Multiple Sclerosis Flashcards
Diagnosis indications for CT
head trauma, acute intracranial hemorrhage, tumor/mass, acute/chronic headaches, meningitis, intracranial calcification, fractures, spinal trauma, bone lesions, degenerative spinal disease.
Diagnosis indications for MRI
head trauma, acute/chronic intracranial hemorrhage, tumor/mass, demyelinating disease/lesion, chronic headache, vascular malformations, aneurysm, infection, degenerative spinal disease.
Indications for CT
lower in cost, speed, claustrophobic, obese (>300lbs) pacemaker or metal fragments in heart or eye
Indications for MRI
anatomical detail needed, nonspecific white matter lesions
MRI pros/cons
pros-sensitivity/specificity, no radiation, safe contrast agents, excellent soft tissue resolution, white matter lesions
cons-slow, claustrophobia, strong magnetic field, poor bone detail
MRI reading: T1
lesions mostly dark
dense bone, air and water all dark
fat bright
MRI reading: T2
looks like a negative
CSF, edema, demyelination are bright white
dense bone and air dark
fat, water, and abnormal tissue bright
Neuroanatomy of MS
CNS
UMN- cortical, brainstem, spinal cord
other- cerebellum, other
Prevalence/incidence of MS
young adults
women more than men
20-40 peak onset
Etiology of MS
unknown
environmental- vit D deficiency
Pathogenesis of MS
inflammatory (autoimmune) degenerative disease
acute CNS inflammation-autoimmune response against CNS antigens, T cells cross blood brain barrier, recognize myelin as foreign and attack, this causes demyleination and axonal injury
hallmark sclerotic plaque
end stage of process-areas of myelin and oligodendrocyte loss filled with inflammatory infiltrate
Disease course
insidious, episodic
initial insidious or acute neurologic sign/symptom (sensory, weakness, vision common), then symptoms resolve, then 2nd neurologic insult, then MRI and other diagnostic testing, then diagnosed with MS
5 diseases courses
clinically isolated syndrome (CIS) relapsing-remitting secondary progressive primary progressive progressive-relapsing
clinically isolated syndrome
first event
risk of developing MS
relapsing-remitting MS (RRMS)
disease attack with subsequent with subsequent recovery
little or no neurologic deficits between attacks
stepwise increase in neurologic deficits over years
90% of patients
secondary progressive MS (SPMS)
relapsing and remitting MS attacks are followed by incomplete recovery
cumulative loss of function and disability
conversion occurs 6-10 yrs after initial symptoms
85-90% of patients with RRMS
primary progressive (PPMS)
10% of patients
slow, steady progress of neurologic deficits
symptoms and signs are usually spinal
no obvious attacks, insidious progression
more common in late onset MS
progressive-relapsing MS (PRMS)
less then 5% of cases
progressive disease with clear acute relapses
initial symptoms
sensory, weakness, visual loss (optic neuritis), ataxia, diplopia, vertigo, fatigue
symptoms during disease course
weakness, sensory, ataxia, bladder, fatigue, cramps, diplopia, visual loss, bowel, dysarthria
parasethesia
abnormal spontaneous sensations; burning, tingling, pins and needles
feeling like the leg is on fire
dysesthesia
unpleasant sensation produced by a stimulus that is usually painless
allodynia
experience of pain from a non painful stimulation
hypoesthesia
loss of sensation/numbness
cerebellar clinical findings
ataxia "lack of order" intention tremor (terminal dysmetria-under/overshoot as limb approaches target)
ataxia
disordered contractions of agonist and antagonist muscles and lack of normal coordination between movements at different joints
includes dysrthythmia (adnormal timing)
includes dysmetria (abnormal trajectory)
appendicular (extremities-cerebellar hemispheres)
truncal (wide BOS-cerebellar vermis)
in order to make a diagnosis
find evidence of damage in at least two separate areas of the CNS
find evidence that the damage occurred at least one month apart
rule out all other possible diagnoses
1-multiple episodes of neurologic symptoms
2-MRI multiple lesions
3-CFS positive oliogoclonal bands
medical management
glucocorticoids for acute exacerbations
disease modifying therapies
symptomatic therapies
look at spasticity, neuorpathic pain, bladder/bowel dysfunction
better prognostic factors
female, onset (relapse-remitting, optic neuritis, sensory, complete recovery), younger are at onset, long attack intervals, low freq attacks early on
worse prognostic factors
male, onset (polysymptomatic, motor, incomplete recovery), increased age at onset, more frequent attacks, high freq attacks early on
intervene
help maintain mobile and prevent secondary complications
help guide recovery after an exacerbation
consider fatigue and heat sensitivity for some patients
