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neuro 210 finallll > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

what is the first cause of non-traumatic disability in young adults of north america and europe

A

MS

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2
Q

where is MS more common geographically?

A

more as you move up and down the equator … in canada its more in the prairies and atlantic

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3
Q

Approx how many people in alberta are diagnosed with MS?

A

14,000

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4
Q

What is average age of onset of MS?

A

15-45 years old (mainly young)

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5
Q

what percentage accounts for paediatric MS? how many of them are less than or equal to age 18?

A

6% of total MS is paediatric and 3-10% of MS patients have their onset before 18

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6
Q

What is the ratio of females to males with MS?

A

females to males ratio of 3:1 (most autoimmune systems are more common in woman than men)

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7
Q

what are possible causes of MS?

A

MS is a multifactorial disease meaning that many things can contribute to its cause

  1. infections like measles and EBV can trigger MS
  2. sun exposure or lack of
  3. smoking can worsen symptoms of MS
  4. more salt can cause activation or over activation of immune cells
  5. genes… and genetic background
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8
Q

What are some clinical manifestations of MS?

A
  1. ocular manifestations include: blurred vision and diplopia
  2. cerebellar manifestations include: nystagmus (fast moving of eyes), ataxia, vertigo
  3. autonomic manifestations include urinary incompetence with bladder
  4. sensory manifestations include severe neuropathic pain
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9
Q

What is the disease course of MS?

A

initially, the symptoms present themselves as waves so they come and ago during periods called relapsing and remissions for about 10 years then it starts to increase in progression and stop remission because conditions get worse

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10
Q

what is the EDSS scale? what does it do?

A

its used to assess disability stage of MS.. its flawed because it focuses too much on the motor disabilities and not much the cognitive

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11
Q

What is the MS disease course in steps?

A
  1. clinically isolated syndrome (CIS) –> people who had their first attack can become or manifest it into MS if theres any chance of another attack
  2. relapsing and remitting periods (approx 80% of people get it) for about 10 years
  3. secondary progressive: 75-80% of relapsing-remitting … this is where the RR’s stop but MS can still develop
  4. primary progressive (10-15%) –> don’t have relapse course
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12
Q

What is focal demyelination?

A

this is where specific areas of the brain have demyelination… includes optic neuritis (you can have this as a symptom or just as a condition alone) and idiopathic transverse myelitis (inflammation of spinal cord that can be due to things other than MS)

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13
Q

what is diffuse demyelination?

A

this is generalized demyelination …

incldues

  • neuromyelitis optica
  • ADEM
  • vasculitis
  • lyme disease
  • viral infection
  • neurolupus
  • neurosarcoidois
  • paraneoplastic syndrome
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14
Q

How do we diagnose MS?

A
  1. History –> through clinical record
  2. neurological examination: looks at weakness and changes in sensation
  3. lumbar puncture to check CSF for proteins
  4. Blood test
  5. MRI to see white spots in the brain
  6. EEG’s to measure brain activity
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15
Q

What is MS?

A

multiple sclerosis means (many scars) –> it is described as demyelination, demyelination and axonal transection

first, myelin start degenerating

  • Then, it can either start to re-myelinate –> not as strong as before but better than nothing
  • OR it can cause axonal transection (axonal cutting) which myelin degenerates and exposes axons to damage
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16
Q

Where in the brain does MS mainly affect?

A

it can cause a lesion around the paraventricular areas and white spots in staining show lesions of degeneration

Decreased axonal density in MS plaques… shows that along with demyelination, theres also neurogeneration of axons as well .. less white matter

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17
Q

What are of the brain is severely affected by MS?

A

the corpus callosum is affected because its a big white matter tract and results for 56% of lost density in the brains of people with MS

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18
Q

What are some examples of neurodegenerative diseases.?

A
  1. parkinson’s diseases
  2. huntington’s disease
  3. ALS
  4. spinocerebellar taxis
  5. alzheimer’s disease

these are important to note because we can compare the symptoms of these disorders to the symptoms of MS to see if MS is a neurodegenerative disorder or not

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19
Q

What are some characteristics of Neurodegenerative diseases? How can these be compared to MS?

A
  1. they affect specific parts or functional systems of the nervous system (MS affects multiple areas and is not specific)
  2. they begin insidiously, after a long period of normal nervous system function and pursue a gradual progressive course (you need a lot of cells to be gone to notice neurodegenerative disorders but thats not the case for MS)
  3. the CSF shows minimal changes (usually mild increase in proteins) but in MS. the CSF seems normal
  4. imaging shows either no change or only a volumetric reduction (atrophy) –> MS shows a lot of white spots that are easily detected initially
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20
Q

In what ways can MS be a disease of immune dysfunction?

A

the destruction within the CNS in MS is through to be immune-mediated

  • many inflam cell types are localized to lesion sites in the MS
  • the activity of several inflam cell types is dysregulated
  • levels of several inflam cytokines are increased in the serum, CSF and CNS of patients with MS (these should NOT be in CSF in the first place)
21
Q

What does genetic testing tell us about MS?

A
  • also in genetic testing it shows that all genes involve din MS are involved in regulation immune responses
  • theres also more % of MS occurring in monozygotic twins showing theres a genetic link
22
Q

What are some immune privileged sites (areas where immunity isn’t present due to preventative measures)?

A
  1. eyes (cornea, anterior chambers, …etc..)
  2. brain –> ventricles, and striatum … BBB
  3. pregnant uterus
  4. ovary
  5. testes
  6. adrenal cortex
  7. hair follicles
23
Q

What is EAE? How was it replicated in animals?

A

mice were injected with myelin basic protein developing demyelinated disease (EAE)

  • the disease is mediated by the TH1 cells which are pro-inflammatory ones
  • the disease can be transferred from animal to animal through transfer of T-cells
  • indicates the involvement of T-cells in the spread of MS-like symptoms?
24
Q

What is the immunology of EAE? and molecular mimicry?

A

immunology:

  1. inject MBP
  2. pool of native t-cells… one T-cell recognizes this MBP
  3. that T-cell makes the pro-inflammatory cells for that specific MBP
  4. these inflam cells replicate
  5. once exposed to the MBP again, these pro-inflam are re-activated in the CNS and products produce the CNS pathology once they enter the CNS
25
Q

What happens once the inflammatory cells get activated due to MBP?

A

they cross the BBB and get to the CNS.. then more inflammation in the CNS occurs due to the cytokines and chemokine … macrophages eat away at the myelin

26
Q

What is perivascular inflammation in the MS plaques?

A

its T-cells accumulating near tissue of inflammation …

27
Q

What do T-cells do once they accumulate in plaques in the brain?

A

they cause axonal transection in acute MS lesions… so they cut the myelin

28
Q

What is the pathology of MS and the brain atrophy presented in MS?

A

the pathology of MS is higher amounts of axonal loss associated with progression of the clinical course of the disease as well as higher myelination loss…

it shows up in the brain as a large loss of white matter (enlarged ventricles)

29
Q

What are two approaches to MS treatment?

A
  1. disease modifying treatments –> these are long term treatments aimed to modify disease course, delay accumulation of disability … this does not have direct impact on the symptoms of MS but it is a MS specific treatment (i.e. its not like advil)
  2. Symptom treatments –> treatments to settle the symptoms of MS … this has NO direct effect on the actual disease (i.e. giving them advil for their headache will relieve their symptoms but NOT get rid of MS).. these are non-specific treatments for MS
30
Q

What is typically given to relieve acute attacks in clinical manifestations of MS (non-specific)?

A

often steroids are given to stop inflammation and get rid of the major clinical manifestations

31
Q

What is mainly given to control the spasticity of nerves in MS?

A

Baclofen … GABA agonist is given or inject directly in the CSF to produce inhibition and stop muscle spasms (works on the inhibitory interneurons)

32
Q

What is one of the worst feelings associated with MS symptoms?

A

tiredness and fatigue and lack of energy distinct from sadness or weakness… severe in up to 74% of patience and worst symptom of the disease in 50-60% of the ppl

33
Q

what is a good treatment for fatigue in MS?

A

stimulants like amantadine or modafinil is good for giving them energy

34
Q

What is trigemnial neuralgia? What are some treatments for it?

A

trigemnial neuralgia is a neuropathic pain of the face which is very disbabling… treatments mainly with seizure reducing medications

35
Q

What are the two main areas that targets for treatment in MS can cover?

A

it can cover existing treatments primarily target in the inflammatory component of MS in the immune system OR in the CNS

36
Q

What are the three main points to treat specific to MS in the CNS?

A
  1. inflammation
  2. neurodegeneration/demylination
  3. failure of repair
37
Q

What are three different MS therapy options targeting immune system?

A
  1. monoclonal antibodies … blocks the function of immune cells
  2. oral therapies
  3. traditional injectables
38
Q

What are traditional immunomodulatory therapies (3)

A
  1. interferon
  2. IFNbeta1a
  3. Glatiramer Acetate (GA) or Copaxone
39
Q

How does GA work?

A

GA is presented as an antigen and generates GA-specific T-cells of TH2 bias

  • the GA affects T cells and TH2 cells to stop pro-inflammatory actions and work more as anti-inflammatory actions
40
Q

How does Interferon-beta work?

A

it acts through the infereron-Beta receptor and inhibits antigen presentation and T-cell activation –> decreases activation of T-cells and immune cells

it causes decrease in pro-inflammatory TH1 cytokines

41
Q

What are some pros to traditional immunomodulatory therapies?

A

its safe

  • 33% relapse reduction
  • reduce GAD enhancement
  • GA is a neuroprotective
  • delay disability progression
42
Q

What are some cons to traditional immunomodulatory therapies?

A

injectables
- BIFN side effects include flu-like symptoms, injection site reactions, liver effects, leukopenia
GA side effects: injection site reactions, rash, panic reaction, lipoatrophy

43
Q

What is diethyl fumarate?

A

oral medication that needs to be taken with food because it can cause upset GI .. it reduces relates for up to 50% and has few side effects, HOWEVER

cons: it can include facial flushing, upset GI, fatigue, headache, leukopenia, increase LFT, minor infections, and monitoring

44
Q

what is teriflunomide? whats its mechanism of action?

A

it decreases the proliferation of T and B cells

45
Q

What are the pros and cons of teriflunomide?

A

pros: its a pill, it reduces annual relapse by 31%
cons: hair loss, nausea, TB reactivation, diarrhea..etc…

46
Q

What is Tysabri? what does it do?

A

tasbri blocks alpha-4 intern and attaches to WBC’s and blocks entrance to BBB (this is the most effective drug)

they do this when the first line fails

47
Q

What is a common disorder associated with Tysabri?

A

PML … its comes from a JC virus and can cause death… PML is more common if tysabri is taken over 2 years so patience only take it for less than 2 years

also not prescribed to patients who have taken antisuppresants

48
Q

What is fingolimod?

A

makes b and t cells stay in the lymph nodes and circulate less

neuro 210 finallll (12 decks)

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