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
what can a relapse of MS be
Optic neuritis, pyramidal problem, sensory problem, brain stem problem, anything really
26
what is the treatment for an acute MS exacerbation
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
what is the symptomatic treatment for pyramidal dysfunction
(e.g. weakness and spasticity) physio occupational therapy anti spasmodic agent (although sometime spasticity can help with walking/ standing where there is weakness)
28
what are the treatment options for spasticity
``` 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
what are the treatment options for sensory symptoms
``` anti convulsants (gabapentin- careful of dependency) anti depressants (amitriptyline) tens machine acupunture lignocaine infusion ```
30
what is detrusor sphyncteric dysfunction dyssenergia
bladder neck and detrusor muscle contracting at the same time
31
what are the treatment options for urinary dysfunction in MS
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
what is the treatment for fatigue in MS
occupational therapist do fatigue management amantadine (can cause heart failure and seizures) modafinil if sleepy hyperbaric oxygen
33
does cannabis work in MS
can work in drug resistant spasticity in some patients
34
when is the best time to intervene in MS management
in relapsing remitting stage
35
what are the first line disease modifying therapies for MS
(given for moderate relapses 2-3 times per year) - interferon beta (avonex, rebif, betaseron, extavia) - glitiramer acetate - tecfedira, aubagio
36
what are the second line disease modifying therapies for MS and when are they given
(if still having relaspes with 1st line treatment or if initial presentation severe) - monoclonal antibody (tysabri, ocrevus) - fingolimod, cladrabine
37
what are the third line disease modifying therapies for MS
- miroxantrone, lemtrada | - HSCT (stem cell transplantation)
38
how are interferons and glitiramer acetate administered and how effective are they
injectable (sc, im) decrease relapse rate by a third decrease severity of relapses by 50%
39
what is tecfidera and what does it do
oral drug 1st line for RR MS 44% reduction in relapse rate
40
what are fingolimod/ cadrabine
oral agents 2nd line for MS >50% reduction in relapse rate, with significant effect of disease progression but more toxic (why 2nd line)
41
who gets monoclonal antibodies (tysabri) in MS
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
how do monoclonal antibodies work in MS
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)