Multiple Sclerosis Flashcards
(146 cards)
1
Q
Multiple sclerosis (MS)
A
is the most common chronic inflammatory, demyelinating and neurodegenerative disease of the central nervous system in young adults.
2
Q
Multiple sclerosis (MS)
(Common)
A
MS has a greater Prevelance in European countries
But most common in people of European (Caucasian) descent.
3
Q
Multiple sclerosis (MS)
(Chronic)
A
You live with this for the rest of your life
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
5
Q
Multiple sclerosis (MS)
(Demyelinating)
A
Oligodendrocytes make myelin in CNS
Schwann cells make myelin in PNS
6
Q
Multiple sclerosis (MS)
(Young adults)
A
20-40s typical age for diagnosis
7
Q
White matter
A
Where axons with myelin sheaths are
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
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)
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
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)
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
13
Q
Immunohistochemistry
Transected axon
A
Beginning of Neurodegeneration
Everything not connected to the cell body will die
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
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
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
17
Q
Multiple
A
Need to have multiple occurrence of symptoms to be diagnosed p, must be spread out in time and space
18
Q
Stats for Canada
A
Canada
1 person in 400
4,377 new diagnosis/year
75% female
90% with Relapsing remitting Multiple sclerosis
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)
20
Q
Pre-symptomatic
A
Inflammation is present but it is below the threshold, the patient likely won’t have notice symptoms
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
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)
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
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
25
Secondary progressive
Symptoms continuous get worse (flair up)
Goals is to reduce the amount of people in this stage
26
Is the true cause of Multiple Sclerosis (MS) known?
No, the true cause of MS is unknown, and it is difficult to identify causes at an individual level.
27
What are the main risk factors associated with MS?
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)
28
What are the main risk factors associated with MS?
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
29
Can MS have a family history, and how do genetic mutations arise?
Yes, MS can have a family history, but genetic mutations can also spontaneously arise or result from environmental exposures, such as radiation.
30
How can exposure to radiation impact genetic mutations related to MS?
Exposure to radiation (e.g., x-rays) can cause damage in sperm and egg cells, potentially leading to genetic mutations before fertilization.
31
What gene family is associated with MS, and how does it relate to autoimmune conditions?
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).
32
Pathophysiology of MS (what is happening)
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
33
Pathophysiology
Blood Brain Barrier
BBB is selective,inflammation makes the BBB leaky, things that are normal up’s circulating in the blood can get in there,
34
Broken wire vs fix wire analogy
Broken wire: demyelination
Fixed wire: remyelination
Oligodendricytes, will try to fix it, but it not not has good has it was originally
35
Location of demyelination affect on symptoms
Presenting symptoms of MS depend on the location of the demyelinating lesions:
● Visual
● Sensory
● Motor
● Cognitive
36
Optic neuritis:
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
37
Focal Lesion location of optic neuritis
Optic nerve
38
Diplopia
Double vision
39
Focal lesion of diplopia
focal lesions are located in the left pons and right middle cerebellar peduncle
40
Vertigo
, a sensation of dizziness, is a symptom of impaired balance.
Problem in the inner ear
41
Focal lesion of vertigo
the cerebellar hemispheres
42
Lhermitte's sign and Paresthesia
Lhermitte's sign: electrical shock radiating down the spine upon neck flexion
Paresthesia: numbness/ tingling
43
Location of focal lesion that cause Lhermitte's sign and Paresthesia
located in the cervical spinal cord
44
sensorimotor hemisyndrome
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)
45
sensorimotor hemisyndrome focal lesion
focal lesion located in the left cerebral hemisphere of a patient will have right sensorimotor hemisyndrome.
46
What are focal lesions?
Areas of demyelination characteristic of all MS phenotypes, typically occurring around post-capillary venules [8] They are also known as plaques.
47
What happens to the blood-brain barrier in areas of focal lesions?
It breaks down
48
Where can focal lesions occur in the brain?
Grey matter and white matter
49
What is the Expanded Disability Status Scale (EDSS)
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
50
What does the EDSS access? (8 functional system)
The EDSS assesses disability across 8 functional systems (subscales):
Pyramidal
Cerebellar
Brainstem
Sensory
Bowel and bladder
Visual
Mental (cognitive)
Other
51
What is an important tool for diagnosing and monitoring MS?
Magnetic resonance imaging (MRI) is an important tool for diagnosing and monitoring MS.
52
Timed 25 foot walk
Gait speed, timing how quickly they can walk, motor impairment, sensory issues and coordination can all slow them down
53
What is the Symbol Digit Modalities Test (SDMT)?
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
54
What are the Fatigue Severity Scale (FSS) and the Modified Fatigue Impact Scale (MFIS)?
Patient-reported outcome measures used to assess the severity and impact of fatigue.
55
What is symptoms tied to
Many signs and symptoms, they are non specific, closely tied to where the Neurodegeneration are affecting in the body
56
Common measures of symptoms
EDSS
Timed 25 foot walk
SDMT (cognitive)
FSS or MFIS (fatigue)
57
What is the pyramidal system?
Also known as the corticospinal tract, the pyramidal system is responsible for controlling voluntary movements.
58
How does the doctor assess pyramidal function in the video?
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
59
How does the doctor assess Cerebellar function in the video?
Coordination test- looking for ataxia
flipping hands back and forth as high and fast as possible
60
How does the doctor assess Brainstem function in the video?
Speech and swallowing can present as from brain stem
Nystagmus ( involuntary eye movement) tracking finger with eye test
61
How does the doctor assess sensory function in the video?
Scratch, vibration, and using a toothpick for nociception (pain sensation).
62
Clonus
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
Optic neuritis
(Typical)
Onset and involvement
Onset: sub acute to chronic (hours to days)
Involvement: unilateral
64
Optic neuritis
(Typical)
Signs and symptoms
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
Optic neuritis
(Typical)
Recovery
Gradual recovery within 2-4 weeks after reaching peak severity
66
Myelitis (inflammation of spinal cord)
*Typical
Onset and involvement
Onset:Sub-acute and/or chronic (hours to days)
Involvement:
incomplete transverse myelitis
Asymmetric involvement
67
Myelitis (inflammation of spinal cord)
*Typical
Signs or symptoms
• 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
Myelitis (inflammation of spinal cord)
*Typical
Recovery
Gradual recovery starting within 2-4 weeks after reaching peak severity
69
FATIGUE SEVERITY SCALE (FSS)
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
Modified Fatigue Index Scale (MFIS)
- 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
How is fatigue measured clinically?
Want to see impact of exercise on fatigue: goal is to reduce score
72
Two domains of Fatigue
Perceptions of fatigue
Performance fatigability
73
Components of perceptions of fatigue
Homeostatic factors
Psychological factors
74
Components of performance fatigability/ the disease associated with the component
Peripheral factors
-Myasthenia Gravis (MG)
Central factors
-Multiple Sclerosis (MS)
75
What is perception of fatigue
● 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
What’s is performance fatigability
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
Homeostatic factors
What is controlling it
It’s normal function
Pathological states
Hypothalamus
Central regulation of activity based on energetic, inflammatory and neural feedback
Unknown, possible PD, hypothalamic lesions
78
Psychological factors
What is controlling it
It’s normal function
Pathological states
Frontal lobes
Mood and motivational influences on feelings of fatigue
Ex. Waking up in a bad mood
Depression, CFS, possible PD, Mood disorder
79
Peripheral factors
Outside of CNS (e.g. muscles)
What is controlling it
It’s normal function
Pathological states
Muscle, nerves, and glycogen stores
Loss of muscle force secondary to energy depletion or EC uncoupling
Myopathies, MG, GSD, GBS
80
Central factors
In the CNS (e.g. brain, brain stem, or spinal cord
What is controlling it
It’s normal function
Pathological states
Domain-specific cortical and subcortical network
Domain-specific task failure secondary to dysfunction in cognitive networks
MS, TBI, CVA, PD, other dementia
81
While separated in this diagram, it should be noted that perceptions of
fatigue and performance fatigability have the potential to influence each other.
Just a fact
82
Homeostatic factors and psycological factors
Capacity to perform past, present, and future actions
The internal perception of our ability to perform
83
Peripheral factors and Central factors
Limits is the current actions
Happening right now
84
Fatigue abbreviations
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
Performance fatigability
Definition
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
Pyramidal and Extrapyramidal Motor Pathways (originates and goes where?)
Descending pathways that originate in midbrain, pons , or medulla and descend down the spinal cord
87
Pyramidal and Extrapyramidal Motor Pathways
Primary motor cortex
Pyramidal cells travel down and cross over
88
Pyramidal Tract (Corticospinal pathway)
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
Primary Motor Cortex (M1)
30-40% of pyramidal tract fibers, only about 20% to spinal cord
90
Cross over occurring
When Layer 5 pyramidal neurons discharge action potentials and transmit this to the spinal cord
91
Time to task failure: Experiment
Performance fatigability task
Measuring how much time they can do this for
Shorter time= higher fatigability
Wall sit
92
Angelo Mosso
Professor of Physiology at the University in Turin
• blood circulation, respiration, physical education, high-altitude physiology, and muscular fatigue
• ergograph
93
Angelo Mosso
Ergograph
Instead of a sustained contraction, intermittent contractions are made at the middle finger (flex it repeated day)
94
Ergographic tracings
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
Anotomy and pathophysiology determines?
What type of fatigue will be experienced
Central/Peripheral fatigue
96
Exercise in the past
This was not encouraged because they were worried about its affects, (fatigue)
Exercise is going to cause relapses.
- increase the amount and intensity
97
G-B syndrome
Autoimmune disease that can affect myelination in the peripheral
98
Central ( explain the diagram)
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
Peripheral (explain the random ass diagram)
Axon
Muscle
- Myasthenia gravis, cause by few post synaptic acetylcholine receptors
100
Exercise therapy for fatigue in multiple sclerosis (Review)
Why is is strong
It’s a systematic review and meta analysis of only randomized
101
Exercise therapy for fatigue in multiple sclerosis (Review)
Population
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
Exercise therapy for fatigue in multiple sclerosis (Review)
Intervention
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
Exercise therapy for fatigue in multiple sclerosis (Review)
Comparison
No exercise or other type of intervention
104
Exercise therapy for fatigue in multiple sclerosis (Review)
Outcome Measure
Self-report questionnaires on fatigue
105
Exercise therapy for fatigue in multiple sclerosis (Review)
Key results
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
What type of exercise reduces fatigue the most in individuals with MS
Mixed (aerobic and strength) Other (e.g. yoga, tai-chi)
107
Conclusion of the exercise study
There is not enough evidence to definitively determine
- more studies with large sample sizes are needed
108
Mechanisms of exercise-induced effects on fatigue
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
Neurotrophins for Neuroprotection
Acute and chronic
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
Inflammation and Cytokines
Effects of exercise on cytokines secretion
Single intense exercise
Increase in pro-inflammatory cytokines
111
Inflammation and Cytokines
Effects of exercise on cytokines secretion
Regular moderate exercise (chronic)
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
HPA Axis
Stress response
Chronic endurance training decreases the stress response.
- Circulating cortisol in response to stress goes down
- Circulating endorphins increase (positive for mood)
113
Analogy
Why does the pathophysiology of MS lead to fatigue, and central fatigue in particular?
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
CSEP-guidelines
Why was 4.5 chosen
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
4.5 vs 5.0 on EDSS
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
CSEP - Guidelines
Based on systematic reviews.
Who?
"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
CSEP - Guidelines
Based on systematic reviews.
What:
● F.I.T.T.
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
CSEP - Guidelines
Vs
Compare with 24-hour Movement Guidelines of the general population
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
National Multiple Sclerosis
American guildlines
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
Lifestyle PA: Guidlines
● Daily accumulation of at least 30 min of activities
● planned/unplanned leisure, work, household, moderate-to-vigorous intensity
121
Exercise
● Planned PA performed repeatedly
with a specific objective (e.g. improvement of fitness ...)
122
Rehabilitation (short term)
:
● 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
O-4.5 (mild impairment)
Exercise (USA Natuonal MS society, their recommendation)
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
Exercise, Body Temperature & MS
Uhthoff’s phenomenon
• Transient worsening of symptoms with increased core temperature
• aka heat intolerance
125
Exercise, Body Temperature & MS
Thermoregulatory impairment
• Autonomic pathology: blunted sweating
Cooling Countermeasures
- cooling vest
126
Barriers and facilitators to exercise and lifestyle physical activity.
Physical
• Physical environment
• Social environment
• Health condition
• Cognitive/behavioral
• Cost
Fatigue
• Time
127
Barriers and facilitators to exercise and lifestyle physical activity.
Facilitators
• Physical environment
• Social environment
• Health condition
• Cognitive/behavioral
• Cost
• Time
128
Regular lifelong exercise
Older at diagnosis
(Delay diagnosis)
Brain volume reduce a little
Older age when you reach secondary progressive
129
Exercise after diagnosis
date of diagnosis is the same if you did not exercise at all
Medium brain volume
Medium delay of onset of secondary progressive
130
Traditional MS course, no exercise (last slide)
Normal date of diagnosis
High loss of brain volume
Younger age for onset of secondary progressive
131
EDSS
0-4.5
Symptoms
• 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
EDSS 0-4.5
Neurological impairments
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
EDSS 0–4.5
Functional limitations:
Functional limitations: Ranging from no limitations to limited endurance, unsteadiness, and impaired information processing and memory
134
EDSS 5.0–6.5
Symptoms
Symptoms: Progression of any or all symptoms mentioned on 0-4.5
135
EDSS 5.0–6.5
Neurologic impairments:
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
EDSS 5.0–6.5
Functional limitations
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
EDSS 7.0–9.
Symptoms:
Continued worsening of all symptoms mentioned 0-4.5
138
EDSS 7.0–9.0
Neurologic impairments:
Significant impairments in many or all systems, as mentioned 0-4.5
139
EDSS 7.0–9.0
Functional limitations
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
Dorsal column lesions there causes issues with
Vibration,light touch, proprioception (sensory information)
141
EDSS 2 (simplified version)
Minimal disability (fully Ambulatory)
142
EDSS 3 (simplified version)
Mild disability (fully ambulatory)
143
EDSS 4 (simplified version)
Moderate Disability (fully ambulatory)
144
EDSS 5 (simplified version)
Disability affect normal routine, if you exercise, you might be too fatigued to do your daily routine
145
EDSS 6 (simplified version)
Individual using at least one assistive device (unilateral)
146
EDSS 6.5 (simplified version)
Often using two devices (bilaterally)
