Multiple Sclerosis Flashcards

1
Q

What is MS?

A

Most common neuroinflammatory disorder in western populations

-T cell mediated disorder

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2
Q

Pathophysiology found in MS?

A

Multiple plaques of demyelination are found throughout the brain and spinal cord occurring sporadically over years

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3
Q

Who gets MS?

A
  • Women
  • Age 20-40 years
  • Genetic predisposition
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4
Q

Pathology of MS?

A
  • Plaques of demyelination (only effects CNS)
  • Plaques can occur anywhere in CNS but certain sites are more commonly affected
  • Acute relapses caused by focal inflammation causing myelin damage and conduction block
  • When damage is severe, secondary permanent axonal destruction occurs
  • Grey matter damage also takes place early pm and the extent of the damage correlates with severity of disability and cognitive involvement
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5
Q

Sites commonly affected with plaques of demyelination in MS?

A
  • Optic nerves
  • Periventricular region
  • Corpus callosum
  • Brainstem
  • Cerebellar connections
  • Cervical spine cord
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6
Q

Pathological basis for MS?

A

Progressive axonal damage, this causes the progressive disability seen in progressive forms of MS

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7
Q

What does presentation of MS depend on?

A

Area of CNS affected

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8
Q

What sign are there in MS?

A

UMN not LMN (because peripheral myelinated nerves are not directly affected)

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9
Q

Types of presentation of MS?

A

Pyramidal dysfunction
Optic neuritis
Sensory nerve involvement
Cerebellar dysfunction

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10
Q

What is pyramidal dysfunction? (+ explain it)

A

Dysfunction of corticospinal tract

  • Increased tone
  • Spasticity
  • Muscle weakness
  • Extensors of upper limbs are weak and flexors of lower limbs
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11
Q

What is optic neuritis?

A

Painful visual loss in an eye develops over 1-2 weeks

  • Painful on eye movements
  • Loss of central vision
  • RAPD positive
  • Most improve
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12
Q

Explain sensory nerve involvement?

A

Unusual symptoms
Reduced vibration and proprioception
Pain
Paraesthesia

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13
Q

DANISH?

A
Dysdiadochokinesia 
Ataxia 
Nystagmus 
Intention tremor 
Scanning dysarthria 
Hypotonia
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14
Q

Brainstem involvement in MS

A

Compression of the 6th and 7th cranial nerves?

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15
Q

Compression of 6th cranial nerve causes?

A

Diplopia

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16
Q

Compression of 7th cranial nerve causes?

A

Facial weakness

17
Q

Diagnosis and investigation for MS?

A
  • 2 or more episodes suggesting demyelination
  • Evidence of damage to CNS that is disseminated in time and space
  • Blood tests should be done to exclude other inflammatory disorders
  • MRI= definitive investigation
18
Q

Types of MS?

A
  • Relapsing and remitting
  • Secondary progressive
  • Primary progressive
  • Relapsing progressive
19
Q

What is relapsing and remitting MS?

A
  • Most common
  • Symptoms occur in attacks which get partially or fully better over weeks
  • Patient may accumulate disability over time
20
Q

What is secondary progressive MS?

A

-75% of people with RRMS evolve into this type within 35 years of onset

21
Q

Primary progressive MS?

A

Gradually worsening disability without relapses or remissions

22
Q

What is relapsing progressive MS?

A

Least common type

-Relapses on pattern of progressive disability from the outset

23
Q

Symptomatic management of MS: Pyramidal dysfunction?

A
  • Physio
  • Occupational Therapy
  • Baclofen for spasticity
24
Q

Symptomatic management of sensory symptoms?

A

Neuropathic pain involved gabapentin, amitriptyline or other agents

25
Q

Symptomatic treatment of urinary tract symptoms?

A

Bladder training advice
Anticholinergics (oxybutynin sometimes given to reduce detrusor instability)
Fatigue: rules out other causes

26
Q

Symptomatic treatment for fatigue in MS?

A

Rule out other causes

  • Do fatigue diaries with OT to ID triggers
  • Amantadine works for some people
27
Q

Treatment of a moderate acute exacerbation?

A

Oral steroids over five days (methylprednisolone)

28
Q

Treatment of a severe acute exacerbation of MS?

A

Admit to hospital and give IV steroids

29
Q

1st line disease modifying therapy for RRMS>

A
Tecfidera (oral) 
OR
Interferons 
OR 
Glutamir acetate injections
30
Q

2nd line treatment for RRMS?

A

Fingolimod
Cladribine
Monoclonal ABs

(More effective at reducing relapses but more toxic)