Multiple Sclerosis Flashcards
features suggestive of MS
onset between 15-50, optic neuritis, Lhermitte sign, internuclear ophthalmoplegia, fatigue, Uhthoff phenomenon, sensory sx of numbness and paresthesia, motor symptoms of paraparesis, spasticity, bowel and bladder dysfunction
Uhthoff phenomenon
heat sensitivity
Lhermitte sign
electrical shocks up the spine
Types of MS
relapsing remitting (majority), primary progressive, secondary progressive, progressive relapsing
Diagnosis of MS
T2 MRI lesions seen in time and space (periventricular juxtacortical and infratentorial or spinal cord.
Oligoclonal IgG bands on CSF fluid
what to see on CSF when diagnosing MS?
oligoclonal IgG bands and elevated IgG index (90%)
manifestations of optic neuritis
acute, peaks at 2 weeks, monocular vision loss, eye pain with movement,
washed out color vision
afferent pupillary defect
diagnosis of optic neuritis
need MRI of orbits and brain
look for MS
treatment of optic neuritis
IV steroids and 35% of cases reoccur
need to rule out MS
Who gets optic neuritis
young women and strongly associated with multiple sclerosis and associated with immune mediated demyelination
can also be a clinically isolated syndrome but can also progress to MS.
acute vision loss, decreased color perception and pupillary defect, headache and pain with eye movement
optic neuritis
may see swelling and hyperemia of disk on funduscopic exam. But 66% of all pts also haven normal funduscopic exam.
If suspecting optic neuritis you need to get a
MRI to rule out signs of demyelinating disease and MS
Optic neuritis may be isolated clinical syndrome and so need to assess risk for progression to MS. High risk for progression is multiple demyelinating plaques and may be started on early disease modifying therapy like interferon or galtiramer acetate for relapse prevention.
Surveillance schedule of MRI with optic neuritis
Get MRI on presentation and then 5 months and 1 year and imaging remaining negative no further imaging
normal brain MRI have a 20% risk of conversion to MS.
Clinically isolated syndrome in MS is a
defined as a 1st episode of CNS dysfunction caused by demyelination and it may progress to MS. All pts should undergo a MRI to evaluate for demyelination plaques and assess MS risk stratification and abnormal MRI findings need to get dx modifying therapy
what is chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)?
this is an acquired inflammatory disorder that has demyelination of peripheral nerves and nerve roots that presents as progressive, symmetric and proximal and distal muscle weakness along with a distal sensory loss affecting the arms and legs. This is NOT MS.
Symptoms last over 8 weeks and help differentiate CIDP from acute inflammatory demyelinating polyneuropathy or AIDP
what is on CIPD presentation
distal sensory loss with vibratory and proprioception loss is seen.
progressive, symmetric proximal and distal muscle weakness
see diminished or absent deep tendon reflexes are also characteristic.
chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) diagnosis
from electrodiagnostic studies which show peripheral nervous system demyelination (reduced conduction velocity and prolonged distal motor latencies and LP can show albuminocytologic disassociations in 90% of pts
nerve biopsy is limited and but it can now be used to help confirm segmental meylin loss when electrodiagnostic studies are indeterminate.
what is AIDP also known as?
guillain barre syndrome
acute inflammatory demyelinating polyneuropathy or AIDP or Guillain Barre syndrome is caused by
prior antecedent illness Campylobacter infection, HIV, infection or vaccination.
See rapid onset of symptoms within 3-4 weeks.
Lambert Eaten myasthenia gravis syndrome
see auto immune PRE synaptic neuromuscular junction disorder associated with malignancy (small cell lung cancer) in 50% of cases
presentation of Lambert Eaten myasthenia gravis syndrome
progressive symmetrical proximal muscle weakness that improves with physical activity and see reflexes become diminished or absent but sensory function is typically preserved.
What do you see on MRI of brain and orbits with gadolinium if patient has MS and presents with optic neuritis?
see periventicular white matter lesions that are >3mm and optic nerve inflammation
relapsing remitting (majority) of MS is defined as
disease relapse after full or partial recovery of initial MS symtpoms
acute MS or relapses are treated with
glucocorticoids but immunomodulatory agents are continued indefinitely to decrease relapse rate and slow accumulative lesions on MRI.
1st line immunomodulator for treatment is
interferons or glatiramer acetate based on side effect profile and clinical data
if MS pts don’t respond to 1st line agent when what are they switched too:
natalizumab = recombinant monoclonal atnibody against alpha 4 integrins that prevent adhesion of inflammatory lymphocytes and monocytes.
side effect of natalizumab
can cause progressive multifocal leukocephalopathy (PML) which is a fatal disease caused by the JC virus
what must be checked prior to starting natalizumab?
JC virus antibody because potential for fatal PML infection.
If JC virus antibodies are positive and MS pt has failed initial interferon therapy with continued relapses, what to start
start fingolimod instead of natalizumab
Which virus increases your predisposition for developing MS?
EBV.
after starting fingolimod, what is there an increased risk of:
HSV infections.
treatment of progressive MS is
limited
mitoxantrone s only FDA approved therapy for secondary progressive MS
ocrelizumab is only FDA approved therapy for primary progressive MS
