Multiple Sclerosis: An imaging review and update on new treatments.

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1 Multiple Sclerosis: An imaging review and update on new treatments. Dr Marcus Likeman Consultant Neuroradiologist North Bristol NHS Trust Bristol Royal Hospital for Children

2 MRI appearances - White Matter Characteristic periventricular WM plaques >3mm Also corpus callosum, juxtacortical and infratentorial FLAIR and Double IR Flame shaped best on sagittal images perivenous inflammation Mostly free diffusion May enhance post Gd in first 6-8 weeks Low T1 intensity black holes may become chronic Confluence of lesions later in the disease

3 MS plaques typical appearance Axial T2 Sagittal T2 Double IR

4 MRI Appearances - Brain Postcontrast T1 axial Chronic Black Holes

5 MRI Appearances White Matter Single Large tumefactive lesion Target appearance on T2W images Peripheral enhancement Restricted diffusion Cellular infiltration Seen early in disease course

6 Tumefactive MS Axial T2 Axial T1 post contrast

7 Restricted Diffusion in MS ADC map ADC map Coronal FLAIR

8 Grey Matter Lesions Best seen on Double Inversion Recovery More common in progressive stages Likely substrate for cognitive decline

9 Later Phase of Disease GM and WM atrophy Iron deposition in basal ganglia

10 Optic Neuritis Clinical diagnosis Reduced acuity/colour vision Papillitis MRI Optic nerve hyperintensity on STIR WM lesions Coronal STIR Orbits

11 Spinal cord Disease Focal T2 Hyperintense lesions in cord WM >3mm but <two vertebral body heights Little or no swelling of the cord Occupy only part of cross section of the cord Best identified in cervical region More specific than brain lesions Long section of inflammation >3 vertebral heights Neuromyelitis Optica (NMO)

12 Spinal cord Disease Axial T2 Sagittal T2 Transverse myelitis

13 Limitations of MRI in MS Normal Appearing White and Grey matter Generally poor correlation between volume of T2WM lesions on MRI and function Chronic black holes on T1 indicate more severe destruction correlate better with disability NAWM better demonstrated by advanced techniques

14 MS Diagnosis Clinical: Neurological signs separated in space and time Radiological: New MRI lesions separated in time and space. Scans>3months apart Enhancement on single scan >3months from clinical onset Diagnostic problems Single clinical episode Clinically isolated syndrome (CIS) Primary progressive disease Need to make diagnosis at an early stage Commence new therapies Clinical trials MRI criteria for dissemination in space - McDonald criteria

15 McDonald Criteria out of 4 of the following: A) One Gd enhancing or nine T2 hyperintense lesions if no enhancement B) At least one infratentorial lesion C) At least on juxtacortical lesion (involving U fibres) D) At least three periventricular lesions One spinal cord lesion can be substituted for one infratentorial lesion.

16 Revised criteria 2005 Revision incorporated precise criteria for use of spinal cord lesions in diagnosis: Cord lesions need to be focal to satisfy criteria One spinal cord lesion can be substituted for one infratentorial lesion. An enhancing spinal cord lesion can be used for an enhancing brain lesion Individual spinal cord T2 Hyperintense lesions can contribute to the 9 required overall

17 The Presentations of Multiple Sclerosis Clinically isolated syndrome Radiologically isolated syndrome Relapsing-Remitting MS (RRMS) Primary Progressive MS (PPMS) (Neuromyelitis optica (NMO))

18 Clinically Isolated Syndrome Single episode - not able to diagnose MS Clinical Features Optic neuritis Sensorimotor High rate of conversion if brain WM lesions Up to 15% no clinical progressive despite MR WML +ve Advantage to early use of DMTs: Delay onset of second clinical episode Reduction in WM lesion accumulation

19 Radiologically Isolated Syndrome Radiological lesion without clinical episode May fulfil McDonald criteria Over 2 year period 33% develop clinical episode (CIS) 66% demonstrated radiological progression Faster conversion from RIS to CIS if: Gd enhancing lesions Spinal cord lesions Oligoclonal bands

20 Relapsing Remitting MS Commonest MS course - 85%. 3:1 F:M Average age of onset 30 years Early disease - relapses and periods of remission Accumulate residual deficits from relapses Development of secondary progressive MS (SPMS) SPMS gait disorder requiring mobility assistance Natural history variable and unpredictable 60-70% conversion to SPMS, most in years 15% escape major attacks or SPMS Most important predictor of future disability - time taken to development of SPMS

21 RRMS - Disease Modifying Therapies DMTs are efficacious only in RR phase of MS Reduce relapse rate Delay onset of secondary progressive phase. DMTs three classes Interferons and glatirmer acetate Oral Agents Monoclonal Antibodies MRI monitoring Breakthrough disease before changing agents Screening for side effects

22 First Generation DMTs Interferon beta and glatirmer acetate IM or sc administration Efficacy: Reduce relapse rate by one third Moderates development of new brain lesions over 1-3 years for CIS and RRMS Slow progress of disability only in first 2-3 years Efficacy reduced by neutralising antibodies Favourable safety profiles/minimal monitoring First line agents

23 Disease Modifying Therapies Oral Agents Fingolimod Sequestrates lymphocytes in lymph nodes ~50% reduction in relapse rate vs placebo Greater reduction in MRI activity vs interferons Increased risk of viral infections Acts on cardiac smooth muscle bradycardia 2 nd line agent Terifunomide Efficacy similar to interferons Dimethyl Fumarate Efficacy similar to Fingolimod Fewer side effects Transient flushes and GI symptoms 1 st or 2 nd line

24 Disease Modifying Therapies - Monoclonal Antibodies Natalizumab (Tysabri) First MAB for MS Prevents transmission of lymphocytes across BBB. Greater efficacy than first generation therapies Reduction in relapses(68%), disability scores and all MRI measures. Complication : Progressive Multifocal Leukoencephalopathy (PML) Risk 1in 100 if JC +ve, prior immunosupression and MAB therapy > 2 years Rare if JC ve pre treatment

25 Disease Modifying Therapies - Monoclonal Antibodies - Natalizumab Complications Other viral infections can occur Indications: Breakthrough disease on first line DMTs Short course first line therapy in early aggressive MS 12 monthly MRI required to screen for PML PML

26 Disease Modifying Therapies - Alemtuzumab MAB against CD52 - depletes B, T and NK cells. 70% Reduction in RR, 42% Reduction in disability Reduction of all MRI measures Significant adverse effects Autoimmune thyroid disease (20-30%), ITP, Herpes infections Second line agent for breakthrough disease Herpes simplex encephalitis

27 Primary Progressive MS 15% of MS presentations Average age at onset 40 years No initial relapsing/remitting phase. Disease progressive from outset Equal M:F involvement Clinical Features Spastic paraparesis (85%) Progressive cerebellar ataxia (10-15%) No imaging differences from RRMS Imaging excludes other causes for spastic paraparesis No response to DMTs

28 MRI Prognosis No specific MRI markers at first presentation to indicate prognosis More rapid accumulation of T2 WM lesions in first 5 years - increased disability at 20 years Later in disease measures of cortical and deep grey matter atrophy become more important for prognosis

29 Neuromyelitis Optica (NMO) Neuroinflammatory disorder Antibody to Aquaporin 4 - water channel molecule expressed on end feet of astrocytes Recurrent inflammation of spinal cord and optic nerves Attacks more disabling than MS No secondary progressive phase Lower frequency oligoclonal bands Interferons, Fingolimod and Natazulimab exacerbate the disease Treatment with Azathioprine, Rituximab second line

30 NMO - Imaging findings Longitudinally extensive transverse myelitis (LETM) T2 Hyperintensity >3 vertebral bodies in height Central cord cf peripheral in MS Optic neuritis Brain lesions Mostly similar to MS but silent Occasionally in specific Aquaporin 4 rich areas Medial thalamus around third ventricle Hypothalamus Periaqueductal region

31 NMO - Imaging findings Axial DIR Axial DIR Sagittal T2

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