Multiple Sclerosis Flashcards

1
Q

What are some key facts about MS?

A

-1/800 of adult population
-Most common cause of neurological disability in
young adults
-Young onset, long duration, limited effect on mortality results in a significant proportion of people with severe disability.
-50 % gait assistance after 10-15 years.

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2
Q

How is MS classified?

A

-Relapsing remitting MS (RRMS)
-Secondary progressive MS (SPMS)
-Primary progressive MS (PPMS)
-Clinically isolated syndrome (CIS)

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3
Q

What is relapsing remitting MS?

A

In relapsing remitting MS, people have distinct attacks of symptoms which then fade away either partially or completely.

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4
Q

What is secondary progressive MS (SPMS)?

A

Secondary progressive MS (SPMS) is a stage of MS which comes after relapsing remitting MS for many people. With this type of MS your disability gets steadily worse.

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5
Q

What is primary progressive MS (PPMS)?

A

Primary progressive MS affects about 10-15% of people diagnosed with MS. It has this name because from the first (primary) symptoms it is progressive. Symptoms gradually get worse over time, rather than appearing as sudden attacks (relapses).

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6
Q

What is clinically isolated syndrome (CIS)?

A

In the years before they’re diagnosed with MS, it’s possible that some people may get a diagnosis of one of two syndromes. These are clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS). Lots of people are diagnosed with these and never go on to get MS. But for some they’re an early sign that they’ll later develop MS.

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7
Q

What are the 4 pathological patterns of MS?

A

MS is not the same pathological process in everyone

I Inflammation & remyelination
II Inflammation & antibody/ complement
III Oligodendrocyteapoptosis
IV Oligodendrocyte damage including normal appearing tissue

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8
Q

What is multiple sclerosis?

A

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) characterized by chronic inflammation, demyelination, gliosis, and neuronal loss.

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9
Q

What is the pathophysiology of MS?

A

Two fundamental processes constitute general pathological process seen in MS patients:
-Focal inflammation resulting in macroscopic plaques and injury to the blood-brain barrier (BBB)
-Neurodegeneration with microscopic injury involving different components of the CNS including axons, neurons, and synapse

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10
Q

How is axonal damage relevant to MS?

A

-Axonal loss is greatest in
areas of active demyelination
but also occurs in normal
appearing white matter
-axons die early in the course of the disease
-Greater correlation between atrophy/ axonal loss
and disability
-Axonal transection occurs predominantly in areas of inflammation

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11
Q

How is MS diagnosed?

A

-MRI
-Immunology
-Evoked Potentials

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12
Q

What are the principles of diagnosis?

A

Dissemination in
-Time i.e. more than 1 attack
-Space lesions in more than 1 area
Clinically separate syndromes
MRI
Independent immune attack in CNS
Exclude mimics

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13
Q

What does MRI show in MS patients?

A

-Inflammatory lesions- diagnosis
-New inflammatory lesions and gadolinium
enhancing lesions = new activity
-T1 Black holes and atrophy = marker of disability

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14
Q

What is the McDonald criteria for MS?

A

-Dissemination in space: T2 lesion or more in at least two MS typical CNS regions: periventricular, juxtacortical, infratentorial and spinal cord.

-Dissemination in time: simultaneous asymptotic contrast-enhancing and non-enhancing lesions at any time OR a new T2 and/or contrast-enhancing lesion (s) on follow-up MRI, irrespective of timing OR await a second clinical attack

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15
Q

How are CSF oligoclonal bands relevant to MS?

A

-Evidence of independent production of antibodies within the blood- brain barrier
97% of PwMS
-OCB negative patients tend to have a better prognosis
Not exclusive to MS- also with other infectious/ inflammatory conditions

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16
Q

How are visual evoked potentials relevant to MS?

A

-Evidence of delayed conduction in visual pathways
-Especially useful if eye asymptomatic

17
Q

What role do genes play in MS?

A

Individual genes-
Twin studies:
monozygotic 30% vs dizygotic 3%
In high prevalence populations (0.3%):
1st degree relatives 2-3%, 2nd degree relatives 1%.
Group genes
-Racial differences
-Isolated communities

18
Q

Is MS more prevalent in women?

A

-MS is more prevalent in women
(2-3F/1M)

19
Q

Does migration play a role in MS?

A

-MS is more common in countries further from the equator

20
Q

What is the hygiene hypothesis?

A

the relative lack of early exposure to common pathogens during childhood in areas of with high levels of sanitation and hygiene may increase the risk for aberrant immune responses and autoimmune diseases if they are exposed to infectious triggers such as EBV later during adolescence and adulthood.

21
Q

What is EBV?

A

Epstein- Barr Virus (EBV)
-Formally known as Human gamma herpesvirus 4, and also known as Human Herpes Virus 4
-Cause of infectious mononucleosis (“mono” or “glandular fever”)
-Most people will get EBV as children and will not experience any symptoms
-Once infected, a person remains a carrier of EBV for life. But the virus normally doesn’t cause any symptoms or problems at all.
-Up to 95% of adults have been exposed to the virus

22
Q

What is the link between EBV and MS?

A

-EBV antibodies were significantly higher
in people who eventually developed MS
than in a matched set of individuals who
did not get the disease
-The risk of MS increased significantly following an EBV infection
MS Patients are almost universally seropositive for
-EBV infection (99.5%) although there is a very high rate of asymptomatic EBV infection amongst control populations too (94.2%)

23
Q

What characterises a ‘GOOD’ prognosis in MS?

A

-young
-female
-Few attacks/ good recovery/ long intervals between attacks

(These apply for groups rather than an individual patient)

24
Q

What characterises a ‘POOR’ prognosis in MS?

A

-Older
-Male
-Motor / cerebellar
-Frequent/ little recovery
-Higher lesion load on MRI
-Progressive course

(These apply for groups rather than an individual patient)

25
Q

How is disability measured in MS?

A

Expanded Disability Status Scale (Kurtzke)

26
Q

Outline the Expanded Disability Status Scale:

A

-Grade 1-3.5 combinations of functional systems (Pyramidal, cerebellar, visual, sensory, brainstem, sphincters, mood/ cognition, other, Graded minimal, mild, moderate)
-4.0: Fully ambulatory without aid, self-sufficient, up 12 hours/ day; able to walk without aid or rest some 500 meters
-5.5: Ambulatory without aid or rest for about 100 meters; disability severe enough to preclude full daily activities
-6.0: Intermittent / unilateral constant assistance to walk about 100 meters with or without resting
-6.5: Constant bilateral assistance to walk 20 meters without resting
-7.0: Unable to walk five meters, wheels self transfers alone.
-8.0: Restricted to bed/ chair; effective use of arms
-9.0: Confined to bed; can still communicate and eat.
-9.5: Unable to communicate effectively or eat/swallow
-10.0: Death due to MS

27
Q

What factors should be considered when deciding the choice of therapy?

A

-Disease Severity
-Relapses
-MRI Disability
-Patient Attitude to risk
-Work/ lifestyle
-Funding
-NICE Guidance

28
Q

What are first-line injectables?

A

Reduce relapses by about 30%
Beta Interferon
Interferons modulate the immune response
Flu symptoms
Subcut: Betaferon, Rebif
IMI: Avonex, Plegridy
Glatyrimer acetate
Polymer of myelin
No blood monitoring
Both safe in pregnancy

29
Q

What are some oral medication options?

A

Teriflunomide (30%)
-Derived from Laquinimod
-Contraindicated in pregnancy
-Rapid elimination
-Hair thinning, liver, low White cells
Dimethyl fumarate (40+%)
-Fumarate was used for psoriasis
-Most widely prescribed >300 000 patients
-Gastrointestinal side effects
-Few cases of PML

30
Q

What are some orals: SIP inhibitors?

A

Fingolimod
-Reduces relapses by 50%
-Daily tablet
-Cardiac: Heart block
-Macular oedema
-Reduced lymphocytes thus infections

Others
-Ponisimod
-Ozanimod
-Siponimod: Licence for SP MS

31
Q

What are the figures for depression in MS patients?

A

50% will have depression at some stage
15% will be depressed at any one time
Rates higher than in RA, with similar pain and disability (brain disease)
Overlap between MS symptoms and “organic” symptoms of depression (sleep/ fatigue/ cognitive)
Respond to conventional antidepressants!
Chose drugs based on other effects (SSRI)

32
Q

What can cause depression in MS?

A

Reactive effects on:
self esteem, family, relationship, work
Practical concerns: Financial, housing
pain

Biological:
-Both are brain diseases
-Disability & duration
Cognitive dysfunction
Frontal & temporal lesion

33
Q

What types of pain are there in MS?

A

-Neuropathic
-Complication of other aspects of the disease

34
Q

What is neuropathic pain like in MS patients?

A

-Trigeminal neuralgia
-Limbs

35
Q

What are other complications of other aspects of the disease?

A

-Spasticity
-Musculoskeletal
-Psychogenic component
-Bladder/ bowel/ bedsores

36
Q

How common is fatigue in patients with MS?

A

-Common at all disease stages (80%)
-Worse with relapses/ immune activation
-Worse in afternoon, with heat or exercise
-Better with rest, cooling
-Limited role for medication amantadine, modafanil, amphetamines

37
Q

Who is involved in the MS team?

A

–Doctors
-Therapy
-Work
-Social services
-Physio, OT
-Extended family/ friends
-Family Patient
-Nurses Ward / MS Continence District
-GP
-Neurologist
-Psychiatrist