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Demyelinating Disease Flashcards

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1
Q

Where are the lesions typically distributed in MS?

A

Perivenous white matter

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2
Q

What is the pathology of acute lesions in MS?

A

Myelin destruction with relative axon sparing
Mononuclear cell and lymphocyte infiltration with interstitial oedema
Breakdown of the BBB

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3
Q

How do acute lesions progress in MS after initial inflammation?

A

Astrocyte proliferation
Old lesions are acellular, clearly demarcated and bare axons surrounded by astrocytes; increasing axonal loss accounts for increasing disability

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4
Q

Is there a prodrome to MS?

A

Sometimes - vague, non-specific e.g. Headaches, lethargy, aches

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5
Q

What should be considered the underlying diagnosis in a young adult presenting with paroxysmal facial pain?

A

Trigeminal neuralgia - MS presentation

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6
Q

What is Lhermitte’s sign?

A

Shock-like sensation in limbs on neck flexion due to cervical posterior column/spinothalamic plaques

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7
Q

What does loss of all sensory modalities at a given spinal level in MS suggest about the location of the lesion?

A

Dorsal root entry zone

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8
Q

What are the most common motor presentation distributions in MS?

A

Monoparesis or paraparesis

Much less commonly hemiparesis or quadraparesis

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9
Q

What reflex is lost in UMNL?

A

Abdominal reflex

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10
Q

What would a plaque of demyelination at the anterior horn cell root cause?

A

A mixed UMNL and LMNL picture

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11
Q

What are the symptoms of optic neuritis?

A

Visual loss with central scotoma

Pain on eye movement may occur due to irritation of dural membrane surrounding optic nerve

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12
Q

What might a mild optic neuritis cause isolated loss of?

A

Colour vision

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13
Q

What does bilateral optic neuritis suggest in terms of differential diagnosis?

A

MS less likely
Neuromyelitis optica
Leber’s hereditary optic neuropathy (mitochondrial)

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14
Q

What is Uhthoff’s phenomenon?

A

Visual Sx of MS (or demyelinating disease generally) worsening following hot bath or exercise

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15
Q

What does fundoscopy show in optic neuritis?

A

Papillitis

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16
Q

2 investigations for optic neuritis?

A

HRCT/MRI - exclude optic nerve tumour and possibly identify plaques
Delayed VERs/VEPs

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17
Q

What does an optic disc with previous optic neuritis look like?

A

Atrophic with a pale, punched out temporal margin

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18
Q

What is internuclear ophthalmoplegia? Where is the lesion?

A

Medial longitudinal fasciculus lesion pathognomonic of MS in young people
Causes a failure of adduction on the affected side and a side-by-side diplopia

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19
Q

When does primary progressive MS more commonly occur?

A

If it presents after that age of 45 or so

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20
Q

What process do unmatched oligoclonal CSF bands indicate?

A

Intrathecal antibody production

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21
Q

What MRI modality best highlights demyelination?

A

T2 - demyelination shows increased signal

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22
Q

What MRI modality is best for showing acute demyelinating lesions?

A

GAD

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23
Q

What does GAD highlight in demyelinating disease?

A

Acute lesions

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24
Q

What criteria is used to diagnose MS with a single clinical episode?

A

McDonald Criteria

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25
Q

What does the McDonald criteria require for a diagnosis of MS?

A

At least one clinical episode
At least 2 episodes attributable to demyelination at least 30 days apart
Exclusion of alternative pathologies

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26
Q

When can PPMS be diagnosed?

A

After 1 year of progressive deficit with MRI plaques and mismatched CSF oligoclonal bands

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27
Q

7 differentials for unmatched CSF oligoclonal bands?

A 
MS
HIV
Lyme disease
Syphilis
Chronic meningitis 
Neurosarcoidosis
Subacute sclerosing panencephalitis
28
Q

How are MS relapses treated?

A

3d IV methylpred

29
Q

How does NMO usually present visually?

A

Rapid bilateral visual loss

30
Q

What is the usual progression of Sx in NMO?

A

Rapid bilateral visual loss
Transverse myelitis with back pain, girdle pain, lower limb paraesthesia and urinary retention
Occasionally ascending sensorimotor loss

31
Q

What antibody is commonly implicated in NMO?

A

Anti-aquaporin 4 Ab

32
Q

What disease does the presence of anti-aquaporin 4 Ab suggest?

A

NMO

33
Q

What may differentiate MS from NMO on CSF analysis?

A

NMO does not have unmatched oligoclonal bands

34
Q

What might you consider in a presumed MS patient without unmatched oligoclonal CSF bands?

A

NMO

35
Q

What is acute disseminated encephalomyelitis otherwise known as?

A

Post-infectious encephalomyelitis

36
Q

What 4 things does ADEM usually follow?

A

Measles
VZV
Occasionally URTIs or GI infections
Live or attenuated vaccines

37
Q

How does ADEM present?

A

Days-weeks after a viral infection resolves, fever headache n+v develop
Progressing on to meningism, drowsiness, multifocal neuro signs and symptoms and myoclonus

38
Q

What is the imaging modality of choice for ADEM?

A

MRI - shows small focal white matter changes which simultaneously enhance with contrast (same degree of acuteness unlike MS)
CT will be normal

39
Q

What suggests ADEM over acute MS?

A

Fever, meningism

40
Q

What does ADEM with raised intracranial pressure and bloodstained CSF suggest?

A

Acute haemorrhagic leukoencephalitis

41
Q

Over what time period does PML occur?

A

3-6m

42
Q

What relapse related side effect is associated with alemtuzumab therapy for MS?

A

Pseudo-relapses - repeats of previous relapses

43
Q

What drug is associated with pseudo relapses in MS?

A

Alemtuzumab

44
Q

What is tecfedira otherwise known as?

A

Dimethyl fumerate

45
Q

What is dimethyl fumerate otherwise known as?

A

Tecfedira

46
Q

What is tysabri?

A

Natalizumab

47
Q

What is Natalizumab otherwise known as?

A

Tysabri

48
Q

What is Campath?

A

Alemtuzumab

49
Q

What is Alemtuzumab otherwise known as?

A

Campath

50
Q

What are the 2 first line drugs for relapse prevention in MS?

A

B interferon and capaxone

51
Q

How is B interferon delivered?

A

Injection

52
Q

What is a rough guideline for need to start relapse prevention therapy in RRMS?

A

2 attacks in 2 years

53
Q

How much do capaxone and B interferon lower relapse rate in RRMS?

A

Roughly 35%

54
Q

What are the 2 second line drugs for RRMS?

A

Fingolomod

Dimethyl fumerate

55
Q

How are fingolomod and Dimethyl fumerate delivered?

A

Oral

56
Q

By how much do Dimethyl fumerate and fingolomod lower relapse rate in RRMS?

A

Roughly 50%

57
Q

What are the major risks associated with Alemtuzumab therapy?

A

Autoimmunity - Goodpastures, thyroid (either way), ITP

Pseudo relapses

58
Q

What is the major risk associated with Natalizumab?

A

PML

59
Q

What drug for RRMS is most associated with PML?

A

Natalizumab

60
Q

How does ocrelizumab work?

A

CD19 inhibitor

61
Q

What radiological signs suggest PML?

A

Multifocal white matter lesions
Leading edge on DWI
Scalloping of cortex

62
Q

What two viruses are mostly associated with PML?

A

JC virus

BK virus

63
Q

What are anti-MOG antibodies? What diseases are they associated with?

A

Anti-Myelin Oligodendrocyte Glycoprotein
May have a role in seroneg NMO, optic neuritis and ADEM
Also adrenoleukodystrophy and vanishing white matter disease

64
Q

What is the owls eye sign and what can it be seen in?

A

Spinal cord - e.g. In long term NMO, chronic ischaemic change in anterior horn cells

65
Q

If NMO patient is AQP4 positive, what does it suggest about their disease course?

A

Relapsing remitting

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