MS and inflammatory CNS disorders Flashcards

1
Q

what is MS?

A

inflammatory demyelinating disorder of the CNS

plaques are disseminated in time and place

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2
Q

who is MS most common in?

A

females
often presents in 30s and 40s
more common as you move away from the equator (more common further north and south - may be linked to Vit D deficiency)

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3
Q

what virus can be associated with MS?

A

EBV

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4
Q

most common form of MS?

A

relapsing, remitting MS (90%)

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5
Q

other types of MS?

A

secondary progressive
- initially like relapsing, remitting, then becomes s progressive slope
- (vision, walking affected)
progressive relapsing
- has flares/relapsing but progressing fairly rapidly
primary progressive
- progressing rapidly without any real specific relapses

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6
Q

clinical features of MS?

A
pyramidal dysfunction 
optic neuritis
sensory symptoms
Lr urinary tract dysfunction
cerebellar and brain stem features
cognitive impairment
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7
Q

how does pyramidal dysfunction present?

A
increased tone
spasticity
weakness
extensors of upper limbs
flexors of lower limbs
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8
Q

how does optic neuritis present?

A

painful visual loss lasting 1-2 weeks
painful on eye movement
RAPD
most will improve

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9
Q

what sensory symptoms might occur in MS?

A

any

e. g
- pain
- paraesthesia
- proprioception and vibration (dorsal column loss)
- numbness
- trigeminal neuralgia

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10
Q

sensory symptoms suspicious of MS?

A

feeling of water running down the leg

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11
Q

how common is sensory presentation in MS?

A

around half of people

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12
Q

how does cerebellar dysfunction present?

A
DANISH
- dysdiadokinesia
- ataxia
- nystagmus
- intention tremor
- slurred speech (dysarthria)
- hypotonia
past pointing
pendular reflexes
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13
Q

brain stem dysfunction may affect which cranial nerves and how may this present?

A

CN VI = diplopia

CN VII = facial weakness

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14
Q

features of internuclear opthalmoplegia?

A

instead of both eyes moving together, one eye moves and the other drags behind, normal eye then has nystagmus
causes distortion of binocular vision and diplopia

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15
Q

where is the problem in internuclear opthalmoplegia?

A

medial longitudinal fasciculus

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16
Q

how can MS affect urinary tract?

A
frequency
nocturia
urgency
urge incontinence
retention
(can affect detrusor muscle)
17
Q

how is fatigue due to MS managed?

A

amantadine
modafinil if sleepy
hyperbaric oxygen

18
Q

how is diagnosis made of MS?

A

at least 2 episodes suggestive of demyelination
dissemination in time and place
exclude alternative diagnosis

19
Q

what investigations are used for MS diagnosis?

A
Clinical diagnosis
MRI
CSF
neurophysiology
blood tests (to exclude other things which may mimic MS)
20
Q

MS differentials?

A
vasculitis
granulomatous disorder
vascular disease (inc. stroke)
structural lesion
infection (HIV, syphilis, lyme disease)
metabolic disorder (e.g B12 folate deficiency)
21
Q

what blood tests are done to exclude other cause in expected MS?

A
PV, FBC, CRP
renal, liver, bone profile
auto antibody screen
borellia, HIV, syphilis serology
B12 and folate
Vit D
22
Q

classical MRI findings in MS?

A

dissemination in time

23
Q

CSF features in MS?

A

oligoclonal bands

24
Q

how is MS managed generally?

A

acute exacerbation/relapse management
symptomatic treatment
disease modifying therapy

25
Q

how is acute relapse managed?

A
mild = symptomatic treatment
moderate = oral steroids (methyloprednisolone) 
severe = admit/IV steroids (1000mg over 3 days)
26
Q

what symptomatic treatment is used in MS?

A

pyramidal dysfunction - physio, OT, antispasmodic agent
sensory - anticonvulsants, antidepressants, tens machine, acupuncture, lignocaine infusion
urinary - bladder drill, anti-cholinergics (oxybutynin), desmopressin, catheterisation

27
Q

is spasticity always treated?

A

no

if patient is weak, spasticity may allow them to stand

28
Q

examples of anti-spasmotic agent?

A
physio
baclofen
tizanidine
botox
intrathecal baclofen/phenol (if bed bound)
29
Q

how does MS affect bladder dysfunction?

A

increased bladder tone at neck
detrusor hypersensitivity
detrusor sphyncteric dyssenergia

30
Q

a lot of the problems in MS are due to what?

A

drug related issues

31
Q

is cannabis effective in MS?

A

in some

around 50% have cannabinoid receptors which respond well in drug resistant spasticity

32
Q

how does MS progress if untreated?

A

increasing cognitive dysfunction

decreasing brain volume

33
Q

first line disease modifying therapy?

A
interferon beta
glatiramer acetate
- decrease relapse rate and severity
- self administered injections
tecfedira aubagio
- oral
- first line indication in RR MS but long term data unknown
34
Q

second line disease modifying therapy?

A
monoclonal antibody
- e.g tysabri
- used in rapidly evolving RR MS despite interferon treatment
- can cause PML
fingolimod, cladribine
- oral
- reduce relapse rate
- effect disease progression
- but more toxic than 1st line
35
Q

third line disease modifying therapy?

A

mitoxantrone, lemtrada

HSCT (stem cell transplant)

36
Q

indication to move on to second line therapy?

A

new lesion formation on imaging or new contrast enhancement despite being on first line treatment

37
Q

how do monoclonal antibodies work in MS?

A

stop trans-endothelial migration of activated T cells across BBB in EAE mediated by integrins

38
Q

inflamamatory cascade in MS?

A

immune cells pass through BBB > immune cells may re-activate and produce cytokines > immune cells mount autoimmune attack against myelin