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Flashcards in Multiple Sclerosis Deck (9)
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1
Q

Etiology/risk factors

A
  • multifactorial
  • genetic predisposition
    • e.g. HLA allele for MHC Class 2 (on APC’s), 100s of other immune system-related loci ID’d
  • immunogenic triggers:
    • viruses (EBV, HHV6)
    • autoimmunity
  • vitamin D deficiency
    • certain alleles for genes involving Vit D metabolism assoc w/ increased risk for MS
  • temperate latitudes
    • environmental –> acquire risk of are you move to when young
2
Q

Clinical presentations (3 types)

A
  • Relapsing-remitting pattern (85%)
    • –> Secondary progressive MS (when neurological deficits persist and progress instead of passing
  • Progressive-relapsing
  • Primary progressive
3
Q

Signs and symptoms (10)

A
  1. Focal weakness –> UMN pattern, weakness in progravity mm (elevators, flexors), monoparesis, hemiparesis, paraparesis –> ** can be subtle
  2. Focal numbness/paresthesias –> often bilateral, band-like sensation, tingling
  3. Optic neuritis –> painful inflammation of optic nerve, +/- scotoma (blind spot in eye)
  4. Speech difficulty –> dysarthria/slurring
  5. Lhermitte’s –> flexion of neck causes paraesthesia
  6. Uhthoff’s –> symptoms excerbated by overheating
  7. Coordination/Gait/Balance issues
  8. Bladder spasticity, frequency
  9. Spasticity –> especially in legs
  10. Internuclear ophthalmoparesis (MLF white matter tract demyelination)

** typical symptoms of white matter dysfunction

4
Q

MRI findings

A
  • White matter enhancing lesions (T2/FLAIR)
    • Dawson’s fingers
    • periventricular and/or perivenular
    • Increased water signal where myelin has been disrupted
    • acute or chronic lesions
  • Hypointense “black holes” (T1)
    • chronic demyelinating lesions w/ localized areas of axonal loss, astrocytosis
    • associated w/ MS disability
  • Gadolinium enhancement of lesions
    • BBB breakdown – acute lesions
  • Brain atrophy - over time, assoc w/ MS disability
  • Spinal cord enhancing lesions MRI (FLAIR)
    • Short white lesions
5
Q

Course of MS for relapsing-remitting type

A
  • starts as a primarily immune-mediated process
  • can take several decades to progress to “secondary progressive” phase
  • Secondary progressive phase is more difficult to treat symptoms effectively –> use combinations of existing drugs or more potent drugs, new drugs in pipeline
  • over time, MS becomes neurodegenerative –> a secondary neurodegerative disease
  • brain volume atrophy is accelerated in MS, treatment helps slow this down
6
Q

Pathogenesis

A
  • Immune-mediated inflammatory disease of CNS
  • WBCs cross BBB & secrete cytokines
    • T and B cells, macrophates –> autoimmune attack against myelin antigens –> due to molecular mimicry (?)
    • T lymphocytes form perivascular infiltrate (white lesions on MRI)
  • Results:
    • Demyelination
    • Axonal Injury – correlates with neurologic disability
    • Brain atrophy
    • Damage doesn’t respect vascular boundaries
7
Q

Clinical criteria for MS diagnosis

A
  • neurological symptoms and signs attributd to myelin dysfunction in different regions of the CNS (dissemination in space) and at different times (dissemination in time)
  • Adjunct studies (MRI, lumbar puncture, evoked potentials)
  • No other explanation:
    • lyme sarcoid, B-12 deficiency, HIV, small strokes
8
Q

Adjunct tools to support diagnosis

A
  • MRI
  • Oligoclonal IgG bands (Lumbar puncture)
    • inflammation
    • thought to represent B cell expansion in CNS in response to demyelination (antigen not known)
    • Pleocytosis NOT common
    • 80% of individuals w/ MS
  • Evoked potentials
    • test for impulse conduction delays
9
Q

Treatment strategies for MS

A
  • type 1 IFN
  • antibodies to immune-related proteins
  • trap T cells in lymph nodes
  • block proliferation of activated B and T cells
  • immunosuppressives
  • ** most act to prevent immune activation/inflammation @ periphery