Demyelinating Disease Flashcards
MS
- Fatal?
- Contagious?
- Directly Inherited?
- Always severely disabling?
NO
MS affects which brain matter
- WHITE
* W/ some gray matter involvement
MS
Where?
Further away from Equator, higher your risk
MS
Cause?
UNKNOWN:
(Maybe):
*Vit D deficiency
*Virus (EBV) kicks off autoimmune
Involvement of cerebellum
Tremor
Ataxia
Involvement of medulla/brainstem
Sensory systems, Lhermitte’s, Pain, Proprioception
Involvement of Pons
Diplopia
Vertigo
Dysarthria
INO
- Parastesia arms/legs
- Monocular blindness
- Slowly progressing motor deficit
- fatigue
- depression
- Focal muscle weakness
- bowel/bladder/sexual
- gait
- lhermitte
MS
MS s/s worse with
Heat, fever, hot water, exercise, menstruation, saunas
EDSS progress
6 = 15 years 8 = 46 years
- New recurrence of symptom
- 24 hrs - weeks/month
- will uncover in interview
MS Relapse
Confirming progression
+1 on EDSS
*2 consecutive visits 3 months apart
Attack, then back to baseline, then attack then back to baseline
*baseline may raise
Relapsing-remitting
Linearly gets worse
Primary progressive
Attack, then baseline (few cycles), then start linear raise
Secondary progressive
1ary progressive
Many will become….
2ary progressive
Overall MS Tx goal
Prevent Disability ACCUMULATION. (W/ increasing lesions/plaques = WHITE + gray matter)
- Younger at onset
- Female
- Low MRI lesion load
- Complete recovery from 1st relapse
- Low relapse rate
- No disability at 5 years
Prognosis?
FAVORABLE
NO to 2ary progressive
- Older age at onset
- Male, AA
- High MRI lesion load
- No complete recovery after 1st relapse
- Early disability of disability
- Insidious motor onset
UNFAVORABLE
–>2ary progression
MS
Major auto-immune attack cells
T cells
Cross BBB and attack myelin on WHITE matter (and grey)
Demyelenation causes
Slower nerve conduction
PARTIALLY REVERSIBLE
Axonal injury + destruction cause
PERMANENT neurological dysfunction
Where are lesions?
- optic nerves
- Periventricular white matter
- Cerebral cortex
- Brain stem
- Cerebellum
- Spinal cord
Crucial evidence in MS dx
Dissemination of lesions in space and time
MS Dx
CSF
- up IgG/albumin (serum + CSF)
- Oligoclonal bands (CSF ONLY)
- Normal glucose, cells, protein
MS s/s
(white matter issues)
Devic’s Dz (NEUROMYELITIS OPTICA)
MIGRAINE
- Infxn- lyme, pml, hiv
- inflammatory - lupus, sjogrens, cns vasculitis, sarcoidosis, bahcet’s dz
- Metabolic - b12, #
- CNS lymphoma
Image
Transverse myelitis more than 3 spinal segments
NOT MS
Neuromyelitis optica?
Auto-immune
- spinal cord= transverse myelitis
- Optic nerves - optic neuritis (bilateral)
- serum- IgG
NMO - Myelitis optica
NMO-IgG antibody
MS Vs. NMO
NMO = bilat optic neuritis, white matter brain lesion, transverse myelitis, NMO IgG antibody
MS= OCB in CSF, White matter brain lesions
Take MRI, see white matter lesions, but see gandolinium contrast enhancements in new area (new lesions)
DX MS
How to confirm dissemination in space and time?
MRI
Enhancing w/ gandolinium contrast
MRI, predicting prognosis
Lesion load
TX goals
Less relapse
Less dz progression
Tx
Acute relapses
- 1 per year untreated
- W/ Menstruation (heat)
1 per year in untreated
HIGH DOSE STEROIDS
Methylprednisone
Shorten episode
Tx long term
Immunomudolating Rxs (started in 90s) Before only injection, now oral
Interfeuron S.E.
- injection site rxn
- flu-like s/s
- Neutropenia
- up liver function tests
- possible antibody formation
Natalizumab
DANGER
JC Virus –> will develop PML (progressive multifocal leukoencephalopathy)
CHECK JC VIRUS ANTIBODY LEVELS ON THIS MED
Relapses
MC reason?
Not taking Rx
Best way to prevent s/s
Early detection/Tx start
T1-weighted scan
- Hypointense lesions *(black holes) - axonal damage
* old lesions
T2 weighted scan
- total disease burden
- myelin damage
- old + new lesions
FLAIR image
- Suppress CSF white color from t2
- Best - dz burden
- subcortical lesion ID
Gandolinium Contrast w/ image
*new Lesion
