MS Flashcards

1
Q

Define MS

A

progressive long term neurological disorder of CNS affecting brain SC and optic nerves

acquired chronic autoimmune mediated inflammatory disease

multiple areas of scarring sclerotic tissue found disseminated throughout the CNS white and grey matter
BS SC optic nerve

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2
Q

prevalance

A

MS is the most prevalent chronic inflammatory disease of the CNS and the most common cause of non-traumatic neurological disability in young adults:

8,000 people living with MS in Ireland
100,000 people in the UK
400,000 people in the US
2.5 million people worldwide

Globally, the median estimated prevalence of MS is 30 per 100,000
(range, 2–80)

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3
Q

epidemiology

A

Peak age onset 25-35 years 70% between 21 and 40
Rarely in childhood and after 60 years

Females > Males (3:1)

White races mostly

Risk 1:750-800 for Northern Europeans

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4
Q

causes

A
not known if it has single or multiple causes 
known risk factors 
genetic environmental 
viral 
immunological
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5
Q

genetic factors

A

Incidence in first-degree relatives is 20 x higher than in general population (2-4% compared to 0.1%)
Risk higher for females
Concordance rate in monozygotic twins is 30%
Women transmit to offspring more frequently than males
Genome-wide association studies from 1000s of patients have
identified >200 gene variants that raise the risk of disease
Most risk alleles are associated with immune-pathway genes

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6
Q

environmental factors

A

Incidence higher with increasing geographic latitude
Europe and North America – 120 per 100,000 population (4-6x higher than south)
Equatorial countries – rare (1 per 100,000)
Differences in the same latitude – lower prevalence in Korea compared to Japan
Reasons unclear

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7
Q

viral factors

A

“Epidemics” after WWII Faroe Islands
Orkney and Shetland Islands
Iceland

Viral agent with long incubation period?

Increased incidence after history of mononucleosis or Epstein- Barr virus?

No proof

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8
Q

immunology

A

Genetically susceptible individuals may have an abnormality in immune response that results in an attack on their own neural tissue

Analysis of active lesions suggests that a single immune- effector mechanism dominates in each person

No single specific antigen

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9
Q

pathophysiology

A

MS attacks myelin in the CNS
Complex interplay between the immune system, glial cells
(myelin-making oligodendrocytes) and neurons
Destruction of oligodendrocytes → Myelin degenerates → Less
effective conduction by neuron

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10
Q

pathology

A

Sclerotic plaques in the cortex (grey and white matter), spinal cord and optic nerve
Acute lesions are inflammatory, mediated by T cells (CD4+ and
CD8+)
Relative sparing of axon itself initially
Possible incomplete re-myelination following acute demyelinating episode
Later stages of disease: damage to axons

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11
Q

investigations

A

no single definitive test
lumbar puncture
visual evoked response
MRI

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12
Q

clinical presentation

initial symptoms

A

Vague: lack of energy, headache, depression, aches in limbs
Precise neurological deficit Sensory disturbance 40% Retrobulbar or optic neuritis 17% Limb weakness 12%
Diplopia 11%
Vertigo, Ataxia, Sphincter disturbance - 20%
FCDE: First clinical demyelinating event

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13
Q

clinical symptoms

motor symptoms and signs

A
Muscle weakness: Often asymmetric paraparesis  Monoparesis
Hemiparesis
Tetraparesis
Spasticity (80%)
Clonus
Spasms
Hyperreflexia, positive Babinski’s sign
Abnormal posture and movement
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14
Q

visual symptoms

A

diplopia
blurred vision
loss of visual activity
sudden onset of optic neuritis without any other CNS signs or symptoms
pupillary abnormalities
irregularities in outline of pupil
partial constriction and loss of light reflex

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15
Q

cerebellar signs

A
hypotonia 
ataxia 
intention tremor 
poor coordination 
nystagmus 
dysarthria
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16
Q

sensory systems

A
somatosensory symptoms 
position sense / proprioception 
vibratory sense 
pain, temp, touch 
Lhermitte's symptoms - flexing head - sensory symptoms 
spine of LL 
paraesthesias and numbness
17
Q

cranial nerves / brainstem

A

visual disturbance
vertigo
UMN signs

18
Q

autonomic

A

bladder dysfunction
bowel
sexual dysfunction
sweating and vascular abnormalities

19
Q

cognitive psycho psychiatric

A

Cognitive dysfunction 43-70%
Affects memory and higher executive functions
Euphoria
Emotional lability
Psychiatric symptoms – mood swings, anxiety, hypomanic states
Depression common (15% to 50%)
Sleeping problems

20
Q

fatigue

A

Common in initial presentation as well as established disease
Relapses often associated with fatigue
33-55% of people with MS report it as a troubling symptom
Worse as day progresses
Link to temperature (Uhthoff’s phenomenon)
Exacerbated by poor sleep, pain, anxiety

21
Q

clinical course
relapsing
remising MS

A

Most common type of MS – up to 85% of cases
Characterized by attacks (relapses) and remissions (recovery).
During remission , fewer or no symptoms. Relapses: unpredictable and unclear etiology
During a relapse new symptoms may occur or previous symptoms may
return
A relapse is usually defined as the appearance of new symptoms lasting more than 24 hours. They can last any length of time.
40% will develop secondary progressive MS

22
Q

primary progressive MS

A

Some people with MS never have distinct relapses and
remissions.
From the onset of disease, individuals experience steadily worsening symptoms and progressive disability.
This may level off at any time, or may continue to get worse.
Around 10-15% of people with MS have PPMS

23
Q

secondary progressive SPMS

A

Starts as RRMS but after repeated attacks the remissions stop
and the disease moves into a progressive phase.
40% of people with initial RRMS develop secondary progressive MS.
The time it takes to move into the secondary progressive phase varies (median 15-20 years from first onset)
Less progression with:
Younger age Early treatment
Fewer spinal cord lesions

24
Q

benign MS

A

Usually starts with mild attacks followed by a recovery
It does not worsen over time and there is rarely permanent
disability. The first symptoms are usually sensory.
It is only possible to classify people as having benign MS when they have little or no sign of disability 10 to 15 years after the onset of the disease. However, occasionally disability may develop even after many years of the disease remaining inactive.
Around 10% per cent of people with MS have the benign form.

25
Q

course of disease

A

Impact on life expectancy depends on course of disease and access to disease-modifying treatments
On average people with MS die 6 years earlier
15 y after diagnosis: 50% use walking aids, 29% need a
wheelchair
In first 10 years 50-80% become unable to work

26
Q

treatment

A

exercise modifying pharmacology
exercise and lifestyle
symptomatic pharmacology and treatment

27
Q

pharm managment

A

Immunomodulators (disease modifiers) Copaxone® (Glatiramer acetate) Novantrone® (Mitoxantrone)
Tysabri® (Natalizumab)
Gilenya® (Fingolimod) Lemtrada® (Alemtuzumab) Leustatin® (Cladribine) Dimethyl fumarate Ocrevus® (Ocrelizumab) Aubagio® (Teriflunomide)

Steroids (treatment of relapses)
0.5g daily orally
1g IV 3-5 days

-Interferons (prevention of  relapses)
Avonex
Rebif
Betaferon
Most effective in FCDE and early  stages
28
Q

symptomatic pharm management

A

Spasticity: Zanaflex, Baclofen, Dantrolene, Baclofen pump
Urinary Symptoms:
Intermittent self catheterisation (Residual vol < 100mls)
Oxybutin, Tolterodine Impramine
Fatigue: Amantadine
Oscillopsia: Gabapentin
Neuropathic pain: Lyrica

29
Q

symptomatic treatment

A
Sexual dysfunction
60-70% of males impotent
90% improved with Viagra
Cognitive problems  neuropsychology
cognitive retraining strategies
Depression
Amitryptilline
30
Q

assessment

A

subjective
objective
outcome measures

31
Q

subjective

A
Presenting Complaint
History of Presenting Complaint
Investigations
Past Medical History
Social History
Family History
Take time
Develop a rapport
Open ended questions
Avoid interrupting (if possible!)
Summarise or paraphrase as you go on
Don’t have to take entire history sitting down face to face

new diagnosis
1. Database
Has the diagnosis been confirmed by a neurologist? Is the patient aware?
How has the neurologist classified the disease?
Currently in a relapse? Medications (steroids, disease modifiers, other)

  1. Subjective questions
    What problems did you notice that
    brought you to hospital?
    Have you ever had anything like this before?
    How is it affecting your daily life (mobility, ADLs, participation)? How are you coping?
    Did the steroids make a difference?
32
Q

subjective assessment in MS:

known diagnosis

A

Since you were last seen or assessed, has any activity you used to undertake been limited, stopped or affected?”

“Are you still able to undertake, as far as you wish:
Your work / employment
Leisure activities
Family roles
Washing, dressing and using the toilet
Getting about and getting in and out of the house
Controlling your environment – opening doors, switching things on and
off, using appliances, using your phone
Shopping, going to church, community activities
Household and domestic activities?”

33
Q

objective assessment

A
observation 
neuro exam 
ROM
functional assessment 
activities
34
Q

outcome measures

A

Impairment
Oxford scale, 10RM, 5TSTS
Modified Ashworth Scale
Nine Hole Peg Test

Activity limitation
Functional Assessment Measure (FAM)
*Multiple Sclerosis Functional Composite (MSFC) scale
Gait tests (Timed 10MWT, 6MWT)
Balance (TUG, Berg Balance Scale, Mini-Best Test)
*MS Fatigue Impact Scale (MFIS)

Participation restriction
* Kurtzke’s Extended Disability Status Scale (EDSS)

35
Q

aims of physio RX

A

Maintain soft tissue length and manage tonal abnormalities
Maximise muscle activity and strength
Education about the importance of exercise
Posture re-education
Gait training
Balance re-education / Vestibular rehabilitation / Falls prevention
Fatigue management
Management of incontinence
Pain management

36
Q

education

A

A wealth of evidence has established that exercise in MS is safe and effective

Aerobic training (low to moderate intensity) can improve fatigue and aerobic fitness
Balance exercises reduce fall rates and improve balance
Resistance training may improve fatigue and ambulation
Flexibility exercises may diminish spasticity and potentially prevent future contractures

37
Q

Lifestyle and exercise

A

encourage to exercise

may have beneficial effects on MS

38
Q

exercise testing in MS

A

6 minute walk test
with HR monitor, RPE
Leg or arm cycle ergometry with HR monitor, RPE (Physiological Cost Index)

30s STS 
10 rep max 
5T STS 
1 min STS 
goniometry 
sit and reach test
39
Q

exercise prescription

A

FITT principle

Considerations:
ICF, patient goals
Feasibility, safety
Patient choice
Facilitators – enjoyment, peers
Barriers – fear, fatigue,  facilities, conflicting advice