1
Q
What is the peak onset for Multiple Sclerosis (MS)?
A
Between 20 and 30 years of age
2
Q
Who is more likely get MS?
A
Women (1.4-3.1 times more likely than men)
3
Q
Where is the incidence of MS the highest?
A
In the northern most latitiudes of northern and southern hemispheres
4
Q
T/F an individual that migrates at the age of 15 to another area will take on the risk profile for that area
A
False; they must have migrated before the age of 15
5
Q
Where are epidemics of MS noted and what is thought to be the cause?
A
The Faroe islands, shetland and Orkney Islands, Iceland, and Sardinia after british occupation in WWII
6
Q
What populations appear resistant to MS?
A
Hutterites and Native Americans (North American), Lapps (Scandanavia)
7
Q
How high is the incidence in first generation relatives?
A
20x than in general population
8
Q
What is the concordance rate between monozygotic twins? Dizygotic twins?
A
30%; <5%
9
Q
What is the etiology?
A
Unknown; autoimmune reaction to oligodendrocytes and myelin (viral connection in genetically predisposed)
10
Q
Where do plaques most frequently occur?
A
- optic nerves
- brainstem
- Cerebellum
- spinal cord
11
Q
T/F edge of plaque forms an abrupt interface with normally myelinated white matter
A
True
12
Q
T/F plaque does not impinge on anything else
A
False. Impinges on gray matter
13
Q
What is typical within plaque
A
Axon sparing (axon is not destroyed)
14
Q
What is the mechanism of plaque evolution?
A
Unclear. Unknown if demyelination precedes or is secondary to inflammation
15
Q
What is the current plaque evolution theory?
A
Acute inflammatory response to T cells, plasma, and macrophages results in demyleination by:
- direct mechanisms (anti-body and cell-mediated immunity)
- Indirect mechanisms (secretion of lymphkines and cytokines)
16
Q
What are ultrastructural characteristics of plaques?
A
- Degenerative changes in myelin
- infiltration with macrophages or microglia with phagocytosis of myelin
- Preservation of axons (axon sparing)
17
Q
What is the possibility of remyelination?
A
Earlier in the disease there are more oligodendrocytes preserved in plaque thus remyelination is more likely. Chances decrease as the disease progresses
18
Q
What are the results of demyelination?
A
- Conduction block at site of lesion
- Slower conduction time
- Increased subjective feeling of fatigue secondary to compensation for neurologic deficits (nerve fiber fatigue)
19
Q
What is nerve fiber fatigue?
A
feeling of fatigue due to the increased energy demand to conduct a nerve impulse
20
Q
What type of diagnosis is MS?
A
Diagnosis of exclusion (must do testing to exclude other causes)
21
Q
What criteria is included in the diagnosis?
A
- Medical hx
- Neurological exam
- Evoked potentials
- MRI
- Lumbar Puncture
22
Q
Characteristics of definite MS:
A
- Relapsing/remitting with at least 2 bouts separated by at least one month; or slow, stepwise progressive course for at least 6 months
- Documented neurological signs in more than one functional system of CNS
- Onset of symptoms between 10 and 50 years
- Absence of other more likely neurologic explanation
23
Q
Characteristics of probable MS:
A
- Hx of relapsing/remitting symptoms
- signs not documented and only one current sign commonly associated with MS
- Documented single bout of symptoms with signs of more than one white matter lesion
- Good recovery, then variable signs and symptoms
- Absence of other more likely neurologic explanation
24
Q
Characteristics of possible MS:
A
- Hx of relapsing/remitting symptoms
- NO documentation of signs establishing more than one lesion
- Absence of other more likely neurologic explanation
25
T/F person experiences major, flucuating, odd symptoms that come and go, but ignores them
False; the symptoms ignored are minor
26
T/F there are no diagnostic lab tests for MS
True
27
What tests are useful for confirming the suspicion of MS?
1. CSFStudies-confirm demyelinating disease in CNS
2. Evoked potential studies- can confirm presence of lesion not picked up by MRI or Identify silient lesion
3. MRI-confirm presence of lesions
4. Blood and urine tests-unremarkable in MS
28
What results would you find in a CSF study that would confim your suspicion of MS?
* Increased in immunoglobulin concentrations present
* increased protein level
* May be slight elevation in cell count (primarily T-lymphocytes)
29
What are the results in an Evoked Potential Studies that would indicate a suspected lesion?
Slow signals to the brain
30
T/F MRI by itself is sufficent to confirm MS diagnosis
False; abnormal MRI without evidence is not sufficient. Neither does negative MRI in the presence of clinical signs disprove diagnosis
31
What is the correlation between size and area of lesions and patient's disability level?
Poor
32
What is the difference between Benign and malignant?
Benign- no loss of function 15 years post onset (20% of benign MS patient).
Malignant- rapdily progressing and significant disabilities culminating in death
33
What category do 85% of MS patients fall in to and what are its characteristics?
* Relapsing-remitting
* Relapses with either full recovery or minor deficits remaining upon recovery
* Periods between relapse characterized by no visible disease progression (stable periods mask the continuing disease process)
34
What are characterisics of primary progressive MS ?
* Contiued progression from onset without remissions or significant plateaus
* might be occasional plateaus with temporary minor improvements then return of progression
35
What are characteristics of secondary progressive?
* Intitial relapsing-remitting course followed by progression at a variable rate
* includes ocassional remission and then relapse
36
What are characteristics of progressive-relapsing?
Progressive disease from onset but with clear, acute relapse, with or without full recover after each relapse
37
What are categories of MS are benign?
* Relapsing-remitting
* Secondary-progressive
* Porgressive-relapsing
38
What are typical early signs/symptoms?
* Fatigue
* Diploplia
* Blurred Vision
* Weakness
* Sensory changes
* intention tremor (cerebellar lesions)
* Problems with bladder control
* Incoordination
* Intolerance to heat
39
What are possible causes of diploplia?
* Usually due to Internuclear opthalmoplegia
* Lesion in MLF carrying fibers from vestibular nuclei for extraocular muscles for controlling ey movements in relation to head movement
* Paresis/palsy of VI can also occur
40
What causes blurred vision and what does it result in?
* Optic neuritis
* Can result in:
* Central Scotoma
* Pain behind eye (headache)
* Visual field defects
* Alteration in color reception
41
What are characteristics of weakness?
* Most often paraparesis, but can be monoparesis or quadraparesis
* Often accompanied by other signs of UMN lesion (spasiticity, hyperreflexia, pathologic signs)
42
What are the common distributions for sensory changes?
1. Ascending numbness starting in the feet
2. Bilateral Hand numbness
3. Hemiparesthesia
4. Dyesthesia in one of the about distributions
43
Where is sensation loss the greatest?
dorsal column (vibration, proprioception, kinesthesia) vs. spinothalamic
44
What are typical later sign/symptoms?
1. Motor- weakness and spasticity increases
2. Cerebellar-incoordination, ataxia, scanning speech, loss of balance
3. Sensory- Lhermitte's sign, dyesthesia, parathesias, numbness increases, increase in loss of dorsal column informaion
4. Emotional lability, depression
45
T/F the number of relapses in first 2 years has prognostic value
False: it has no prognostic value
46
What are unfavorable prognostic signs?
* Initially progressive course
* Male
* Higher basal EDSS scores
* More functional system involved at onset
* Higher residual motor system deficits in pyramidal, visual, sphinteric, and cerebellar systems
47
What are favorable prognostic signs?
* Onset before 30
* Female
* Complete recoveries (no disability in remission period)
* Sensory system involved at onset
* Longer first inter-attack interval
48
What are 3 ways for medical managment?
* Treatment of relapses
* Prevention of relapses
* Spasticity
49
What meds are use for treatment of relapses
* Corticosteriods of immunosuppression (inflammation)
* Milder relapses usually get oral prednisone
* More significant bouts- with IV methylprednisone (Solu-Medrol)
50
What meds are used to prevent relapses?
Interferon (reducess number and severity of relapses)
51
What meds are used to treat Spasticity?
Baclofen, Dantrolene, Diazepam
52
What is used to evaluate MS?
Standard neuro exam, Scales (EDSS, MFIS)
53
What is EDSS used to look for?
* monitor progression of disablility associated with MS
* insure that all participants in a clinical trial are in the same class/type/phase of MS
54
T/F there is not evidence that any PT intervention is effective on the underlying pathology associated with MS
True
55
What do goals center on ?
maximizing independence and quality of life
56
What are typical areas of intervention?
Fatigue, weakness,spasticity, sensory of dysfunction, ambulation/mobility
57
What are primary approaches to MS?
1. Teaching energy conservation
2. Adapting work environments for energy conservation
3. Cardiovascular endurance program
58
What are steps for energy conservation techniques?
1. plan ahead and organize to alternate light and heavy tasks throughout the day
2. do only as much as you can then stop
3. allow time for each task and stop before fatigued
4. use a schedule for planning activities
5. alternate sitting and standing tasks
6. get help when needed (family education)
59
What steps for cardiovascular endurance program?
1. Used during stable periods, not during an exacerbation (not for malignant)
2. Exercise tolerance test is recommended before beginning
3. Evidence indicates that up to 80% of predicted MHR is acceptable
1. submax exercise
4. Keep in mind
1. safety
2. thermal regulation
60
What causes weakness and how is it treated?
* UMNL, fatigue, disuse
* pool, PNF techniques, resistance exercises
61
What are general principles of resistance exercises?
1. begin with stretching to maintain ROM and decrease spasticity
2. unaffected muscle groups should be maximally strengthened to allow maximal use of compensatory techniques that involve unaffected limbs
3. use adaptive devices to allow patient to remain ambulatory as long as possible
4. teach patient to balance workout with rest periods (1-5 minute rests throughout session to facilitate reovery of neurotransmission)
5. progression should be slow (start at 8-10 reps,add 1-2 reps every 2-3 weeks until 20-25 reps; add weight untill back down to 8-10 reps)
6. focus on proximal strength
7. workout in a cool envirionment
62
How do you treat spasticity?
teach patient to stretch and encourage daily stretching sessions
63
How do you to treat sensory dysfunction?
1. teach patient to do twice daily skin inspections
2. appropriate cushioningon w/c and matresses
3. Pressure relief for w/c bound patient
64
How do treat ambulation and mobility issues?
work on underlying impairments and on problem solving for mobility, consider AFOs, think about contraindications, and consider scooter or w/c
65
When do you consider AFOs?
* consisten foot drop and to drag
* poor knee control (hyperextension)
* lateral insability of ankle (air splint)
66
What are contraindications to AFO?
* Moderate or severe spasticity in lower extremities (creates lesions, decrease ROM, make spasticity worse)
* Severe edema in the foot
Multiple Sclerosis
flashcards
Decks in class (1)
# Cards
