Multiple Sclerosis

FACTS

  • idiopathic inflammatory disorder affecting optic nerves, cerebrum, spinal cord
  • demographics: 20-40, F > M
  • symptoms disseminated in space and time
  • pathogenesis: oligodendrocytes damage →loss of myelin sheath

HPI

  • parasthesias
  • bladder symptoms
    • urinary frequency, urgency, incontinence
    • libido symptoms
  • visual disturbances
    • double vision, blurring, field cuts
    • acute vision loss, pain with movement
  • spastic paraparesis

    PHYSICAL EXAM

    standard neuro exam
    • internuclear ophthalmoplegia (plaque in MLF)
    • vision tests (optic neuritis)
    • Lhermitte’s sign
    • bilateral trigeminal neuralgia

    IMAGING

    • evaluate for lesions of the optic nerves, brain white matter (esp. periventricular)
    • look for incomplete ("open ring") enhancement on MRI to distinguish demyelinating processes from actual gliomas/abscesses 
    1750163699355-425.png
    Figure 1: open ring enhancement
    1750163715134-356.png

    A/P

    Diagnosis: McDonalds criteria (see below)
    LP for CSF
    • OP normal typically
    • can support diagnosis in some cases

    Notes

    McDonalds Criteria

    # clinical attacks
    lesions
    Additional criteria to make Diagnosis
    ≥ 2
    objective e/o ≥ 2 lesions OR 1 lesion with hx prior attack
    None
    ≥ 2
    objective e/o 1 lesion
    Disseminated in space
    1
    objective e/o 2 lesions
    Disseminated in time
    1
    objective e/o 1 lesion
    Disseminated in space or wait for further clinical attack
    0
    none
    on

    Schilder’s Disease (Myelinoclastic Diffuse Sclerosis)

    • mass-like demyelinating lesion that can mimic glioma or abscess radiographically.
    • Biopsy may be required when diagnosis uncertain
    • MS variant in children with bilateral, large (>2cm) parieto-occipital WM lesions and subacute cognitive/motor decline
    • Pathology: destruction of myelin with relative axonal preservation; perivascular lymphocytic infiltration similar to MS.
    • Etiology: unclear; likely autoimmune with environmental or infectious trigger in genetically susceptible individuals.
    • Differs from MS in its solitary or few large lesions rather than multiple small plaques.
    • Acute management: High-dose IV corticosteroids (e.g., methylprednisolone 1 g/day for 3–5 days), followed by oral taper, Plasma exchange for steroid-refractory cases.
    • Long-term: Immunomodulatory therapy (interferon beta or other MS-directed agents) in relapsing forms.