Demyelinating Diseases Flashcards
Name three characteristic MS syndromes
- optic neuritis
- transverse myelitis
- intranuclear ophthalmoplegia
How can optic neuritis present?
loss of acuity
red desaturation (decreased ability to distinguish color)
optic disc atrophy/pallor
RAPD
How can transverse myelitis present?
PATCHY inflammatory demyelination in spinal cord…partial lesion does not mimic complete cord transection
can present with unilateral/bilateral weakness or sensory loss below lesion. Can have bowel/bladder incontinence. Tingling/pain around torso at level of lesion.
How does INO present?
inability to adduct eye during contralateral gaze with nystagmus of abducting eye; convergence is SPARED
tingling electric sensation down the spine when patient flexes neck
Lhermitte’s sign
worsening of MS symptoms in the heat
Uhthoff’s phenomenon
discrete episodes of neurologic dysfuction that resolve after a period of time
relapsing remitting MS
relapses = “flares”
recovery from each MS relapse is incomplete and baseline function deteriorates
secondary progressive
relentlessly progressive course from onset of MS with superimposed relapses
progressive relapsing
relentlessly course from MS onset with NO relapses
primary progressive
features predicting good prognosis for MS
young age of onset female primarily sensory symptoms mild relapses with little/no residual deficits optic neuritis WITHOUT MOTOR SYMPTOMS
what imaging modality good for picking up new MS lesions
T2 MRI
FLAIR
t2 hyperintesne ovoid lesions are classic
Classic CSF finding MS
oligoclonal bands
mechanism of oligoclonal bands on CSF
intrathecal production of IgG antibodies by plasma cell clones
Besides oligoclonal bands what else can MS CSF show?
moderate pleiocytosis and elevated protein
what can visual evoked potentials be used for?
document evidence of old optic neuritis
chronic treatment options for MS
interferon beta 1a/1b
glatiramer acetate
natalizumab
fingolimod
natalizumab increases risk of?
progressive multifocal leukoencephalopathy
What labs to get before starting interferon?
CBC and LFTs
can cause leukopenia and transaminitis
MOA natalizumab
monoclonal antibody against alpha 4 integrins that prevents lymphocytes and monocytes from crossing BBB
MOA fingolimod
mixed agonist/antagonist of sphingosine 1p1 receptor (first oral MS med; all others are injectable)
what must be monitored when patient is on fingolimod
ECG watch out for bradycardia and heart block
symptomatic treatment options for MS spasticity
baclofen, tizanidine, diazepam
symptomatic treatment for MS bladder dysfunction
anticholinergic agents and intermittent self cath
presents similarly to MS except usually after viral antecedent or vaccine
acute disseminated encephalomyelitis
acute disseminated encephalomyelitis vs. MS
Unlike MS, ADEM patients will…
- only have one phase (monophasic) and will usually recover well
- rarely show oligoclonal bands
- have more cells with lymphocytic pleocytosis
neuromyelitis optica (NMO) = ? + ?
development of optic neuritis and transverse myelitis
MS vs. NMO
NMO patients unlike MS, will have
- greater pain component in ON/transverse myelitis
- CSF pleocytosis sometimes neutrophilic predominance
How to confirm diagnosis of NMO
antibodies to the aquaporin 4 channel
dementia, focal cortical dysfunction, cerebellar abnormaliteis
progressive multifocal leukoencephalopathy (PML)
What conditions associated with PML?
immunosuppressed states, AIDS, leukemia/lymphoma
causative agents PML
JC virus! (leads to demyelination by infecting oligodendrocytes)
patient presents with aucte confusion and cortical vision loss (blindness with preserved pupil reactivity) in the setting of rapid HTN or on transplant immunosuppressants?
posterior reversible encephalopathy syndrome
PRES
