MS and inflammatory CNS disorders Flashcards
what is MS?
inflammatory demyelinating disorder of the CNS
plaques are disseminated in time and place
who is MS most common in?
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)
what virus can be associated with MS?
EBV
most common form of MS?
relapsing, remitting MS (90%)
other types of MS?
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
clinical features of MS?
pyramidal dysfunction optic neuritis sensory symptoms Lr urinary tract dysfunction cerebellar and brain stem features cognitive impairment
how does pyramidal dysfunction present?
increased tone spasticity weakness extensors of upper limbs flexors of lower limbs
how does optic neuritis present?
painful visual loss lasting 1-2 weeks
painful on eye movement
RAPD
most will improve
what sensory symptoms might occur in MS?
any
e. g
- pain
- paraesthesia
- proprioception and vibration (dorsal column loss)
- numbness
- trigeminal neuralgia
sensory symptoms suspicious of MS?
feeling of water running down the leg
how common is sensory presentation in MS?
around half of people
how does cerebellar dysfunction present?
DANISH - dysdiadokinesia - ataxia - nystagmus - intention tremor - slurred speech (dysarthria) - hypotonia past pointing pendular reflexes
brain stem dysfunction may affect which cranial nerves and how may this present?
CN VI = diplopia
CN VII = facial weakness
features of internuclear opthalmoplegia?
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
where is the problem in internuclear opthalmoplegia?
medial longitudinal fasciculus
how can MS affect urinary tract?
frequency nocturia urgency urge incontinence retention (can affect detrusor muscle)
how is fatigue due to MS managed?
amantadine
modafinil if sleepy
hyperbaric oxygen
how is diagnosis made of MS?
at least 2 episodes suggestive of demyelination
dissemination in time and place
exclude alternative diagnosis
what investigations are used for MS diagnosis?
Clinical diagnosis MRI CSF neurophysiology blood tests (to exclude other things which may mimic MS)
MS differentials?
vasculitis granulomatous disorder vascular disease (inc. stroke) structural lesion infection (HIV, syphilis, lyme disease) metabolic disorder (e.g B12 folate deficiency)
what blood tests are done to exclude other cause in expected MS?
PV, FBC, CRP renal, liver, bone profile auto antibody screen borellia, HIV, syphilis serology B12 and folate Vit D
classical MRI findings in MS?
dissemination in time
CSF features in MS?
oligoclonal bands
how is MS managed generally?
acute exacerbation/relapse management
symptomatic treatment
disease modifying therapy
how is acute relapse managed?
mild = symptomatic treatment moderate = oral steroids (methyloprednisolone) severe = admit/IV steroids (1000mg over 3 days)
what symptomatic treatment is used in MS?
pyramidal dysfunction - physio, OT, antispasmodic agent
sensory - anticonvulsants, antidepressants, tens machine, acupuncture, lignocaine infusion
urinary - bladder drill, anti-cholinergics (oxybutynin), desmopressin, catheterisation
is spasticity always treated?
no
if patient is weak, spasticity may allow them to stand
examples of anti-spasmotic agent?
physio baclofen tizanidine botox intrathecal baclofen/phenol (if bed bound)
how does MS affect bladder dysfunction?
increased bladder tone at neck
detrusor hypersensitivity
detrusor sphyncteric dyssenergia
a lot of the problems in MS are due to what?
drug related issues
is cannabis effective in MS?
in some
around 50% have cannabinoid receptors which respond well in drug resistant spasticity
how does MS progress if untreated?
increasing cognitive dysfunction
decreasing brain volume
first line disease modifying therapy?
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
second line disease modifying therapy?
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
third line disease modifying therapy?
mitoxantrone, lemtrada
HSCT (stem cell transplant)
indication to move on to second line therapy?
new lesion formation on imaging or new contrast enhancement despite being on first line treatment
how do monoclonal antibodies work in MS?
stop trans-endothelial migration of activated T cells across BBB in EAE mediated by integrins
inflamamatory cascade in MS?
immune cells pass through BBB > immune cells may re-activate and produce cytokines > immune cells mount autoimmune attack against myelin
