Multiple sclerosis

  1. What is multiple sclerosis
    MS is an immune mediated progressive demyelinating disease of the CNS
  2. What is Demyelinaton
    Destruction of myelin the fatty and protien materila that surrounds certain nerve fiber in the brain and spinal cords 
  3. What is the result of Demyelination
    impaird transmissin of nerve impulses
  4. What ages and sex does MS affect
    Age 15-50 and it affect women more often than men.
  5. How is the myelin destroyed?
    T and B lymphocytes cross teh blood brain barrier they are supposed to check the NCS for antigens and leave.  But T cells remain.  The immune system attacks causing randomly scatterd plaques of sclerotic tissues 
  6. What causes MS
    Cause is unknow: environmental exposure at a young age and immunologic causes are implicated.  
  7. Where is it most prevelant?
    Europe, New Zealand, Southern australia, teh norther USA and southern Canada.
  8. How are genetic prediopositons incicated 
    By the presence of specific cluster (haplotype) of human leukocyte andtines on the cell walls
  9. Other factors that can increase symptoms
    • Onset in early adult life,
    • Female 
    • caucasion living in temperte limates 
    • Trigeminal neuralgia 
    • Fatigue, stress, and heat 
  10. Areas most affected by Demyelination
    • optic nerves
    • chiasm 
    • and tracts 
    • the cerebrum
    • the brain stem 
    • cerevellum 
    • spinal cord 
    • The Axons
  11. Relapsing-remitting (RR)
    Acute episodes with almost a complete recovery
  12. Primary-progressive (PP)
    Steady dgenerative progression without exacerbation
  13. Secondary-Progressive (SP)
    Initally RR followed by steady deterioration later in disease process 
  14. Progressive-relapse (PR)
    Progressive but with periodic acute exacerbations
  15. What % of patients have (RR)
    80-85% with each relapse recovery is complete with residual deficits 
  16. Signs and Symptoms of MS
    • varied and multiple reflecting location of he lesion (plaque) 
    • faigue
    • depression
    • weakness
    • numbness 
    • difficultiy in coordination
    • loss of balance 
    • PAIN
    • visual disturbances 
    • blurring visoin
    • diplopia (double vision)
    • Scotoma (patchy blindness
    • total blindness
  17. The most disabiling symptom
  18. What contributes to fatigue
    • Heat
    • Depression
    • anemia
    • deconditioning
    • medications
  19. Pain can lead to what?
    Social isolation
  20. additonal sensory manifestations include?
    • paresthesias
    • dysesthesias
    • propioception loss
  21. medication tx of pain
    • opiods 
    • anti-seisure 
    • antidepressants 
  22. Perimenopausal women have pain related too?
    • osteoporosis 
    • estrogen loss
    • immobility
    • corticosteriod therapy
  23. Spasticity is?
    Muscle hypertonicity 
  24. how does Spasticity affect extremites?
    muscle hypertonicity of the extremites and loss of teh abdominal relexes from involvment of teh main motor pathways (pyramidal tracts) of the spinal cord. 
  25. How is fronal or parietal love involvment seen?
    Cognitive and psychosocial problems 
  26. Severe cognitive changes with dementia are?
  27. Ataxia
    impaird coordination of movements
  28. Involvement of teh cerebellum or basal ganglia can produce?
  29. Objective clinical findings?
    • Charot Triad 
    • intention tremors 
    • nystagums 
    • scalling 
    • clipped speech
    • ataxia
    • shuffling gait
    • increased deeptendon reflexes
    • spastic paralysis 
    • impaired bowl and bladder function 
    • impotance
    • cognitive loss in advanced stage 
    • pallor of optic discs blindness
    • Increaased immunoglobulin G (IgG) levels in the CSF
    • MRI indicates demyelinatin and presence of MS
  30. Life expectancy for PT with MS?
    not dramatically diffrent from those with out MS.
  31. DX of MS is based on?
    Presence of multiple plaques in the CNS Observed in MRI.
  32. Electorphoresis of CSF identified sthe presence of?
    oligoclonal banding (several bands of imunoglobulin G bonded together) which indicates an immune system abnormality.
  33. What is the cure for MS?
  34. Individual TX of MS
    • indicated to relieve the patient symptoms 
    • provide continuing support 
  35. The goal of treatment is?
    • Delay progression 
    • manage chronic symptoms 
    • treat acute exacerbations
  36. Meds for MS include?
    • those for modification and those for symptom managment
    • such as immunomdulatin therapies, immunosuppressive agents.
  37. Disease-Modifying Therapies
    • reduce the frequency of relapse 
    • the duration of relapse 
    • and number and size of plauques 
    • all mes require injection
  38. Interferon beta 1a (Rebif) inerferon 1b (Betaseron) are and admin how?
  39. Avenox is admin how?
    IM q wk
  40. Side effects of interferon beta meds
    • flulike symptoms 
    • potential liver damage
    • fetal abnormalites
    • depressin
  41. Glatiramer acetate (copaxone)
    • Reduces rate of relape in RR 
    • decreases the number of plaques
    • increases the time between relapses
    • admin SQ Q D
    • Side effects are minimal and manageble
    • may take 6 months for evidence of immune response to appear
  42. IV methylprednisolone 
    • the key in treating acute relapse in the RR
    • shorten duration of relapse 
    • exerts anti-inflammatory effect vy acting on T cells
    • 1 gram is adim IV Q D doe 3 days followed by  a oral taper of predenisone. 
    • Side effects include 
    • mood swings
    • weight gain
    • electrolye imbalance 
  43. Mitoxantone (Novantrone)
    • Admin via IV every 3 months
    • reduce frequency of clincia relapses in PT with SP or worseing RR
    • Montior for side effects of cardiac toxicity
  44. Med for Symptom managment?
    • Baclofen 
    • GABA agonis - tx of spasticity
    • Benzodiazepines (valium)
    • Tizanidine (Zanaflex)
    • Dantrolene (Dantrium)
    • Symmeterel 
    • Cylert
    • Prozac 
    • Inderal 
    • Neurontin
    • Klonopin
  45. Assessment/Analysis
    • History of onset and progression of motor and sensory loss
    • factor that intensify symptoms
    • neurologic status 
    • Glasgow Coma scale
  46. Planning and goals 
    • The major goals may include 
    • promotion of physical movility 
    • avoidance of of injury
    • achievement of bladder and bowel continece 
    • promotion of speech
    • swallowing mechanisms 
    • improvement of cognitive function
    • develpompent of coping skills 
    • improved home maintence management 
    • adaptation to sexual dysfunction
  47. Promote physical mobility by?
    • Relaxation and coordination exercises promee muscle efficency.
    • Progressive resistive exercies to strengthen weak muscles.
  48. Exersices?
    • Walking to improve gait
    • if muscle groups are iffeversibley affecte other muscle can be trained to compenste. 
    • teach use of assistive device.
  49. minimizing spasticity and contractures?
    • Severe adductor spasm of the hips wieh flexor spasm of the hips and kness
    • Warm packs can be applied 
    • no hot baths due to risk for injury secondary to sensorly loss
    • increaed temp can incre symptoms
    • Daily exercises for streaching to min contractures
    • Swimming and bicycleing are useful 
    • weight bearing can relive spasticity in th elegs
    • PT should not be hurried may increase spasticity
  50. Activity and rest 
    • work to just short of fatigue 
    • strenous exersice not advised due to increased body temp
    • take short rest periods,preferably lying down 
    • Extreme fatigue may contribute to exacerbation.
  51. Minimize effects of immobility.
    • effects such as 
    • pressure ulcers
    • expiratory muscle weakness 
    • accumulaton of brochial secretions 
    • conduct coughing and deep breathing 
  52. Prevent injury
    • teach to walk with feet apart to widen the base of support and increase stability
    • if positon sense is lost have PT watch feer while walking
    • gait training with assistive devices
    • if gait is ineffective may use wheelchair or motro scooter
    • weighted braclets for movement control
  53. hyperfelexic uninhibited
    inability to store urine
  54. hyporeflexic hypotonic 
    inability to empty bladder 
  55. bladder training 
    • voiding schedule 1.5-2 hrs and increase time
    • drink measured amount of fliud Q2hr and void 30 min later
    • use timer 
    • take meds to TX bladder spasticity
    • intermittent self cath to maintain bladder control
    • bowel problems include fecal impaction constipation and incontince
  56. Commucnication and swallowing difficulties
    • speech therapy
    • take small bites 
    • chew well 
    • use straw with liquied 
    • eat food of more solid consistancy
  57. Vision
    • if cranial nerve affecting vision may use an eye patch
    • for diplopia
    • Prism glasses 
    • talking books
  58. expected outcomes
    • Improve physical mobilit
    • is free of injury
    • attains or maintaind control of bladder and bowel patterns
    • participate 
    • in stratiges to imporve speech and swallowing
    • compenstes for alter thought process
    • demonstrates effective coping stratagies
    • adheres to plan for home maintenace managment
    • adapt to changes in sexual function
Card Set
Multiple sclerosis
Spc Nursing Multiple sclerosis