Differentiating diagnosis of WMLs Flashcards
MS Differential Diagnosis
No single clinical feature or test is sufficient
What are the diagnostic criteria for MS?
- Dissemination in space
- Dissemination in time
- Reasonable exclusion of alternative
What is dissemination in space?
Two or more parts of CNS= in brain not always the same area
What is dissemination in time?
Damage that occurs on different dates
Symptoms should not happen at the same time
Why is misdiagnosis of MS an issue?
- Often common conditions with non-specific symptoms, signs, MRI findings
- NMOSD
What does NMOSD stand for?
Neuromyelitis optica spectrum disorder
What is NMOSD?
Inflammatory disorder of CNS characterised by severe, immune-mediated demyelination and axonal damage targeting optic nerves and spinal cord
What are the clinical diagnosis of MS?
- Age
- Signs
- Symptoms
- CSF
What are the MR diagnosis of MS?
- Pattern
- Shape
- Enhancement
- SWI
- Other
What are examples of pattern?
- PV
- Cortical
- Sub-cortical
- ON
- CC
- Spinal cord
What are the shape of MS?
- Oval
2. Dawson’s finger
MR MS pattern: location
Immediately adjacent to PV, within cortex (cortical), below subcortical, Optic nerve, CC, Spinal cord
MR MS pattern: shape
- Oval
2. Dawson’s finger
MR MS pattern: Enhancement
4-6 weeks, sometimes 3 months, usually 4 weeks
MR MS pattern: SWI
CVS
Iron deposition
Where do lesions develop?
Around the vein with the vein at the centre
What are immediately adjacent to cortex?
U fibres
What are the function of U fibres?
Connect one gyrus to another
When do enhancing and non-enhancing lesions happen?
Enhancing: 3-4 weeks
Non-enhancing: much older
In posterior fossa, where are lesions?
Along intermedullary course
What are silent lesions?
Patients can have lesions not manifesting themselves clinically
Where are focal demyelinated plaques found?
White matter
Where are demyelinated lesions found?
Deep grey matter
What would typically fit with an MS lesion?
If a lesion is observed that has a venule in its centre
What does intralesional susceptibility signal represmet?
Iron-rich macrophages/microglia
Myelin loss also contributes
What are spinal cord divided into?
- Typical
2. Atypical
What are examples of typical for SC?
- Unifocal
2. Multifocal
What are examples of Atypical SC?
- Tumefactive
2. Diffuse
What are the pathology for NMO?
- Inflammation
- Astrocytopathy
- Myelin relatively preserved
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%
What is Aquaporin 4?
most abundant CNS water channel
• concentrated in astrocytic foot
processes
What is astrocytopathy?
Conversion of antibodies to AQP4
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
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)
What is SC lesion of NMO?
Extent > 3 segments • Central grey matter • Swelling • Partial enhancement • Atrophy & cavity formation
What involved in neuromyelitis optica?
Preferential spinal central gray matter
Specific brain lesions in NMO
Medullary periaqueductal grey
• Bilat hypothalamus
Cloud-like enhancement
NMO - 90%
MS - 8%
Cortical lesions
NMO- 0%
MS - 67%
What is considered MS lesion?
If more than half of the lesions have a central vein
Acute myelitis
Intramedullary lesions
≥ 3 contiguos segments (LETM)
≥ 3 contiguous segments SC atrophy (history of myelitis)
Area postrema syndrome
Dorsal medulla/area postrema
lesions
Acute brainstem syndrom
Periependymal brainstem lesions
MOG-ab Similar to AQP4-ab
Conus involvement (isolated sphincter and erectile
dysfunction)
• Fluffy lesions (adults, or ADEM attacks childhood)
• Bilateral cerebellar peduncle
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)
What pathology is not directly visualised?
Small vessel disease
MR of SVD
White matter hyperintensities •Recent subcortical infarcts Lacunes •Microhaemorrhages •Perivascular spaces •Atrophy
Where do WMH appear?
Vascular end zones
progress proximally along perforating arteries
Where do lacunes appear?
WMH edge
Where do WMH expand?
around lacune
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
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
What are causes of micrbobleeds?
SVD (leakage) ● Cerebral amyloid angiopathy (CAA) Aβ amyloid deposition in vessel wall Cortical & leptomeningeal arteries, arterioles (veins)
T2*-Microbleeds
Occur in the asymptomatic elderly (6.4%) Associated with hypertension, age, lacunes, confluent WMC • MS Absent • SVD Present • CADASIL Present