Flashcards in Multiple sclerosis Deck (23):
What is MS?
an inflammatory demyelinating disorder the central nervous system
Plaques disseminated in time and place
Female:Male = 3:1
Initial presentation in 30s & 40s
What is the pathophysiology of MS?
Lymphocytes cross the BBB and get into brain
Attack myelin cells
Inflammation and plaques
What is the aetiology of MS?
What are the 4 different courses of MS?
Relapsing remitting 90% :
-relapses over weeks and weeks, progressively gets worse then better
Secondary progressive 60%:
Primary progressive 10-15%
-older males, never relapse
60% of relapsing remitting patients develop secondary progressive disease after 10 years
features of MS
optic neuritis: common presenting feature
Uhthoff's phenomenon: worsening of vision following rise in body temperature
-Dorsal column loss
-Proprioception & vibration: Rhombergs test positive (proprioception)
-Lhermitte's syndrome: paraesthesiae in limbs on neck flexion
Motor (due to pyramidal dysfunction)
spastic weakness: most commonly seen in the legs
-weak extensors and strong flexors in the upper limbs and opposite in the lower limbs
-ataxia: more often seen during an acute relapse than as a presenting symptom
-Pendular reflexes – when -patellar tapped the leg swings
Describe what optic neuritis is?
painful visual loss
1 to 2 weeks
RAPD -relative afferent pupilllary defect
common presenting feature
in 1 eye rather than 2
colour vision goes first
What is internuclear ophthalmoplegia?
Caused by Medial longitudinal fasciculus dysfunction
Distortion of binocular vision
Failure of adduction- diplopia
Nystagmus in abducting eye
In MS one eye may quickly look at something and then the other may have nystagmus.
If have problem in LHS, left medial LF problem so when looking right, left eye fails to adduct and right eye has nystagmus.
Describe the lower urinary tract dysfunction seen in MS?
(similar to BPH)
What is the diagnosis of MS?
At least 2 episodes suggestive of demyelination
Dissemination in time and place
MRI - diagnosis shows plaques
CSF: oligoclonal bands
Blood tests – these should all be negative
What blood tests are carried out in the investigations of MS?
Plasma viscosity, FBC, CRP
Renal liver bone profile
Auto anti body screen
Borellia, HIV, syphilis serology
B12 and folate
What is a clinically isolated syndrome in MS?
-First presentation suggestive of MS
-can't tell until second event whether they definitely have MS
How to treat a:
exacerbration of MS?
-Usually will get better
-Oral methylprednisolone 500mg per day for 5 days and lansoprazole to protect stomach
Severe-Admit / IV steroids
-Come into hospital and IV methylprednisolone 1’000 mg 3 days
But steroids = side effects so ideally only do this once a year, no more than once every 3 months
-only reduces period of exacerbation
How can spasticity be managed?
Oral medication - baclofen,tizanidine(anti-spasmodics): start low go slow
Side effects: tired/drousy/hypotension so sometimes do nothing due to s/e of treatment
I.M. Botulinum toxin – this is uncommonly used in MS as not a long term solution
Nerve blocks – not long term solution
Intrathecal baclofen / phenol - end stage treatment
Spasticity may be helpful for pt e.g. so weak that can’t stand without spasticity so don’t want to take it all away.
How is MS pain treated?
anti convulsant eg. gabapentin
anti depressant eg. amitriptyline
How is lower urinary tract dysfunction treated in MS?
bladder drill (training)
anti cholinergics eg., oxybutynin (if old tolteridine as oxybutynin can cause dementia)
catheter - clean self intermittent or permanent
there are bladder clinics for MS patients, they do a post micturition ultrasound and see if it’s over 100 – if it is and given anticholinergics (oxybutynin) this can give urinary retention.
If someone has retention >100mls – catheter
can do this themselves 2-3 times a day
can put a permanent catheter for end stage management
How can fatigue be managed in MS?
Modafinil if sleepy
Occupational therapists can help people understand about their fatigue
Describe the 1st, 2nd and 3rd disease modifying therapy for MS?
First line therapy
-Interferon Beta – Avonex, Rebif, Betaseron, Extavia
-Glitiramer Acetate (Copaxone)
Second line therapy
Third line therapy
Second and third line drugs work better but risk death, 1st line aren’t great but are safe
What is the 1st line:
-does this work?
Interferon beta and copaxone: 1st line
This is common, safe and patients can self administer
Injectable agents – sc, im
Decrease relapse rate by 1/3
Decrease severity of relapses by 50%, for mild it’s less effective
Effect on disability
All comparable re efficacy
What is the step up from 1st line for MS disease modifying therapy?
Tecfidera: step up from 1st line
First line indication in RR MS
44% reduction in relapse rate
Long term data unclear
Bad side effects such as stomach upset and flushing
If have attack on the first line drugs can step up to this
What is the role of tysabri and fingolimod?
= Single disease modifying therapies in highly active relapsing remitting multiple sclerosis (RRMS)
-Patients with rapidly evolving severe relapsing remitting multiple sclerosis
-Patients with high disease activity despite treatment with a interferon
What is assoc. with tysabri?
progressive multifocal leukoencephalopathy (PML) associated with tysabri:
JC virus positive
Single Vs dual therapy
Estimated risk 1/385 after 2 years
what is this?
sphingosine 1-phosphate (S1P) modulator
>50% reduction in relapse rate
Significant effect on disease progression
NICE SMC approved as second line