Multiple Sclerosis Flashcards

1
Q

what is multiple sclerosis

A

inflammatory dymyelinating disorder of the CENTRAL nervous system

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2
Q

what is a MS plaque

A

area of inflammation- this inflammation causes demyelination

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3
Q

is there a gender bias in MA

A

females: males
3: 1

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4
Q

what is the usual age of onset of MS

A

30s/40s

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5
Q

plaques in MS are disseminated in time and place- what does this mean

A

affects different areas at different times

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6
Q

what is your chance of getting MS if your identical twin has it

A

one in 3

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7
Q

what increases your chances of getting MS

A

living further from the equator (both north and south)
having epstein barre virus
low vit D
if born in summer months (mother vit D deficient during pregnancy)

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8
Q

what are the clinical courses of MS

A
relapsing remitting (90%)
secondary progressive (relapsing remitting but start nor getting fully better)
progressive relapsing (progresisvely gets worse will occasional relapses ans slight remissions) 
primary progressive (constant decline)
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9
Q

what are the clinical features of MS

A
pyramidal dysfunction- hypertonicity, weakness, hyper-reflexity
optic neuritis 
sensory symptoms 
urinary tract dysfunction 
cerebellar and brain stem features 
cognitive impairment
mental and physical fatigue
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10
Q

what are the features of pyramidal dysfunction

A
increased tone
spasticity (veolcity dependant, spastic catch)
brisk reflexes
weakness
extensors of upper limb weak 
flexors of lower limbs weak
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11
Q

what are the features of optic neuritis

A
painful (sore on eye movements) visual loss
lasts for 1-2 weeks 
most will improve
RAPD
(is inflammation of the optic nerve)
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12
Q

how many patient with MS will have/ have had optic neuritis

A

half

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13
Q

what sensory symptoms can you get in MS

A
pain, 
parasthesia, 
dorsal column loss (proprioception and vibration), 
numbess (very sugestive of MS), 
trigeminal neuralgia 

common to have burning feeling, or feel like water running down leg

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14
Q

can you have pain and numbness at the same time

A

yes

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15
Q

what do you look for in all patients with trigeminal neuralgia

A

scan for MS

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16
Q

what do most people with MS present with

A
optic neuritis (50%)
sensory symptoms (50%)
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17
Q

what are the clinical features of cerebellar dysfunction (can happen in MS)

A

dysarthia
ataxia
nystagmus
intention tremor
post pointing (finger over shooting mark when eyes closed)
pendular reflexes (hyporeflexia and hypotonia)
dysdiadokinesis (inability to perform rapid alternating movements)

18
Q

what are the features of brian stem dysfunction seen in MS

A
diplopia (CN VI palsy)
facial weakness (CN VII palsy)
internuclear ophthalmoplegia
19
Q

what is affected in internuclear ophthalmoplegia

A

medial longitudinal fasciculus

failure of adduction, nystagmus is aBducting eye (opposite side of lesion)

20
Q

what urinary tract dysfunction can you get in MS

A

increased tone of bladder + irritability of detrusor muscles:

  • frequency
  • nocturia
  • urgency
  • urge incontinence
  • retention
21
Q

how is MS diagnosed

A
at least 2 episodes suggestive of demyelination 
dissemination in place and time 
exclude other diagnoses via blood tests 
MRI (done for every patient)
CSF (LP)
neurophysiology
22
Q

what are your MS differentials

A
vasculitis
granulomatous disoder (neurosarcoidosis)
vascular disease, stroke/ TIA
structural lesion 
infection- HIV, syphilis, lyme disease
metabolic- B12/ folate deficiency
23
Q

what is included in the blood test to exclude other diagnoses in MS

A
plasma viscosity (will be raised in vasculitis), FBC, CRP 
renal live bone profile 
auto anti body screen 
borellia, HIV, syphilis serology 
B12 and folate 
vitamin D
24
Q

what is seen in 90+% of MS patients in CSF

A

oligoclonal bands

25
Q

what can a relapse of MS be

A

Optic neuritis, pyramidal problem, sensory problem, brain stem problem, anything really

26
Q

what is the treatment for an acute MS exacerbation

A

mild- symptomatic
mod- oral steriods (methylprednisolone 500mg for 5 days- not more than 1/2 per year)
severe- admit, IV steroids (1000mg over 3 days)

27
Q

what is the symptomatic treatment for pyramidal dysfunction

A

(e.g. weakness and spasticity)
physio
occupational therapy
anti spasmodic agent (although sometime spasticity can help with walking/ standing where there is weakness)

28
Q

what are the treatment options for spasticity

A
physio 
oral meds (baclofen, tizanidine= can cause floppiness and tiredness) 
bo tox (into muscles if severe) 
intrathecal baclofen/ phenol (end stage bed bound Tx)
29
Q

what are the treatment options for sensory symptoms

A
anti convulsants (gabapentin- careful of dependency) 
anti depressants (amitriptyline)
tens machine 
acupunture 
lignocaine infusion
30
Q

what is detrusor sphyncteric dysfunction dyssenergia

A

bladder neck and detrusor muscle contracting at the same time

31
Q

what are the treatment options for urinary dysfunction in MS

A

depends on symptoms- can just be lifestyle changes
bladder drill (training)
anti cholinergics (oxybutynin- for detrusor irritability and overactivity, can cause retention)
desmopressin
catheterisation

32
Q

what is the treatment for fatigue in MS

A

occupational therapist do fatigue management
amantadine (can cause heart failure and seizures)
modafinil if sleepy
hyperbaric oxygen

33
Q

does cannabis work in MS

A

can work in drug resistant spasticity in some patients

34
Q

when is the best time to intervene in MS management

A

in relapsing remitting stage

35
Q

what are the first line disease modifying therapies for MS

A

(given for moderate relapses 2-3 times per year)

  • interferon beta (avonex, rebif, betaseron, extavia)
  • glitiramer acetate
  • tecfedira, aubagio
36
Q

what are the second line disease modifying therapies for MS and when are they given

A

(if still having relaspes with 1st line treatment or if initial presentation severe)

  • monoclonal antibody (tysabri, ocrevus)
  • fingolimod, cladrabine
37
Q

what are the third line disease modifying therapies for MS

A
  • miroxantrone, lemtrada

- HSCT (stem cell transplantation)

38
Q

how are interferons and glitiramer acetate administered and how effective are they

A

injectable (sc, im)
decrease relapse rate by a third
decrease severity of relapses by 50%

39
Q

what is tecfidera and what does it do

A

oral drug
1st line for RR MS
44% reduction in relapse rate

40
Q

what are fingolimod/ cadrabine

A

oral agents
2nd line for MS
>50% reduction in relapse rate, with significant effect of disease progression but more toxic (why 2nd line)

41
Q

who gets monoclonal antibodies (tysabri) in MS

A

highly active relapsing remitting multiple sclerosis:
-Patients with rapidly evolving severe relapsing remitting multiple sclerosis

-Patients with high disease activity despite treatment with a interferon

42
Q

how do monoclonal antibodies work in MS

A

activated T cells cross BBB via VCAM1 mediated by integrins (transendothelial migration)
then cause autoimmunne attack against myelin
tysabri stops the activation of these leukocytes (t cells)