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Flashcards in Exam 3 ppt 3 MS & ALS Deck (37)
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1

Multiple Sclerosis (everything below, but not detailed types and clinical manifestations):

What is it?

Epidemiology:

Etiology:

Pathophysiology:

Clinical Course (general):

Exacerbating Factors:

Non PT treatment:

PT Treatment:

 

What is it?

  • Chronic inflammatory demyelinating disease of CNS

Epidemiology:

  • Adult onset typically 20-40 years old
  • Race: white 2x more likely than African Americans
  • Sex: Females 2x more likely than males

Etiology:

  • Unknown
  • Best accepted theory is some sort of underlying viral disorder that causes autoimmune response
    • Some have suspected chalmydia, but this has not been proven and is debatable
  • Possible geneitc connection (15%)

Pathophysiology:

  • Autoimmune resonse sets of Immune system
  • •Something crosses BBB and causes demyelination (that can stop at any point)
    • attacks to myelin cause inflammation and then scar tissue develops,
    • oligodendrocytes are the glial cells that myelinate CNS axons and experience damage
      • shappy said they are the ones that are activated to respond (but microglial cells are like the phagocytes of the CNS, so I would think they have a large role in the innflammation and immue response - maybe oligodendrocytes try to regenerate?
    • You get inflammation first, then you will get the scar tissue after on the site (treat with inflammatory first)

  • •Slows conduction
  • •Decreasing transmission
  • •Results in weakness
  • Sort of like a CNS version of chronic Gillian Barre.

Clinical Course (general):

  • May be progressive or not, may have remissions and relapses. Very unpredictable.
  • optic nerve, motor and sensory cortex- not limited to these areas.

  • symptoms wax and wane which may or may not have an element of progression

Exacerbating Factors:

  • –Heat
  • –Stress

Non PT Treatment:

  • Anti-inflammatory at first to stop inflammatory response
  • may use IVIG to attack anitbodies that are created.
  • Oligodendrocytes can be repaired (remyelination can happen).

    • Remyelination can stop at any point.

  • For an Exacerbation:
    • Exacerbation (attack): symptoms get worse, treat immediately with anti-inflammatory (steroids), controls edema, after edema goes away the symptoms may also reduce. It is an argument to be as fit as possible before the attack

PT Treatment:

  1. –Help them avoid exacerbating factors
  2. –Exercise is okay, but not in hot environments (pools must be cool)
  3. –May need specialized outcome measures
    • Think of things that you can measure to show progress
      • Sensations (semmes weinstein, temperature, etc.)
    • •Need more research
      • •Including more short term and long term outcome measures
    • –Insurance companies don’t want to reimburse for maintenance
      • •Insurance companies like short term outcome measures
  4. Work on balanc and overall conditioning
  5. ”Strategic Weighting” Weighted belt can improve ability to move. There is certain spots for the weights on the belts. (sort of like jackets for scared dogs)

  6. Don’t forget wound care stuff

2

Multiple Sclerosis

What is it?

What is it?

Chronic inflammatory demyelinating disease of CNS

3

Multiple Sclerosis

Epidemiology:

 

 

Epidemiology:

  1. Adult onset typically 20-40 years old
  2. Race: white 2x more likely than African Americans
  3. Sex: Females 2x more likely than males

4

Multiple Sclerosis

Etiology:

 

 

Etiology:

  • Unknown
    • Best accepted theory is some sort of underlying viral disorder that causes autoimmune response
      • Some have suspected chalmydia, but this has not been proven and is debatable
    • Possible geneitc connection (15%)

5

Multiple Sclerosis

Pathophysiology:

 

Pathophysiology:

  • Autoimmune resonse sets of Immune system
  • •Something crosses BBB and causes demyelination (that can stop at any point)
    • attacks to myelin cause inflammation and then scar tissue develops,
      • oligodendrocytes are the glial cells that myelinate CNS axons and experience damage
        • shappy said they are the ones that are activated to respond (but microglial cells are like the phagocytes of the CNS, so I would think they have a large role in the innflammation and immue response - maybe oligodendrocytes try to regenerate?
    • You get inflammation first, then you will get the scar tissue after on the site (treat with inflammatory first)
      • •Can see Plaque build up
      • •Plaque is scar tissue
      • •Related to death of neuron
  • •Slows conduction
  • •Decreasing transmission
  • •Results in weakness
  • Sort of like a CNS version of chronic Gillian Barre.

6

Multiple Sclerosis

Clinical Course (general):

 

 

 

Clinical Course (general):

  1. May be progressive or not, may have remissions and relapses. Very unpredictable.
  2. optic nerve, motor and sensory cortex- not limited to these areas.
  3. symptoms wax and wane which may or may not have an element of progression

7

Multiple Sclerosis

Exacerbating Factors:

 

 

Exacerbating Factors:

–Heat
–Stress

8

Multiple Sclerosis

PT Treatment:

 

PT Treatment:

  1. –Help them avoid exacerbating factors
  2. –Exercise is okay, but not in hot environments (pools must be cool)
  3. –May need specialized outcome measures
    • Think of things that you can measure to show progress
      • Sensations (semmes weinstein, temperature, etc.)
    • •Need more research
      • •Including more short term and long term outcome measures
    • –Insurance companies don’t want to reimburse for maintenance
      • •Insurance companies like short term outcome measures
  4. Work on balanc and overall conditioning
  5. ”Strategic Weighting” Weighted belt can improve ability to move. There is certain spots for the weights on the belts. (sort of like jackets for scared dogs)
  6. Don’t forget wound care stuff

 

9

Multipule Sclerosis: Clinical Manefestations/What does MS affect? (9 examples)

 

 

Anywhere CNS nerves are

  1. –Sensory Cortex
  2. –Pain
  3. –Visual Changes (optic nerve)
  4. –Motor dysfunction (motor cortex)
  5. –Speech/swallowing
  6. –Cognitive
  7. –Depression
  8. –Affective
  9. •Autonomic changes
  • –Cardiovascular
  • –Bladder
  • –Bowel
  • –Sexual dysfunction


•Basically everything in CNS

10

Multiple Sclerosis: Four autonomic functions affected

 

Autonomic changes

  1. –Cardiovascular
  2. –Bladder
  3. –Bowel
  4. –Sexual dysfunction

11

Multiple Sclerosis

Non-PT Treatment

What about for an exacerbation?

 

Non PT Treatment:

  1. Anti-inflammatory (steroid) at first to stop inflammatory response
  2. may use IVIG to attack anitbodies that are created.
  3. Oligodendrocytes can be repaired (remyelination can happen).

    1. Remyelination can stop at any point.

For an Exacerbation:

  1. Exacerbation (attack): symptoms get worse, treat immediately with anti-inflammatory (steroids), controls edema, after edema goes away the symptoms may also reduce. It is an argument to be as fit as possible before the attack

12

Can you see plaques on an MRI for someone with MS?

 

Scars plaque can be found anywhere in CNS

13

Is MS easy or hard to diagnose?

 

Manifestations can be hard to put a label on because the symptoms are vague. Easy to miss the diagnosis

14

How many categories of MS are there?

 

6 categories of Primary Progressive MS

15

What are the 6 Categories of Primary Progressive MS?

 

 

  1. .Benign MS (about 20%)
    • •Mild disease with full function greater than 15 years)
  2. 2Malignant MS (also called Marburg Disease ) – malignant does not mean cancer, just that it is fast and hard
    • •Rapid onset, continued progression. Significant disability or death
  3. Relaxing Remitting MS (70%) – she likes to test on this one
    • •Acute episodes followed by remission/improvement without disease progression
  4. Secondary Progressive MS
    • •Develops from relaxing remitting
    • •However is more progressive
    • •Occasional relapses to differentiate it with minor remissions
      • •A lot of these people will plateau during the remission period (you will not see them return to full function)
    • •pts are older at this age 
  5. Progressive Relapsing
    • •Intervals between relapses actually show disease progression (so in between exacerbations you are still getting worse)
    • •Occurs with aging
  6. Primary Progressive (the little version of the big category of all of this)
    • •Disease progression without or with progression
    • •If you don’t fit into one of the other 5 categories, so you just say that it is Primary Progressive
       

16

Characteristics of Benign MS? (2)

 

.Benign MS

  • (about 20% of MS
  • •Mild disease with full function greater than 15 years)

17

Characteristics of Malignant MS? (3)

 

Malignant MS

  1. also called Marburg Disease ) – malignant does not mean cancer, just that it is fast and hard
  2. •Rapid onset, continued progression.
  3. Significant disability or death

18

characteristics of relaxing Remitting MS: (2)
 

 


Relaxing Remitting MS

  1. 70% of all MS – she likes to test on this one
  2. •Acute episodes followed by remission/improvement without disease progression

19

characteristics of Secondary Progressive MS: (4)

 

Secondary Progressive MS:

  1. •Develops from relaxing remitting
  2. •However is more progressive
  3. •Occasional relapses to differentiate it with minor remissions
    • •A lot of these people will plateau during the remission period (you will not see them return to full function)
  4. •pts are older at this age

20

Characteristics of Progressive Relapsing MS: (2)

 

Progressive Relapsing

  1. •Intervals between relapses actually show disease progression (so in between exacerbations you are still getting worse)
  2. •Occurs with aging

21

characteristics of Primary Progressive MS (the little version of the big category of Primary Progressive MS): (2)

 

Primary Progressive (the little version of the big category of all of this)

  1. •Disease progression without or with progression
  2. •If you don’t fit into one of the other 5 categories, so you just say that it is Primary Progressive

22

what does ALS stand for?

Amyotrophic Lateral Sclerosis

23

what is an alternate name for ALS?

 

Lou Gheric's Disease

24

What is ALS ?

 


•Motor neuron disease

  1. –Degenerative spinal cord, brain, brainstem motor neuron loss.
  2. –Typically develops in UE first, then progresses to lower
    • •One of few conditions where Diplegia is present in UE

25

ALS Epidemiology

Epidemiology

  1. –Men more common than women (2:1)
  2. –10-15% seem to have familial link
  3. –30K cases in USA (15 diagnosed per day)

26

ALS Etiology

 

 

  • Unkown
  • –A number of theories
    1. •Free radical build up
      • –Enzymes whose job it is to elimiate free radicals are dysfunctional (superoxide)
    2. •Neurotransmitter issues
      • –Glutamate is typically elevated
    3. •Motor neuron degeneration
    4. •Autoimmune
    5. •Unscheduled apoptosis
       

27

ALS: prognosis

From onset of symptoms to death: 5-10 years (usually from respiratory problems)

28

What are the 5 theories of ALS Etiology?

 

 

  1. •Free radical build up
    • –Enzymes whose job it is to elimiate free radicals are dysfunctional (superoxide)
  2. •Neurotransmitter issues
    • –Glutamate is typically elevated
  3. •Motor neuron degeneration
  4. •Autoimmune
  5. •Unscheduled apoptosis++
     

29

ALS Pathophysiology

 


•Pathophysiology

  1. –Motor neuron progressive degeneration
  2. progression
    1. – from cranial nerves
    2. –Can progress to sensory
    3. –Bowel and bladder
  3. –Typically develops in UE first, then progresses to LE
    • •One of few conditions where Diplegia is present in UE
  4. –Distal to proximal
  5. –Ultimately can affect breathing
     

30

What are three types of motor neurons that ALS affects?

 

  1. LMN
  2. UMN
  3. Bulbar neurons