1. Parkinson's disease is a chronic degenerative disorder of the _________ that produces _______ problems

  2. What is the cause of PD?
  3. Primary or idiopathic PD thought to have ______ and ______ factors

  4. T/F: exposure to specific viruses and toxins can damage cells and activate PD
  5. Characteristics of secondary PD (not true PD)



    vascular disease

    exposure to toxins

    antipsychotic medications

    over-dose of narcotics

    repeated chronic head trauma
  6. Risk factors of PD (4)



    exposure to environmental toxins
  7. Incidence/prevalence of PD
    increases with age

    men are more likely to develop PD
  8. PD is the disruption of which motor system?
    extrapyramidal motor system
  9. Pathophys of PD
    substania nigra in basal ganglia contain dopamine, dopamine is an inhibitory NT that controls movement, cells that have decreased dopamine become overly excited
  10. Overly excited neurons cause what?
    movement and postural abnormalities
  11. Lewy bodies are what?
    clumps of proteins found in the brain of most PD patients

    result from decreased NE
  12. Early signs/symptoms (5) of PD

    muscle weakness

    muscle aching

    decreased flexibility

    less spontaneous change in facial expression
  13. Clinical features (5) of PD
    pill rolling

    increased muscle rigidity

    difficulty initiating movements


    loss of automatic movements
  14. Tremors (affect where first?)
    affect hands, arms, leg first

    then progress to jaw tongue forehead eyelids
  15. PD posture
    stooped, leaning forward, head and neck flexed
  16. non-motor functions

    voice low

    chewing/swallowing issues

    masked face


    memory loss
  17. co-morbidities (4) of PD

    UTI/ respiratory infections


    disturbed sleep, fatigue
  18. Tests of PD
    currently no diagnostic tests but can use MRI, EEG, CAT
  19. Stages of PD (5)


    3-balance problems develop, ambulate w/o assistance

    4-assistance needed during ambulation

    5-w/c bound
  20. Sub-types of PD
    juvenile-extremely rare

    early onset-rare
  21. prognosis of PD
    no cure

    case by case basis
  22. treatments of PD
    meds (levidopa, dopamine agonists, anti-cholinergics, MAO-Binhibs, NMDA, glutamate)

    deep brain stimulation-brain pacemaker

  23. causes of Alzheimers
    exact cause is unknown

    genetic, environmental, lifestyle factors can contribute
  24. mutations on which chromosomes contribute to Alzheimers?
    1, 14, 21, 19
  25. T/F: People with Down syndrome have an increased chance in developing Alzheimers?
  26. which lifestyle factors can contribute to Alzheimers?
    obesity, smoking, diabetes, stress
  27. Environmental factors which can cause Alzheimers?
    viruses, metals (zinc, aluminum)
  28. Prevalence of Alzheimers
    1 in 8 people over 65 has AD

    more women then men

    more education = less chance for AD
  29. 7 stages of AD
    • 1-none
    • 2-very mild cognitive decline
    • 3-mild cognitive decline (friends family become aware of decline)
    • 4-moderate cognitive decline-(detectable by medical interview)
    • 5-moderately severe cognitive decline-noticeable gaps in memory/thinking, need assistance w/ ADLs
    • 6-severe cognitive decline-decline in memory, may have personality changes
    • 7-very severe cognitive decline-
  30. amyloid plaques
    beta-amyloid proteins

    found in extracellular CNS

    stimulates production of free radicals
  31. neurofibrillary tangles
    tau proteins

    lead to cell death
  32. NT's affected
    decrease in Ach in baslis nucleus of meynert

    decrease in serotonin in median raphe

    decrease in NE in locus cerulues
  33. Tests of AD
    only true test is by an autopsy
  34. Early signs of AD
    language problems (foregetting names of common things)

    forgetting where you placed an object

    lost on familiar trips

    personality changes/social impairments

    loss of interests
  35. middle signs of AD
    forgetting details about current events/past events

    change in sleep patterns

    reading/writing impairments


    increased difficulty with ADLs
  36. severe AD
    cant understand language

    cant recognize family members

    cant perform ADLs
  37. subtypes of AD
    • early onset
    • -progresses rapidly
    • appears before 60
    • hereditary link

    • late onset
    • -more common
    • develops after 60
    • may be hereditary
  38. co-morbidities of AD


    muscle contractures

    broken bones

    loss of social instabilities
  39. treatments of AD
    Ach esterase


    Vitamin E


  40. background of MS
    demyelination of brain, spinal cord, cranial nerves

    characterized by remissions, exacerbations
  41. etiology of MS
    unknown cause but may appear as autoimmune

    has genetic, immunlogic and environmental components

    viral infections

    climate can impact a person
  42. incidence/prevalence of MS
    more common in white people

    more common in women

    occurs between 20-40
  43. Relapsing-remitting MS
    most common form

    characterized by exacerbations and remissions followed by partial or complete recovery

    85% of people being with this one
  44. Primary progressive MS
    progression of disability from onset without plateaus of remissions but can have periods of stabilization

    does not experience acute attacks

    10-15% people with MS have this
  45. Secondary progressive MS
    begins as relapsing remitting followed by progression of disability that may include occasional relapses , minor remissions and plateaus

    of the 85% that start out as RRMS more than 50% will develop SPMS within 10 years, 90% within 25 yrs
  46. progressive-relapsing MS
    least common

    shows progression of disability from onset but with clear acute relapses with w/o full recovery

    5% of people have this
  47. Pathophys of MS

    loss of myelin sheath causing loss of saltatory conduction

    affects all types of nerve fibers: sensory and autonomic

    earliest lesions occur as inflammation of myelin sheath lost in white matter of brain and spinal cord
  48. plaques are what and where are they found?
    seen in lateral ventricles of brain, brain stem and optic nerve

    larger areas of inflammation and demyelination
  49. Testing for MS

    neuro exam

    visual/auditory/somatosensory testing


    lumbar puncture
  50. Clinical features of MS
    blurred vision is common 1st sign due to plaques on corticospinal tract

    diplopia, nystagmus, vertigo,

    numbness, tingling, tightness


    progressive weakness, paralysis in UE
  51. motor symptoms of MS
    paraperesis or paraplegia more common than UE weakness

    spasticity more common in legs than arms

    amyotrophy can occur
  52. coordination symptoms of MS
    gait imbalance

    slurred speech
  53. co-morbidities of MS

    complications of immobility

    respiratory infections

    bed sores

  54. Treatments of MS
    no specific treatment at this time

    medications (corticosteroids,beta interferons, copaxone, tysabri,novantrone)

    plasma exchange

  55. Goals of MS (4)
    improve speed of recovery from attacks

    reducing number of attacks and lesions

    slow progression of disease

    find relief from other complications
  56. What happens to nerve axons of patients with MS during remission?
    limited remyelination
  57. definition of ALS is....?
    progressive neurodegenerative disease that attacks nerve cells in the brain and spinal cord resulting in muscle weakness and atrophy
  58. amyotrophic =?
    muscle wasting
  59. sclerosis =?
    hardening of the lateral corticospinal tract
  60. cause of ALS
    90% is unknown

    10% genetic
  61. Incidence of ALS
    40-60 yrs old



    smoking, family history

    males more likely to have it than females

    whites more common
  62. course of ALS
    no 2 people go through the same course of ALS

    death usually occurs within 3-5 years
  63. ALS is a _________ disease
  64. ALS degenerates both _________ and ________motor neurons
    upper and lower
  65. as motor neurons degenerate the anterior and lateral columns of the spinal cord are replaced by fibrous ______ causing hardening of these areas
  66. Wallerian Degeneration =?
    process by which motor axons die

    death in anterior horn of cell body

    degeneration of associated motor axons

    Schwann cells break down myelin

    axon breaks into pieces

    macrophages clean up axon
  67. Upper motor neurons
    degeneration of corticospinal upper motor neurons

    • loss of these leads to:
    • spastic paralysis
    • hyperreflexia
    • stiffness
  68. lower motor neurons
    degeneration of lower motor neurons that reside in anterior horn of spinal cord and in brainstem

    • loss of these leads to:
    • flaccid paralysis
    • decreased muscle tone
    • decrease reflexes
    • muscle weakness
    • muscle atrophy
  69. progressive bulbar palsy
    bulbar involvment (facial muscles)
  70. progressive muscle atrophy
    pure lower motor neuron degeneration
  71. primary lateral sclerosis
    pure upper motor neuron degeneration
  72. ALS do not affect (4)
    1-cranial nerves

    2-sensory neurons

    3-cognitive function

    4-bowel and bladder function
  73. diagnostic tests for ALS
    determined by ruling out all other tests

    family history, lab tests, CT/MRI, EMG, blood tests, gene testing
  74. early stage clinical features of ALS
    painless, weakness and difficulty breathing

    soft/spastic muscles


    atrophy of muscles

    localized or sporadic symptoms

    muscle imbalance

    weak grip
  75. middle stage features of ALS
    symptoms worsen

    muscle paralysis


    joint pain/deformity

    difficulty swallowing
  76. final stage clinical features of ALS
    paralysis of voluntary muscles

    severe breathing insufficiency

    susceptible to lung infections

    speech failure

    problems eating/speaking due to dysphagia

    death after 3-5 years
  77. Sporadic ALS
    most common form

    accounts for 90-95% reported cases
  78. Familial ALS
    gene related

    connected to defective gene on chromosome 21
  79. Guamanian ALS
    extremely high incidence in Guam
  80. co-morbidities

    weight loss





    pressure sores

    lung failure
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