  67. Case 3

  68. Case 3 4 • What is it? • What else would help?

  69. Case 3

  70. Case 3 4 • ? diagnosis

  71. Case 3 • CLIPPERS syndrome

  72. Case 3

  73. Case 3 • CLIPPERS – Pontocerebellar dysfunction – Responsive to steroids – Homogenous GAD enhancing nodules without ring enhancement or mass effect predominant in cerebellum or pons <3mm in diameter

  74. Case 3 • CLIPPERS is very rare – Largest case series is 19 – Consider if clinical, radiological features add up – Commonly relapses when steroids stopped – Second line immunosuppression

  75. MRI in MS MS Masterclass, Sheffield, September 2016 Dr David Paling Royal Hallamshire Hospital, Sheffield University of Sheffield

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