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Decision Making In DMTs and Symptomatic Therapy for MS: Lessons From Case Studies
PVA Summit-August 2019Orlando, FLMitchell Wallin, MD, MPHChetan Gandhy, MDVonda Ford-Stites, PharmDHeidi Maloni, NP, PhDTerry Lee-Wilk, PhD
DisclosuresMitchell Wallin, MD, Heidi Maloni, PhD, Terry Lee-Wilk, PhD and Vonda Ford-Stites, PharmD has no financial or non-financial interest to disclose.
This continuing education activity is managed and accredited by AffinityCE in cooperation with PVA. AffinityCE, PVA, as well as all accrediting organizations, do not support or endorse any product or service mentioned in this activity. Disclosure will be made when a product is discussed for an unapproved use.
AffinityCE staff and PVA Staff, as well as Planners and Reviewers, have no relevant financial or non-financial interests to disclose.
Commercial Support was not received for this activity
DisclosuresChetan Gandhy, MD
• Grant/research support: None currently• Speaker’s Bureau: Biogen, Genentech, Formerly EMD Serono,
Sanofi• Advisory Board: Biogen, Genentech, Alexion, Sanofi• First Degree Relative that is Medical Director at Genentech
This continuing education activity is managed and accredited by Affinity CE in cooperation with PVA. AffinityCE, PVA, as well as all accrediting organizations, do not support or endorse any product or service mentioned in this activity. Disclosure will be made when a product is discussed for an unapproved use.-AffinityCE staff and PVA Staff, as well as Planners and Reviewers, have no relevant financial or non-financial interests to disclose.Commercial Support was not received for this activity.
Learning OutcomesAt the conclusion of this activity, the participant will be able to:1. Understand the current MS Center of Excellence structure and approaches to care management2. Describe the current MS disease modifying medications and understand their criteria for use in the VA health care system3. Become familiar with challenging MS case presentations and optimizing both MS disease modifying and symptomatic therapy4. Understand how providers in other specialties can assist with the care of patients with MS
CE/CME CreditIf you would like to receive continuing education credit for this activity, please visit:
https://pva.cds.pesgce.com
Topical Outline• Introduction• Case Discussion #1 (Panel & Audience)• Case Discussion #2 (Panel & Audience)• Case Discussion #3 (Panel & Audience)• Case Discussion #4 (Panel & Audience)
• Panel Members: • Heidi Maloni, PhD, NP• Terry Lee-Wilk, PhD • Vonda Ford-Stites, PharmD• Mitchell Wallin, MD, MPH• Chetan Gandhy, MD
Multiple Sclerosis Care• Whole Heath Approach• MSCoE-Primary Care• MS Disease Modifying Therapy and Criteria for Use• MS Symptomatic Therapy• MSCoE-SCI Centers and Multidisciplinary Care
CASE 1
Case 1 - History• 37 year old man of mixed heritage with active RRMS.• Symptom Onset and Diagnosis
• 9/2017 presents to Gen Neuro for left leg weakness/numbness with more falls describes progressive worsening of falls
• 10/21/2017 presents to the ER for room spinning dizziness that is positional with blurry vision – diagnosis is made
• Seen in MS clinic 10/26/2017• EDSS - 3
Case 1 - Symptoms• Cognitive dysfunction• Fatigue• Dysphagia subjective• Left leg weakness with foot drop• Left leg numbness• Room Spinning Dizziness• Intermittent Blurry Vision
Case 1 - medications• Meclizine - Dizziness
Case 1 -ImagingMRI Brain 10/2017Flair SequenceSagittal
Case 1 -ImagingMRI Brain 10/2017Flair SequenceSagittal
Case 1-ImagingCervical Spine MRI SagittalStir
Case 1 -ImagingCervical Spine MRIAxial T2 Arrow shows a dorsal lateral lesion level of C6
Case 1 –ImagingCervical Spine MRIAxialT1 with contrastCentral enhancement at C2
Case 1 – Lab work up• ANA panel negative• RF negative• Lupus Anticoagulant negative• B12: 423• Initial JCV Stratify Ab: 1.38 (positive)• HIV negative• Hep B and C negative• Vitamin D: 49
Neuropsychological Consultation• Cognitive testing indicates primary difficulties in domains of
working memory, processing/psychomotor speed, and verbal learning and memory. Some difficulties in aspects of language, and executive function. Reasoning abilities are largely normal.
• Memory difficulties are likely due to encoding rather than retrieval difficulties. It is possible that slowed processing speed and deficits in working memory are hindering the encoding process.
• Significant decline in verbal learning and memory, working memory, and processing speed compared to results 3 years ago.
• History of depression, chronic pain, and migraine may confound results.
Case 1 – Questions• How do you classify the severity of the patient’s MS?• How would you utilize the severity of the patient’s MS in
treatment decisions?• Is Induction therapy appropriate for this patient?• Thoughts about treatment course taken?
CASE 2
Case 2• 33 year old AA male with active relapsing-remitting MS• Symptom onset and diagnosis:
• 2005 ED without bladder symptoms (age 21yrs)• 2006 bilateral optic neuritis• 2007 (leg weakness and foot drop)-diagnosis made
• Initiated care at DCVA 2009• 2017
• EDSS: 5.5/6.0• Evidence for disease activity clinical and on MRI• Relapses free since 2011
Case 2-Symptoms• Cognitive dysfunction• Fatigue• Dysphagia (mild)• Dysarthria- staccato speech)• Neurogenic bowel and bladder (behavioral management)• Bilateral intention tremor • Left leg weakness with foot drop• Asymmetric spastic paraparesis
• Gait: independent; wears 4lb ankle weight
Case 2-Medications• Calcium carbonate 1.25mg daily• Cholecalciferol 2000IU daily• Fish oil 1000mg twice a day• Quarterly pulse steroid infusions
Case 2-Relapse History• 2009: left foot drop- initiates Ampyra• 3/2010: poor hand dexterity resolved untreated; fatigue• 7/2010 foot drop worsens; note LLE atrophy; difficulty
sleeping (EDSS 6)• 9/2010: orange flashing in left eye; blurred vision;
resolved no tx.• 1/2011 DC Ampyra and improvement in balance and
sleep• 7/2011:retrobulbar optic neuritis with bitemporal
hemianopsia; VA: 0/30; OS: 20/200; steroid tx• 9/2011: several enhancing lesions MRI; tx. Steroids
(EDSS 7.0)
Case 2-MS DMT History• IM Interferon beta 1a: 2007 (clinical break through; flu-like
sx.)• SQ interferon beta 1 b: 2008-7/2011 (dz. break through)• Fingolimod: 10/2011- 3/2012 (PLEVA rash)• Natalizumab: 9/2012- 9/2014 total 24 infusions
• (JCV AB + Index value: 4.21)
• Pulse steroids (three months)• Rituximab: 5/2015 single dose- infusion reaction and
refuses further treatment with rituximab.• Quarterly pulse steroids 2015- to present • Wellness focus (diet- modified Paleo; dark chocolate)
JCV Ab Index Reference:<0.20 negative0.20-0.40 Indeterminate>0.40 Positive
DMT Associated Benefits and Harms• 3/2012: viral syndrome preceded papular rash on trunk
and spread to legs- stopped fingolimod and rash resolved within a month
• 2013: vision 20/20 OU; EDSS: 6 on natalizumab• 6/2013: worsening symptoms; rash on feet, face, palms;
associated with with fever (natalizumab 10 doses); dx.: leukocytoclastic vasculitis; natalizumab held but resumed when rash resolved; rash treated: prednisone, doxycycline, acyclovir
• 9/2014: herpes zoster infection following steroid infusion subsequent to natalizumab discontinuation.
PATHOLOGY REPORT- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -Date obtained: Apr 2012 Gross Description
Specimen #1 is additionally labeled "right abdomen (upper)" andconsists of a single punch biopsy of tan skin (0.3 x 0.3 x 0.4 cm). The undersurface of the specimen is inked blue and the specimen issubmitted in its entirety into cassette 1A.
Specimen #2 is additionally labeled "right medial thigh" and consistsof a single punch biopsy of tan skin (0.3 x 0.3 x 0.4 cm). Thespecimen is submitted in its entirety into cassette 2A.
DIAGNOSIS1. SKIN, RIGHT ABDOMEN, PUNCH BIOPSY:
CONSISTENT WITH PITYRIASIS LICHENOIDES VARIOLOFORMIS ACUTA (PLEVA).
2. SKIN, RIGHT MEDIAL THIGH, PUNCH BIOPSY: MILD SUPERFIVIAL PERIVASCULAR DERMATITIS.
Rash #1
Rash #2
• Biopsy of lesion on left lateral foot consistent with early leukocytoclastic vasculitis
• Skin with moderate perivascular inflammatory cell infiltration including mononuclear cells
• Occasional polymorphonuclear leukocytes and rare eosinophils and focal infiltration in the vascular wall.
• Occasional vessel with fibrinoid necrosis.
• Unknown etiology- either r/t viral etiology or natalizumab
2010Axial T2 FLAIR
2017Axial T2 FLAIR
20172010
T1 post GD-2017T1 pre GD-2010
2010 2017
Discussion• How should we best manage medication side effects?
• What are the next steps with this risk adverse, complicated by autoimmunity, young, African American male patient?
• What nondrug approaches are available and is his current wellness plan and intermittent steroids enough for life?
CASE 3
Case 3 70 year old man with 32 year history of Multiple Sclerosis.• Symptom Onset and Diagnosis
• 1987 presents to Neurologist for bilateral leg numbness• Seen by Neurology – MRI/VEP/SSEP/LP confirmed diagnosis• Minimal relapses and mostly sensory symptoms• 2004 – Sensory loss in LE progresses to weakness• 2009 – He progressed to use of wheel chair• Same time developed bladder incontinence• He notices worsening constipation• Told during this time his MRIs are unchanged• EDSS – 6.5
Case 3 – Clinical Course• 2009 – wheelchair bound/ bladder
incontinence/constipation• 2011 – patient’s wife notices low volume to voice and
weak cough• 2013 – more trouble with pain and hand weakness• 2014 – mild dysarthria• 2015 – worsening cognitive function and sleep
disturbances• 2017 – PFT shows neuromuscular weakness
Case 3 - ImageSagittal Flair – several ovoid lesions
Case 3 -imagesMRI axial T2 – shows atrophy of brainstem and cerebellum
Case 3 -ImagesCervical Sagittal T2 Stir – Shows several lesions with frank spinal cord atrophy
Case 3 -ImagesAxial T2 Cervical spine MRI – shows cord atrophy
Case 3 – DMT History• 2000 – Trialed Copaxone • 2004 – Trialed IFN• 2015 – Discussed oral therapy vs High Efficacy therapy• Patient decided risk does not outweigh benefit of therapy
Case 3 - Symptoms• Paraplegia• Chronic neuropathic pain• Speech study – showed mild dysphagia, weak cough, and
hypophonia, mild dysarthria• PFT – Shows neuromuscular weakness• Bladder incontinence• Constipation• Cognitive fatigue• Central Sleep Apnea• Fine motor weakness of bilateral hands
Case 3-Questions for Discussion?• Patient opted to focus on quality of life, what is the impact
his secondary symptoms have on his functionality?• What methodology and medications might you use to
improve a patient’s quality of life?• What non medication and holistic approaches would you
recommend?• What should the providers be concerned about when
prescribing medications for this patient?• Are there situations where medication could worsen
quality of life for this patient?
CASE 4
Case 453 year old W Hispanic female with history of secondary progressive MS. Onset symptoms were transient numbness and tingling in both legs in 2003, diagnosis 2011 with onset of paraparesis and ataxia. MRI of brain and spinal cord c/w MS and CSF revealed +OCB. Increased gait ataxia forced patient to use cane permanently in 2012. Weight gain increased with development of comorbid DM and HTN.
• PMH: Hyperlipidemia, Obesity, Diabetes mellitus II, HTN• MEDS: Interferon beta 1a, metformin, oxybutynin, lisinopril,
tamsulosin, vitamin D• SH: Married, living with spouse and one teenage daughter,
working as a DoD contractor, no smoking or alcohol
Case 4
Case 4 (continued)• PE:• MSt: alert, orientated to time/place, some deficits in
complex attn tasks and delayed recall• CN: normal• Reflexes: L sided hyperreflexia with + Babinski• Motor: spastic paraparesis (R>LLE)• Sensory: hypoesthesia RUE/R trunk/RLE, mild stocking
loss to pain/temperature bilaterally• CSG: R sided ataxia with FNF and HKS, uses cane to
walk short distance (50-100’) and wheelchair for longer distances
Case 3 (cont.)• 2016-2017: Worsening symptoms fatigue, leg weakness,
bladder urgency/incontinence, and moderate cognitive changes. SDMT: Raw Score:48, Normed Score:82, Percentile Rank:11.7
• Attempts at reasonable accomodations, EEO complaint, fired from DoD contracting job in later 2017
• Poor glucose control (HgbA1c: 11)• Bladder urgency, frequency and incontinence• Depressed mood
Discussion• How do co-morbid conditions influence disability? How
might these issues be managed?• Cognitive dysfunction and mood changes appear to be a
factor in the patient’s job loss. What could be done to intervene?
• What are ways to assess and manage the patient’s neurogenic bladder symptoms
• How would a multidisciplinary care team assist in the management of this patient?
Conclusions• Whole health principle important in approaching patients
with MS• Understanding the risk-benefit of MS DMTs critical for
guiding treatment decisions• Symptomatic care requires an understanding of MS and
the impact of comorbid conditions• MSCoE hub and spoke system of care along with SCI/D
centers offers important spectrum of expertise throughout the life cycle of patients with MS
Decision Making in DMTs and Symptomatic Therapy for MS
Thank you!
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