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Multiple Sclerosis

Background

  • Progressive inflammatory disorder primarily manifesting with demyelination of the central white matter

  • Optic neuritis and transverse myelitis (spinal cord lesion) are common presentations

  • Generally develop over a few days; very uncommon to happen suddenly (e.g., patients will complain about a dark spot appearing in their vision that expands over several days)

Evaluation

  • MRI w/ and w/o contrast can identify plaques and determine if they are more acute

    • “Active” MS plaque will enhance, and continues to for weeks (even after treatment)

  • Modified MacDonald Criteria: ≥3 characteristic demyelinating lesions (>1 cm, periventricular, infratentorial (brainstem/cerebellum/cord) or juxtacortical in location) with evidence of separation in time (active and chronic)

  • LP with studies for oligoclonal bands, IgG index, cell count and protein, anti-mog, anti-aqp4

Management

  • Treat flares and optic neuritis with steroids

    • Speeds up recovery, but does not improve the degree of recovery

    • Often dosing starts with methylpred 1g

  • If a patient with known MS has worsening symptoms that are not new, then recrudescence is the likely cause infectious/toxic/metabolic workup and imaging is needed

  • There are several long-term medications; common side effects listed below:

    • Interferon (SQ injections) – flu-like symptoms, injection site reactions

    • Glatiramer acetate (SQ) – injection site reactions

    • Fingolimod (PO) – macular edema, liver injury, increased risk of skin cancer

    • Teriflunomide (PO) – liver injury, hair loss, immunosuppression, teratogenic

    • Dimethyl fumarate (PO) – GI side effects, lymphocytopenia, liver injury

    • Natalizumab (IV) – PML concern, immunosuppression

    • Ocrelizumab (IV) – contraindicated in active HBV infection, cannot give live vaccines

    • Alemtuzumab (IV) – autoimmune disease, rash, headache

Neuromyelitis Optica and Spectrum Disorder

  • Demyelinating disease due to Ab against aquaporin-4 (on oligodendrocytes)

  • Classically causes optic neuritis and longitudinally extensive transverse myelitis

    • Can be more aggressive than MS

  • Diagnose with NMO antibodies and MS workup as above

  • Treated with steroids, but in severe or refractory cases may require PLEX