Clinical Features of MS Flashcards

1
Q

Define MS

A

Chronic, inflammatory, multifocal, demyelinating disease of the CNS of unknown cause

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2
Q

Briefly describe how MS occurs

A

Autoimmunity -> inflammation -> neurodegeneration (irreversible axonal loss)

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3
Q

Describe the geographical distribution of MS

A

Latitude effect: the higher the latitude, the higher the incidence and the greater number of MS cases

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4
Q

MS epidemiology in sexes?

A

More in women than men

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5
Q

MS disease duration

A

40-50 mean years

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6
Q

Social impact of MS

A

Only 1 third of patients remain actively employed 15 years after MS onset

Only 1 third of patients remain in a relationship 24 years of MS onset

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7
Q

Describe cognitive impairment in MS

A
  • memory
  • speed of information processing
  • attention
  • executive functioning
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8
Q

Aetiology of MS?

A

Multifactorial

  • genetically susceptible
  • environmental factors (latitude, vitamin D, sunlight exposure)
  • hormones
  • viral infections (EBV)
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9
Q

Evidence of the role of Vit D in MS?

A
  • Low 25 (OH) D serum level-> higher risk of acute attacks
  • Low 25 (OH) D serum level -> higher risk of MS
  • Low Vit D intake (w/ high latitude) -> higher risk of MS
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10
Q

Potential factors affecting MS incidence?

A

Latitude effect: greater MS prevalence at higher latitudes; role of Vit D; exceptions to both

Time of exposure: period of susceptibility (<15yrs- original risk & >15 new risk; month of birth effect (May births); more in Spring

Viral Hypothesis: MS triggered by e.g. EBV; more in EBV seropostitive (-ve has 0 risk); higher anti EBV titres has more MS

Genetics: 30% risk, HLA Class II has strongest effect: FHx- 10x risk

Hormones: pregnancy -> less relapses, 3 months post-part has more relapses

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11
Q

Confounding factors for role of Vit D in MS

A

Black people are more likely to have Vitamin D deficiency, but less likely to develop MS

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12
Q

Confounding evidence to the latitude effect?

A
  • Norway’s North-South gradient is inverted

- Black people are more likely to have Vitamin D deficiency, but less likely to develop MS

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13
Q

Month of Birth effect in MS?

A

MS higher incidence for May born

Lower incidence for November born

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14
Q

Role of EBV in MS

A

Similarities in epidemiology:

Young pts (esp women)
High income countries
EBV has a similar latitude distribution

(EBV postive pts are 13x more likely to develop MS)

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15
Q

Confounding evidence to the correlation between EBV and MS

A

90-95% of world is EBV positive

BUT: MS is virtually absent, among EBV seronegative subjects

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16
Q

Relationship between titres of EBV antibodies and MS?

A

Higher anti-EBNA IgG titres = higher risk of MS

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17
Q

Relationship between infectious mononucleosis and MS

A

History of IM = higher risk of MS (2.3 relative risk higher in those with infectious mononucleosis)

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18
Q

Evidence that there are genetic factors for MS

A
  • first degree relatives are 10-25x more likely to develop MS

(HLA-DRB1*15 seems to play a large role)- HLA-clas sII genes have the strongest effect

19
Q

The role of hormones in MS (2)

A
  • Incidence of MS in women has almost doubled in the last 50 years
  • Relapse frequency decreases in pregnancy, but increases in first 3 months post partum
20
Q

How MS clinically manifests (2)

A
  • Relapses: episodic, acute neuro symptoms lasting over 24 hrs
  • Progression: insidious, steady accumulation of irreversible disability for at least 1 yr- needs retrospective assessment (NB: minor/temporary improvement can happen)
21
Q

Symptoms of relapses (based on lesion location)?

A
  • optic neuritis
  • spinal cord lesion: limb weakness, paraesthesia, Lhermitte’s (electric shock), urgency/incontinence, sexual dysfunction
  • brainstem lesion: diplopia, paraesthesia, vertigo/nystagmus, dysarthria
  • cerebellar lesion: incoordination of limbs, ataxia
  • cerebral lesion: impaired conc., hemiparesis, hemisensory, SEIZURES., PSYCH DISTURBANCE
  • fatigue
22
Q

Most common relapse symptoms? (3)

A
  • optic neuritis
  • motor weakness
  • sensory disturbances
23
Q

Why are MS symptoms so varied?

A

Amount and location of damage to nervous system varies between each patient

24
Q

Subtypes of MS? (3)

and incidence of them

A
  • Relapsing-remitting MS (80-85%)
  • Secondary progressive MS (follows RRMS)
  • Primary progressive MS (15-20%)
25
Q

Relationship between RR-MS and SP-MS

A

85% of RR-MS convert to SP-MS after 25 years from onset (10-15 median years)

26
Q

How to diagnose MS?

A

[DIAGNOSIS OF EXCLUSION]

Lesions that are:
- Disseminated in time

  • Disseminated in space
27
Q

How to confirm suspicion of MS?

A
  • MRI
  • CSF analysis: increased production of Ig in CSF- oligoclonal bands in CSF only, NOT serum
  • Electrophysiology- visually evoked potentials (VEP)-> for DIS criteria
28
Q

How to use MRI to identify MS?

A

Use gadolinium contrast to identify how recent the lesion is…

Enhanced contrast at newer lesions from previous 6 weeks (due to faulty BBB)

29
Q

What is McDonald’s diagnostic criteria for MS?

A

Uses MRI in conjunction w/ DIT and DIS criteria:

2 attacks (DIT) + neuro exam abnormal

2 attacks +MRI

MRI + 1 attack + neuro exam abn

1 attack + MRI

1 yr disease progression + MRI

30
Q

Features of MRI-T2 lesions in MS

A
  • round, ovoid
  • few mm, 1 cm
  • perventricular, around corpus callosum, cerebellum, brainstem
31
Q

Relationship between MRI lesions and clinical attacks

A

Most lesions are clinically silent (asymptomatic)

32
Q

How long does GAD enhancement last for?

A

2-6 weeks

33
Q

CSF abnormalities in MS?

A

White cells: normal/mild increase (10-20 cells/mm3) -90% lymphocytes

IgG oligoclonal bands: +ve in CSF only, NOT serum

34
Q

Oligoclonal bands in serum pathophysiology?

A

Inflammation of BBB, allowing Igs to move into CSF

35
Q

Red flags for alternative diagnosis to MS?

A
  • Lack of oligoclonal bands

- V. high lymphocytes (white cells >20cells/mm3)

36
Q

What do visually evoked potentials (VEP) show?

A

Looks at evidence of delayed conduction (that might not show symptoms)

37
Q

MS DDx

A

ADEM (Acute Disseminated Encephalomyelitis)
Acute/subacute monophasic inflammatory and demyelinated process of CNS

Single event -6months-> inflammation resolves

Mainly in paeds, low frequency oligoclonal bands, variable symptoms

NMO (Neuromyelitis Optica)
CNS demyelination w/ optic neuritis and Acute myelitis (mainly spinal cord involved)

monophasic/relapsing (more disabling than MS)

38
Q

Differentiating between ADEM and MS?

A

MS has much smaller lesions (and lesions are in hallmark areas)

39
Q

Difference in symptoms of NMO and MS?

A

MS has unitlateral optic neuritis, but NMO has bilateral optic neuritis

MRI for NMO shows lesion >3 vertebrae

Auto-Ab for AQP4 channel

40
Q

How is disability graded in MS patients?

A

Expanded Disability Status Scale (EDSS)

Scale from 1-10

0: complete normal examination
10: death from MS

41
Q

What is clinically isolated syndrome (CIS)?

A

First presentation in MS (DIS but NO DIT)

NB: this is at risk of conversion to clinically defined MS

NBII: If demyelinating attack w/ no lesions on MRI -> low probability of a new inflammatory attack

42
Q

MS prognostic indicators: Good VS Bad?

A

GOOD Prognostic Indicators

  • young onset
  • female
  • optic neuritis/ only sensory symptoms
  • low freq of early attacks
  • complete remission of symptoms
  • long first inter-attack interval
BAD Prognostic Indicators
[more likely to gain progressive MS]
- >40yrs at onset
- male insidious pyramidal tract involvement
- prominent cerebellar involvement
- frequent early attacks
- rapid dvpmt of fixed disability
43
Q

Main cause of death in MS patients?

A

A cause related to their MS