Module 6: Central Nervous, head and neck Flashcards
Incomplete ring enhancement think
demyelination
does stroke restrict
yes
do hypercellular tumours restrict
yes
Herpes encephalitis, does it restrict
yes
Don’t restrcit examples
met
atypical infeciton (toxo)
GBM vs lymphoma
lymphoma enhances homogenously
GBM - heterogenous, aggressive
dawson fingers
Calloso-septal interface
MS
Define for MS
seperation in space and time
MS relationship with which virus
EBV
MS is rarer closer to
the equator
MS trickery
calssic differentials
Vasculitius
Lyme
Vasculitis favours the
basal ganglia
spares the collosal septal interface
Lymes involves more of the
cranial nerves
ADEM stands for
acute disseminated encephalomyelitis
ADEM present in
childhood after vaccination
ADEM appears as
large T2 bright
enhance in ring nodular pattern
though incomplete as demyelination
not invovle the collosal
demyelinating disorder of the spine and optic
NMO (Devic)
neuomyelitis optica
CSF is dark can be
Flair
or
T1
causes of T1 bright basal ganglia
liver failure
hyperlaminetation
high blood sugar
wilsons
does stroke restrict
yes
PRES is what
vascular autoregulation BBB disruption
PRES affects where
bilateral
posterior circulation
watershed areas
PRES history
who gets it
HTN
Pregnancy
chemo
Central Pontine Myeloonitis
rapidly corrected low sodium level
CPM involves which type of cells
oligodendroglial cells
distinguish OM from PRES
DWI
but location more of a giveaway
Wernickes encephalopathy is caused by
thiamine deficiency
Wernickes get enhancement of the
mammillary bodies
T2/Flair signal in bilateral medial thalamus
periaqueductal gray
wernickes ddx
think thalamic insult
artery of percheron infarction
internal cerebral vein thrombosis
high signal crossing the corpus collosum
Marchiafava-Bignami
Marchiafava-Bignami
seen in
drunks
carbon monoxide poisoning
CT hypdensity
T2 bright globus pallidus
why would things in the brain NOT enhance
the BBB
- extra axial
- disrupted the BBB (aggressive infection or high grade tumour)
enahcnement of low vs high grade tumours
high grade DO enhance
- though JPA, grade 1 WHO, this does enhance
- also ganglioglioma
Do low grades enhance
NO
Do high grades enhance
YES
astrocytomas
- two types
diffuse
circumscribed
circumbscribes astrocytoma
JPA - cyst with nodule
Subependymal giant cell
- arise from lateral ventricle
- ax with TS
any intraventricular tumour will enhance or not enhance
will enhance
escapes the BBB
Gliomatosis cerebri
diffuse
involves at least 3 lobes
extensive T2 signal
no mass effect
low grade so doesn’t enhance
tumour that is crossing the midline
GBM
Lymphoma
Tumofactive MS plaque
Radiation
Tumours that restrict diffusion
lyphoma
GBM
medulloblastoma
lymphoma will enhance
uniformaly
choroid plexus xanthogranulomas
benign
7% of people have it
GBM vs Lymphoma
enhancement
GBM - heterogenous rim enhancement
vs
lympohma - homogeous
GBM vs Lymphoma
crossing miudline
both can
restrict
GBM vs Lymphoma
GBM can restrict but lymphoma is classic for restricting
intravascular angiocentric lymphoma
stroke presentation
mutlifocal infarcts
calcium in a brain tumour
most common
Oligodendroglioma
- always calcify
but in real life Astrocytoma so much more common that it could be this
which tumours calcify
Oligodendrogliomas
Ependyomomas
Astrocytoma
GBM
oligodendrogliomas trivia
Ca+2
cortically based
expands the cortex
frontal lobe
has calcium within it
Oligodendrogliomas, prognostic facotr
1P, 19Q deletion, how responsive to radiotherapy
Cortically based tumour
Dysembryolploastic neuroepithelial Tumour (*DNET)
Oligdendrogliomas
gangliogliomas
refactroy seizures
bubbly T2 lesion
DNET
Oligodendroglioma
calcified tumour expands the cortex of frontal lobe
gangliogliomas
cyst with a nodule
differentials for Cyst with a nodule
by location
INfratent
JPA
Haemangioblastomas
Supratent
Pleomorhpic Xanthoastrocytoma
Ganglioglioma
dural tail
PXA
- invades leptomeninges
CP angle tumour
does not go into auditory canal
Meningioma
-0 enhances homogenously
CP angle tumour
goes into the auditory cancal
schwannoma
CP angle tumour
restrict
epidermoid
if CP angle tumour schwanna and bilateral think of
NF-2
low enhancing pituitary lesion
microadenoma
if T2 bright go with RCC
large pituitary
macroadinoma - more than 10mm
Apoplexy will be
T1 bright
sheehans syndrome is
post partum haemorrhage
cant lactate
next step pituitary quesiton
often CT
- for a craniopharyngioma
types of craniopharyngioma
childhood
- calcifies
adult
- pappillary subtype
hypothalamic hamartoma
hamartoma of the tuber cinereum (part of the hypothalamus)
gelastic seizures
precoscious puberty
toothpaste tumour
ependymoma
hard ball tumour
medulloblastoma
age for medulloblastoma
under 10
medulloblastoma are highly cellular and therefore
restrict diffusion
Ependymoma age group
bimodal <5 and > 30
subependymoma
how does it enhance
size
it doesn’t
<2cm
subependymoma age
adult
most paeds tumours
are infratentorial
most paeds are infratentorium except for
Choroid plexus papilloma
lateral trigone
why hydrocephalus in choroid plexus papilloma
secrete CSF
Features in NF1
sphenoid dysplasia
renal vascular stenosis
lateral meningocele
antermedial tibial bowing
NF1 CNS tumour
optic pathway
pilocytic astrocytomas
NF2 cranial features
meningiomas
ependymomas
schwannomas
T2 bright
nodules along ventricles
Subependymal giant cell tumour
renal AML
lung thin walled cysts
Tuberous sclerosis
- subependymal nodules
Cortical tubers
- t2 bright bands
endolymph sac tumour found in
temporal bone
features fo VHL in pancreas
serous cystadenoma
regular cysts
islet cell tumours
features of VHL in CNS
haemangioblastomas in brain and spine
endolymphatic sac tumour
vHL in abdo
phaeo
RCC
renal cysts
corduroy sign, next step
get a mammogram
then thyroid exam
Cowden syndrome
Hamartomas
Breast Ca
Thyroid Ca
Lhermitte-Dulcos
wears corduroy.
enlarged cerebellar hemisphere
SAH along the vertex
truama or vasculopathy
SAH
Basilar
think aneurysm
interpeduncular cistern haemorrhage can be from which aneurysm location
basilar tip
PICA bleeds will go
posterior fossa or intraventricular
MCA aneurysm bleeds go where
sylvian fissure
early s.e of SAH
hydrocephalus due to blood blocking the csf
mid timeframe of SAH
absent vessels
diffuse vasospasms
Vasospasm
- Fischer score
grades risk of vasospasm
1mm of SAH thickness risk of
vasospasm
fleishcherscore of II
why vasospasm with blood
Oxyhemoglobin fownregulates the NO
othe irritants to cuase vasospasm
meningitis - pus
PRES
Reversible cerebral vasospasm syndrome (pregnant thunderclap headache)
Migraine
when does vasospasm happen after SAH
4- 14 days
Late complications of SAH
superficial siderosis
Superfical siderosis appears as
curvilinear low signal on gradient coating the surface of the brain
sensorineurla hearing loss and ataxia and SAH
haemosiderin deposits causes it as a longer term complication of SAH
How does pseudo SAH manifest
brain is dark due to oedema
dura look bright in comparison, mistaken for SAH
look at the sulci, no sulcal density
SAH HU is
60
common locations of hypertensive haemorrhage
basal ganglia (putamen)
pons
cerebellum
T1, white matter is
white
scattered microbleeds on gradient
subcorticol location
lobar bleed with normal BP
dialysis patient
amyloid
how does cytotxic oedema end up hitting the brain
death of sodium potasssium transporter
end up leaking with oedema resultant
normally seen about 3 hours after a stroke
area of restricted diffusion
- its a stroke
but FLAIR is normal.
what could that mean
hyperacute - within first 6 hours
MCA infarcts will normally involve which structure
basal ganglia
(herpes woudn’t)
hypothalamic bilateral infarct
artery of Percharon
wernicker
internal cerebral vein thrombosis
recurrent artery of heubner
branch of proximal ACA
infarct to caudate head
haemorrhagic conversion after strokes
who is at risk
TPA
Anti caog
large territories (1/3MCA distribution)
venous infarcts more likely to bleed
t1 bright
sub acute blood
fat
melanin
proteinacious material
halonised calcium
kids T1 won’t look like an adults until age
1
kids wont’ have the same T2 brain as an adult until
2
types of watershed areas
external and internal
external watershed from
embolic
better prognosis.
internal watershed from
hypoxia
arterial occlusion
deep perforators have few collatorals
i say sickle cell
you say
Moya moya
what is moya moya
proximal ICA / supraclinoid stenosis, chronic so multiple collaterols.
high grade narrowing/occlusion
kid - stroke
adult - bleed
haemosiderin MRI sequence to look for what option
Amyloid
Cavernoma
Blood
Venous malformation in the pons
Capillary telangiectasia
40 year old with migraine
temporal lobe
white matter scarring
normal MRA
not involving the occipital
Cadasil
Cerebral AD arteriopathy subcorticol infarcts and leukencephalopathy
central sulcus seperates which lobes
frontal from parietal
how to find central sulcus
pars bracket sign is immediately behind the central sulcus
inverted omega on the central sulcus represents the
motor hand
Homonculous, the legs are supplied by the
ACA
why does hippocampus look brighter on FLAIR compared to normal cortex
cortex is 6 layers
hippo is 3
what are virchow robins spaces
fluid filled spaces next to perforating vessles.
CSF gets reabsorbed at the
arachnoid granulations
cavum velum interpositum
extension of quadrigeminal plate cistern to foramen of munro
supracellar cisterns look like a
pentagon
sylvian vs ambient cisterns
what are their location
sylvian point anteriorly
ambient point posteriory
MRi appearance of babies
T1 looks like an adult T2
T2 looks like an adult T1
immature myelin has what component compared to mature myelin
more water
therefore is brighter on T2 and darker on T1
last part of the brain to myelinate?
subcortical
which bits of brain are myelinated at birth?
braisntem and posterior limb of the internal capsule
corpus collosum forms in what direction
front to back
cortpus collosum hypoplasia will be absence of which bit ?
splenium
what goes through foramen ovale
V3 Accessory meingeal artery
what goes through Foramen rotundum
V2
what goes through superior orbital fissure
CN3 Cn4 CN V1 CNVI