Multiple Sclerosis Flashcards
what is multiple sclerosis
inflammatory dymyelinating disorder of the CENTRAL nervous system
what is a MS plaque
area of inflammation- this inflammation causes demyelination
is there a gender bias in MA
females: males
3: 1
what is the usual age of onset of MS
30s/40s
plaques in MS are disseminated in time and place- what does this mean
affects different areas at different times
what is your chance of getting MS if your identical twin has it
one in 3
what increases your chances of getting MS
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)
what are the clinical courses of MS
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)
what are the clinical features of MS
pyramidal dysfunction- hypertonicity, weakness, hyper-reflexity optic neuritis sensory symptoms urinary tract dysfunction cerebellar and brain stem features cognitive impairment mental and physical fatigue
what are the features of pyramidal dysfunction
increased tone spasticity (veolcity dependant, spastic catch) brisk reflexes weakness extensors of upper limb weak flexors of lower limbs weak
what are the features of optic neuritis
painful (sore on eye movements) visual loss lasts for 1-2 weeks most will improve RAPD (is inflammation of the optic nerve)
how many patient with MS will have/ have had optic neuritis
half
what sensory symptoms can you get in MS
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
can you have pain and numbness at the same time
yes
what do you look for in all patients with trigeminal neuralgia
scan for MS
what do most people with MS present with
optic neuritis (50%) sensory symptoms (50%)
what are the clinical features of cerebellar dysfunction (can happen in MS)
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)
what are the features of brian stem dysfunction seen in MS
diplopia (CN VI palsy) facial weakness (CN VII palsy) internuclear ophthalmoplegia
what is affected in internuclear ophthalmoplegia
medial longitudinal fasciculus
failure of adduction, nystagmus is aBducting eye (opposite side of lesion)
what urinary tract dysfunction can you get in MS
increased tone of bladder + irritability of detrusor muscles:
- frequency
- nocturia
- urgency
- urge incontinence
- retention
how is MS diagnosed
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
what are your MS differentials
vasculitis granulomatous disoder (neurosarcoidosis) vascular disease, stroke/ TIA structural lesion infection- HIV, syphilis, lyme disease metabolic- B12/ folate deficiency
what is included in the blood test to exclude other diagnoses in MS
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
what is seen in 90+% of MS patients in CSF
oligoclonal bands
what can a relapse of MS be
Optic neuritis, pyramidal problem, sensory problem, brain stem problem, anything really
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)
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)
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)
what are the treatment options for sensory symptoms
anti convulsants (gabapentin- careful of dependency) anti depressants (amitriptyline) tens machine acupunture lignocaine infusion
what is detrusor sphyncteric dysfunction dyssenergia
bladder neck and detrusor muscle contracting at the same time
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
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
does cannabis work in MS
can work in drug resistant spasticity in some patients
when is the best time to intervene in MS management
in relapsing remitting stage
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
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
what are the third line disease modifying therapies for MS
- miroxantrone, lemtrada
- HSCT (stem cell transplantation)
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%
what is tecfidera and what does it do
oral drug
1st line for RR MS
44% reduction in relapse rate
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)
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
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)
