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CNS CLERKSHIP > Multiple Sclerosis and Inflammatory CNS Diseases > Flashcards

Multiple Sclerosis and Inflammatory CNS Diseases Flashcards

1
Q

What is multiple sclerosis?

A

An autoimmune, inflammatory demyelinating disorder of the CNS.

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2
Q

In MS, patches of scar tissue known as plaques form over the demyelinated areas preventing what?

A

Nerve communication.

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3
Q

Progression of symptoms in MS correlates to what?

A

Plaque dissemination of areas of the brain/spinal cord controlling affected areas.

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4
Q

MS is more common in which sex?

A

Females 3:1.

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5
Q

Initial presentation of MS typically in which decades?

A

30s and 40s.

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6
Q

What are the various clinical courses of MS?

A
  • Relapsing remitting.
  • Secondary progressive.
  • Progressive relapsing.
  • Primary progressive.
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7
Q

What are the clinical features of Multiple Sclerosis?

A
  • Pyramidal dysfunction.
  • Optic neuritis.
  • Sensory symptoms.
  • Lower urinary tract dysfunction.
  • Cerebellar and brain stem features.
  • Cognitive impairment.
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8
Q

What are the symptoms of pyramidal dysfunction seen in MS?

A

In the extensors of upper limbs and the flexors of lower limbs, there will be:

  • Increased tone.
  • Spasticity.
  • Weakness.
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9
Q

Describe optic neuritis?

A

Painful progressive visual loss over 1-2 weeks.

Often associated with MS.

If unilateral, RAPD (relative afferent pupillary defect) may be observed.

Most cases improve over time.

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10
Q

What are the sensory symptoms experienced in MS?

A
  • Pain.
  • Paraesthesia (pins + needles).
  • Dorsal column loss: impaired/lost ability to sense vibration and proprioception.
  • Numbness.
  • Trigeminal neuralgia.
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11
Q

If cerebellar dysfunction is present in MS, what signs will be observed?

A
  • Ataxia.
  • Intention tremor.
  • Nystagmus.
  • Past pointing.
  • Pendular reflexes.
  • Dysdiadochokinesia.
  • Dysarthria.
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12
Q

What is ataxia?

A

Lack of voluntary coordination of muscle movements e.g. gait abnormality, changes to speech and eye movement abnormalities.

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13
Q

What is past pointing?

A

Pointing beyond the finger in the finger-nose test.

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14
Q

What are pendular reflexes?

A

When reflex is elicited, limb stimulated swings like a pendulum.

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15
Q

What is dysdiadochokinesia?

A

Inability to perform rapid alternating movement, e.g. tapping the right hand fast on the back of the left hand.

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16
Q

What is dysarthria?

A

Difficult or unclear articulation of speech that is otherwise normal.

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17
Q

What features of brain stem dysfunction may be seen in MS?

A
  • Diplopia: CN VI palsy.

- Facial weakness: CN VII palsy.

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18
Q

What is internuclear ophthalmoplegia?

A

Disorder of conjugate lateral gaze resulting in impaired adduction.

Attempting to gaze contralaterally (in relation to affected eye) results in minimal adduction - if any.

The contralateral eye abducts with nystagmus.

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19
Q

What causes internuclear ophthalmoplegia?

A

Injury or dysfunction (MS) in the medial longitudinal fasciculus.

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20
Q

What signs and symptoms are seen in internuclear ophthalmoplegia?

A
  • Distortion of binocular vision.
  • Failure of adduction resulting in diplopia.
  • Nystagmus in adducing eye.
  • Eye lag.
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21
Q

What features of lower urinary tract dysfunction are seen in MS?

A
  • Frequency.
  • Nocturia.
  • Urgency.
  • Urge incontinence.
  • Retention.
22
Q

How is fatigue managed in MS?

A
  • Amantadine.
  • Modafinil if sleepy.
  • Hyperbaric oxygen.
23
Q

By what criteria is MS diagnosed?

A
  • At least 2 episodes suggestive of demyelination.
  • Dissemination in time and place.
  • McDonald criteria.
24
Q

What are the various differential diagnosis of MS?

A
  • Vasculitis.
  • Granulomatous disorder.
  • Vascular disease.
  • Structural lesion.
  • Infection.
  • Metabolic disorder.
25
Q

How is a diagnosis of MS made clinically?

A
  • MRI.
  • CSF.
  • Neurophysiology.
  • Blood tests.
26
Q

What blood tests will come back negative in MS?

A
  • Plasma viscosity, FBC, CRP.
  • Renal liver bone profile.
  • Auto anti-body screen.
  • Borellia, HIV, syphilis serology.
  • B12 and folate.
27
Q

What findings in CSF may suggest MS?

A

Oligclonal bandS i.e. more than one.

28
Q

Why are oligoclonal bandS present in CSF of MS?

A

In MS antibodies cross the BBB to attack myelin surrounding nerves resulting in high level of antibodies in CSF.

Oligoclonal bandS shows >2 bands and thus presence of disease activity - though this may not necessarily be MS. But is MS in >90% of cases.

29
Q

Management of mild acute exacerbation of MS?

A

Manage symptoms.

30
Q

Management of moderate acute exacerbation of MS?

A

Oral steroids.

31
Q

Management of severe acute exacerbation of MS?

A

Admit to hospital/ IV steroids.

32
Q

Management of pyramidal dysfunction in mild acute exacerbation of MS?

A

For weakness and spasticity:

  • Physio.
  • Occupational therapy.
  • Anti-spasmodic agent.
33
Q

Management of spasticity in mild acute exacerbation of MS?

A
  • Physio.
  • Oral meds: Baclofen, Tizanidine.
  • Botulinum toxin.
  • Intrathecal Baclofen/ Phenol.
34
Q

How are intrathecal drugs administered?

A

Into the spinal canal or subarachnoid space.

35
Q

Management of sensory symptoms in mild acute exacerbation of MS?

A
  • Anti-convulsant e.g. Gabapentin.
  • Anti-depressants e.g. Amitriptyline.
  • TENS machine.
  • Acupuncture.
  • Lignocaine infusion.
36
Q

What causes lower urinary tract dysfunction in MS?

A
  • Increased tone at bladder neck.
  • Detrusor hypersensitivity.
  • Detrusor sphincter dyssenergia.
37
Q

What is detrusor sphincter dyssenergia?

A

Bladder outlet obstruction from detrusor muscle contraction with concomitant involuntary urethral sphincter activation.

Associated with neurologic conditions.

38
Q

Management of lower urinary tract dysfunction in MS?

A
  • Bladder drill.
  • Anti-cholinergics e.g. Oxybutynin.
  • Desmopressin.
  • Catheterisation.
39
Q

What is bladder drill/training?

A

Aims to slowly stretch the bladder to hold larger volumes and make the bladder muscle less overactive with time to allow more bladder control.

40
Q

First line disease modifying therapy in multiple sclerosis?

A
  • Interferon-beta: Avonex, Rebif, Betaseron, Extavia.
  • Glitiramr Acetate (Copaxone).
  • Tecfedira.
41
Q

Second line disease modifying therapy in multiple sclerosis?

A
  • Monoclonal antibody: Tysabri, Lemtrada, Zymbrata.

- Fingolimod.

42
Q

Third line disease modifying therapy in multiple sclerosis?

A

Mitoxantrone.

43
Q

Describe Interferon-beta & Copaxone, and their effect on multiple sclerosis?

A
  • Injectable: SC, IM.
  • Decrease relapse rate by 1/3.
  • Decrease severity of relapses by 1/3.
  • Some effect on disability.

Both comparable efficacy.

44
Q

Describe Tecfidera and its role in MS?

A
  • Oral drug.
  • First line indication in relapsing remitting MS.
  • 44% reduction in relapse rate.
  • Unclear long term data.
45
Q

Describe Fingolimod and its role in MS?

A
  • Oral drug.
  • Sphingosine 1-phosphate (S1P) modulator.
  • > 50% reduction in relapse rate.
  • Significant effect on disease progression.
  • NICE & SMC approved as second line in MS.
46
Q

Describe the monoclonal antibodies: Tysabri, Lemtrada & Ocrelizumab, and their role in MS?

A
  • Single disease modifying therapies in highly active relapsing remitting multiple sclerosis.
  • Used in those with rapidly evolving severe relapsing remitting MS.
  • Those with high disease activity despite interferon treatment.
47
Q

Describe the use of the monoclonal antibody Ocrelizumab in MS?

A
  • Used in early primary, progressive MS.

- Delays progression by 25%.

48
Q

Integrins α4β1 mediates what in MS?

A

Trans-endothelial migration of activated T-cells across the BBB in Experimental autoimmune encephalomyelitis.

49
Q

Describe the inflammatory cascade in MS?

A
  • Immune cells pass through BBB from systemic circulation.
  • Immune cells may reactivate and produce cytokines.
  • Immune cells mount autoimmune attack against myelin in the CNS.
50
Q

What is the mode of action of Tysabri in MS?

A
  • Binds to Integrin-α4β1 to block its interaction with VCAM-1 and prevent leukocyte migration into brain tissue. This reduces inflammation and prevents lesion formation.
  • Inhibits ongoing CNS inflammation by mediating leukocytes already present in CNS by interrupting interaction between α4-integrin-expressing leukocytes and extracellular matrix proteins to cause apoptosis.

CNS CLERKSHIP (43 decks)

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