MS Flashcards
cause
discrete plaques of demyelination occur at multiple CNS sites
due to T-cell mediated immune response (trigger unknown, ?vit D)
demyelination heals poorly, hence relapsing/remitting
prolonged demyelination causes axonal loss and progressive Sx
prevalence
commoner in temperate areas (eg more in scotland than england)
rarer in black africa/asia
risk of where you live rather than your heritage
demographics
mean age of onset 30yo
female:male 3:1
early exposure to sunlight/vit D is important, and vit D status relates to prevention of MS, fewer Sx and fewer new lesions on MRI in established MS
presentation
usually monosymptomatic, eg:
unilateral optic neuritis (pain on eye movement and rapid decrease in central vision)
numbness or tingling in the limbs
leg weakness
brainstem or cerebellar disturbance (eg diplopia, ataxia)
Sx may worsen with heat eg hot bath, or with exercise
rarely polysymptomatic
progression
early on, relapses (which can be stress induced) may be followed by remission and full recovery
with time, remissions are incomplete, so disability accumulates
steady progression of disability from the outset also occurs, while some patients experience no progressive disablement at all
poor prognostic signs: older female motor signs at onset many relapses early on many MRI lesions axonal loss
diagnosis
this is clinical
no test is pathognomonic
requires lesions disseminated in time and space unattributable to other causes
therefore after 1 episode further evidence is needed
early diagnosis and Tx reduce relapse rates and disability
take a good Hx, it may reveal previously unrecognised episodes
Rx for MS
encourage a happy, stress free life if possible (stress can trigger the development f new lesions)
minimize disability (disabled living foundation)
if poor diet, or low sun exposure, give vit D
steroids
methylprednisolone 0.5-1g/24h for <3days shortens acute relapses
use sparingly - 2 times or less per year
no overall prognostic effect
interferons
IFN-1B & IFN-1A
decrease relapses by 30% in active relapsing/remitting MS
decrease lesion accumulation on MRI
the power to delay disability is modest at best, as is their role in progressive MS
SE: flu Sx, depression, abortion
NB can cause lesions ass. w/ more severe disability 15yrs later
monoclonal antibodies
alemtuzumab acts against T-cells in relapsing/remitting
shown to be better than IFN
SE: infections while the immune system reconstitutes itself, autoimmune disease (thyroid, skin, kidney)
natalizumab acts against VLA-4 receptors that allow immune cells to cross the blood-brain barrier
decreases relapses in relapsing/remitting MS by 68% and decreases lesions on MRI by 92%
SE: progressive leucoencephalopathy, antibody-mediated resistance
non-immunosuppressives
glatiramer, mitoxantrone
other drugs
azathioprine may be as effective as interferons for relapsing/remitting MS but 20x cheaper
there are no effective drug therapies for progressive MS
palliation
spasticity - baclofen, diazepam, dantrolene, tizanidine
tremor - botulinum toxin type A
urgency/freq - teach intermittent self-catheterisation
sensory consequences of MS
dysaesthesia pins and needles loss of vibration sense trigeminal neuralgia swallowing disorders constipation diplopia, hemianopia, optic neuritis, visual phenomena (eg on exercise), bilateral inter-nuclear ophthalmoplegia
motor consequences of MS
spastic weakness
myelitis
cerebellum: trunk and limb ataxia, intention, tremor, scanning (monotonous) speech, falls
