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C2 Modules CLINICAL > Differentiating diagnosis of WMLs > Flashcards

Differentiating diagnosis of WMLs Flashcards

1
Q

MS Differential Diagnosis

A

No single clinical feature or test is sufficient

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2
Q

What are the diagnostic criteria for MS?

A
  1. Dissemination in space
  2. Dissemination in time
  3. Reasonable exclusion of alternative
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3
Q

What is dissemination in space?

A

Two or more parts of CNS= in brain not always the same area

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4
Q

What is dissemination in time?

A

Damage that occurs on different dates

Symptoms should not happen at the same time

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5
Q

Why is misdiagnosis of MS an issue?

A
  1. Often common conditions with non-specific symptoms, signs, MRI findings
  2. NMOSD
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6
Q

What does NMOSD stand for?

A

Neuromyelitis optica spectrum disorder

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7
Q

What is NMOSD?

A

Inflammatory disorder of CNS characterised by severe, immune-mediated demyelination and axonal damage targeting optic nerves and spinal cord

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8
Q

What are the clinical diagnosis of MS?

A
  1. Age
  2. Signs
  3. Symptoms
  4. CSF
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9
Q

What are the MR diagnosis of MS?

A
  1. Pattern
  2. Shape
  3. Enhancement
  4. SWI
  5. Other
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10
Q

What are examples of pattern?

A
  1. PV
  2. Cortical
  3. Sub-cortical
  4. ON
  5. CC
  6. Spinal cord
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11
Q

What are the shape of MS?

A
  1. Oval

2. Dawson’s finger

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12
Q

MR MS pattern: location

A

Immediately adjacent to PV, within cortex (cortical), below subcortical, Optic nerve, CC, Spinal cord

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13
Q

MR MS pattern: shape

A
  1. Oval

2. Dawson’s finger

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14
Q

MR MS pattern: Enhancement

A

4-6 weeks, sometimes 3 months, usually 4 weeks

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15
Q

MR MS pattern: SWI

A

CVS

Iron deposition

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16
Q

Where do lesions develop?

A

Around the vein with the vein at the centre

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17
Q

What are immediately adjacent to cortex?

A

U fibres

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18
Q

What are the function of U fibres?

A

Connect one gyrus to another

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19
Q

When do enhancing and non-enhancing lesions happen?

A

Enhancing: 3-4 weeks

Non-enhancing: much older

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20
Q

In posterior fossa, where are lesions?

A

Along intermedullary course

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21
Q

What are silent lesions?

A

Patients can have lesions not manifesting themselves clinically

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22
Q

Where are focal demyelinated plaques found?

A

White matter

23
Q

Where are demyelinated lesions found?

A

Deep grey matter

24
Q

What would typically fit with an MS lesion?

A

If a lesion is observed that has a venule in its centre

25
Q

What does intralesional susceptibility signal represmet?

A

Iron-rich macrophages/microglia

Myelin loss also contributes

26
Q

What are spinal cord divided into?

A
  1. Typical

2. Atypical

27
Q

What are examples of typical for SC?

A
  1. Unifocal

2. Multifocal

28
Q

What are examples of Atypical SC?

A
  1. Tumefactive

2. Diffuse

29
Q

What are the pathology for NMO?

A
  1. Inflammation
  2. Astrocytopathy
  3. Myelin relatively preserved
30
Q

What are the diagnosis of NMO?

A

Optic neuritis initial event in the young
• Acute myelitis initial event in the older
• AQP4 AB but negative 20-30%

31
Q

What is Aquaporin 4?

A

most abundant CNS water channel
• concentrated in astrocytic foot
processes

32
Q

What is astrocytopathy?

A

Conversion of antibodies to AQP4

33
Q

AQP4 Channelopathy

A 
Female > 80%
• Non-Caucasian predominance
• Relapsing if untreated
• Severe disability and high mortality
• Associated with other auto-immunity
• Onset with both ON + TM uncommon
34
Q

Myelin Oligodendrocyte

Glycoprotein (MOG)-AB Disease

A 
Female : Male equal
• No non-caucasian predominance
• ~ 50% monophasic
• Better outcome than AQP4-Ab
disease
• Not associated with other autoimmunity
• Onset with both ON + TM
common
• Overlap with ADEM (monophasic
& relapsing)
35
Q

What is SC lesion of NMO?

A 
Extent > 3 segments
• Central grey matter
• Swelling
• Partial enhancement
• Atrophy & cavity formation
36
Q

What involved in neuromyelitis optica?

A

Preferential spinal central gray matter

37
Q

Specific brain lesions in NMO

A

Medullary periaqueductal grey

• Bilat hypothalamus

38
Q

Cloud-like enhancement

A

NMO - 90%

MS - 8%

39
Q

Cortical lesions

A

NMO- 0%

MS - 67%

40
Q

What is considered MS lesion?

A

If more than half of the lesions have a central vein

41
Q

Acute myelitis

A

Intramedullary lesions
≥ 3 contiguos segments (LETM)
≥ 3 contiguous segments SC atrophy (history of myelitis)

42
Q

Area postrema syndrome

A

Dorsal medulla/area postrema

lesions

43
Q

Acute brainstem syndrom

A

Periependymal brainstem lesions

44
Q

MOG-ab Similar to AQP4-ab

A

Conus involvement (isolated sphincter and erectile
dysfunction)
• Fluffy lesions (adults, or ADEM attacks childhood)
• Bilateral cerebellar peduncle

45
Q

Best classifiers between MOG and MS

A 
MS Ovoid lesions PV (body of lateral ventr)
Dawson’s fingers
T1 hypointense lesions
•MOG Fluffy lesions
3≤ lesions (MOG AB)
46
Q

What pathology is not directly visualised?

A

Small vessel disease

47
Q

MR of SVD

A 
White matter hyperintensities
•Recent subcortical infarcts Lacunes
•Microhaemorrhages
•Perivascular spaces
•Atrophy
48
Q

Where do WMH appear?

A

Vascular end zones

progress proximally along perforating arteries

49
Q

Where do lacunes appear?

A

WMH edge

50
Q

Where do WMH expand?

A

around lacune

51
Q

Perivascular spaces

A

● Fluid-filled spaces, follow typical course of a
vessel, in GM/WM; SI similar to CSF
As they follow the course of perforators, they are
-linear when imaged parallel
round or ovoid, when imaged perpendicular
to the course of the vessel
- <3mm

52
Q

Microbleeds

A

Small areas of signal void
● 2–5 mm in diameter, but up to 10 mm
● Associated blooming on T2*-w
Perivascular collections of hemosiderinladen macrophages

53
Q

What are causes of micrbobleeds?

A 
SVD (leakage)
● Cerebral amyloid angiopathy (CAA)
Aβ amyloid deposition in vessel wall
Cortical &amp; leptomeningeal arteries,
arterioles (veins)
54
Q

T2*-Microbleeds

A 
Occur in the asymptomatic elderly (6.4%)
Associated with hypertension, age, lacunes,
confluent WMC
• MS Absent
• SVD Present
• CADASIL Present

C2 Modules CLINICAL (26 decks)

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