MS, SVD - Differential diagnosis Flashcards
What is the diagnostic criteria for MS?
Dissemination in time and space. Reasonable exclusion of alternatives.
What disease is a an example of misdiagnosis in MS?
NMOSD.
What are some things you should look at before making a clinical diagnosis?
age, signs, symptoms, CSF
What will you see on MR for MS?
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
What is the location of MS on MR?
adjacent periventricular, cortical, sub-c, ON, CC, spinal cord
What can you see on SWI for MS?
can see vessel or vein. CVS (central vein sign - lesion has venual in centre), iron deposition
What locations can we have on posterior fossa for MS?
facial colliculus - nerve 5 and 6 middle cereberlar peduncle white matter 5th nerve trigemnial intramedullary
Where are cortical lesions as seen from pathology in RRMS, SPMS, PPMS
focal demyelinated plaques in the WM
cortical demyelination
demyelinated lesions in the deep GM
How much enhancing does SWI, intralesional susceptibility signal (ISS) show at 3T for MS? What does it represent?
non-enhancing - 48%
enhancing - 58%
represents iron-rich macrophages/microglia. myelin loss also contributes
What does SWI show in focal lesions over time?
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.
What is typical to see on imaging on the spiral cord for MS? What is atypical?
unifocal/multifocal
tumefactive disease
What is the pathology for NMO?
Inflammation
Astrocytopathy - affects astrocides
Myelin relatively preserved - damaged in secondary phase
What are diagnosis for older and younger people for NMO?
Optic neuritis - initial event in young
Acute myelities - intial event in the older
measure body against AQP4 AB.
What is AQP4 AB? How many people is it negative in? Why is it important?
Negative in 20-30%. most abundant CNS channel. concentrated in astrocytic foot processes. Important to channel water as regulates water going in and out.
What people is AQP4 channelopathy seen in? what happens with it?
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
What people are Myelin Oligodendrocyte Glycoprotein (MOG)-AB disease seen in and what can happen?
female-male equal no non-caucasian predominance 50% monophasic onset with both ON and TM common overlap with ADEM (monophasic and relapsing)
Where/what are subcortical lesions seen on NMO?
see on more than 3 segments central GM swelling partial enhancement atrophy and cavity information (volume loss in cavity)
Where are specific brain lesions in NMO?
Medullary periaqueductal grey
Bilat hypothalamus
What does brain lesions looks like in NMO and where seen?
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
How much % is cloud like enhancement in NMO and MS?
NMO - 90%
MS - 8%
How much % is cortical lesions in NMO/MS?
NMO - 0
MS - 67%
What is the diagnostic criteria (2015) for NMO (including for NMOSD with/without AQP4)?
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.
What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute optic neuritis?
brain is normal.unspecific
optic nerve > 1/2 length or optic chiasm
What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute myelitis?
intramedullary lesions
> 3 contiguous segments SC atrophy
What are MR requirments for NMO when AQP4-IgG is negative/unknown - area postrema syndrome?
dorsal medullar/ area postrema lesions
What are MR requirments for NMO when AQP4-IgG is negative/unknown - acute brainstem syndrome?
periependymal brainstem lesions
What is similar in AQP4-ab and MOG-ab
conus involvement(isolalated sphincter and erectile dysfunction) fluffy lesions (adults or ADEM attacks childhood) bilateral cerebellar peduncle
What is differential diagnosis for MS?
> 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
What is DD for MOG?
Fluffy lesions
3< lesions (MOG AB)
What’s more common than MS?
Incidental focal WML - not related to any disease 5-10% in 20-40 years
What is seen on MR for SVD?
wm hyperintensities recent subcortical infarcts lacunes microhaemorrhages enlargement of perivascular spaces atrophy - volume loss
What is seen in MR or white matter hyperintensities of presumed vascular orign - SVD
signal abnormality of variable size in WM
T2/FLAIR hyperintensity, without cavitation
lesions in subcortical GM or brainstem not included
what is affected in SVD?
small arteries and arterioles
capillaries
small veins
often silent, develops over years before manifesting clincally
what is the appearance for WM hyperintensities on PV and SC?
heterogeneous
PV - caps, pencil-thin lining, halo
SC - punctuate, early/confluent
If U-fibres are spared in MS, what might the disease be?
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
if there are pontine lesions, is it MS
in medial lemiscus
symmetrical
not MS
if temporal lobe is spared, is it MS
no
maybe cadasil if not around anterior temporal lobe
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
no
could be SVD
explain the evolution of wmh and lacunes
WMH appear in vascular end zones
progress proximally along perforating arteries
lacunes appear at WMH edge
WMH expand around lacune
where can you see CADASIL
subcortical lacunar lesions
what do you see on perivascular spaces, imaging shape, size
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
what are size of microbleeds seen on what imaging
small areas of signal void
2-5 mm in diameter but up to 10mm
associated blooming on T2*
causes of microbleeds?
SVD (leakage)
cerebral amyloid angiopathy (CAA)
AB amyloid deposition in vessel wall
cortical and leptomeningeal arteries, arterioles
What is distribution of SVD and CAA
svd - lobar and deep
caa - lobar
what else is seen on spinal MR with DD of intramedullary lesions on MS/SVD/CADASIL?
MS - diffuse changes
svd/cadasil - no lesions
are microbleeds on t2* in ms/svd/cadasil
absent in MS
Present in svd/cadasil
what % is central vein sign in ms and migraine
ms - 84%
migraine - 22%
What is DD of MS
subcortical, periventriular, PF, curvilinear, central vein sign, ISS, spinal cord
what is DD of NMOSD
optic nerve, spinal cord, fluffy, cloud, conus (anti mog), no CVS, no ISS
what is DD of SVD
no subcortical no spinal cord pons PVS lacunes MCB no CVS no ISS
