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C2 > MS, SVD - Differential diagnosis > Flashcards

MS, SVD - Differential diagnosis Flashcards

1
Q

What is the diagnostic criteria for MS?

A

Dissemination in time and space. Reasonable exclusion of alternatives.

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2
Q

What disease is a an example of misdiagnosis in MS?

A

NMOSD.

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3
Q

What are some things you should look at before making a clinical diagnosis?

A

age, signs, symptoms, CSF

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4
Q

What will you see on MR for MS?

A 
pattern - PV, cortical, Sub-c, ON, CC, spinal cord
shape - oval, Dawson's finger
enhancement
SWI - hypointensity, MCB, central vein
anything unsuual - lacunes, VR spaces
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5
Q

What is the location of MS on MR?

A

adjacent periventricular, cortical, sub-c, ON, CC, spinal cord

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6
Q

What can you see on SWI for MS?

A

can see vessel or vein. CVS (central vein sign - lesion has venual in centre), iron deposition

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7
Q

What locations can we have on posterior fossa for MS?

A 
facial colliculus -  nerve 5 and 6
middle cereberlar peduncle
white matter
5th nerve trigemnial
intramedullary
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8
Q

Where are cortical lesions as seen from pathology in RRMS, SPMS, PPMS

A

focal demyelinated plaques in the WM
cortical demyelination
demyelinated lesions in the deep GM

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9
Q

How much enhancing does SWI, intralesional susceptibility signal (ISS) show at 3T for MS? What does it represent?

A

non-enhancing - 48%
enhancing - 58%
represents iron-rich macrophages/microglia. myelin loss also contributes

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10
Q

What does SWI show in focal lesions over time?

A

As lesion develops, will enhance for 3-6 weeks then will go
Low signal- dark rim will happen quick then slowly increase then slowly decrease after 2-3 years.
Magnetic susceptibility increases rapidly as it changes from enhanced to non-enhanced. High susceptibility values during first 2-4 years. Then gradually decreases.

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11
Q

What is typical to see on imaging on the spiral cord for MS? What is atypical?

A

unifocal/multifocal

tumefactive disease

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12
Q

What is the pathology for NMO?

A

Inflammation
Astrocytopathy - affects astrocides
Myelin relatively preserved - damaged in secondary phase

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13
Q

What are diagnosis for older and younger people for NMO?

A

Optic neuritis - initial event in young
Acute myelities - intial event in the older
measure body against AQP4 AB.

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14
Q

What is AQP4 AB? How many people is it negative in? Why is it important?

A

Negative in 20-30%. most abundant CNS channel. concentrated in astrocytic foot processes. Important to channel water as regulates water going in and out.

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15
Q

What people is AQP4 channelopathy seen in? what happens with it?

A 
Female > 80%
non-Caucasian predominace
relapsing if untreated
Severe disability and high mortality
Associated with other auto-immunity
onset with both ON and TM uncommon
10% monophasic
90% relapsing
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16
Q

What people are Myelin Oligodendrocyte Glycoprotein (MOG)-AB disease seen in and what can happen?

A 
female-male equal
no non-caucasian predominance
50% monophasic
onset with both ON and TM common
overlap with ADEM (monophasic and relapsing)
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17
Q

Where/what are subcortical lesions seen on NMO?

A 
see on more than 3 segments
central GM
swelling
partial enhancement
atrophy and cavity information (volume loss in cavity)
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18
Q

Where are specific brain lesions in NMO?

A

Medullary periaqueductal grey

Bilat hypothalamus

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19
Q

What does brain lesions looks like in NMO and where seen?

A

60% present
located in periventricular (aqp4 positive?)
extensive
multiple, patchy, enhancing (cloud like - dots of different sizes) in 90& of pat with CE
in more diffused way in corpus callosum - splenium, oedematous, heterogenous

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20
Q

How much % is cloud like enhancement in NMO and MS?

A

NMO - 90%

MS - 8%

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21
Q

How much % is cortical lesions in NMO/MS?

A

NMO - 0

MS - 67%

22
Q

What is the diagnostic criteria (2015) for NMO (including for NMOSD with/without AQP4)?

A

with - positive test and 1 clinical characteristic
without - 2 core clinical characteristics, dissemination in space, negative test
clinical characteristics - optic neuritis, acute myelitis, acute brainstem syndrome etc.

23
Q

What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute optic neuritis?

A

brain is normal.unspecific

optic nerve > 1/2 length or optic chiasm

24
Q

What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute myelitis?

A

intramedullary lesions

> 3 contiguous segments SC atrophy

25
Q

What are MR requirments for NMO when AQP4-IgG is negative/unknown - area postrema syndrome?

A

dorsal medullar/ area postrema lesions

26
Q

What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute brainstem syndrome?

A

periependymal brainstem lesions

27
Q

What is similar in AQP4-ab and MOG-ab

A 
conus involvement(isolalated sphincter and erectile dysfunction)
fluffy lesions (adults or ADEM attacks childhood)
bilateral cerebellar peduncle
28
Q

What is differential diagnosis for MS?

A

> 1 ovoid lesions PV adjacent to body of lateral ventricle and in inferior temporal lobe
S-shaped u-fibre lesions
T1 hypointense lesions
Dawson’s finger-type lesion

29
Q

What is DD for MOG?

A

Fluffy lesions

3< lesions (MOG AB)

30
Q

What’s more common than MS?

A

Incidental focal WML - not related to any disease 5-10% in 20-40 years

31
Q

What is seen on MR for SVD?

A 
wm hyperintensities
recent subcortical infarcts
lacunes
microhaemorrhages
enlargement of perivascular spaces
atrophy - volume loss
32
Q

What is seen in MR or white matter hyperintensities of presumed vascular orign - SVD

A

signal abnormality of variable size in WM
T2/FLAIR hyperintensity, without cavitation
lesions in subcortical GM or brainstem not included

33
Q

what is affected in SVD?

A

small arteries and arterioles
capillaries
small veins
often silent, develops over years before manifesting clincally

34
Q

what is the appearance for WM hyperintensities on PV and SC?

A

heterogeneous
PV - caps, pencil-thin lining, halo
SC - punctuate, early/confluent

35
Q

If U-fibres are spared in MS, what might the disease be?

A

between cortex and white matter there is a black band
always white matter in between
so suspicious of ms
typical to involve u fibres

if spares u fibres might be small vessel disease

36
Q

if there are pontine lesions, is it MS

A

in medial lemiscus
symmetrical
not MS

37
Q

if temporal lobe is spared, is it MS

A

no

maybe cadasil if not around anterior temporal lobe

38
Q

does CADASIL(Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, usually called CADASIL, is an inherited condition that causes stroke and other impairments. This condition affects blood flow in small blood vessels, particularly cerebral vessels within the brain) involve ant temporal pole

A

no

could be SVD

39
Q

explain the evolution of wmh and lacunes

A

WMH appear in vascular end zones
progress proximally along perforating arteries
lacunes appear at WMH edge
WMH expand around lacune

40
Q

where can you see CADASIL

A

subcortical lacunar lesions

41
Q

what do you see on perivascular spaces, imaging shape, size

A

fluid-filled spaces, follow typical course of a vessel, in GM/WM,
linear when imaged parallel
round or avoid, when imaged perpendicular to the course of the vessel
< 3 mm

42
Q

what are size of microbleeds seen on what imaging

A

small areas of signal void
2-5 mm in diameter but up to 10mm
associated blooming on T2*

43
Q

causes of microbleeds?

A

SVD (leakage)
cerebral amyloid angiopathy (CAA)
AB amyloid deposition in vessel wall
cortical and leptomeningeal arteries, arterioles

44
Q

What is distribution of SVD and CAA

A

svd - lobar and deep

caa - lobar

45
Q

what else is seen on spinal MR with DD of intramedullary lesions on MS/SVD/CADASIL?

A

MS - diffuse changes

svd/cadasil - no lesions

46
Q

are microbleeds on t2* in ms/svd/cadasil

A

absent in MS

Present in svd/cadasil

47
Q

what % is central vein sign in ms and migraine

A

ms - 84%

migraine - 22%

48
Q

What is DD of MS

A

subcortical, periventriular, PF, curvilinear, central vein sign, ISS, spinal cord

49
Q

what is DD of NMOSD

A

optic nerve, spinal cord, fluffy, cloud, conus (anti mog), no CVS, no ISS

50
Q

what is DD of SVD

A 
no subcortical
no spinal cord
pons
PVS
lacunes
MCB
no CVS
no ISS

C2 (24 decks)

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