Demyelination, Cohen Flashcards by Amanda Beach

presenting Sx of MS

visual loss, diplopia, dysarthria, ataxia, paralysis, sensory loss, bladder and sexual dysfunction
loss of cognitive abilities

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type of destruction in MS

myelin destruction in oligodendrocytes

axons destroyed

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age onset MS

late 20s

female >M

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gender prognosis MS

male worse prognosis

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geography Ms

north equator more common

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twin studies MS

more common in monozygotic than dizygotic

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HLA MS

DR15

D3 D4

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pathology MS

T cell mediated against CNS myelin
inflammation
some B cells
macrophages!
cytokines and chemokines

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what cytokines and chemokines are released in MS

INF beta and gamma

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tyeps of courses of MS

benign MS
relapsing remitting
secondary chroni
primary progressive

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majority MS is what pattern

relapsing remitting

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course of benign MS

small number of mild attacks and regain full function eventually

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why are legs affected more in MS than arms

more myelin

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what amount of attacks in first few years of MS suggests poor prognosis

> 1 attack/year

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life expenctancy shortage in MS patients

5-10 years

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Kurtzkes rule

90% disability in MS occurs within 10 years initial dx

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Common Sx in first attack of MS

visual loss or double vision
weakness
paresthesia

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Dx of MS

easier when patients have 2+ attacks of CNS dysfunction
MRI! old and new lesions
LP!!! most specific b/c oligoclonal bands

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What shows recent area demyelination in CNS

MRI with gadolinium enhancement

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Optic neuritis

sudden loss vision in one or both eyes
painful
lose pupillary reaction

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what causes optic neuritis

swelling of nerve

very painful

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Marcus Gunn reaction or Pupillary afferent defect

when flashlight quickly moved form normal eye to affected eye and seems to dilate

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disc in optic neuritis

pallor

yellow coloring

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what to give to patient with optic neuritis

IV corticosteroids

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patients with optic neuritis tend to develop

Signs of internuclear ophthalmoplegia

adduction cannot reach medial edge abductin goes part way with nystagmus b/l

location lesion of internuclear ophthalmoplegia

damage to medial longitudinal fasciculus in brain stem linking CN VI with contra CNIII

causes of internuclear opthalmoplegia

MS | or brainstem stroke

Diagnostic criteria MS

2+ attacks in brain or spinal cord at 2+ times

MRI findings in MS

9+ hyperintense T2 lesions with 1+ gadolinium enhancing lesion 1+ lesion of cerebellum or brain stem 3+ periventricular lesions

if almsot meet MRI findings MS in brain do what

MRI of cervical or thoracic to see discrete cord lesions

lesions in brain are usually in what location compared to lateral ventricles in MS

right angles

MS thoracic spine

<3 consecutive segment lesions

LP os MS patient

oligoclonal bands IgG increased levels myelin basic protein increased wBC (not super high)

Goal Tx MS

limit attacks and disability

beta interferons used in MS

avenox betaseron rebif

glatiramer actate is indicated for what form MS

relapsing remitting | acts as decoy for immune system

use of Natalizumab

PML except have to stop if think have JC virus

Fingolimod

once day capsule limit circulation lymphocytes (keep inside lymph nodes) muss less likely to cross BBB

side effects fingolomid

cardiac: brady and CAD

Tx for MS symptoms

antispasmodics antidepressants corticosteroids

Neuromyelitis optica "Devic"

optic neuritis and spinal cord demyelination | not brain demyelination!!!!!

MRI devics or NMO

>3 vertebral segments show demyelination

devics reaches C3 C4

respiratory crisis

CSF in devic disease

seldom oligoclonal bands | >50 WBC

Tx devic disease

corticosteroids!! chronic with azathioprine!! not INF

Ab in devic disease

against aquaporin 4 channels which more common in optic nn and spinal cord

age affected by NMO

young- very elderly

bilateral optic neuritis more likley to be

NMO

time frame NMO

shortly after infection | monophasic illness

Acute inflammatory demyelinating Polyneuropathy

Guillain Barre after infection (upper respiratory or GI) rapidly progressive paralysis ascending

where is immune attack in guillain barre

roots of peripheral and sometimes CN usually just motor not sensory DTR completely lost

death in guillain barre

respiratory arrest

Nerve conduction in guillain barre

dec velocity and delayred F waves

LP in guillain barre

high high CSF protein slight elevation WBC cellular chemical dissociation

meningitis encephalitis LP

both WBC and protein increased!

outcome guillian barre

full recovery in weeks to mo | soemtimes permanent weakness or pain

Chronic Inflammtory Demyleinating Polyneuropathy

``` slower 3-6 mo mild weakness dec reflexes increased CSF protein ```

Tx Chronic Inflammatory Demyelinating Polyneuropathy

oral corticosteroids plasma exchange IVIgG

does guillain barre respond to corticosteroids

Tx Guillain barre

plasma exchange IV IgG most effective if begun within first 3 weeks!!!!!!