Multiple sclerosis Flashcards

1
Q

What is MS?

  • M:F
  • initial presentation?
A

an inflammatory demyelinating disorder the central nervous system

Plaques disseminated in time and place

Female:Male = 3:1

Initial presentation in 30s & 40s

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2
Q

What is the pathophysiology of MS?

A

Lymphocytes cross the BBB and get into brain

Attack myelin cells 

Inflammation and plaques 

MS
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3
Q

What is the aetiology of MS?

A
  • genetic disposition
  • environmental factors
  • immune mediated
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4
Q

What are the 4 different courses of MS?

A

Relapsing remitting 90% :
-relapses over weeks and weeks, progressively gets worse then better

Secondary progressive 60%:
-gradually worsens

Relapsing progressive

Primary progressive 10-15%
-older males, never relapse

60% of relapsing remitting patients develop secondary progressive disease after 10 years

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5
Q
Describe the:
-visual
-sensory
-motor
-cerebellar
-other
features of MS
A

Visual
optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia

Sensory

  • pins/needles
  • pain
  • Paraesthesia
  • Dorsal column loss
  • Proprioception & vibration: Rhombergs test positive (proprioception)
  • Numbness
  • trigeminal neuralgia
  • 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

Cerebellar

  • ataxia: more often seen during an acute relapse than as a presenting symptom
  • Intention Tremor
  • Nystagmus
  • Past pointing
  • Pendular reflexes – when -patellar tapped the leg swings
  • Dysdiadokinesis
  • Dysarthria

Others

urinary incontinence
sexual dysfunction
intellectual deterioration
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6
Q

Describe what optic neuritis is?

A

painful visual loss

1 to 2 weeks 

most improve 

RAPD -relative afferent pupilllary defect 

common presenting feature 

in 1 eye rather than 2 

colour vision goes first
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7
Q

What is internuclear ophthalmoplegia?

A

Caused by Medial longitudinal fasciculus dysfunction

Distortion of binocular vision 

Failure of adduction- diplopia 

Nystagmus in abducting eye 

Lag 

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.

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8
Q

Describe the lower urinary tract dysfunction seen in MS?

A

-frequency
-nocturia
-urgency
-urge incontinence
-retention
(similar to BPH)

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9
Q

What is the diagnosis of MS?

A

(mcdonald criteria)

At least 2 episodes suggestive of demyelination

Dissemination in time and place 

Clinical

MRI - diagnosis shows plaques

CSF: oligoclonal bands 

Neurophysiology 

Blood tests – these should all be negative
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10
Q

What blood tests are carried out in the investigations of MS?

A

Plasma viscosity, FBC, CRP

Renal liver bone profile 

Auto anti body screen 

Borellia, HIV, syphilis serology 

B12 and folate
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11
Q

What is a clinically isolated syndrome in MS?

A
  • First presentation suggestive of MS

- can’t tell until second event whether they definitely have MS

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12
Q
How to treat a:
-mild
-moderate
-severe
exacerbration of MS?
A

Mild-symptomatic treatment:
-Usually will get better

Moderate-Oral steroids:
-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

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13
Q

How can spasticity be managed?

A

Education

Physiotherapy 

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 

Surgery 

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.

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14
Q

How is MS pain treated?

A

anti convulsant eg. gabapentin

anti depressant eg. amitriptyline 

tens machine 

Acupuncture 

Lignocaine infusion
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15
Q

How is lower urinary tract dysfunction treated in MS?

A

bladder drill (training)

anti cholinergics eg., oxybutynin (if old tolteridine as oxybutynin can cause dementia)

Desmopressin 

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

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16
Q

How can fatigue be managed in MS?

A

Fatigue management

Amantadine 

Modafinil if sleepy 

Hyperbaric oxygen 

Occupational therapists can help people understand about their fatigue

17
Q

Describe the 1st, 2nd and 3rd disease modifying therapy for MS?

A

First line therapy

- Interferon Beta – Avonex, Rebif, Betaseron, Extavia 
- Glitiramer Acetate (Copaxone) 
- Tecfedira 

Second line therapy 

- Tysabri 
- Fingolimod 

Third line therapy 
-Mitoxantrone 

Second and third line drugs work better but risk death, 1st line aren’t great but are safe

18
Q

What is the 1st line:

-does this work?

A

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
19
Q

What is the step up from 1st line for MS disease modifying therapy?

A

Tecfidera: step up from 1st line

Oral agent 

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

20
Q

What is the role of tysabri and fingolimod?

A

= 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
21
Q

What is assoc. with tysabri?

A

progressive multifocal leukoencephalopathy (PML) associated with tysabri:

JC virus positive 

Single Vs dual therapy 

Estimated risk 1/385 after 2 years
22
Q

Fingolimod:

what is this?

A

Oral agent

sphingosine 1-phosphate (S1P) modulator 

>50% reduction in relapse rate 

Significant effect on disease progression 

NICE SMC approved as second line
23
Q

Mitoxantrone:

  • what is this used for?
  • how is this administereD?
  • what is this related to?
A

Relapsing progressive MS

12 infusions over 2 years 

Cardiac toxicity dose related