Multiple sclerosis and inflammatory CNS disorders Flashcards Preview

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Flashcards in Multiple sclerosis and inflammatory CNS disorders Deck (24)
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1
Q

What is multiple sclerosis (MS)?

A

An inflammatory demyelinating disorder of the CNS

2
Q

When does MS typically present?

A
  • 30s and 40s
  • Female>Male (3:1)
3
Q

What are the clinical features of MS?

A

Pyramidal dysfunction, optic neuritis, sensory symptoms, LUT dysfunction, cerebellar & brain stem features, cognitive impairment

4
Q

What are the signs of pyramidal dysfunction?

A

Increased tone, spasticity and weakness in the extensors of the upper limbs and flexors of the lower limbs

5
Q

What are the signs of optic neuritis?

A

Painful visual loss, 1-2 weeks, most improve, relative afferent pupillary defect (RAPD)

6
Q

What are the sensory symptoms associated with MS?

A

Pain, paraesthesia, dorsal column loss (proprioception and vibration), numbness and trigeminal neuralgia

7
Q

What are the symptoms associated with cerebellar dysfunction in MS?

A

Ataxia, intention tremor, nystagmus, past pointing, pendular reflexes, dysdiadokinesis, dysarthria

8
Q

What are the symptoms associated with brain stem dysfunction in MS?

A
  • Diplopia - CN VI palsy
  • Facial weakness - CN VII palsy
9
Q

What occurs as a result of internuclear ophthalmoplegia?

A
  • Involves the medial longitudinal fasciculus
  • Distortion of binocular vision
  • When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus.
  • Divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will “see double” when looking to the left
  • Lag also occurs
10
Q

What are the symptoms associated with lower urinary tract dysfunction in MS?

A

Frequency, nocturia, urgency, urge incontinence and retention

11
Q

What can be used to manage fatigue in MS?

A

Amantadine, modafinil if sleepy and hyperbaric oxygen

12
Q

How is MS diagnosed?

A
  • At least 2 episodes suggestive of demyelination
  • Dissemination in time and place
  • McDonald criteria
  • MRI, CSF, neurophysiology
  • Blood tests
13
Q

What blood tests are done to investigate MS?

A

PV, FBC, CRP, renal liver bone profile, auto-antibodies, borellia, HIV, syphilis serology, B12 and folate - negative

14
Q

What is usually present in the CSF in MS patients?

A

Oligoclonal bands in 90% of cases

15
Q

How is an acute exacerbation of MS managed?

A
  • Mild - symptomatic treatment
  • Moderate - oral steroids
  • Severe - admit/IV steroids
16
Q

How is pyramidal dysfunction managed?

A

Physiotherapy, occupational therapy, anti-spasmodic agent e.g. baclofen, tizanidine

Botulinum toxin

17
Q

How are sensory symptoms in MS managed?

A
  • Anti-convulsant e.g. gabapentin
  • Anti-depressant e.g. amitriptyline
  • Tens machine
  • Acupuncture
  • Lignocaine infusion
18
Q

How is lower urinary tract dysfunction managed?

A
  • Bladder drill, anti-cholinergics e.g. oxybutynin
  • Desmopressin, catheterisation
19
Q

What are first and second line disease modifying agents used in MS?

A

1st line:

  • Interferon beta - avonex, betaseron
  • Glitiramer acetate (copaxone)
  • Tecfedira

2nd line:

  • Monoclonal antibody - tysabri, lemtrada, ocrelizumab
  • Fingolimod
20
Q

What is the route of administration and how effective are interferon beta and copaxone in treating MS?

A
  • Injectable agents - SC or IM
  • Decrease relapse rate by 1/3
  • Decrease severity by 50%
  • Effect on disability
21
Q

What is the route of administration and how effective is tecfidera in treating MS?

A
  • Oral agent
  • First line in relapsing remitting MS
  • 44% reduction in relapse rate
22
Q

What is the route of administration and how effective is fingolimod in treating MS?

A
  • Oral agent
  • >50% reduction in relapse rate
  • Significant effect on disease progression
  • Second line therapy
23
Q

How effective are monoclonal antibodies in treating MS?

A

Used in patients with rapidly evolving RRMS and in patients with high disease activity despite treatment with an interferon

Ocrelizumab delays progression by 25%

24
Q

Describe the inflammatory cascade in MS

A
  1. Immune cells pass through BBB
  2. Immune cells may re-activate and produce cytokines
  3. Immune cells mount autoimmune attack against myelin