Karpatkin spring 2013 2

  1. therapeutic nihilism
    "a disbelief in the efficacy or value of therapy, as of drugs, psychotherapy, etc/" ... the doctrine that given a pt's condition, it makes no diff if therapy is given
  2. fem:male ratio of MS pts
  3. I'm going much more minimal in these notes...
    so reread the slides. It's a lot of stuff you basically know, but a review wouldn't hurt.
  4. current thinking on the basica etiology of MS
    interaction btwn genetic predisposition & an inciting environmental antigen --> autoimmune demyelinating response
  5. briefly describe the types of MS: relapsing-remitting, relapsing-progressive,
    chronic progressive, secondary progressive,
    benign, fulminant
    • relapsing-remitting: episodes of deterioration followed by partial recovery
    • relapsing-progressive: episodes of deterioration followed by slower deterioration or plateaus
    • chronic progressive:steady deterioration
    • secondary progressive: begins as R-R, becomes CP
    • benign: occasional symptoms w/o functional impairment
    • fulminant: rapidly progressing --> early severe disability and death

    NOTE: these describe behavior over time, but not the speed or severity
  6. 4 things to look for when diagnosing MS
    • MRI-enhancing lesions: gadolinum is injected, and it'll enhance a lesion if there was a recent inflammation
    • CSF analysis: shows signs of tissue destruction
    • symptoms spatially & temporally distinct: diff locations, 6 months apart
    • history/exclusion: r/o stroke, trauma, tumors, etc
  7. MS can present in so many ways based on where lesions are located. A useful division is spinal cord vs cerebral structures. How will a pt w SC lesions present?
    like an SCI pt, but different bc of heat sensitivity & fatigue
  8. primary vs secondary fatigue
    • primary: general lassitude/lethargy, decreased conductivity (aka fatiguablility out of proportion to the task causing it, decreased endurance)
    • secondary: due to side effects of MS, such as infection, spasticity, depression...
  9. causes for secondary fatigue
    • infection
    • spasticity (increases energy costs of activity)
    • ataxia (increases energy costs of activity)
    • weakness
    • depression (extrinisic, or intrinsic due to poorly placed lesions)
    • sleep deprivation (due to lesions in brain, spasticity, pain...)
    • polypharmacy (as you take more meds, more side effects)
  10. measures of fatigue
    • Fatigue Severity Scale and Fatigue Impact Scale
    • Visual analog scale for fatigue (this is real time)
    • endurance tests (6 min walk test)
  11. can exercise cause further neurologic damage?
    NO! it'll make a pt tired, and it could lead to inappropriate movement patterns and increased falls risk, but it won't worsen the MS
  12. L'Hermitte's Sign
    indicates what?
    • a shock-like sensation in the spine or LEs produced by rapid neck flexion (like in a sneeze or cough)
    • posterior column demyelinating damage
  13. sensory changes in MS pts
    • anaesthesia: rare
    • paraesthesia & dysesthesia: 65% of pts initially present with these ((diff from vascular troubles bc here you won't have claudication or skin changes)
    • BUT, a pt with these may still test normally on a sensory test - able to feel stim, just also feels tingling
  14. trigeminal neuralgia
    • cranial n V palsy
    • due to MS's affinity for trigeminal tracts
    • uncommen
    • extremely painful
  15. primary and secondary cause of weakness in MS
    • primeary: plaques in motor cortex or pyramidal tracts (bi or unilat, UE or LE, mimicking other diseases)
    • secondary: due to disuse
  16. most common initial complaint in MS
    optic neuritis: blurred vision, diplopia, usually transient (2-3 days)
  17. why is there spasticity, hyperreflexia, and pathologic reflexes in MS?
    bc those are caused by UMN lesions
  18. 2 drugs to treat spasticity
    • baclofen (can get it as a surgically inserted pump) ... side effect of lethargy if it's a big dose
    • tizanidine aka zanaflex
  19. weather's impact on MS
    • heat & humidity give transient symptom wersening
    • some pts will benefit from ice vests or drinking cold water before/during/after exercise

    • BUT
    • can use focal heat to treat musculoskeletal disorders (but don't do heated therapeutic pools)
  20. ataxia is due to what region involvement
    cerebellar, occasionally from posterior column involvement

    if vertigo is present, may have ataxic symptoms that are actually due to peripheral vestibular issues
  21. causes of pain in MS
    • sensory disturbances: dysesthesia, L'Hermitte's sign, trigeminal neuralgia)
    • spasms from spasticity
    • musculoskeletal pain due to inappropriate movement patterns due to weakness, disuse atrophy, contractures
  22. psychiatric symptoms of MS
    • in late stages: euphoria
    • depression: reactive, but can be primary (lesions in brain) ... can lead to fatigue, so is usually treated w antidepressants
    • memory loss
    • impaired safety awareness
    • diminished attention
    • frontal affect (Homer Simpson)
    • psychosis: a rare complication, usually due to complications from steroids
  23. bladder presentation in MS
    • it's affected in 80-90% of pts
    • frequent, urgent urinations
    • failure to empty
    • failure to store
    • --> UTI (which can be mistaken for exacerbation
  24. speech and language complications in MS
    • aphasia (Broca's/nonfluent > Wernicke's/fluent)
    • dysarthria (disturbance in muscular control of mouth)
    • poor breath control
    • dysphagia (difficulty swallowing)
  25. breathing changes in MS pts
    • primary - loss of motor control to muscles of respiration
    • secondary - decondition, prolonged positioning that compresses/constricts lungs
  26. gliosis
    proliferation of nervous scar tissue

    in final stages of MS, myelin is replaced by fibrous scarring called gliosis, which inhibits transmission of impulses
  27. oligodendrocyetes
    cells that produce CNS myelin (they also get destroyed in MS)
  28. basic pathology behind MS
    • an autoimmune demyelinating disease characterized by a course of demyelination, slowing down, eventual stopping of saltatory conduction in CNS
    • CNS inflammation --> compression --> ischemia
    • destruction of oligodendrocytes
    • axonal loss
    • gliosis
  29. "plaques" in MS lingo
    demyelinating lesions - they're sharply delineated and can be viewed on MS
  30. which myelin in CNS is a target for MS?
    all of it
  31. typical location of lesions in MS
    periventricular region of lateral ventricals and the optic nerve (that's why optic neuritis is often the first complaint)
  32. what happens to the BBB in MS?
    becomes more permeable, allowing antibodies and immunie cells easier penetration ito the area of the plaques
  33. cytotoxic T-cells and macrophages are present where, leading to what in MS
    in the plaques, leading to edema that can have a mass (displacing)effect, simulating a tumor
  34. how do steroids help in MS
    control the edema resulting from the inflammatory response
  35. a hypothesis on the remission part of MS
    • oligodendrocytes are remyelinating
    • but in later MS no oligs are preserved, and remyelination occurs only at borders of plaques, if at all
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Karpatkin spring 2013 2
Karpatkin spring 2013