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
What does intralesional susceptibility signal represmet?
Iron-rich macrophages/microglia | Myelin loss also contributes
26
What are spinal cord divided into?
1. Typical | 2. Atypical
27
What are examples of typical for SC?
1. Unifocal | 2. Multifocal
28
What are examples of Atypical SC?
1. Tumefactive | 2. Diffuse
29
What are the pathology for NMO?
1. Inflammation 2. Astrocytopathy 3. Myelin relatively preserved
30
What are the diagnosis of NMO?
Optic neuritis initial event in the young • Acute myelitis initial event in the older • AQP4 AB but negative 20-30%
31
What is Aquaporin 4?
most abundant CNS water channel • concentrated in astrocytic foot processes
32
What is astrocytopathy?
Conversion of antibodies to AQP4
33
AQP4 Channelopathy
``` 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
Myelin Oligodendrocyte | Glycoprotein (MOG)-AB Disease
``` 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
What is SC lesion of NMO?
``` Extent > 3 segments • Central grey matter • Swelling • Partial enhancement • Atrophy & cavity formation ```
36
What involved in neuromyelitis optica?
Preferential spinal central gray matter
37
Specific brain lesions in NMO
Medullary periaqueductal grey | • Bilat hypothalamus
38
Cloud-like enhancement
NMO - 90% | MS - 8%
39
Cortical lesions
NMO- 0% | MS - 67%
40
What is considered MS lesion?
If more than half of the lesions have a central vein
41
Acute myelitis
Intramedullary lesions ≥ 3 contiguos segments (LETM) ≥ 3 contiguous segments SC atrophy (history of myelitis)
42
Area postrema syndrome
Dorsal medulla/area postrema | lesions
43
Acute brainstem syndrom
Periependymal brainstem lesions
44
MOG-ab Similar to AQP4-ab
Conus involvement (isolated sphincter and erectile dysfunction) • Fluffy lesions (adults, or ADEM attacks childhood) • Bilateral cerebellar peduncle
45
Best classifiers between MOG and MS
``` MS Ovoid lesions PV (body of lateral ventr) Dawson’s fingers T1 hypointense lesions •MOG Fluffy lesions 3≤ lesions (MOG AB) ```
46
What pathology is not directly visualised?
Small vessel disease
47
MR of SVD
``` White matter hyperintensities •Recent subcortical infarcts Lacunes •Microhaemorrhages •Perivascular spaces •Atrophy ```
48
Where do WMH appear?
Vascular end zones | progress proximally along perforating arteries
49
Where do lacunes appear?
WMH edge
50
Where do WMH expand?
around lacune
51
Perivascular spaces
● 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
Microbleeds
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
What are causes of micrbobleeds?
``` SVD (leakage) ● Cerebral amyloid angiopathy (CAA) Aβ amyloid deposition in vessel wall Cortical & leptomeningeal arteries, arterioles (veins) ```
54
T2*-Microbleeds
``` Occur in the asymptomatic elderly (6.4%) Associated with hypertension, age, lacunes, confluent WMC • MS Absent • SVD Present • CADASIL Present ```