Multiple sclerosis Flashcards
1
Q
Types of MS?
A
- neuromyelitis optica ( devic’s)- severe opric neuritis and extensive transverse myelitis extending > 3 vetrebral segments ( NMO antibody posetive)
- clinically isolated syndrome ( CIS)- single MS-like episode, which may progress to MS.
- Tumefactive MS -isolated lesion >2 cm mimicking neoplasms on MRI
- Fulminant MS ( Marburg) - progressive and fetal MS assoiated with several axonal damage, inflammation and necrosis.
- Acute disseminated encephalomyelitis (ADEM)- monophasic demyelinating disorder with multifocl neurologic symptoms seen mainly in children often following infection or vaccine.
2
Q
Etiology of MS?
A
- Genetic- polygenetic HLA-DRB1 gene
- Enviromental- Regions with less sun exposure and low vitamin D.
- Infection- certain viruses (EBV)
3
Q
Clinical patterns of MS?
A
- RRMS ( Relapsing-remitting pattern) - 85% Exacerbation alternate with remission. Remission can last months to year. Excavation can occur spontaneously or can be triggered by infection.
- PPMS ( primary progressive pattern) -10% progresses gradually without remission. No clear exacerbations.
- SPMS ( secondary progressive pattern)- first relapses alternating with remission followed by gradual progression of disease.
- PRMS ( progressive relapsing pattern ) -5% progresses gradually but progression is interrupted by sudden clear relaps.
* most RRMS goes on to become SPMS
4
Q
Charcots neurologic triad
A
- Dysarthria ( difficult or unclear speech) plaques on brain stem ( cerebellar) that effects nerve fibers that control muscles of mouth and throat and this can interfere with conscious movement ( eating , talking ) and unconscious movement (swallowing )
- Nystagmus ( involuntary rapid eye movement) plaques around nerves controlling eye movement.
can cause pain during eye movement or diplopia
-Plaques around the optic nerve causes loss of vision ( optic neuritis) blurring or graying of vision, dark point in center of vision. - Intention tremor- Plaques along motor pathway of spinal cord. Effects outbound signals like skeletal muscle control ( Weakness, spasms, tremors, ataxia )
paralysis in severe cases.
5
Q
Diagnosis of MS?
A
- clinical criteria
- McDonald criteria
- Brains and spinal MRI
- Alternatively contrast-enhanced CT
- CSF -igG levels, cell count, protein and albumin, myelin protein ( should be elevated during active demyelination) , glucose.
6
Q
what is McDonald criteria?
A
- Dissemination in space and in time.
Dissemination in space requires-T2 bright lesions in two or more of the following locations : periventricular (≥ 3 lesions) cortical or juxtacortical (≥1 lesion) optic nerve (≥1 lesion) infratentorial (≥1 lesion) spinal cord (≥1 lesion)
Dissemination in time can be established in one of two ways:
-a new lesion when compared to a previous scan (irrespective of timing)
-T2 bright lesion and/or gadolinium-enhancing
presence of asymptomatic enhancing lesion and a non-enhancing T2 bright lesion on any one scan
7
Q
Treatment of MS
A
- acute treatment- treatment of disabling relapses with objective findings of neurological impairment to speed recovery IV methylprednisolone 500-1000 mg od for 3-7 days +/- short oral prednisone taper
- Disease-modifying therapy (DMT)- interferon-beta (Betaseron, Avonex, Rebifâ ) and glatiramer acetate (Copaxone) 2nline-, natalizumab (Tysabriâ„¢)
- clinically isolated syndrome - Avonex ( single attacks and abnormal brain MR )
- relapsing-remitting MS-Interferon-beta and glatiramer acetate
- secondary progressive MS-interferon-beta may slow the progression of disability
- primary progressive MS-immunosuppressive agents eg: methotrexate 7.5mg q weekly
symptomatic treatment
Spasticity (baclofen, tizanidine, dantrolene, BDZ )
Bladder dysfunction (oxybutynin)
Pain (TCA, carbamazepine, gabapentin)
Fatigue (amantadine, modafinil, methylphenidate)
Depression (antidepressants)
physiotherapy, speech therapy, occupational therapy, nutrition
