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Kin 372 > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

Multiple sclerosis (MS)

A

is the most common chronic inflammatory, demyelinating and neurodegenerative disease of the central nervous system in young adults.

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2
Q

Multiple sclerosis (MS)

(Common)

A

MS has a greater Prevelance in European countries

But most common in people of European (Caucasian) descent.

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3
Q

Multiple sclerosis (MS)

(Chronic)

A

You live with this for the rest of your life

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4
Q

Multiple sclerosis (MS)

(Inflammatory)

A

It’s inflammatory, it’s is autoimmune, immune cells (T cells and B cells) are attacking tissues that are ours

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5
Q

Multiple sclerosis (MS)

(Demyelinating)

A

Oligodendrocytes make myelin in CNS

Schwann cells make myelin in PNS

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6
Q

Multiple sclerosis (MS)

(Young adults)

A

20-40s typical age for diagnosis

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7
Q

White matter

A

Where axons with myelin sheaths are

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8
Q

White matter having grey spots

A

Indicate a loss of myelin on the axon

The freckles are called plaques, and can be seen using MRI

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9
Q

Luxol fast blue stain

A

What it does is that it sticks to anywhere that there is myelin,

Histology:
Some white matter areas are blue (indicating myelin)

others have no blue stain (indicating demyelination)

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10
Q

Immunohistochemistry
Colours

A

Anti body with fluorescent probe that lights up green or red

Myelin- Red

Neurofilament- green

Yellow: myelin is starting to be affected

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11
Q

Immunohistochemistry

Green gaps

A

Red (myelin) should cover the green (axon), the gaps with just green means that there is demyelination

Can see different stages of demyelination (more/less green visible)

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12
Q

Immunohistochemistry
Green blob

A

Growth cone to try to grow back, forming that big green part, axon got cut, so there is degeneration

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13
Q

Immunohistochemistry
Transected axon

A

Beginning of Neurodegeneration

Everything not connected to the cell body will die

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14
Q

Progression of disability

A

Normal nerve cell

Phagocytes cells start to degrade the myelin

Transected cell (nuerodegenerative process) -may be the reason for progressive disability

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15
Q

MRI and Histology
What happens to the ventricles (filled with cerebral spinal fluid)

A

Expanded volume of ventricles and decreased amount of gray matter and white matter

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16
Q

Ventricle expansion explained

A

Later MS, When the axons dies, the dead tissue applies resistance to ventricle,

ventricles begin to expand,

they usually trace the brain to compare how much brain volume is loss

Losing brain volume and gaining CSF is another indication of nuerodegenerstion

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17
Q

Multiple

A

Need to have multiple occurrence of symptoms to be diagnosed p, must be spread out in time and space

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18
Q

Stats for Canada

A

Canada
1 person in 400

4,377 new diagnosis/year

75% female

90% with Relapsing remitting Multiple sclerosis

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19
Q

Clinical Patterns of MS
(the four stages And three types)

A

PPMS- PRIMARY PROGRESSIVE (ms)

Pre-symptomatic

Clinically isolated syndrome

Relapsing-remitting (ms)

Secondary progressive (ms)

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20
Q

Pre-symptomatic

A

Inflammation is present but it is below the threshold, the patient likely won’t have notice symptoms

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21
Q

Clinically isolated syndrome

A

First event that caused a symptom, but not sufficient to cause a diagnosis, need to have multiple presentations of this

First symptoms distinct, but goes away

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22
Q

Relapsing-Remitting
(DMT involment and both definition)

A

Relapse: active stage of inflammation

Remitting: non active stage of inflammations

Time between relapse and remitting vary

DMTs tries to keep the person in earlier RRMS phase

Symptoms starts to stay near the end of this phase ( likely when neurodegeneration is happening)

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23
Q

Diagnosis for MS

A

Start of Relapsing-remitting

Two events that affect different part of the body, and are separated in time, they are sufficient enough to diagnose for MS

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24
Q

Relapsing-Remitting
Re-myelination

A

Process can happen when in remission

Once the symptoms starts to stay the is process no longer works

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25
Q

Secondary progressive

A

Symptoms continuous get worse (flair up)

Goals is to reduce the amount of people in this stage

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26
Q

Is the true cause of Multiple Sclerosis (MS) known?

A

No, the true cause of MS is unknown, and it is difficult to identify causes at an individual level.

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27
Q

What are the main risk factors associated with MS?

A

The risk factors include lifestyle, environmental exposures, and genetic factors.

Smoking, sedentary behaviour, diet

Mutation in the germ cell

Vitamin D deficiency is a risk factor (lifestyle / Environmental)

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28
Q

What are the main risk factors associated with MS?

A

The risk factors include lifestyle, environmental exposures, and genetic factors.

Smoking, sedentary behaviour, diet

Mutation in the germ cell

Vitamin D deficiency is a risk factor, lifestyle / Environmental

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29
Q

Can MS have a family history, and how do genetic mutations arise?

A

Yes, MS can have a family history, but genetic mutations can also spontaneously arise or result from environmental exposures, such as radiation.

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30
Q

How can exposure to radiation impact genetic mutations related to MS?

A

Exposure to radiation (e.g., x-rays) can cause damage in sperm and egg cells, potentially leading to genetic mutations before fertilization.

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31
Q

What gene family is associated with MS, and how does it relate to autoimmune conditions?

A

The HLA (Human Leukocyte Antigen) gene family is associated with MS, as it plays a role in the immune system and is linked to autoimmune conditions through its connection to white blood cells (leukocytes).

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32
Q

Pathophysiology of MS (what is happening)

A

The presence of demyelinationnlesssions in the brain, spinal cord and optic nerve.

These lesions are characterized by breakdown of the BBB and the presence of inflammatory cells

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33
Q

Pathophysiology
Blood Brain Barrier

A

BBB is selective,inflammation makes the BBB leaky, things that are normal up’s circulating in the blood can get in there,

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34
Q

Broken wire vs fix wire analogy

A

Broken wire: demyelination

Fixed wire: remyelination

Oligodendricytes, will try to fix it, but it not not has good has it was originally

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35
Q

Location of demyelination affect on symptoms

A

Presenting symptoms of MS depend on the location of the demyelinating lesions:
● Visual
● Sensory
● Motor
● Cognitive

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36
Q

Optic neuritis:

A

pain that is worsened by eye movement, as well as vision loss that can be partial or total

Honestly a lot of eye issues, another slide goes in detail

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37
Q

Focal Lesion location of optic neuritis

A

Optic nerve

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38
Q

Diplopia

A

Double vision

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39
Q

Focal lesion of diplopia

A

focal lesions are located in the left pons and right middle cerebellar peduncle

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40
Q

Vertigo

A

, a sensation of dizziness, is a symptom of impaired balance.

Problem in the inner ear

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41
Q

Focal lesion of vertigo

A

the cerebellar hemispheres

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42
Q

Lhermitte’s sign and Paresthesia

A

Lhermitte’s sign: electrical shock radiating down the spine upon neck flexion

Paresthesia: numbness/ tingling

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43
Q

Location of focal lesion that cause Lhermitte’s sign and Paresthesia

A

located in the cervical spinal cord

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44
Q

sensorimotor hemisyndrome

A

sensory and motor deficits affecting one side of the body, which can include hemiparesis (weakness on one side of the body) and hemisensory deficits (sensory issues on one side of the body)

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45
Q

sensorimotor hemisyndrome focal lesion

A

focal lesion located in the left cerebral hemisphere of a patient will have right sensorimotor hemisyndrome.

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46
Q

What are focal lesions?

A

Areas of demyelination characteristic of all MS phenotypes, typically occurring around post-capillary venules [8] They are also known as plaques.

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47
Q

What happens to the blood-brain barrier in areas of focal lesions?

A

It breaks down

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48
Q

Where can focal lesions occur in the brain?

A

Grey matter and white matter

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49
Q

What is the Expanded Disability Status Scale (EDSS)

A

The EDSS is the most widely accepted measure of clinical disability in MS. It is a scale that ranges from 0 (a normal neurological examination) to 10 (death due to MS).

Goes up in increments of 0.5

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50
Q

What does the EDSS access? (8 functional system)

A

The EDSS assesses disability across 8 functional systems (subscales):

Pyramidal

Cerebellar

Brainstem

Sensory

Bowel and bladder

Visual

Mental (cognitive)

Other

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51
Q

What is an important tool for diagnosing and monitoring MS?

A

Magnetic resonance imaging (MRI) is an important tool for diagnosing and monitoring MS.

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52
Q

Timed 25 foot walk

A

Gait speed, timing how quickly they can walk, motor impairment, sensory issues and coordination can all slow them down

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53
Q

What is the Symbol Digit Modalities Test (SDMT)?

A

A neuropsychological test often used to assess cognitive function, particularly processing speed, attention, and visual-motor coordination. It involves matching symbols to numbers according to a key

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54
Q

What are the Fatigue Severity Scale (FSS) and the Modified Fatigue Impact Scale (MFIS)?

A

Patient-reported outcome measures used to assess the severity and impact of fatigue.

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55
Q

What is symptoms tied to

A

Many signs and symptoms, they are non specific, closely tied to where the Neurodegeneration are affecting in the body

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56
Q

Common measures of symptoms

A

EDSS

Timed 25 foot walk

SDMT (cognitive)

FSS or MFIS (fatigue)

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57
Q

What is the pyramidal system?

A

Also known as the corticospinal tract, the pyramidal system is responsible for controlling voluntary movements.

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58
Q

How does the doctor assess pyramidal function in the video?

A

Evaluating her leg strength, such as her ability to lift her leg against gravity and push down against resistance. [2, 3]

Testing her reflexes, as brisk reflexes can indicate an issue with the pyramidal system.

Clonus, dorsiflex ankle, and fooot vibrates indicate clones, it being present is pyramidal sign

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59
Q

How does the doctor assess Cerebellar function in the video?

A

Coordination test- looking for ataxia

flipping hands back and forth as high and fast as possible

60
Q

How does the doctor assess Brainstem function in the video?

A

Speech and swallowing can present as from brain stem

Nystagmus ( involuntary eye movement) tracking finger with eye test

61
Q

How does the doctor assess sensory function in the video?

A

Scratch, vibration, and using a toothpick for nociception (pain sensation).

62
Q

Clonus

A

involuntary vibration (origin different than tremor)

  • ex at ankle: forcefully dorsiflexes ankle and holding it to see if clonus (vibration) is present
  • if it is present, is considered a pyramidal sign
63
Q

Optic neuritis
(Typical)

Onset and involvement

A

Onset: sub acute to chronic (hours to days)

Involvement: unilateral

64
Q

Optic neuritis
(Typical)

Signs and symptoms

A

Signs or Symptoms:
- Afferent pupillary defect
- Central visual blurteng or scotoma
- Reduced visual acuity
• Dyschromatopsia (colour blindness)
• Normal optic disc or optic disc swelling
• Mild unilateral orbital pain that is worsened by eye movements

65
Q

Optic neuritis
(Typical)

Recovery

A

Gradual recovery within 2-4 weeks after reaching peak severity

66
Q

Myelitis (inflammation of spinal cord)
*Typical

Onset and involvement

A

Onset:Sub-acute and/or chronic (hours to days)

Involvement:

incomplete transverse myelitis

Asymmetric involvement

67
Q

Myelitis (inflammation of spinal cord)
*Typical

Signs or symptoms

A

• Sensory involvement: paresthesias (numbness, tingling, pins-and-needles feeling, tightness, coldness and/or swelling of the limbs or trunk), Lhermitte sign, impairment of vibration and joint position sense, decreased pain and light touch perception and Uhthoff phenomenon

• Motor deficits: pyramidal signs (Babinski sign, bright reflexes and clonus), spastic paresis and/or weakness (asymmetric) and spasticity

• Sphincter dysfunction: urinary urgency, hesitancy, urge incontinence, constipation and faecal incontinence

• Sexual dysfunction: erectile dysfunction and impotence

68
Q

Myelitis (inflammation of spinal cord)
*Typical

Recovery

A

Gradual recovery starting within 2-4 weeks after reaching peak severity

69
Q

FATIGUE SEVERITY SCALE (FSS)

A

9 questions
- mostly dealing with physical element of fatigue
- reflects on events of past week
- calculate an average score from scores on each question
-clinically significant is score: >/=4
- minimally important difference (MID)/clinically important difference
(CID)
- score must change by a certain amount to be meaningful change
- 0.5-0.89 point change is CID
- significant enough change that symptoms can be partially alleviated

Visual analogue fatigue scale (VAFS)
- worded the way it is to ensure that the patient is actually reading the questionnaire

70
Q

Modified Fatigue Index Scale (MFIS)

A
  • over the past 4 weeks
  • scale goes from 0-4
  • 21questions
  • questions at end can give indication of what domains fatigue is having the most impact on
  • total MFIS: max score is 84
  • Clinically significant fatigue: >= 38
  • CID/MID: 4-6 points

Physical sub scale: 9 (0-36)

Cognitive sub scale: 10 (0-40)

Psychosocial sub scale: 2 (0-8)

71
Q

How is fatigue measured clinically?

A

Want to see impact of exercise on fatigue: goal is to reduce score

72
Q

Two domains of Fatigue

A

Perceptions of fatigue

Performance fatigability

73
Q

Components of perceptions of fatigue

A

Homeostatic factors

Psychological factors

74
Q

Components of performance fatigability/ the disease associated with the component

A

Peripheral factors
-Myasthenia Gravis (MG)

Central factors
-Multiple Sclerosis (MS)

75
Q

What is perception of fatigue

A

● refers to subjective sensations of weariness, increasing sense of effort, mismatch between effort expended and actual performance, and exhaustion.

● Measured using self-report instruments (Fatigue Severity Scale OR Modified Fatigue Impact Scale)

76
Q

What’s is performance fatigability

A

defined as the magnitude or rate of change in a performance criterion relative to a reference value over a given time.

● In the motor domain, measured during motor tasks by tracking a decrease in peak force over time.

● In the cognitive domain, measured by declines in reaction time or accuracy over time on continuous performance tasks

77
Q

Homeostatic factors

What is controlling it
It’s normal function
Pathological states

A

Hypothalamus

Central regulation of activity based on energetic, inflammatory and neural feedback

Unknown, possible PD, hypothalamic lesions

78
Q

Psychological factors

What is controlling it
It’s normal function
Pathological states

A

Frontal lobes

Mood and motivational influences on feelings of fatigue
Ex. Waking up in a bad mood

Depression, CFS, possible PD, Mood disorder

79
Q

Peripheral factors
Outside of CNS (e.g. muscles)

What is controlling it
It’s normal function
Pathological states

A

Muscle, nerves, and glycogen stores

Loss of muscle force secondary to energy depletion or EC uncoupling

Myopathies, MG, GSD, GBS

80
Q

Central factors
In the CNS (e.g. brain, brain stem, or spinal cord

What is controlling it
It’s normal function
Pathological states

A

Domain-specific cortical and subcortical network

Domain-specific task failure secondary to dysfunction in cognitive networks

MS, TBI, CVA, PD, other dementia

81
Q

While separated in this diagram, it should be noted that perceptions of
fatigue and performance fatigability have the potential to influence each other.

A

Just a fact

82
Q

Homeostatic factors and psycological factors

A

Capacity to perform past, present, and future actions

The internal perception of our ability to perform

83
Q

Peripheral factors and Central factors

A

Limits is the current actions

Happening right now

84
Q

Fatigue abbreviations

A

CFS = chronic fatigue syndrome; CVA = cerebro-
vascular accident; EC = excitation/contraction; GBS = Guillain-Barré syndrome; GSD = glycogen storage diseases; MG = myasthenia gravis; MS = multiple sclerosis; PD = Parkinson disease; TBI = traumatic brain injury.

85
Q

Performance fatigability
Definition

A

A reduced ability of a muscle (or group) to continue to produce contractile output (measureable), relative to initial maximal starting strength, following sustained or intermittent contractions (voluntary or otherwise). The initial strength is regained following a variable period of rest (distinct from injury).

86
Q

Pyramidal and Extrapyramidal Motor Pathways (originates and goes where?)

A

Descending pathways that originate in midbrain, pons , or medulla and descend down the spinal cord

87
Q

Pyramidal and Extrapyramidal Motor Pathways

Primary motor cortex

A

Pyramidal cells travel down and cross over

88
Q

Pyramidal Tract (Corticospinal pathway)

A

Very important for ongoing control of purposeful movement

• The ~ 1 million fibers originate in primary motor and premotor and other areas of cortex

• Large pyramidal cells within layer 5 of neocortex

• Interneurons and motor neurons (α and γ)

89
Q

Primary Motor Cortex (M1)

A

30-40% of pyramidal tract fibers, only about 20% to spinal cord

90
Q

Cross over occurring

A

When Layer 5 pyramidal neurons discharge action potentials and transmit this to the spinal cord

91
Q

Time to task failure: Experiment

A

Performance fatigability task

Measuring how much time they can do this for

Shorter time= higher fatigability

Wall sit

92
Q

Angelo Mosso

A

Professor of Physiology at the University in Turin
• blood circulation, respiration, physical education, high-altitude physiology, and muscular fatigue
• ergograph

93
Q

Angelo Mosso

Ergograph

A

Instead of a sustained contraction, intermittent contractions are made at the middle finger (flex it repeated day)

94
Q

Ergographic tracings

A

Size of the contractions indicated by height of curve

Shows performance fatigability

You can train fibre tho conversion/ development to improve endurance (type 1 fibres)

95
Q

Anotomy and pathophysiology determines?

A

What type of fatigue will be experienced

Central/Peripheral fatigue

96
Q

Exercise in the past

A

This was not encouraged because they were worried about its affects, (fatigue)

Exercise is going to cause relapses.
- increase the amount and intensity

97
Q

G-B syndrome

A

Autoimmune disease that can affect myelination in the peripheral

98
Q

Central ( explain the diagram)

A

M1 (motor cortex)

Axon
- Central demyelination causes Multiple sclerosis

Peraminal (corticospinal track)

Motorneuron pool(all motor neurons that goes to the muscles)
- Post-poliomyelitis syndrome caused by motorneuron death

99
Q

Peripheral (explain the random ass diagram)

A

Axon

Muscle
- Myasthenia gravis, cause by few post synaptic acetylcholine receptors

100
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Why is is strong

A

It’s a systematic review and meta analysis of only randomized

101
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Population

A

People diagnosed with MS

  • 18 yrs +
  • most participants had Relapsing Remitting MS - EDSS<6

Level 6: need to use assistant device to walk 100 m
- these studies primarily recruited people with a lower level of physical impairment

102
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Intervention

A

Exercise (supervised or unsupervised; in any setting, no restrictions on duration, frequency, or intensity)

  • For analysis: split up into endurance, muscle power, task-oriented, mixed training (aerobic and strength) , or other

Wanted to study various types of exercise to see if one type has a greater effect or not

103
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Comparison

A

No exercise or other type of intervention

104
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Outcome Measure

A

Self-report questionnaires on fatigue

105
Q

Exercise therapy for fatigue in multiple sclerosis (Review)

Key results

A

We used 36 studies, involving 1603 people with MS, in an analysis. Combined, these 36 trials supported the idea that exercise therapy may be a promising treatment to reduce fatigue without side events.

Only reported 1 fall

106
Q

What type of exercise reduces fatigue the most in individuals with MS

A

Mixed (aerobic and strength) Other (e.g. yoga, tai-chi)

107
Q

Conclusion of the exercise study

A

There is not enough evidence to definitively determine

  • more studies with large sample sizes are needed
108
Q

Mechanisms of exercise-induced effects on fatigue

A

Fatigue may be brought by exercise Acutely, but in the longer term, fatigue levels are shown to be improved

Can be challenging for clients to understand

Neurotrophins for Neuroprotection

109
Q

Neurotrophins for Neuroprotection

Acute and chronic

A

Acute (2 significant neurotrophins)

  • BDNF (decrease but inconclusive) and VEGF(increase but inconclusive)

Chronic

Over time, BDNF goes up, the nervous system is getting this vitamin, does neuroprotection via changes to the permeability of the blood brain barrier

110
Q

Inflammation and Cytokines

Effects of exercise on cytokines secretion

Single intense exercise

A

Increase in pro-inflammatory cytokines

111
Q

Inflammation and Cytokines

Effects of exercise on cytokines secretion

Regular moderate exercise (chronic)

A

Long term exercise, the things that cause inflammation will go down (pro-inflammatory cytokines)

The amount of the inflammation suppressor goes up (anti-inflammatory cytokines)

112
Q

HPA Axis

Stress response

A

Chronic endurance training decreases the stress response.
- Circulating cortisol in response to stress goes down
- Circulating endorphins increase (positive for mood)

113
Q

Analogy

Why does the pathophysiology of MS lead to fatigue, and central fatigue in particular?

A

Pump: motor cortex
Hose: axon going to tire
- if there is a hole, nothing will be happening but your brain will be getting tired trying to send information (pumping)

  • getting no result from your effort
114
Q

CSEP-guidelines

Why was 4.5 chosen

A

4.5 chosen because the guidelines are recommended to be done in ADDITION to daily activities -> people with more impairment than 4.5 may be more negatively impacted by exercise (fatigued in other areas of life due to exercise)

115
Q

4.5 vs 5.0 on EDSS

A

4.5 on EDSS: fully ambulatory without aid, may have some limitation for long-term activities, can be active most of the day
- able to walk without aid or rest for 300 ml

5: walk without aid or resting for 200m, disability severe enough to impair full-day activity (hard for them to work for a full day)

116
Q

CSEP - Guidelines

Based on systematic reviews.

Who?

A

“adults (aged 18-64 years) with minimal to moderate disability (suggested 0-4.5 on EDSS scale by Kelvin although there is no actual correlation listed by CSEP) resulting from either relapsing remitting or progressive forms of multiple sclerosis”

  • audience: “people living with multiple sclerosis, their families, health care professionals and organizations that promote exercise or serve adults with multiple sclerosis”
117
Q

CSEP - Guidelines

Based on systematic reviews.

What:
● F.I.T.T.

A

Frequency: 2x/ week

Intensity: moderate (5-6 on RPE scale of 10)

Time: in sessions of 30( 60 minutes of moderate activity a week)

Type: aerobic activity

118
Q

CSEP - Guidelines

Vs

Compare with 24-hour Movement Guidelines of the general population

A

General population is 150 mins per week at moderate to vigorous intensity

Why is it less for MS
-cautious about both intensity and amount accumulated—-> no set answer for why this is reduced though

119
Q

National Multiple Sclerosis
American guildlines

A
  1. Endorse and promote benefits/safety
  2. Early evaluation (physical/occupational therapist or exercise/sport
    scientists), individualized exercise program
  3. ≥150 min/week exercise and/or ≥150 min/week lifestyle PA
  4. Progressive based on ability, preferences, safety
  5. If disability increases, referral to specialists
  6. Limited mobility, facilitated by trained assistant
120
Q

Lifestyle PA: Guidlines

A

● Daily accumulation of at least 30 min of activities

● planned/unplanned leisure, work, household, moderate-to-vigorous intensity

121
Q

Exercise

A

● Planned PA performed repeatedly
with a specific objective (e.g. improvement of fitness …)

122
Q

Rehabilitation (short term)

A

:
● Intermittent or ongoing use of interdisciplinary strategies to regain or maintain optimal physical function, promote functional independence, prevent complications, and improve QoL.

Not lifestyle changes

123
Q

O-4.5 (mild impairment)

Exercise (USA Natuonal MS society, their recommendation)

A

Exercise may temporarily worsen symptoms in patients who are heat sensitive

Aerobic: 10-30 min x 2-3/week = 20-90 min, moderate

Resistance: 2-3/week, 1-3 sets (8-15 reps), 5-10 exercises

Flexibility: daily

Neuromotor: 3-6/week, 20-60 minutes = 60-360 min

Csep has not caught up, reason why recommendations are lower

124
Q

Exercise, Body Temperature & MS

Uhthoff’s phenomenon

A

• Transient worsening of symptoms with increased core temperature

• aka heat intolerance

125
Q

Exercise, Body Temperature & MS

Thermoregulatory impairment

A

• Autonomic pathology: blunted sweating

Cooling Countermeasures
- cooling vest

126
Q

Barriers and facilitators to exercise and lifestyle physical activity.

Physical

A

• Physical environment

• Social environment

• Health condition

• Cognitive/behavioral

• Cost

Fatigue

• Time

127
Q

Barriers and facilitators to exercise and lifestyle physical activity.

Facilitators

A

• Physical environment

• Social environment

• Health condition

• Cognitive/behavioral

• Cost

• Time

128
Q

Regular lifelong exercise

A

Older at diagnosis
(Delay diagnosis)

Brain volume reduce a little

Older age when you reach secondary progressive

129
Q

Exercise after diagnosis

A

date of diagnosis is the same if you did not exercise at all

Medium brain volume

Medium delay of onset of secondary progressive

130
Q

Traditional MS course, no exercise (last slide)

A

Normal date of diagnosis

High loss of brain volume

Younger age for onset of secondary progressive

131
Q

EDSS
0-4.5
Symptoms

A

• Symptoms: Ranging from no symptoms to mild-to-moderate fatigue, unsteadiness/imbalance, sensory changes, mild walking impairment, and reduced visual acuity; bowel and/or bladder symptoms; altered mood state; and cognitive impairment

132
Q

EDSS 0-4.5
Neurological impairments

A

Neurologic impairments: Ranging from normal neurologic exam to mild-to-moderate impairments in proprioception, cerebellar function, vision, muscle strength/tone/endurance, bladder function, and cognition

133
Q

EDSS 0–4.5

Functional limitations:

A

Functional limitations: Ranging from no limitations to limited endurance, unsteadiness, and impaired information processing and memory

134
Q

EDSS 5.0–6.5

Symptoms

A

Symptoms: Progression of any or all symptoms mentioned on 0-4.5

135
Q

EDSS 5.0–6.5

Neurologic impairments:

A

May include an increase in the impairments mentioned 0-4.5, worsening gait (unilateral to bilateral spastic paresis, foot drop with compensatory hip hike, and circumduction with progression from unilateral to bilateral assistance and/or use of manual wheelchair), and upper extremity coordination

136
Q

EDSS 5.0–6.5

Functional limitations

A

Limited walking distance (20–200 m); falls; inability to safely complete dual motor/cognitive tasks; work/home activities require adaptations, compensatory strategies, and mobility aids (ranging from cane to wheeled walker for daily use to a manual wheelchair for distances); transfers on/off the floor and into/out of chairs increasingly challenging; and requires assistance from support partner for more complex daily activities

137
Q

EDSS 7.0–9.

Symptoms:

A

Continued worsening of all symptoms mentioned 0-4.5

138
Q

EDSS 7.0–9.0

Neurologic impairments:

A

Significant impairments in many or all systems, as mentioned 0-4.5

139
Q

EDSS 7.0–9.0

Functional limitations

A

Gait—from 10 ft with a walker to restricted to bed and wheelchair;

Transfers—from minimal assist to total assist;

Bed mobility—from minimal assist to total assist;

Seated balance—from independent to total assist;

Standing balance—from independent with bilateral support to unable to stand unaided

140
Q

Dorsal column lesions there causes issues with

A

Vibration,light touch, proprioception (sensory information)

141
Q

EDSS 2 (simplified version)

A

Minimal disability (fully Ambulatory)

142
Q

EDSS 3 (simplified version)

A

Mild disability (fully ambulatory)

143
Q

EDSS 4 (simplified version)

A

Moderate Disability (fully ambulatory)

144
Q

EDSS 5 (simplified version)

A

Disability affect normal routine, if you exercise, you might be too fatigued to do your daily routine

145
Q

EDSS 6 (simplified version)

A

Individual using at least one assistive device (unilateral)

146
Q

EDSS 6.5 (simplified version)

A

Often using two devices (bilaterally)

Kin 372 (7 decks)

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